Field Crop Diseases

Page iii
Field Crop Diseases
Third Edition
Robert F. Nyvall
Iowa State University Press / Ames

Page iv
Robert F. Nyvall, Professor of Plant Pathology, University of Minnesota, specializes in diseases of cultivated wild rice and in the development of mycoherbicides to
control weeds. After receiving his Ph.D. in plant pathology from the University of Minnesota, he did research on vegetable diseases at Washington State University.
While an Extension Plant Pathologist for 15 years at Iowa State University, he specialized in diseases of maize and soybean. Dr. Nyvall also served as Superintendent
of the North Central Experiment Station of the University of Minnesota.
© 1999 Iowa State University Press
All rights reserved
Iowa State University Press
2121 South State Avenue, Ames, Iowa 50014
Orders: 18008626657
Office: 15152920140
Fax: 15152923348
Web site: www.isupress.edu
Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by Iowa State University Press, provided
that the base fee of $.10 per copy is paid directly to the Copyright Clearance Center, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have
been granted a photocopy license by CCC, a separate system of payments has been arranged. The fee code for users of the Transactional Reporting Service is 0
81382070/99 $.10.
Printed on acidfree paper in the United States of America
First edition © 1979 AVI. Field Crop Diseases Handbook
Second edition © 1989 Van Nostrand Reinhold, New York. Field Crop Diseases Handbook
Third edition, 1999. Field Crop Diseases
Library of Congress CataloginginPublication Data
Nyvall, Robert F.
Field crop diseases / Robert F. Nyvall.—3rd ed.
p. cm.
Rev. ed. of: Field crop diseases handbook. 2nd ed. c1989.
Includes bibliographical references (p. ) and index.
ISBN 0813820790
1. Field crops—Diseases and pests—Handbooks, manuals, etc. 2. Plant
diseases—Handbooks, manuals, etc. 3. Phytopathogenic microorganisms—
Control—Handbooks, manuals, etc. I. Nyvall, Robert F. Field crop diseases
handbook. IL Title.
SB731.N94 1999
632—dc21 9918995
The last digit is the print number: 9 8 7 6 5 4 3 2 1

Page v
To
my grandchildren, Emily and Grant
my children, Martha and Chris, Tracey and Nathan
my wife, Sandra
my mother, Gertrude
and especially to the memory of my father, Robert

Page vii
Contents
Preface xxxi
1. Diseases of Alfalfa (Medicago sativa) 3

Diseases Caused by Bacteria
Alfalfa Sprout Rot 3
Bacterial Leaf Spot 3
Bacterial Stem Blight 4
Bacterial Wilt 4
Crown Gall 5
Dwarf 6
Root and Crown Rot Complex 6

Diseases Caused by Fungi
Acrocalymma Root and Crown Rot 7
Anthracnose 8
Aphanomyces Root Rot 8
Black Patch 9
Black Root Rot 9
Brown Root Rot 9
Common Leaf Spot 10
Corky Root Rot 10
Crown Wart 10
Cylindrocarpon Root Rot 11
Cylindrocladium Root and Crown Rot 11
Damping Off 11
Downy Mildew 12
Forked Foot Disease 13
Fusarium Crown and Root Rot 13
Fusarium Wilt 14
Lepto Leaf Spot 15
Marasmius Root Rot 15
Mycoleptodiscus Crown and Root Rot 15
Myrothecium Root Rot 16
Oidiopsis Powdery Mildew 16
Oidium Powdery Mildew 16
Phoma Root Rot 17
Phymatotrichum Root Rot 17
Phytophthora Root Rot 18
Powdery Mildew 19
Rhizoctonia Foliage Blight 19
Rhizoctonia Root Rot 20
Rhizoctonia Stem Blight 20
Rhizopus Sprout Rot 21
Root and Crown Rot Complex 21
Rust 22
Sclerotinia Crown and Stem Rot 23
Southern Blight 24
Spring Black Stem 25
Stagonospora Leaf Spot 25
Stagonospora Root Rot 26
Stemphylium Leaf Spot 27
Summer Black Stem 28
Verticillium Wilt 29
Violet Root Rot 31

Page viii
Winter Crown Rot 31
Yellow Leaf Blotch 32

Diseases Caused by Nematodes
Alfalfa Stem 33
Cyst 33
Dagger 34
Pin 34
Reniform 34
Root Knot 34
Root Lesion 35
Spiral 35
Stubby Root 35
Stunt 36

Diseases Caused by Phytoplasmas
Aster Yellows 36
Witches' Broom 36
Unknown Phytoplasma Causing a Witches' Broom 36

Diseases Caused by Viruses
Alfalfa Enation 37
Alfalfa Latent 37
Alfalfa Mosaic 37
Bean Leaf Roll 38
Lucerne Transient Streak 38
Red Clover Vein Mosaic 39
Selected References 39
2. Diseases of Barley (Hordeurn vulgare) 45

Bacterial Blight 45
Bacterial Leaf Blight 46
Bacterial Stripe 46
Barley Basal Kernel Blight 47
Basal Glume Rot 47

Anthracnose 48
Arthrinium arundinis Kernel Blight 49
Ascochyta Leaf Spot 49
Barley Stripe 50
Blast 51
Cephalosporium Stripe 52
Ceratobasidium gramineum Snow Mold 52
Common Root Rot 53
Covered Smut 54
Crown Rust 55
Downy Mildew 55
Dwarf Bunt 56
Ergot 57
Eyespot 57
False Loose Smut 58
Fusarium Head Blight 60
Gibberella Seedling Blight 61
Gray Snow Mold 61
Halo Spot 62
Kernel Blight 62
Leaf Rust 62
Leaf Speckle 63
Leaf Spot 64
Leptosphaeria Leaf Spot 65
Loose Smut 65
Net Blotch 66
Pink Snow Mold 68
Powdery Mildew 69
Pythium Root Rot 69
Rhizoctonia Root Rot 70
Scald 71
Sclerotinia Snow Mold 72
Septoria Speckled Leaf Blotch 72
Sharp Eyespot 73
Southern Blight 74
Speckled Snow Mold 74
Spot Blotch and Associated Seedling and Crown Rots 75
Stagonospora Blotch 76
Stem Rust 77
Stripe Rust 79
TakeAll 79
Verticillium Disease 80
Wirrega Blotch 80
Yellow Leaf Spot 81

Cereal Cyst 82
Root Gall 82
Root Knot 83
Root Lesion 83
Stunt 84

Page ix

Disease Caused by Phytoplasmas
Aster Yellows 84

African Cereal Streak 85
American Wheat Striate Mosaic 85
Australian Wheat Striate 86
Barley Mosaic 86
Barley Stripe Mosaic 86
Barley Yellow Dwarf 87
Barley Yellow Mosaic 88
Barley Yellow Streak Mosaic 88
Barley Yellow Striate Mosaic 89
Barley Yellow Stripe 89
Brome Mosaic 89
Cereal Chlorotic Mottle 90
Cereal Tillering 90
Eastern Wheat Striate 90
Enanismo 90
Flame Chlorosis 91
High Plains Virus 91
Hordeum Mosaic 92
Maize Yellow Stripe 92
Northern Cereal Mosaic 92
Oat Blue Dwarf 93
Oat Pseudorosette 93
Oat Sterile Dwarf 93
Rice BlackStreaked Dwarf 94
Rice Stripe 94
Russian Winter Wheat Mosaic 94
Soilborne Wheat Mosaic 94
Wheat Dwarf 95
Wheat Streak 95
Wheat Yellow Leaf 96
3. Diseases of Buckwheat (Fagopyrum esculentum) 101

Ascochyta Leaf Blight 101
Blight 101
Botrytis Rot 101
Chlorotic Leaf Spot and Stipple Spot 102
Collar Rot 102
Downy Mildew 102
Fusarium Wilt 103
Leaf Spot 103
Powdery Mildew 104
Pythium palingenes Disease 104
Ring Spot 104

Broad Bean Wilt 104
Turnip Mosaic 105
4. Diseases of Canola (Rapeseed) and Mustard (Brassica campestris, B. juncea, 107
B. napus, B. nigra, and B. rapa)

Bacterial Black Rot 107
Bacterial Pod Rot 107
Bacterial Soft Rot 107
Bacterial Wilt and Rot 108
Crown Gall 108
Unnamed Seedling Root Rot 109
Xanthomonas Leaf Spot 109

Alternaria Black Spot 109
Alternaria Leaf Spot 110
Anthracnose 110
Blackleg 111
Black Mold Rot 113
Black Root 113
Brown Girdling Root Rot 113
Cercospora Leaf Spot 114
Charcoal Rot 114
Clubroot 115
Damping Off 115
Downy Mildew 116
Foot Rot 116
Fusarium Seed Infection 117
Fusarium Wilt 117
Gray Mold 118

Page x
Leaf Spot 118
Light Leaf Spot 118
Pod Drop 119
Powdery Mildew 119
Rhizoctonia Crown Rot 120
Ring Spot 120
Sclerotinia Stem Rot 121
Smut, Root Gall 122
Southern Blight 122
Storage Molds 123
White Blight 123
White Leaf Spot 123
White Rust 123
Winter Decline Syndrome 124
Wirestem 125
Yeast Infection of Seed 125

Disease Caused by Nematodes
Root Knot 125

Aster Yellows 126
Green Petal Disease 126

Cauliflower Mosaic 126
Crinkle 127
Mosaic 127
Phyllody 127
Rai Mosaic 127
Yellows 128

Diseases Caused by Unknown Factors
Brown Girdling Root Rot 128
Pollen Necrosis 128
Unknown 129
5. Diseases of Common Bean (Phaseolus vulgaris) 133

Bacterial Brown Spot 133
Bacterial Wilt 134
Bean Wildfire 134
Common Blight 135
Erwinia nulandii Leaf Spot 136
Fuscous Blight 136
Halo Blight 137
Pseudomonas blatchfordae Leaf Spot 139

Angular Black Spot 140
Angular Leaf Spot 140
Anthracnose 141
Aphanomyces Root and Hypocotyl Rot 143
Ascochyta Blight 143
Ashy Stem Blight 144
Aspergillus nidulans Disease 145
Bipolaris sorokiniana Leaf and Pod Lesions 145
Black Node Disease 145
Black Pod Disease 146
Black Root Rot 147
Cercospora Leaf Blotch 147
Chaetoseptoria Leaf Spot 148
Floury Leaf Spot 148
Fusarium Root Rot 148
Fusarium Yellows 150
Gray Leaf Spot 151
Gray Mold 151
Phyllosticta Leaf Spot 152
Pink Pod Rot 153
Pod Rot, Seed Rot, and Root Rot 153
Powdery Mildew 154
Pythium Root and Hypocotyl Rot 154
Pythium Wilt 155
Rhizoctonia Root Rot and Damping Off 155
Rust 156
Smut 157
Southern Blight 158
Speckle Disease 158
Stem Rot 159

Page xi
Web Blight 159
White Leaf Spot 160
White Mold 160

Awl 162
Bulb and Stem 162
Cyst 162
Dagger 162
Lance 163
Lesion 163
Nematode Angular Leaf Spot 163
Pin 163
Reniform 164
Ring 164
Root Knot 164
Spiral 165
Sting 165
Stubby Root 165
Stunt 165

Machismo 166
Witches' Broom 166

Bean Calico Mosaic 166
Bean Common Mosaic 167
Bean Curly Dwarf 167
Bean Dwarf Mosaic 168
Bean Golden Mosaic 168
Bean Mild Mosaic 169
Bean Pod Mottle 169
Bean Red Node 169
Bean Rugose Mosaic 170
Bean Southern Mosaic 170
Bean Yellow Mosaic 170
Bean Yellow Stipple 171
Clover Yellow Vein 171
Cowpea Mild Mottle 172
Cowpea Severe Mosaic 172
Cucumber Mosaic 172
Curly Dwarf Mosaic Disease 172
Curly Top 173
Dwarfing Disease 173
Peanut Mottle 173
Peanut Stunt 174
Southern Bean Mosaic 174
Soybean Yellow Shoot 174
Stipple Streak 175
6. Diseases of Cotton (Gossypium barbadense and G. hirsutum) 183

Agrobacterium Root Rot and Wilt 183
Bacterial Blight 183
Bacterial Lint Discoloration 184
Crown Gall 184
Erwinia Internal Necrosis 185
Pantoea agglomerans Cotton Lint Rot 185
Pseudomonas Leaf Spot 185

Aerolate Mildew 186
Alternaria Stem Blight and Leaf Spot 187
Anthracnose 188
Ascochyta Blight 190
Ashbya Fiber Stain 191
Aspergillus Boll Rot 191
Black Boll Rot 192
Black Root Rot 192
Botryodiplodia Seedling Blight and Boll Rot 193
CercosporaAlternaria Leaf Blight Complex 194
Charcoal Rot 195
Choanephora Mold 196
Cochliobolus Leaf Spot 196
Colletotrichum Boll Rot 196
Corynespora Leaf Spot 197
Cylindrocladium Black Rot 197
Diplodia Boll Rot 198
Escobilla 198

Page xii
Fusarium Boll Rot 199
Fusarium Damping Off 199
Fusarium nygami Root Colonization 200
Fusarium Seed Infection 200
Fusarium Wilt 200
Helminthosporium Leaf Spot 201
Myrothecium Leaf Spot 201
Nematospora Boll Stain 202
Nigrospora Lint Rot 203
Phomopsis Leaf Spot 203
Phytophthora Boll Rot 205
Phytophthora boehmeriae Boll Rot 205
Powdery Mildew 206
Pythium Damping Off 206
Ramulose 207
Rhizoctonia Leaf Spot 207
Rhizopus Boll Rot 208
Rust 208
Sclerotium Boll Rot 209
Sclerotium Stem and Root Rot 209
Soreshin 210
Southwestern Cotton Rust 211
Stemphylium Leaf Spot 211
Tropical Cotton Rust 212

Dagger 214
Lance 21449p4.045
Lesion 215
Needle 215
Pin 215
Reniform 216
Ring 216
Root Knot 216
Scutellonema spp. 217
Spiral 217
Sting 217
Stubby Root 218
Stunt 218

Phyllody 218
Small Leaf 218

Abutilon Mosaic 219
Anthocyanosis 219
Blue Disease 220
Cotton Leaf Crumple 220
Cotton Small Leaf 220
Cotton Terminal Stunt 221
Leaf Curl 221
Leaf Mottle 222
Leaf Roll 222
Mosaic 222
Psylosis 222
Terminal Stunt 223
Tobacco Streak 223
Vein Clearing 223
Veinal Mosaic 223
7. Diseases of Crambe (Crambe abyssinica) 229

Disease Caused by Bacteria

Fusarium Wilt 230

Beet Western Yellows 231
Turnip Mosaic 232
8. Diseases of Flax (Linum usitatissimum) 233

Alternaria Flower and Stem Blight 233
Anthracnose 233
Basal Stem Blight 234
Brown Stem Blight 235
Browning and Stem Break 235
Dieback 236

Page xiii
Fusarium Secondary Rot 236
Gray Mold 237
Pasmo 237
Phytophthora Root Rot (Phytophthora aphanidermatum) 238
Phytophthora Root Rot (Phytophthora nicotianae vat. parasitica) 238
Powdery Mildew 239
Rhizoctonia Seedling Blight and Root Rot 239
Rust 240
Scorch 241
Seed Rot, Seedling Blight, and Root Rot 241
Stem Mold and Rot 242
Thielaviopsis Root Rot 242
Wilt 243

Aster Yellows 244

Crinkle 244
Curly Top 244

Diseases Caused by Physiologic or Weatheroriented Problems
Boll Blight 245
Heat Canker 245
Top Dieback 245
9. Diseases of Maize (Zea mays) 247

Bacterial Leaf Blight and Stalk Rot 247
Bacterial Stalk and Top Rot 248
Bacterial Stripe 248
Chocolate Spot 249
Goss's Bacterial Wilt and Blight 249
Holcus Spot 250
Pseudomonas fuscovaginae Disease 251
Purple Leaf Sheath 251
Seed Rot and Seedling Blight 252
Stewart's Wilt 252

Alternaria Leaf Blight 253
Anthracnose Leaf Blight 254
Anthracnose Stalk Rot 255
Ascochyta Leaf and Sheath Spots 256
Aspergillus Ear Rot 256
Banded Leaf and Sheath Spot 258
Black Bundle Disease 258
Black Kernel Rot 259
Borde Blanco 259
Brown Spot and Stalk Rot 259
Brown Stripe Downy Mildew 260
Cephalosporium Kernel Rot 261
Charcoal Rot 261
Common Corn Rust 262
Common Smut 263
Corticium Ear Rot 264
Crazy Top Downy Mildew 265
Curvularia Leaf Spot 265
Didymella Leaf Spot 266
Diplodia Ear Rot 266
Diplodia Ear Rot and Stalk Rot 267
Diplodia Leaf Spot 268
Diplodia Seedling Blight 268
Diplodia Stalk Rot 269
Dry Ear Rot 271
Ergot 271
Eyespot 272
False Smut 272
Fusarium avenaceum Stalk Rot and Seedling Root Rot 273
Fusarium globosum Kernel Infection 273
Fusarium Kernel Rot 273
Fusarium Leaf Spot 276

Page xiv
Fusarium scirpi in Grain 276
Fusarium Stalk Rot 277
Fusarium thapsinum Infection 278
Gibberella Ear Rot 279
Gibberella Stalk Rot 281
Gray Ear Rot 282
Gray Leaf Spot 282
Green Ear Downy Mildew 284
Head Smut 284
Hormodendrum Ear Rot 285
Hyalothyridium Leaf Spot 285
Java Downy Mildew 286
Late Wilt 286
Nigrospora Stalk Rot 287
Northern Leaf Blight 287
Northern Leaf Spot 289
Penicillium Rot 290
Phaeocytostroma Stalk Infection 291
Phaeosphaeria Leaf Spot 291
Philippine Downy Mildew 291
Phomopsis Seed Rot 292
Physalospora Ear Rot 292
Pyrenochaeta Stalk Rot and Root Rot 292
Pythium Root Rot 293
Pythium Seed and Seedling Blight 293
Pythium Stalk Rot 294
Red Kernel Disease 295
Rhizoctonia Ear Rot 295
Rhizoctonia Root Rot and Stalk Rot 295
Rostratum Leaf Spot 295
Sclerotium Ear Rot 296
Seed and Seedling Blight Other than Pythium 296
Selenophoma Leaf Spot 297
Septoria Leaf Blotch 297
Sheath Blight 297
Sheath Rot 298
Shuck Rot 298
Silage Mold 298
Sordaria fimicola Stalk Infection 299
Sorghum Downy Mildew 299
Southern Corn Leaf Blight 300
Southern Corn Rust 301
Spontaneum Downy Mildew 302
Sugarcane Downy Mildew 302
Tar Spot 303
Trichoderma Ear Rot and Root Rot 304
Tropical Corn Rust 304
Yellow Leaf Blight 304
Zonate Leaf Spot 305

Awl 306
Bulb and Stem 306
Burrowing 306
Columbia Lance 307
Corn Cyst 307
Dagger 307
False Root Knot 307
Lance 307
Lesion 308
Needle 308
Ring 308
Root Knot 309
Spiral 309
Sting 309
Stubby Root 309
Stunt 310

Corn Stunt 310
Maize Bushy Stunt 311
Unnamed Disease 311

Australian Maize Stripe 312
Brome Mosaic 313

Page xv
Cereal Tillering Disease 313
Corn Chlorotic Vein Banding 314
Corn Lethal Necrosis 314
Cucumber Mosaic 314
Cynodon Chlorotic Streak 315
Elephant Grass Mosaic 315
High Plains Virus 315
Johnsongrass Mosaic 316
Maize Chlorotic Dwarf 317
Maize Chlorotic Mottle 318
Maize Dwarf Mosaic 319
Maize Leaf Fleck 320
Maize Line 320
Maize Mosaic 320
Maize Mottle 321
Maize Necrotic Lesion 321
Maize Pellucid Ringspot 321
Maize Raya Gruesa 322
Maize Rayado Fino 322
Maize Red Stripe 322
Maize Ring Mottle 323
Maize Rio Cuarto Disease 323
Maize Rough Dwarf 323
Maize Sterile Stunt 323
Maize Streak 324
Maize Stripe 324
Maize Tassel Abortion 325
Maize Vein Enation 325
Maize Wallaby Ear 326
Maize White Line Mosaic 326
Mal de Rio Cuarto 327
Millet Red Leaf 327
Oat Pseudorosette 328
Rice BlackStreaked Dwarf 328
Rice Stripe 329
Sorghum Stunt Mosaic 329
Sugarcane Fiji Disease 329
Sugarcane Mosaic 329
Vein Enation 330
Wheat Spot Mosaic 330
Wheat Streak Mosaic 331
Wheat Striate Mosaic 331
Unknown Virus 331

Disease Caused by Unknown Factors
North Queensland Stripe 332
10. Diseases of Millet 343

Bacterial Leaf Streak 343
Bacterial Leaf Stripe 344
Bacterial Spot 344
Pantoea agglomerans Leaf Spot 344

Bipolaris Leaf Spot 345
Blast 345
Brown Leaf Spot 346
Dactuliophora Leaf Spot 347
Downy Mildew (Plasmopara penniseti) 347
Downy Mildew (Sclerospora graminicola) 348
Downy Mildew (Sclerospora macrospora) 349
Drechslera Leaf Spot 350
Ergot 350
Exserohilum Leaf Blight 351
False Mildew 351
Fusarium nygamai Disease 351
Head Mold 352
Head Smuts 352
Helminthosporiosis 353
Kernel Smuts 354
Leaf Spot (Drechslera setariae) 354
Leaf Spot (Helminthosporium frumentacei) 355

Page xvi
Long Smut 355
Phyllosticta Leaf Blight 356
Pyricularia Leaf Spot 356
Rhizoctonia Blight 357
Rust (Puccinia substriata vat. indica) 358
Rust (Puccinia substriata var. pennicillariae) 358
Smut 358
Other Smuts Reported on Millet 359
Southern Blight 359
Top Rot 360

Burrowing 361
Cyst 361
Dagger 361
Lance 362
Ring 362
Root Knot 362
Root Lesion 362
Sting 362
Stubby Root 363
Stunt 363

Bajra (Pearl Millet) Streak 363
Guinea Grass Mosaic 364
Maize Streak 364
Panicum Mosaic 364

Brown Leaf Mottle 365
Red Leaf Spot 365
11. Diseases of Oat (Avena sativa) 369

Bacterial Blight (Acidovorax avenae subsp. avenae) 369
Bacterial Blight (Pseudomonas syringae pv. coronafaciens) 369
Bacterial Stripe Blight 370
Black Chaff 370

Anthracnose 371
Covered Smut 373
Crown Rust 374
Downy Mildew 375
Ergot 376
Eyespot 376
Fusarium Foot Rot 377
Head Blight 378

Helminthosporium Seedling Blight, Crown, and Lower Stem Rot
Leaf Blotch and Crown Rot 379
Loose Smut 380
Microdochium Root Rot 381
Pink Snow Mold 381
Powdery Mildew 382
Pythium Seed and Seedling Rot 382
Scoliocotrichum Leaf Blotch 383
Sharp Eyespot 383
Speckled Blotch 384
Stem Rust 385
TakeAll 387
Victoria Blight 387

Bulb and Stem 388
Cyst 388
Dagger 388
Lesion 389
Needle Nematode 389
Oat Cyst Nematode 389
Ring 390
Root Gall 390
Root Knot 391

Page xvii
Sheath 391
Spiral 391
Sting 392
Stubby Root 392
Stunt 392

Aster Yellows 392

Flame Chlorosis 396
Oat Blue Dwarf 396
Oat Golden Stripe 397
Oat Mosaic 397
Oat Necrotic Mottle 397
Oat Soilborne Mosaic 398
Oat Striate Mosaic 398
Orchardgrass Mosaic 399

Disease Caused by Physiological Disorders
Blast 400
12. Diseases of Peanut (Arachis hypogaea) 403

Bacterial Wilt 403

Aerial Blight 404
Alternaria Spot and Veinal Necrosis 404
Anthracnose 405
Aspergillus Crown Rot 405
Blackhull 406
Black Root Rot 406
Botrytis Blight 407
Charcoal Rot and Macrophomina Leaf Spot 407
Choanephora Leaf Spot 408
Collar Rot 408
Colletotrichum Leaf Spot 409
Cylindrocladium Black Rot 409
Cylindrocladium Leaf Spot 411
Diplodia Infection 411
Early Leaf Spot 411
Fusarium Peg and Root Rot 412
Fusarium Stem Canker 413
Fusarium Wilt (Fusarium martii var. phaseoli) 413
Fusarium Wilt (Fusarium oxysporum) 414
Late Leaf Spot 414
Macrophoma Leaf Spot 415
Melanosis 416
Myrothecium Leaf Blight 416
Neocosmospora Root Rot 416
Net Blotch 417
Olpidium Root Rot 417
Pepper Spot and Scorch 417
Pestalotia Leaf Spot 418
Pestalotiopsis Leaf Spot 418
Phanerochaete omnivorum Association 419
Phomopsis Foliar Blight 419
Pod Wart 420
Powdery Mildew 420
Pythium Pod Rot 421
Pythium Wilt 422
Rhizoctonia Diseases 423
Rhizopus Seed and Preemergence Seedling Rot 424
Rust 425

Page xviii
Scab 426
Sclerotinia Blight 426
Sclerotinia Leaf Spot 427
Southern Blight or Stem Rot 428
Web Blotch 430
Yellow Mold 430

Aphasmatylenchus straturatus 431
Dagger 432
Pod Lesion or Kalahasti Malady 432
Ring 432
Root Knot 432
Root Lesion 433
Seed and Pod 434
Spiral 434
Sting 434
Testa 435

Peanut Yellows 435
Witches' Broom 435

Disease Caused by Rickettsia
Rugose Leaf Curl 436

Cowpea Chlorotic Mottle 436
Cucumber Mosaic 437
Eyespot 437
Groundnut Crinkle 437
Groundnut Eyespot 437
Groundnut Rosette 438
Groundnut Streak 439
Indian Peanut Clump 439
Marginal Necrosis 440
Peanut Bud Necrosis 440
Peanut Chlorotic Ringspot 442
Peanut Chlorotic Streak 442
Peanut Green Mosaic 442
Peanut Mild Mottle 442
Peanut Mottle 443
Peanut Stripe 443
Peanut Stunt 445
Peanut Yellow Mottle 445
Unnamed Virus Disease 445
13. Diseases of Red Clover (Trifolium pratense) 451


Anther Mold 451
Black Patch Disease 452
Black Root Rot 452
Brown Root Rot 453
Common Leaf Spot 453
Curvularia Leaf Blight 453
Cylindrocarpon Root Rot 454
Cylindrocladium Root and Crown Rot 454
Downy Mildew 454
Gray Stem Canker 455
Leaf Gall 456
Midvein Spot 456
Mycoleptodiscus Crown and Root Rot 456
Myrothecium Root Rot 457
Northern Anthracnose 458
Powdery Mildew 458
Pseudoplea Leaf Spot 459
Rust 459
Sclerotinia Crown and Root Rot 460
Seed Mold 460
Seed Rot and Damping Off 461
Sooty Blotch 461
Southern Anthracnose 461
Southern Blight 462

Page xix
Spring Black Stem and Leaf Spot 463
Stagonospora Leaf Spot 463
Summer Black Stem 464
Target Spot 464
Violet Root Rot 465
Winter Crown Rot 465

Bulb and Stem 465
Clover Cyst 466
Dagger 466
Lance 466
Lesion 466
Pin 467
Ring 467
Root Knot 467
Spiral 468

Phyllody 468
Proliferation 468
Witches' Broom 468
Yellow Edge 469

Alfalfa Mosaic 469
Alsike Clover Mosaic 469
Clover Yellow Mosaic 470
Common Pea Mosaic 470
Cowpea Mosaic 471
Cucumber Mosaic 471
Dwarf 471
Red Clover Vein Mosaic 471
Ringspot 472
Streak 472
Wilt 472
14. Diseases of Rice (Oryzae sativa) 475

Bacterial Glume Blotch 477
Bacterial Halo Blight 477
Bacterial Sheath Brown Rot 478
Bacterial Sheath Stripe 479
Foot Rot 480
Grain Rot 480
Seedling Blight 481
Sheath Brown Rot 481

Aggregate Sheath Spot 482
Bakanae Disease 482
Basal Node Rot 483
Black Kernel 483
Blast 484
Brown Blotch 485
Brown Spot 486
Collar Rot (Ascochyta oryzae) 487
Collar Rot (Pestalotiopsis versicolor) 487
Crown Sheath Rot 487
Dead Tiller Syndrome 488
Downy Mildew 488
Eyespot 489
False Smut 489
Fusarium Diseases 490
Fusarium Leaf Blotch 490
Fusarium Sheath Rot 491
Kernel Smut 491
Leaf Scald 492
Leaf Smut 493
Narrow Brown Leaf Spot 493
Pecky Rice 493
Phoma Seedling Blight 494
Pithomyces Glume Blotch 494
Rust 495
Sheath Blight 495
Sheath Blotch 497
Sheath Rot 497
Sheath Spot 498
Stackburn Disease 499
Stem Rot 499

Page xx
Water Mold Disease 500
White Leaf Streak 500

Lesion 501
Rice Root 501
Root Knot 501
Stem 502
Summer Crimp 503

Rice Orange Leaf Disease 503
Rice Yellow Dwarf 504

Giallume Disease 505
Grassy Stunt B 505
Grassy Stunt Y 506
Rice Black Streak Dwarf 506
Rice Dwarf 506
Rice Gall Dwarf 507
Rice Grassy Stunt 507
Rice Hoja Blanca 508
Rice Necrotic Mosaic 508
Rice Ragged Stunt 509
Rice Stripe 510
Rice Stripe Necrosis 511
Rice Transitory Yellowing 511
Rice Yellow Mottle 512
Tungro 512
Unknown VirusCaused Disease 514
Waika Disease 514
Wilted Stunt Disease 515

Diseases Caused by Unknown or Abiotic Factors
Panicle Blight 515
Sekiguchi Lesion 515
Straighthead 516
15. Diseases of Rye (Secale cereale) 523

Bacterial Streak 523
Halo Blight 524

Anthracnose 525
Bunt 525
Common Root Rot 527
Cottony Snow Mold 528
Dilophospora Leaf Spot 528
Downy Mildew 529
Dwarf Bunt 530
Ergot 531
Eyespot 531
Halo Spot 534
Karnal Bunt 534
Leaf Rust 535
Leaf Streak 536
Loose Smut 537
Pink Snow Mold 538
Platyspora Leaf Spot 538
Powdery Mildew 539
Scald 539
Septoria tritici Blotch 541
Sharp Eyespot and Rhizoctonia Root Rot 542
Snow Scald 542
Spot Blotch and Associated Seedling and Crown Rots 543
Stalk Smut 545
Stem Rust 546
Strawbreaker 547
Stripe Rust 548
TakeAll 548
Tan Spot 549

Cereal Cyst 550
Leaf and Stem 550
Root Gall 551
Root Knot 551
Root Lesion 551
Seed Gall 552
Stubby Root 552

Page xxi

Aster Yellows 553

Soilborne Mosaic 554
16. Diseases of Safflower (Carthamus tinctorius) 559

Bacterial Leaf Spot and Stem Blight 559
Stem Soft Rot 559

Botrytis Head Rot 561
Charcoal Rot 562
Colletotrichum Stem Rot 563
Damping Off 563
Downy Mildew 563
Fusarium Wilt 563
Phytophthora Root and Stem Rot 564
Powdery Mildew 565
Ramularia Leaf Spot 566
Rhizoctonia Blight and Stem Canker 566
Rust 566
Sclerotinia Stem Rot and Head Blight 568
Septoria Leaf Spot 568

Root Knot 569

Phyllody 569

Alfalfa Mosaic 570
Chilli Mosaic 570
Cucumber Mosaic 570
Lettuce Mosaic and Necrosis 571
Tobacco Mosaic 571
Turnip Mosaic and Necrosis Severe Mosaic 571
17. Diseases of Sorghum (Sorghum bicolor) 575

Bacterial Leaf Stripe 577
Erwinia Soft Rot 577
Pseudomonas fuscovaginae Disease 578

Acremonium Wilt 578
Banded Leaf and Sheath Blight 580
Charcoal Rot 580
Cochliobolus Leaf Spot 581
Covered Kernel Smut 581
Crazy Top 582
Curvularia Kernel Rot 583
Ergot 583
False Mildew 585
Fusarium Root and Stalk Rot 586
Fusarium thapsinum Infection 587
Gray Leaf Spot 588
Green Ear 589
Head Smut 589
Ladder Leaf Spot 590
Leaf Blight 590
Leaf Spot 591
Long Smut 592
Loose Kernel Smut 592
Milo Disease 593

Page xxii
Oval Leaf Spot 593
Panicle and Grain Anthracnose 594
Phoma Leaf Spot 595
Pokkah Boeng 595
Pythium Seed and Seedling Blight 596
Red Rot 597
Red Spot 598
Rhizoctonia Stalk Rot 598
Rough Leaf Spot 598
Rust 599
Sooty Stripe 600
Sorghum Downy Mildew 600
Southern Leaf Blight 602
Southern Sclerotial Rot 602
Tar Spot 603
Target Leaf Spot 603

Awl 604
Cereal Root Knot 605
Dagger 605
Lesion 605
Needle 605
Pin 606
Reniform 606
Ring 606
Root Knot 606
Spiral 607
Sting 607
Stubby Root 607
Stunt 607

Yellow Sorghum Stunt 608

Australian Maize Stripe 608
Brome Mosaic 608
Cucumber Mosaic 609
Elephant Grass Mosaic 609
Johnsongrass Mosaic 609
Maize Chlorotic Dwarf 610
Maize Chlorotic Mottle 610
Maize Dwarf Mosaic Head Blight 611
Maize Rough Dwarf 612
Maize Streak 612
Maize Stripe 612
Peanut Clump 613
Red Stripe Disease 613
Rice Stripe 613
Sorghum Mosaic 614
Sorghum Stunt Mosaic 614
Sorghum Yellow Banding 615
Sugarcane Chlorotic Streak 615
Sugarcane Fiji Disease 615
Unknown Virus 616

Weak Neck 616
18. Diseases of Soybean (Glycine max) 621

Bacillus Seed Decay 621
Bacterial Crinkle Leaf 623
Bacterial Pustule 623
Bacterial Tan Spot 624
Bacterial Wilt (Curtobacterium flaccumfaciens) 625
Bacterial Wilt (Curtobacterium sp.) 625
Bacterial Wilt (Pseudomonas solanacearum) 626
Pseudomonas Seed Decay 626
Wildfire 627

Acremonium Wilt 628
Anthracnose 628
Aspergillus Seedling Blight 631
Brown Spot 631
Brown Stem Rot 632

Page xxiii
Cercospora Leaf Spot and Blight 633
Cercospora Seed Decay 634
Charcoal Rot 634
Choanephora Leaf Blight 636
Cotyledon Spot 636
Downy Mildew 636
Drechslera Blight 637
Essex Disease 638
Frogeye Leaf Spot 638
Fusarium graminearum Seed Infection 639
Fusarium oxysporum Seed Infection 639
Fusarium pallidoroseum Seed Infection 640
Fusarium Wilt 641
Leptosphaerulina Leaf Spot 641
Mycoleptodiscus Root Rot 642
Myrothecium Disease 642
Neocosmospora Stem Rot 643
Phomopsis Seed Rot 643
Phyllosticta Pod Rot 645
Phytophthora Root and Stem Rot 646
Pod and Stem Rot 648
Pod Rot and Collar Rot 649
Powdery Mildew 650
Purple Stain 650
Pyrenochaeta Leaf Spot 652
Pythium Damping Off and Rot 653
Red Crown Rot 654
Rhizoctonia Aerial Blight 655
Rhizoctonia Damping Off, Root, and Stem Rot 656
Rust 657
Scab 658
Southern Blight 659
Stem Canker 660
Stemphylium Leaf Blight 662
Sudden Death Syndrome 662
Target Spot 665
Thielaviopsis Root Rot 665
Top Dieback 666
Twin Stem Abnormality Disease 666
Verticillium Pod Loss 666
Yeast Spot 668

Columbia Lance 668
Lance 669
Lesion 669
Reniform 669
Ring 670
Root Knot 670
Sheath 671
Soybean Cyst 671
Spiral 672
Stem 672
Sting 672

Machismo 673
Soybean Bud Proliferation 673
Witches' Broom 674

Alfalfa Mosaic 674
Bean Pod Mottle 674
Brazilian Bud Blight 675
Bud Blight 675
Cowpea Chlorotic Mottle 676
Cowpea Mosaic 677
Cowpea Severe Mosaic 677
Delayed Maturity 677
Indonesian Soybean Dwarf 678
Mung Bean Yellow Mosaic 678
Peanut Mottle 678
Peanut Stripe 679
Peanut Stunt 679
Soybean Chlorotic Mottle 679
Soybean Crinkle Leaf 680

Page xxiv
Soybean Dwarf 680
Soybean Mosaic 680
Soybean Severe Stunt 681
Soybean Yellow Shoot 682
Tobacco Mosaic 682
Tobacco Necrosis 682
Yellow Mosaic 683

Diseses Caused by Unknown Factors
Pod Necrosis 683
19. Diseases of Sugar Beet (Beta vulgaris) 695

Bacterial Pocket 695
Bacterial Vascular Necrosis and Soft Rot 696
Corynebacterium Infection 697
Crown Gall 697
Scab 697

Aspergillus fumigatus Storage Rot 698
Beet Rust 699
Beet Tumor 699
Black Root 700
Botrytis Storage Rot 700
Charcoal Rot 702
Downy Mildew 703
Dry Rot Canker 703
Fusarium Tip Rot 704
Fusarium Yellows 705
Fusarium, Miscellaneous Species 706
Penicillium Storage Rot 706
Phoma Leaf Spot 706
Phoma Root Rot and Storage Rot 707
Phytophthora Root Rot 708
Powdery Mildew 709
Ramularia Leaf Spot 711
Rhizoctonia Crown and Root Rot 711
Rhizoctonia Foliage Blight 713
Rhizopus Root Rot 714
Sclerotium Root Rot 714
Seedling Rust 715
Violet Root Rot 715

Clover Cyst 716
False Root Knot 717
Nebraska Root Gall 717
Needle 717
Root Knot 718
Stem and Bulb 718
Stubby Root 719
Sugar Beet 719

Rosette Disease 720

Diseases Caused by Rickettsia
Beet Latent Rosette 720
Yellow Wilt 720

Beet Crinkle 721
Beet Curly Top 721
Beet Distortion Mosaic 722
Beet Leaf Curl 722
Beet Marble Leaf 723
Beet Mild Yellowing 723
Beet Mosaic 723
Beet PseudoYellows 724
Beet Ring Mottle 724
Beet Soilborne 725
Beet Soilborne Mosaic 725
Beet Western Yellows 726
Beet Yellow Net 727

Page xxv
Beet Yellow Stunt 728
Beet Yellow Vein 728
Beet Yellows 728
Cucumber Mosaic 729
Lettuce Chlorosis 730
Lettuce Infectious Yellows 730
Rhizomania Disease 730
Savoy 732
Yellows 732
20. Diseases of Sugarcane (Saccharum officinarum) 737

Bacterial Mottle 737
Gumming Disease 738
Leaf Scald 739
Mottled Stripe 740
Ratoon Stunting Disease 740
Red Stripe and Top Rot 741

Banded Sclerotial Leaf Disease 742
Black Rot 743
Black Stripe 743
Brown Rot 743
Brown Spot 744
Brown Stripe 744
Collar Rot 745
Common Rust 745
Covered Smut 746
Culmicolous Smut 746
Other Fungi Reported to Cause Smut 748
Curvularia Leaf Spot and Seedling Blight 749
Downy Mildew (Peronosclerospora sacchari) 749
Downy Mildew (Peronosclerospora spontanea) 750
Downy Mildew LeafSplitting Form 750
Drechslera Seedling Blight and Leaf Spot 751
Dry Top Rot 751
Ergot 752
Eyespot 753
Foliage Blight of Seedlings 753
Fusarium Sett and Stem Rot 754
Iliau 754
Leaf Blast 755
Leaf Blight 755
Leaf Scorch (Leptosphaeria bicolor) 756
Leaf Scorch (Stagonospora sacchari) 756
Marasmius Sheath and Shoot Blight 756
Myriogenospora Leaf Binding 757
Northern Poor Root Syndrome 757
Orange Rust 758
Pachymetra Root Rot 758
Philippine Downy Mildew 759
Phytophthora Rot of Cuttings 759
Pineapple Disease 760
Pokkah Boeng 761
Purple Spot of Sugarcane 761
Red Leaf Spot 762
Red Rot 762
Red Rot of Leaf Sheath and Sprout Rot 763
Red Spot 764
Red Spot of Leaf Sheath 764
Rhizoctonia Sheath and Shoot Rot 764
Rind Disease 765
Ring Spot 765
Ring Spot of Sugarcane 766
Sclerophthora Disease 766
Sheath Rot 767
Sooty Mold 767

Page xxvi
Sugarcane Stubble Decline 767
Tar Spot 768
Target Blotch 768
Veneer Blotch 768
White Rash 769
Wilt 769
Yellow Spot 770

Lance 771
Lesion 771
Root Knot 771
Spiral 771

Grassy Shoot 772
White Leaf 772

Banana Streak 773
Chlorotic Streak 773
Dwarf 774
Fiji Disease 774
Mosaic 775
Sereh 776
Streak Disease 776
Striate Mosaic 777
Sugarcane Bacilliform 777
Sugarcane Mild Mosaic 777
Sugarcane Red Leaf Mottle 778
Sugarcane Yellow Leaf Disease 778

Yield Decline 778
21.Diseases of Sunflower (Helianthus annuus) 783

Apical Chlorosis 783
Bacterial Leaf Spot (Pseudomonas spp.) 783
Bacterial Leaf Spot (Pseudomonas syringae pv. helianthi) 784
Bacterial Wilt 784
Crown Gall 784
Erwinia Stalk Rot and Head Rot 785

Achene Blemish Syndrome 785
Alternaria Leaf Blight, Stem Spot, and Head Rot 786
Botrytis Head Rot 787
Cephalosporium Wilt 788
Charcoal Rot 788
Cladosporium Leaf Spot 789
Downy Mildew 789
Fusarium moniliforme Wilt 791
Fusarium oxysporum Wilt 791
Fusarium Pith Canker 791
Helminthosporium Leaf Blight 792
Myrothecium Leaf and Stem Spot 792
Phialophora Yellows 792
Phoma Black Stem 793
Phoma Leaf Blight 793
Phomopsis Brown Stem Canker 793
Phytophthora Stem Rot 795
Powdery Mildew 795
Rhizopus Head Rot 796
Rust 797
Sclerotinia Basal Stalk Rot and Wilt 798
Sclerotinia Basal Stalk Rot and Wilt, and Midstalk Rot 798
Sclerotinia Head Rot 799
Sclerotium Basal Stalk and Root Rot 801
Septoria Leaf Spot 801

Page xxvii
White Rust 802
Yellow Rust 803

Dagger 803
Lesion 803
Pin 804
Reniform 804
Root Knot 804
Spiral 805
Stunt 805

Aster Yellows 805

Sunflower Mosaic 806
Yellow Leaf Spot Mosaic 806

Disease Caused by Nonparasitic Factors
Bract Necrosis 806
22 Diseases of Tobacco (Nicotiana tabacum) 811

Angular Leaf Spot 811
Barn Rot 812
Black Rust 813
Blackleg 813
Crown Gall 813
Frenching 814
Granville Wilt 815
Hollow Stalk 815
Leaf Gall 816
Philippine Bacterial Leaf Spot 817
Wildfire 817
Wisconsin Bacterial Leaf Spot 818

Anthracnose 819
Barn Spot 820
Black Mildew 820
Black Root Rot 821
Black Shank 822
Blue Mold 823
Botryosporium Barn Mold 825
Brown Spot 825
Charcoal Rot 826
Collar Rot 826
Corynespora Leaf Spot 827
Damping Off 828
Dead Blossom Leaf Spot 829
Frogeye 829
Fusarium Wilt 830
Gray Mold 831
Olpidium Seedling Blight 831
Powdery Mildew 832
Rhizoctonia Leaf Spot 833
Rhizopus Stem Rot 833
Rust (Puccinia substriata) 834
Rust (Uredo nicotianae) 834
Sooty Mold 834
Soreshin 835
Southern Stem and Root Rot 835
Target Spot 836
Tobacco Stunt 837

Brown Root Rot 838
Bulb and Stem 839
Cyst 840
Dagger 840
Foliar 840
Lesion 840
Reniform 841
Root Knot 841
Spiral 842
Stubby Root 842
Stunt 843

Aster Yellows 843
Bigbud 844
Stolbur 844
Yellow Dwarf 845

Page xxviii

Disease Caused by Viroids
Nicotiana glutinosa Stunt Viroid 846

Alfalfa Mosaic 846
Beet Curly Top 847
Bushy Top 847
Clubroot 848
Cucumber Mosaic 848
Eggplant Mosaic 849
Leaf Curl 849
Nicotiana velutina Mosaic 850
Peanut Chlorotic Streak 850
Peanut Stunt 851
Pepper Veinal Mottle 851
Ringspot 851
Tobacco Etch 851
Tobacco Leaf Curl 853
Tobacco Mosaic 853
Tobacco Necrosis 854
Tobacco Rattle 855
Tobacco Ringspot 855
Tobacco Rosette Disease 856
Tobacco Streak 856
Tobacco Stunt 857
Tobacco Veinal Necrosis 857
Tobacco VeinBanding Mosaic 858
Tobacco Vein Mottling 859
Tomato Spotted Wilt 859
Wound Tumor 860

Disease Caused by Higher Plants
Broomrape 860
23. Diseases of Wheat (Triticum aestivum) 865

Bacterial Mosaic 867
Bacterial Sheath Rot 868
Basal Glume Rot 868
Black Chaff 868
Pink Seed 870
Spike Blight 870
Stem Melanosis 871
Wheat Leaf Blight 871
White Blotch 872

Anthracnose 873
Aureobasidium Decay 874
Black Head Molds 874
Black Point 874
Brown Root Rot 875
Ceratobasidium gramineum Snow Mold 877
Common Bunt 878
Common Root Rot 879
Cottony Snow Mold 881
Crater Disease 881
Dilophospora Leaf Spot 882
Disease Caused by Fusarium sporotrichioides 883
Downy Mildew 883
Dry Seed Decay 884
Dwarf Bunt 884
Epicoccum Glume Blotch 885
Ergot 886
Eyespot 887
Flag Smut 888
Fusarium Glume Spot 889
Fusarium Leaf Blight 890
Fusarium Rot 892
Halo Spot 893
Karnal Bunt 894
Leaf Rust 895
Leaf Spot (Ascochyta spp.) 896
Leaf Spot (Phaeoseptoria urvilleana) 896
Loose Smut 897
Microscopica Leaf Spot 898
Patchy Stunting 898
Phialophora TakeAll 898
Phoma Spot 899
Pink Snow Mold 899
Platyspora Leaf Spot 900
Powdery Mildew 900

Page xxix
Prematurity Blight 901
Red Smudge or Pink Smudge 903
Rhizoctonia Bare Patch 903
Sclerotinia Snow Mold 906
Sharp Eyespot 908
Snow Rot 908
Southern Blight 909
Spot Blotch 910
Stem Rust 912
Stripe Rust 914
TakeAll 915
Tan Spot 917
Tar Spot 919
Typhulalike Snow Mold 919
Wheat Blast 920
Zoosporic Root Rot 920

Bulb and Stem 921
Cerel Cyst 921
Columbia Root Knot 922
Dagger 922
Grass Cyst 922
Lesion 923
Ring 923
Root Gall 923
Root Knot 924
Seed Gall 924
Spiral 925
Stubby Root 925
Stunt 926

Aster Yellows 926

Disease Caused by Virolds
Seedborne Wheat Yellows 927

Agropyron Mosaic 927
Australian Wheat Streak Mosaic 928
Barley Yellow Streak Mosaic 930
Barley Yellow Striate Mosaic 931
Barley Yellow Stripe 931
Brome Mosaic 931
Cereal Tillering 932
Cocksfoot Mottle 932
Cucumber Mosaic 932
Eastern Wheat Striate 933
Enanismo 933
European Wheat Striate Mosaic 933
Flame Chlorosis 934
High Plains Disease 934
Indian Peanut Clump 935
Maize Streak 935
Maize White Line Mosaic 935
Mal de Rio Cuarto 936
Orchardgrass Mosaic 937
Rice Blackstreaked Dwarf 937
Rice Hoja Blanca 938
Russian Winter Wheat Mosaic 938
Tobacco Mosaic 939
Wheat (Cardamom) Mosaic Streak 939
Wheat Chlorotic Streak 939
Wheat Dwarf 939
Wheat Rosette Stunt 940
Wheat Soilborne Mosaic 940
Wheat Spindle Streak Mosaic 941
Wheat Spot Mosaic 943
Wheat Yellow Leaf 945
Wheat Yellow Mosaic 945
Unknown Virus 945

Page xxx

Physiologic Leaf Spot 945
Unknown 946
24. Diseases of Wild Rice (Zizania palustris) 959

Bacterial Brown Spot 959

Anthracnose 960
Ergot 960
Fungal Brown Spot 960
Phytophthora Crown and Root Rot 962
Smut 962
Spot Blotch 963
Stem Rot 963
Stem Smut 964
Zonate Eyespot 965
Miscellaneous Fungi 965

Miscellaneous Nematodes 965

Disease Caused by Viruses
Index 969

Page xxxi
Preface
The purpose of Field Crop Diseases, Third Edition, remains the same as it has been in previous editions: to provide a basic knowledge of the diseases of many of
the world's important field crops. Each disease description is meant to stand alone, or to be a selfcontained story, and to give a good working knowledge of a
disease. However, each description is not intended to be comprehensive. If further information is desired, indepth knowledge may be found in sources such as
research journals or in compendia that are published by the American Phytopathological Society (APS).
Some things about the book have changed:
The title is now Field Crop Diseases instead of Field Crop Diseases Handbook because the word ''handbook" lends a different connotation to the contents than is
intended.
The common names of host plants, such as rapeseed and corn, have changed. Since the term "rape" has awkward connotations today, "canola" is now commonly
used to identify this crop. "Corn" has been changed to "maize," which most of the world uses, even though my American mentality often found it awkward to use
"maize" throughout the book.
The authority behind each Latin binomial of the causal microorganism has been dropped to simplify reading by nonplant pathologists.
More than 400 diseases and 1900 references have been added. This edition discusses 1614 plant diseases of 24 field crops.
There are frustrations associated with writing such a book. One is the variety and overlap of common names of diseases. The APS has attempted to alleviate this
problem by publishing a standard list of common disease names. Where possible, I have used the names on this list. However, the names of diseases commonly used
in the literature do not always coincide with the APS list, thereby contributing to the general confusion. I have attempted to list other names of a disease in the
description, but these lists may not always be comprehensive.

Page 3
1.
Diseases of Alfalfa (Medicago stiva)
Alfalfa Sprout Rot
Cause.
Erwinia chrysanthemi survives for up to 2 weeks on inoculated dried seeds. Air, the water supply, or greenhouse workers may introduce bacteria into a sprouting
house. Spread within a tray is by seedtoseed contact. Rot is most severe at high moisture and temperatures of 28°C and above. Little disease occurs below 21°C.
Distribution.
The United States (California).
Symptoms.
Radicles are a translucent yellow as they emerge from the seed. In 24 to 48 hours, seeds stop growing and turn into a yellowish, odiferous mass that contains
numerous bacteria. Disease initially occurs in a few trays, but it may spread throughout all trays in a few days.
Management
1. Control temperature in the sprouting house.
2. Practice sanitation. Bacteria likely survive in water remaining in tanks used for soaking seeds.
3. Soak seeds for 2 hours in 0.5% sodium hypochlorite or calcium hypochlorite. However, hypochlorite is not currently registered for alfalfa seed treatment in the
United States.
Bacterial Leaf Spot
Cause.
Xanthomonas campestris pv. alfalfae (syn. X. alfalfae and Phytomonas alfalfae) survives in infected residue that has been incorporated into soil or is lying on the
soil surface, in hay, and in debris associated with seed. During warm, wet weather, bacteria are splashed or blown onto leaves and enter them through small wounds
that have been made by any means. During dry weather, bacteria may enter leaves through wounds made by

Page 4
windblown soil particles. The bacteria multiply inside the leaf and frequently ooze to the leaf surface, where they may be splashed by rain or rubbed by leaftoleaf
contact onto adjacent healthy leaves.
Distribution.
Wherever alfalfa is grown under warm, wet conditions.
Symptoms.
Diseased seedlings are often killed or stunted at high temperatures. Initially, small, watersoaked spots occur in chlorotic areas on leaflets. The spots enlarge to
irregularshaped lesions (23 mm in diameter) with chlorotic margins that are pronounced on the underside of leaflets. Eventually, the lesions become light yellow to
tan, often with a lighter center, and have a translucent, papery texture. Lesions often glisten because of the dried bacterial exudate on their surface. Diseased leaves
defoliate prematurely. Stem lesions are watersoaked initially, then turn brown or black.
Management
1. Grow resistant cultivars. Plants within a cultivar differ in susceptibility
2. Sow in the spring.
Bacterial Stem Blight
Cause.
Pseudomonas syringae pv. syringae (syn. P. medicaginis and Phytomonas medicaginis) survives in infested residue in soil. During wet weather, bacteria enter a
host plant through stem wounds previously caused by frost.
Distribution.
Western North America.
Symptoms.
Bacterial stem blight occurs from early spring until the first harvest. Normally, only the lower five internodes are diseased.
Initially, lesions are watersoaked and chlorotic at the point of leaf attachment to the stem, leaflet midribs, and petioles. Lesions become linear, are discolored light to
dark brown or black, and extend down one side of the stem for one to three internodes and into the crown and roots of older plants. Bacterial exudate may be
present on leaf surfaces. Leaves attached to diseased areas on the stem become chlorotic and die. Diseased stems are thin, brittle, and shorter than healthy stems.
Management
1. Hardy cultivars are less prone to frost injury; therefore, they will be less likely to become infected.
2. Harvest after all danger of frost is past.
Bacterial Wilt
Cause.
Clavibacter michiganense subsp. insidiosus (syn. Corynebacterium michiganense subsp. insidiosum, C. insidiosum, and Aplanobacter insidiosum). The
Clavibacter subspecies insidiosus sometimes is spelled "insidiosum" in the literature and considered a pathovar.

Page 5
Clavibacter michiganense subsp. insidiosus survives in plant tissue and soil for several years and is seedborne. Bacteria are spread from plant to plant by mowing
machinery, irrigation water, or surface rainwater. Longdistance spread is by hay and seed.
Plants are normally infected the second or third year of growth. Bacteria enter roots through wounds made by a variety of causes, including winter injury and insects.
Bacteria then proceed into the xylem tissue of stems, crowns, and roots, where they rapidly increase in number and prevent water from moving up the plant.
Eventually, diseased tissues disintegrate and release bacteria into the surrounding soil, where, over time, they are distributed to adjacent healthy host plants.
The greatest incidence of bacterial wilt occurs in low, poorly drained areas of fields and over larger geographic areas during periods of continuous wet weather.
Presence of the root knot nematode, Meloidogyne hapla, increases the severity of bacterial wilt.
Distribution.
Wherever alfalfa is grown, but alfalfa wilt is considered to be more important in the United States than in other countries.
Symptoms.
Bacterial wilt is first noticed as scattered dead plants in a field. Initially, diseased plants are stunted; stems and leaves remain small after cutting and give plants a
dwarfed, bunchy appearance. Leaves are somewhat thickened, rounded at the tip, and tend to cup upward. Plants initially wilt during moisture stress caused by
daytime heat but recover their turgidity at night. Later, permanent wilt symptoms develop as leaflet margins become yellowish or bleached, followed by entire leaflets
becoming chlorotic, then necrotic. Eventually, the entire plant dies.
The outer vascular tissue of crowns and taproots is yellow to tan and appears as a discolored ring. The entire root then becomes rotted. Diseased plants are more
prone to winterkill than healthy plants.
Management.
Grow resistant cultivars.
Crown Gall
Cause.
Agrobacterium tumefaciens.
Distribution.
It is likely that crown gall is widespread, but it is not a serious disease of alfalfa.
Symptoms.
Galls present on crowns are irregularshaped and light green when actively growing but are discolored light to dark tan when not growing.
Management.
Not necessary.

Page 6
Dwarf
Cause.
Xylella fastidiosa is a nutritionally fastidious, gramnegative, xyleminhabiting bacterium. Bacterial cells are single, straight rods (1.04.0 × 0.250.5 m).
Several species of leafhoppers carry the bacterium to susceptible hosts and inject it into the plants during feeding. In California, Draeculacephala minerva and
Carneocephala fulgida are important vectors. Other potential vectors include xylemfeeding insects with piercing, sucking mouthparts. Leafhoppers of the subfamily
Cicadellinae and spittlebugs (family Cercopidae) are known vectors in which bacteria multiply in their foreguts, but the bacteria are not retained after molting and are
not transovarial. Grassy weeds apparently provide a favorable habitat for development of vector populations.
Bacterial cells are limited to the xylem tissue of host plants. Once bacteria are established in the xylem tissue, they can systemically colonize both roots and shoots.
Disease expression is caused by vascular occlusions in the xylem tissue, which cause water stress and, eventually, plant wilting.
Xylella fastidiosa also causes Pierce's disease of grape and almond leaf scorch.
Distribution.
The United States (California, Georgia, Mississippi, and Rhode Island). Dwarf occurs sporadically and is considered to be an uncommon disease of alfalfa.
Symptoms.
Diseased plants are normally stunted and have smallerthannormal, dark bluishgreen leaves. Blooming may be retarded or inhibited and fewer buds develop after
each harvest, which results in a diminished number of stems. Infrequently, stem tips may wilt.
Diseased roots initially have a slight yellow vascular discoloration beneath the bark of the taproot. Later, the entire stele may be diseased with a yellowishbrown
discoloration extending into the surrounding tissue. Taproot xylem tissue becomes brown when exposed to air.
Management
1. Grow resistant varieties. 'California Common 49' is resistant to dwarf but is susceptible to the spotted alfalfa aphid.
2. Control grassy weeds.
Root and Crown Rot Complex
This disease is sometimes called Pseudomonas viridiflava root and crown rot or P. viridiflava root and crown rot complex.
Cause.
Pseudomonas viridiflava.
Distribution.
Not known.

Page 7
Symptoms.
The crown and upper taproot have a light brown "dry rot." Light brown streaks extend beyond the rot into the vascular system for about onethird the length of the
diseased root.
Management.
Not reported.
Acrocalymma Root and Crown Rot
Cause.
Acrocalymma medicaginis, teleomorph Massarina walkeri, presumably overseasons as pycnidia on residue.
Distribution.
Australia (southeastern Queensland), where the disease is common in plants more than 1 year old.
Symptoms.
Redflecked cortical and wood tissues occur at the extremity of a wedgeshaped lesion that commences in the crown branches and extends into the taproot. Bark of
diseased areas is often fissured. Later a "dry rot" develops and older, diseased tissue darkens.
Management.
Not known.
Anthracnose
Anthracnose is also called southern anthracnose.
Cause.
Colletotrichum trifolii. Colletotrichum destructivum, C. dematium f. truncata, and C. gloeosporioides have also been reported as causal agents of anthracnose.
Colletotrichum trifolii survives as acervuli and mycelia in residue associated with fields, feedlots, storage areas, and machinery, and on live stems and crowns. During
warm, moist or humid weather, spores are produced in acervuli and disseminated by wind and splashing water to stems and crowns. Secondary inoculum is provided
by spores borne in acervuli that are produced on new lesions.
Two physiologic races, labeled as race 1 and race 2, of C. trifolii occur. In general, disease caused by both races is more severe as temperatures increase. Light
quality and duration have no effect on disease incidence or severity.
Distribution.
Canada and the United States. Race 1 is present wherever alfalfa is grown. Race 2 has been reported from Maryland, North Carolina, and Virginia. Colletotrichum
destructivum is present primarily in Ontario.
Symptoms.
Anthracnose is first detected in summer or autumn by the presence of wilted and dead, yellow or light brown shoots that are scattered

Page 8
throughout a field. The disease is considered to be a major cause of midand latesummer yield reductions and plant mortality as a result of the general reduction of
shoot and crown bud numbers and of overall crown size and health.
Large, diamondshaped lesions with bleached or white centers form on the lower portions of diseased stems. Under magnification, several small, black acervuli,
appearing as upright "hairy" structures due to the presence of numerous dark setae, can be seen in the center of most lesions. Young, dead shoots may droop to form
"shepherd's crooks," which is a useful diagnostic symptom.
Colletotrichum trifolii grows from diseased stems into crowns, causing tissue to become bluish black or black. Diseased crowns are weakened, resuiting in plants
that are predisposed to winter injury or are killed prematurely. In South Africa, C. trifolii has been reported to cause a root rot primarily in areas under irrigation.
Both C. destructivum and C. dematium f. truncata are mildly pathogenic on petioles and leaves but are primarily secondary invaders in stem lesions caused by C.
trifolii.
Management.
Anthracnose cannot be managed in established stands.
1. Grow resistant cultivars.
2. Cut alfalfa before losses become too severe.
3. Under experimental conditions, the fungicides benomyl, copper hydroxide, and mancozeb reduced disease severity.
Aphanomyces Root Rot
This disease is sometimes called Aphanomyces seedling blight and root disease.
Cause.
Aphanomyces euteiches and A. cochlioides. Infection of plants is caused by zoospores that are motile in wet soils over a wide temperature range (3° to 39°C).
However, lower temperatures are most favorable to infection. Zoospores have been reported to be more motile for up to 24 hours in water at temperatures of 3° to 5
°C.
Distribution.
Canada (Ontario and Quebec) and the United States.
Symptoms.
Typical symptoms include postemergence death of seedlings, root and hypocotyl browning, and chlorosis of foliage. Sometimes, seedlings are only stunted. Later, a
root rot of mature plants may occur. Dry weight of live diseased plants that survive the first growing season is reduced.
Management.
Grow the least susceptible cultivars. Resistance has been identified in several alfalfa cultivars.

Page 9
Black Patch
Cause.
Rhizoctonia leguminicola is seedborne and survives as mycelia in infested residue.
Distribution.
The United States (West Virginia).
Symptoms.
Lesions on foliage vary in color from brown to grayblack and may have concentric rings. Seedlings are often blighted and overgrown with coarse, black mycelia.
Similarappearing aerial mycelial growth later occurs on stems and petioles and frequently girdles the stems. Dark lesions and similar dark mycelia may occur on
flowers and seeds.
Management.
Not reported.
Black Root Rot
Cause.
Thielaviopsis basicola, synamorph Chalara elegans, survives as chlamydospores in residue and soil. When soil conditions are moist during the growing season,
chlamydospores germinate to form mycelia that penetrate roots. Later in the season, chlamydospores form within the diseased tissues and either remain in infested
residue that has fallen to the soil surface at harvest time or return to the soil upon the disintegration of residue.
Distribution.
The United States (Maine, Maryland, New Jersey, and Texas).
Symptoms.
The cortex of the hypocotyl below the soil line and taproots and fibrous roots become discolored dark brown and necrotic. A severe root rot may develop, resulting
in wilting of the foliage and eventual plant death.
Management.
Not reported.
Brown Root Rot
Brown root rot is also called Plenodomus root rot.
Cause.
Phoma sclerotioides (syn. Plenodomus meliloti) overwinters as pycnidia in soil residue. Roots are infected when soils either thaw out in the spring or before they
freeze in the winter. Later in the growing season, plants become resistant to infection.
Distribution.
Canada, Finland, and the United States (Alaska).
Symptoms.
Slightly sunken, brown lesions occur on both lateral roots and the taproot. Numerous dark pycnidia develop on or just below the lesion surface. Plants die when rot
proceeds to the crown. However, plants may recover if rot stops and enough taproot remains to produce new branch roots below the crown.
Management.
Rotate alfalfa with resistant crops, such as small grains.

Page 10
Common Leaf Spot
Common leaf spot is also called Pseudopeziza leaf spot.
Cause.
Pseudopeziza medicaginis. Pseudopeziza trifolii f. sp. medicaginissativae is sometimes considered a synonym of P. medicaginis but is not reported in Fart et al.
(1989).
Pseudopeziza medicaginis survives either as mycelia or apothecia in leaf residue on the soil surface. During abundant moisture and temperatures of 15° to 24°C,
ascospores are produced on apothecia and "ejected" into the air, where they are carried by wind currents to healthy leaflets. Seedling stands grown under a thick
cover crop that retains moisture, such as oat, can be severely diseased.
Distribution.
Wherever alfalfa is grown.
Symptoms.
Plants are normally not killed but defoliation reduces hay quality and yield. Circular, dark brown spots (2 mm in diameter) develop on leaflets. There is a sharp line
delineating spots and healthyappearing tissue. When spots are fully developed, the centers become thickened and tiny, light brown, cupshaped apothecia form on the
upper leaflet surface.
Management
2. Cut diseased stands in the prebloom or bud stage before diseased leaves defoliate. This maintains hay quality and removes diseased leaves that will be a later
source of infection.
Corky Root Rot
Corky root rot is called corchosis.
Cause.
Xylaria sp. Little is known of the life cycle of the fungus.
Distribution.
Argentina.
Symptoms.
Lateral roots are destroyed, then a dry, brown, sunken canker develops on the taproot and increases in size until the root is encircled. Fungus growth into roots can
also occur from diseased crowns. Eventually, the entire root is invaded and the plant dies. The root retains its original shape but is light in weight and corky, with areas
of white mycelia growing on the darkened areas of the root. Finally, stands are thinned out and fail to recover after harvest.
Management.
Not reported.
Crown Wart
Cause.
Physoderma alfalfae (syn. Urophlyctis alfalfae and Cladochytrium alfalfae) survives as resting spores in soil. Zoospores are liberated in warm, wet

Page 11
soil and "swim" to the developing buds of crown branches, where they germinate to form infection hyphae that infect buds.
Distribution.
Australia, Ecuador, Europe, New Zealand, and the United States. Crown wart is common in the western United States but is less common in the eastern and
northeastern United States.
Symptoms.
Crown wart is most common in the spring when soils are excessively moist. Irregularshaped, white galls are formed on the crown near the soil surface. Galls rarely
develop on leaves. Upon maturity, galls become gray to brown and have mottled brown interiors (350 mm in diameter) that contain masses of resting spores. Galls
decompose later in the growing season and release spores into the soil.
Management.
Not practiced since crown wart is not considered to be a serious disease.
Cylindrocarpon Root Rot
Cause.
Cylindrocarpon magnusianum (syn. C. ehrenbergii), teleomorph Nectria ramulariae. Cylindrocarpon magnusianum survives as sclerotialike stromata in
infested soil residue. Infection occurs through wounds at the base of branch roots during the end of winter dormancy. Plants become resistant later in the growing
season.
Distribution.
Canada and the United States (Minnesota).
Symptoms.
A watersoaked area that eventually becomes discolored dark brown may occur only on a portion of a root or may involve the entire root. Stromata develop in
cracks in the bark of diseased roots and give them a dark and rough appearance.
Management.
Rotate alfalfa with resistant crops, such as small grains.
Cylindrocladium Root and Crown Rot
Cause.
Cylindrocladium crotalariae. Cylindrocladium clavatum and C. scoparium are also reported to cause disease.
Distribution.
The United States (Hawaii).
Symptoms.
Black and sunken lesions occur on diseased roots and crowns. A brown root rot is sometimes present.
Management.
Not reported.
Damping Off
Damping off is sometimes called Pythium seed and seedling blight.
Cause.
Fusarium acuminatum, Rhizoctonia solani, and Pythium spp. The pri

Page 12
mary Pythium species reported to be involved in damping off are P. debaryanum, P. irregulare, P. splendens, and P. ultimum. Other Pythium species reported
to be pathogenic to alfalfa include P. aphanidermatum, P. myriotylum, P. pulchrum, and P. rostratum.
Oospores and sporangia survive in infested residue and germinate either directly, by forming a germ tube, or indirectly, by producing zoospores that ''swim" through
soil water to roots and seeds. Disease caused by most Pythium species occurs in cold, wet soils; however, higher temperatures favor disease caused by P.
aphanidermatum and P. myriotylum.
Distribution.
Symptoms.
Preemergence damping off frequently occurs but is rarely observed because rapid seed and seedling decay below the soil surface "obscures" symptoms. If seeds
germinate, the seedling radicle and cotyledons turn brown and soft.
Postemergence seedling blight is characterized by hypocotyls and roots becoming light brown and watersoaked. Eventually, plants collapse and dry up. Surviving
seedlings are stunted. In South Africa, P. paroecandrum does not cause severe damping off but infects rootlets, thereby reducing shoot growth and development.
Management
1. Apply a fungicide seed treatment.
2. Seedlings become immune after a few days; plants older than 2 weeks usually do not become infected.
Downy Mildew
Cause.
Peronospora trifoliorum. Peronospora aestivalis has been reported to be a synonym. Peronospora trifoliorum overwinters as perennial mycelia in crown buds
and shoots and as oospores in infested residue. In the spring, conidia are formed in darkness during high relative humidity and are disseminated by wind or splashed
onto leaves. Optimum germination occurs in free water at a temperature of 18°C.
Distribution.
Temperate areas of the world.
Symptoms.
A rapidly growing plant has few symptoms. Downy mildew is most damaging the first year of plant growth during cool, wet springs. Symptoms disappear during
warm, dry weather but may return during cool weather.
Young leaflets, especially at the tips of stems, are dwarfed and twisted or rolled downward and contain light green to yellow blotches. A grayish, cottony growth
consisting of mycelia, conidiophores, and conidia is often visible on the underside of diseased leaflets during moist, cool weather or during periods of high humidity.

Page 13
When the entire stem is diseased, all leaves and stem tissue are chlorotic. Diseased stems are larger in diameter and much shorter than healthy stems.
Management
1. Grow cultivars that have a high percentage of resistant plants.
2. Cut alfalfa in prebloom stage to save foliage.
3. Sow in spring to reduce seedling infection.
Forked Foot Disease
Cause.
Pythium ultimum is frequently associated with this condition.
Distribution.
Not known for certain but likely wherever alfalfa is grown.
Symptoms.
Six or more adventitious roots develop above lesions on seedling radicles and give roots a "forked" appearance. Seedlings are dwarfed or stunted.
Management
2. Seedlings become immune after a few days; plants older than 2 weeks do not become infected.
Fusarium Crown and Root Rot
Cause.
Fusarium acuminatum, F. avenaceum, F. oxysporum, F. sambucinum, and F. solani. Other Fusarium species are presumably involved.
Fungi survive as chlamydospores in infested residue and soil and as saprophytic mycelia in infested residue. Fusarium species enter alfalfa roots by direct penetration
or through wounds caused by feeding of nematodes, insects, or other agents. Feeding injury by the insect Sitona hispidula has been reported to result in root infection
and severe root rot caused primarily by F. oxysporum. The primary role of wounding is not to breach the root surface but to alter the hostpathogen interaction to
favor fungal development in the root. Some Fusarium species, such as F. oxysporum f. sp. medicaginis, F. oxysporum f. sp. lycopersici, F. sambucinum, and F.
solani, produce substances that are toxic to living plant tissues.
Distribution.
Symptoms.
Seedlings may damp off either before or after emergence, especially during warm, wet weather. Diseased plants are usually stunted. Leaves are chlorotic, have a
bleached appearance, curl at the edges, and proceed to wilt.
The disease is characterized by a discolored light brown to black, wedgedshaped necrotic area that spreads from the diseased crown downward into the taproot.
Necrotic areas often occur in the cortex of the branch roots and taproot, often in association with wounds.

Page 14
Management.
No practical means of management is practiced; however, frequent harvesting of plants late in the growing season increases the possibility of root rot.
Fusarium Wilt
Cause.
Fusarium oxysporum f. sp. medicaginis is considered to be the main pathogen. Fusarium oxysporum f. sp. vasinfectum, races 1 and 2, and F. oxysporum f. sp.
cassia are also reported to cause similar symptoms.
Fusarium oxysporum f. sp. medicaginis survives for several years as chlamydospores in soil and residue and as mycelia in infested residue and diseased live plants.
Infection occurs by fungi growing into wounds on small roots and taproots and progressing up the xylem tissue. The nematode Meloidogyne hapla is reported to
increase the virulence of F. oxysporum f. sp. medicaginis. The clover root curculio, Sitona hispidulus, increased the severity of Fusarium wilt in greenhouse
experiments.
Disease is favored by high soil temperatures. Variable soil moisture is not considered an important factor in disease development.
Distribution.
Wherever alfalfa is grown but Fusarium wilt is more severe in tropical and semitropical alfalfagrowing areas of the world.
Symptoms.
Fusarium wilt occurs in irregularsized and shaped areas within a field; however, only a small percentage of plants in the affected area display symptoms at one time.
The greatest loss occurs approximately 2 years after stand establishment. Scattered plants continue to wilt and die throughout a field the remaining years of the stand.
Plants that have been affected by wilt, but have not died, will be dwarfed or stunted.
The first symptom is a rapid wilting of stems on one side of a diseased plant. Later, stems and leaves appear chlorotic or bleached. Leaves at the bottom of the stem
often are a light pink. Tips of stems wilt during hot days or periods of soil moisture deficiency but recover during cool nights or when soil moisture is replenished.
Plants die slowly, often over a period of several months. Frequently leaves of diseased plants become dry and brittle but retain their green color and somewhat
resemble the leaves of freshly cut hay.
The interior of a diseased taproot is a cinnamon brown to red color that is often apparent only as streaks in the woody area. As the disease progresses, the entire
outer portion of the woody cylinder becomes a light brown to redbrown discolored rot that extends from the crown into the taproot.
Management.
There is no satisfactory management. Individual plants have been reported to have some resistance. Seedlings inoculated with vesiculararbuscular mycorrhizal fungi
had a lower incidence of wilt than nonmycorrhizal plants.

Page 15
Lepto Leaf Spot
Lepto leaf spot is also called Leptosphaerulina leaf spot, halo spot, pepper spot, brown leaf spot, and Pseudoplea leaf spot.
Cause.
Leptosphaerulina trifolii (syn. L. briosiana, Pleosphaerulina briosiana, Pseudoplea briosiana, and Pseudoplea medicaginis) overwinters as mycelia and
pseudothecia in infested leaves on the soil surface. During cool, moist weather, spores are discharged from pseudothecia and disseminated by wind to young leaves.
Optimum germination occurs at temperatures of 22° to 25°C in the laboratory. Following moist weather, leaf spot is most severe on young leaves that have grown
back after the first cutting.
Distribution.
Symptoms.
At first, numerous small, reddishbrown flecks appear on both leaf surfaces and the petioles. The flecks enlarge to spots that have a tan center surrounded by an
irregular brown border and halo. Optimum lesion development is reported to occur under high light conditions. Diseased leaves eventually die and become necrotic
but continue to cling to the stem. On older growth, the upper leaves become infected and have typical symptoms but seldom die.
Management.
Effective management measures are not known; however, the following may reduce disease incidence and severity:
1. Grow cultivars that are reported to have some disease resistance.
2. Sow certified diseasefree seed.
3. Cut plants in the prebloom plant stage.
4. Rotate alfalfa with a resistant host, such as soybean, maize or a small grain, for at least 2 years.
5. The fungicides benomyl, copper hydroxide, and mancozeb were effective in reducing disease severity under experimental conditions.
Marasmius Root Rot
Cause.
Marasmius sp.
Distribution.
Egypt.
Symptoms.
In greenhouse pathogenicity tests, roots are brown and watersoaked. Marasmius sp. grows in ropelike strands over the entire root system. Diseased plants are
killed in the field.
Management.
Not reported.
Mycoleptodiscus Crown and Root Rot
Cause.
Mycoleptodiscus terrestris (syn. Leptodiscus terrestris) overwinters as sclerotia in infested residue and soil. Conidia form in summer and are dissem

Page 16
inated by wind to plant hosts when they are forcibly ejected from the fruiting structure, called an acervulus, by setae that unfold as mucilage dries out. Disease is
favored by warm, humid weather.
Distribution.
The central and eastern United States.
Symptoms.
Preemergence and postemergence damping off occurs. A brown to black rot occurs in lateral roots, taproots, and crowns of older plants. The margin of decayed
tissue is black while tissue behind the margin is lighter in color. Numerous sclerotia are formed in decayed tissue. Small spots develop on leaves; reddishbrown lesions
that occur on stems develop into crown rot.
Management.
Not reported.
Myrothecium Root Rot
Cause.
Myrothecium roridum and M. verrucaria. Mycelia penetrate intact roots but will enter through wounds in some situations.
Distribution.
The United States (Pennsylvania and Wisconsin); however, Myrothecium root rot is probably more widely distributed.
Symptoms.
In laboratory tests, brown, watersoaked rots with poorly delineated margins were initially evident on roots. Root growth, in general, was inhibited. In other
greenhouse tests, entire diseased roots had a dark brown rot with occasional streaks that extended upward in the vascular system. However, rotted roots remained
firm and were not watersoaked. Foliar symptoms were chlorosis; purpling of leaflet margins; leaf curling, mottling, and stunting; and death of diseased leaves and
petioles.
Management.
Not reported.
Oidiopsis Powdery Mildew
Cause.
Oidiopsis sp.
Distribution.
Asia, Brazil, and Egypt.
Symptoms.
Initially, white, powdery patches occur on the underside of leaflets. Eventually, the whole leaf is involved and becomes necrotic when disease becomes severe.
Management.
Not reported.
Oidium Powdery Mildew
Cause.
Oidium sp. is the conidial stage of many species in the Erysiphaceae.
Distribution.
The United States (Hawaii).

Page 17
Symptoms.
Not well known, but a symptom is generally presumed to be the typical white to gray "powderish" appearance on upper leaflet surfaces.
Management.
Not reported.
Phoma Root Rot
Phoma root rot is the root rot phase of spring black stem.
Cause.
Phoma medicaginis (syn. Ascochyta imperfecta, P. herbarum f. medicaginum, and P. medicaginis var. medicaginis) overwinters as pycnidia in infested residue
and is seedborne as mycelia on the seed coat. Pycnidia are produced on lesions of diseased tissue in late summer and autumn but rarely during the growing season.
Spores, which are produced in pycnidia in the spring during wet weather and temperatures of 18° to 24°C, are disseminated by wind.
Some researchers have reported that wounds are not required for fungal entry into the roots but more extensive rot occurred when roots were wounded than not
wounded. However, others report wounding is necessary for infection. Stem stubble provides a suitable infection court for the pathogen to invade crown tissues.
Inoculations caused larger lesions on lateral roots than on diseased main roots.
Distribution.
Not reported, but the disease is presumably widespread.
Symptoms.
Main and lateral roots have a black, dry necrosis and eventually disintegrate. Dry weight of foliage and roots is reduced.
Management.
Not reported.
Phymatotrichum Root Rot
This disease is also called cotton root rot, Ozonium root rot, and Texas root rot.
Cause.
Phymatotrichopsis omnivora (syn. Phymatotrichum omnivora, P. omnivorum, and Ozonium omnivorum) survives, primarily in alkaline soils, as sclerotia and
brown sclerotial strands to depths of 2 m in the soil. Sclerotia germinate in early summer when soil temperatures are high and infect roots. Low soil temperatures will
kill the fungus. Conidia are produced on spore mats formed on the soil surface, particularly after a summer rain or during humid weather; however, they are not
thought to be important either in infection or dissemination.
Distribution.
Mexico and the southwestern United States.
Symptoms.
Infested areas within a field may appear as circles of dead plants, but alfalfa in the center of the circle may not be diseased. If alfalfa is diseased, dead plants are
replaced by grasses. Lesions on the taproots are yel

Page 18
low to brown, sunken, and clearly defined, although irregularshaped. Leaves of diseased plants become chlorotic and bronze. Eventually, diseased plants wilt and die
if lesions encircle the root or crown. Irregularshaped, white to tan spore mats sometimes appear on the soil surface.
Management
1. Plow under green manure crops or animal manure.
2. Grow resistant crops, such as a grass, for at least 3 years. However, if sclerotia persist for a long time, this management measure is relatively ineffective.
3. Add sodium salts to soil. This helps to reduce disease severity.
4. Grow cultivars whose plants vigorously produce new roots. These cultivars have some tolerance to the disease.
Phytophthora Root Rot
Phytophthora root rot is also called wet foot disease.
Cause.
Phytophthora megasperma f. sp. medicaginis. In some literature, P. medicaginis and P. megasperma have been referred to synonymously with P. megasperma
f. sp. medicaginis, but Farr et al. (1989) do not consider them to be synonyms. Phytophthora drechsleri and P. cryptogea have also been reported as causal fungi.
Additionally, P. sojae f. sp. medicaginis has been ascribed to be a causal fungus, but a report based on mitochondrial DNA relatedness indicates that the alfalfa
Phytophthora is not related to P. sojae, which is specific to soybean.
Survival is primarily by oospores in infested residue and soil. Mycelia in residue and chlamydospores have also been reported to be survival mechanisms; however,
only oospores are capable of longterm survival. Hyphae from diseased alfalfa plants grow through soil to colonize roots of other plants including black medic,
birdsfoot trefoil, and maize. These plant colonizations increase survival potential and serve as sources of inoculum to infect alfalfa.
Eventually oospores, chlamydospores, and sporogenous hyphae are produced in diseased tissue. In the presence of moisture, sporogenous hyphae bear sporangia
that germinate directly, forming either mycelia or sporangia, or indirectly, producing zoospores, at temperatures of 24° to 27°C. Infection occurs at the tips of small
roots and the bases of fine lateral roots.
Watersaturated soil predisposes roots to infection by increasing root damage. More damage increases the exudation of nutrients, which, subsequently, increases the
chemolactic attraction of zoospores to the roots. Root rot is more severe when susceptible plants are also infected with the nematode Meloidogyne hapla at 28°C
(the optimum temperature).
The optimum growth of a hightemperature cultivar of P. medicaginis

Page 19
from the desert areas of the southwestern United States (designated as cultivar HTI and reported as P. megasperma) occurs at temperatures of 27° to 33°C. In
South Africa, P. drechsleri has been isolated from alfalfa roots with symptoms similar to those caused by P. medicaginis.
Distribution.
Canada and the north central and eastern United States. Phytophthora drechsleri was reported from South Africa.
Symptoms.
Symptoms occur in wet soils. Seeds and seedlings damp off. Leaves become chlorotic or reddish and defoliate from diseased plants. Eventually plants become
stunted, wilt, and die.
Rootlets and taproots are rotted. There is a sharp line that delineates diseased from healthy tissue on roots. Such diseased tissue can occur on the taproot at any depth
below the soil line. The taproot itself may be rotted off at any depth below the crown and has a yellowishbrown discoloration that eventually becomes black.
Rot stops as soils dry and if enough taproot remains alive, side roots are produced and the plant remains alive. Such plants have a shallow root system and produce
abundant forage when surface moisture is plentiful, but little or no forage when surface moisture is depleted.
Management
2. Improve water drainage in soils that tend to be poorly drained.
3. Coating seed with Bacillus cereus significantly increased emergence.
Powdery Mildew
Cause.
Erysiphe polygoni.
Distribution.
Italy and the United States (Massachusetts and Wyoming).
Symptoms.
Typical white to gray, powderlike growths that consist of conidia, conidiophores, and mycelia occur primarily on the upper surfaces of diseased leaflets.
Management.
Not reported.
Rhizoctonia Foliage Blight
Rhizoctonia foliage blight is also called web blight.
Cause.
Rhizoctonia solani AG1 IB survives by forming sclerotia or by growing saprophytically on plant residue. During high temperatures and abundant moisture—
conditions that are frequently found in thick stands of alfalfa—mycelia grow from a precolonized substrate to infect crowns or stems just below the soil line. Sclerotia,
infested residue, and soil that contains propagules of R. solani may be splashed onto the plant foliage. During flooding or irrigation, host plants are infected above the
soil line.

Page 20
Distribution.
Wherever alfalfa is grown in hot, humid weather; however, the disease is seldom severe.
Symptoms.
Rhizoctonia foliage blight is a progression of Rhizoctonia stem blight. Lower leaves and stems are initially affected but the disease may eventually progress halfway up
the plant. Diseased leaves appear watery and "bluish" in color. Eventually, leaves wilt, become brown, and shrivel. A weblike growth of fungus mycelia may be seen
growing over shriveled leaves and stems.
Management.
Increase air movement by proper grazing or by cutting to allow stems to dry out.
Rhizoctonia Root Rot
Rhizoctonia rot is also called Rhizoctonia root rot canker and black root canker.
Cause.
Rhizoctonia solani AG4 survives by forming sclerotia or by growing saprophytically in plant residue. During periods of high temperatures and moisture, R. solani
infects the areas where the lateral roots emerge from the taproot, and the taproot itself.
Distribution.
Australia, Iran, and the irrigated areas of the United States (Arizona and California).
Symptoms.
Affected areas in a field are circular to irregularshaped and have healthy plants next to diseased plants that are wilting. Taproots are covered by a large number of
cankers that are oval to round (612 mm in diameter) and vary in color from yellow to tan, often with a slightly darker border. Taproots may be girdled, but plants are
damaged most by cankers formed on the crowns. When soil temperatures decrease during the winter, diseased areas heal and lesions or cankers turn dark brown to
black.
Management.
Growers in irrigated areas of the southwestern United States have reestablished stands by resowing infested fields in October or November.
Rhizoctonia Stem Blight
Rhizoctonia stem blight is also called Rhizoctonia blight and stem canker.
Cause.
Rhizoctonia solani AG4 survives by forming sclerotia or by growing saprophytically in plant residue. During high temperatures and moisture, mycelia that originate
from a precolonized substrate will infect crowns or stems just below the soil line. Sclerotia, infested residue, and soil containing propagules of R. solani may be
splashed onto the plant foliage and stems. During flooding or irrigation, plants are infected above the soil line.
Distribution.

Page 21
Symptoms.
Dead stems are scattered throughout a stand. Sunken cankers found at the base of diseased stems vary in color from tan to reddish brown to dark brown. Stems are
girdled, causing leaves and tips of stems to yellow and wilt.
Management
1. Sow certified, highquality seed in a wellprepared seedbed with good drainage.
2. Proper mowing and grazing practices are effective means of partially managing the disease since the drying effects of direct sunlight and good air circulation retard
disease development.
Rhizopus Sprout Rot
Cause.
Rhizopus stolonifer. This is the common ubiquitous bread mold fungus.
Distribution.
Potentially any place where alfalfa is grown for sprouts. It is more common on trays or screens than in vats.
Symptoms.
Diseased tissue is soft and translucent. Coarse gray to brown, "cottony" mycelia with large, black sporangia develop in rotted areas.
Management
1. Practice good sanitation.
2. Avoid injuring plants.
3. Change to a vat system.
Root and Crown Rot Complex
This disease complex is sometimes called crown rot.
Cause.
Several bacteria and fungi, including Cylindrocladium crotalariae, Erwinia amylovora var. alfalfae, Flexibacter sp., Fusarium acuminatum, F. avenaceum, F.
solani, F. tricinctum, F. oxysporum, Myrothecium spp., Phoma medicaginis, Pseudomonas marginalis var. alfalfae, Rhizoctonia solani, Serratia
marcescens, and Thielaviopsis basicola.
These fungi and bacteria normally persist either as saprophytes or as resting structures in plant residue and soil. Cutting alfalfa for hay or an injury by machinery, frost,
insects, and animals causes a small portion of stem to be killed, thus allowing bacteria and propagules of saprophytic fungi to begin growing on the dead tissue.
Infection spreads down the dead cut stem into the crown.
Distribution.
Symptoms.
The crowns of most alfalfa plants 1 year old or older may be rotted and have a brown to black discoloration interspersed with live tissue. Tissue that produces crown
buds is often killed, resulting in a plant with

Page 22
few live stems. Because crown rot progresses slowly for a number of years after the disease is initiated, there is a gradual thinning of the stand from year to year.
Management
1. The last cutting of alfalfa should be timed to allow the plant to build up a large enough supply of carbohydrates to overwinter successfully.
2. Grow cultivars adapted to an area.
3. Use good management, fertilize properly, and adjust soil pH between 6.2 and 7.0.
4. Avoid placing livestock in an alfalfa field after the last cutting because wounded crowns provide an entrance for pathogens to grow into the crown.
Rust
Cause.
Uromyces striatus (syn. U. medicaginis, U. oblongus, and U. striatus var. medicaginis). In warmer alfalfagrowing areas of North America, U. striatus survives
as urediniospores and perennial, systemic mycelia in infected plants. Uromyces striatus is capable of surviving and reproducing on a large number of plant species in
the tribes Cicereae, Galegeae, Genisteae, Hedysareae, Trifolieae, and Vicieae.
In the summer, urediniospores are disseminated by wind to northern alfalfagrowing areas where healthy plants are infected during periods of high humidity. Reported
optimum temperatures for disease development vary. Some researchers reported that infection occurred at 21° to 30°C; however, in Iowa, infection efficiency was
greater at 17.5°C than at 28.0°C. In the midwestern United States, rust may build up on plant regrowth in the autumn and on unharvested alfalfa in fencerows.
Uromyces striatus is a heteroecious rust with the presence of the aecial and pycnial stages reported on Euphorbia species in Europe and Canada. Only the uredinial
and telial stages have been reported on alfalfa in the United States.
Distribution.
Wherever alfalfa is grown under warm or temperate conditions; however, rust is most prevalent later in the summer and autumn.
Symptoms.
Rust may cause severe defoliation late in the growing season if harvest is delayed or stands are held for seed production. Autumnsown stands may be weakened,
thinned or lost due to winter injury.
Uredinial pustules are reddish brown and sometimes are surrounded by a yellow halo. Pustules are most abundant on the undersides of leaflets but also occur on
petioles and stems. Rusted leaves yellow, shrivel, and defoliate prematurely or are more likely to be injured by an early frost than are healthy leaves.
Aecia develop on leaves and stems of Euphorbia species and may kill stem apices. Witches' brooms and hypertrophy may occur on stems.

Page 23
Management
1. Grow the most resistant cultivars.
2. Harvest on time to reduce leaf loss and remove inoculum.
Sclerotinia Crown and Stem Rot
Cause.
Sclerotinia sclerotiorum and S. trifoliorum. Sclerotinia trifoliorum is more widespread and is the better known of the two pathogens on alfalfa.
Sclerotinia sclerotiorum survives as sclerotia in infested residue and on the soil surface. Sclerotia germinate during cool, wet weather in the spring and early summer
to produce either apothecia or mycelia that infect crowns, leaves, and stems. Pollen also becomes infected by ascospores, which suggests that pollen may play a
significant role in the epidemiology of blossom blight in alfalfa, especially in seedgrowing areas. Sclerotia are produced on the host surfaces, in the pith, and under
decaying plant parts on the soil surface. Disease is most severe in fields where infested residue remains on the soil surface from the last harvest.
Sclerotinia trifoliorum survives during the winter and high summer temperatures as sclerotia on the soil surface, imbedded in diseased stems and crowns, and
adhering to the plant surface. During cool, wet weather in the growing season, sclerotia germinate to form mycelial strands or apothecia in which asci and ascospores
are produced. However, most primary infection of alfalfa has been reported to occur in the late autumn and early winter when oversummered sclerotia in soil
germinate to form apothecia. Ascospores are then disseminated by wind to host plants, where they infect crowns, leaves, and stems. Pollen grains can also become
infected and cause blossom blight, similar to S. sclerotiorum.
Subsequent disease development then occurs from winter through early spring in most locations. From midwinter through early spring, growth of mycelia commences
within and between host plants; however, mycelia grow only a short distance in soil and normally do not cause infection.
Disease is favored by frequent rainfall, prolonged high humidity, and mild temperatures during winter months. Disease is especially severe when alfalfa is sown into
untilled sod in which numerous alternative hosts for S. trifoliorum are growing.
Distribution.
Cool, humid areas of Europe and North America. Sclerotinia trifoliorum is more widespread on alfalfa than S. sclerotiorum and is found primarily in the South
central and southeastern United States. Sclerotinia sclerotiorum has been reported mainly as a pathogen during the summer months in Canada, the Pacific
Northwest, and the state of Georgia in the United States.
Symptoms.
Symptoms caused by the two fungi are similar and appear at the same time in early spring. Sclerotinia crown and stem rot is most destruc

Page 24
tive on new seedlings and can be recognized by small circular patches of dead or dying plants within a field. The first symptoms occur in the autumn as small brown
spots on diseased leaves and stems. Eventually, spots expand and diseased leaves and stems wilt and die. The fungus then spreads to the crown, where disease is
most destructive the following spring when the crown becomes soft and has a graygreen discoloration. A white, ''fluffy" mass of mycelia, in which small, black
sclerotia are formed, grow over dead plant parts.
Sclerotinia trifoliorum may cause extensive or complete loss of stands particularly on firstyear, autumnsown crops.
Management
1. Rotate alfalfa with a resistant host. Do not grow alfalfa for 3 years.
2. Plow under residue to bury sclerotia.
3. Sow seed that is free of sclerotia.
4. Autumn or winter burning of stubble reduces numbers of sclerotia of S. sclerotiorum, thereby reducing incidence and severity of disease. Autumn burning has been
reported to be more effective in southeastern Washington in reducing the numbers of sclerotia in the dense layer of surface plant residue and in the surface soil at
depths of 0 to 2 cm.
5. Sow in spring because mature plants are relatively resistant.
6. Grow the least susceptible cultivar. No cultivar is completely resistant or tolerant to disease.
Southern Blight
Southern blight is also called Sclerotium blight.
Cause.
Sclerotium rolfsii survives for several years in the soil or in plant residue as small, brown sclerotia that are disseminated by water and wind. Sclerotia germinate under
hot, humid conditions to form mycelial strands that infect plants. Southern blight is not an important disease of alfalfa except in some silty or sandy soils.
Distribution.
Southern Europe and the southern alfalfagrowing areas of the United States.
Symptoms.
From a distance, the symptoms of southern blight within a field appear as scattered patches of dead plants. Plants are bleached to a light tan color and have a white,
cottonlike mycelial growth on stems near the soil surface. Numerous small, tan to brown sclerotia that resemble "seeds" are formed in mycelia growing on diseased
stems, crowns, and infested residue on the soil surface.
Management
1. Plow under infested residue.
2. Practice proper mowing and grazing. The causal fungus does not grow well when exposed to direct sunlight and air movement.

Page 25
Spring Black Stem
Spring black stem is also called Ascochyta leaf spot and spring leaf spot.
Cause.
Phoma medicaginis (syn. P. herbarum f. medicaginum and Ascochyta imperfecta) overwinters as pycnidia in infested tissue and as mycelia on the seed coat.
Spores are produced in the spring during wet weather and temperatures of 18° to 24°C and are disseminated by wind to host plants. Pycnidia are produced on
lesions of diseased tissue in late summer and autumn but rarely during the growing season.
Distribution.
Europe, North America, and South America. Spring black stem is normally not present on firstyear alfalfa unless the fungus was seedborne or spores were
disseminated from nearby fields by wind.
Symptoms.
Yield losses caused by spring black stem are due primarily to defoliation of the first cutting of hay. Disease may also be extensive during the autumn, but symptoms
are less pronounced.
The most severe disease symptoms occur on lower leaves, but upper leaves may also be diseased. Diseased leaves have dark brown or black spots with irregular
borders that enlarge and merge to cover most of the leaf area. Leaves eventually become chlorotic and defoliate.
Stem and petiole lesions initially are dark green and watery. Lesions then become dark brown to nearly black and have a "wateryappearing" margin. Stem lesions
enlarge and merge until most of the lower stem is blackened. Young shoots are often girdled and killed, and the fungus may grow into the crown and upper root.
Seedpods may discolor and shrivel during wet, humid conditions.
Management
1. Harvest hay before defoliation is severe. This also allows plants to dry out, making fungal sporulation and infection more difficult.
2. Plow under plants in cases of severe disease.
3. Treat seed with a fungicide to prevent seedborne introduction of the disease.
4. Sow seed produced in an arid area.
5. Grow moderately resistant cultivars. Highly resistant cultivars are not available.
Stagonospora Leaf Spot
Cause.
Stagonospora meliloti is one of three phases of the same fungus on alfalfa and other clovers. Stagonospora meliloti is associated mainly with the leaf spot phase
during the summer. Phoma meliloti has been reported as one of the causal agents of the root rot phase and is found as pycnidia produced on stems during low
autumn temperatures. Farr et al. (1989) consider P. meliloti to be a synamorph of S. meliloti. The teleomorph, Leptosphaeria pratensis, is found as perithecia on
stems in the spring and occasionally in the late autumn.

Page 26
The fungi overwinter only in residue as mycelia and pycnidia of S. meliloti and perithecia of L. pratensis. During wet spring weather, conidia are extruded from
pycnidia and disseminated by rain and irrigation water and infrequently by wind to serve as primary inoculum. Secondary spread is also by conidia during wet summer
conditions. Pycnidia of S. meliloti are produced on residue later in the growing season. Little is known about the role of the perithecial stage in the epidemiology of
Stagonospora leaf spot.
Distribution.
Widespread, but Stagonospora leaf spot is most common in warm, humid areas or where alfalfa is grown under irrigation.
Symptoms.
Spots on leaves and stems are 3 to 6 mm in diameter and circular to irregularshaped. The spot is pale buff to almost white in the center and has a light to dark brown
diffuse margin. In some instances, spots have faint concentric zones the same color as the margin. Diseased leaves defoliate soon after spots form. Pycnidia, which
appear as small, dark specks, are scattered throughout the older spots.
Management
1. Rotate with a resistant host for 2 to 3 years.
Stagonospora Root Rot
This disease is sometimes called Stagonospora crown and root rot.
Cause.
Stagonospora meliloti, teleomorph Leptosphaeria pratensis. Phoma meliloti is also reported as a cause and Farr et al. (1989) consider P. meliloti to be a
synamorph of S. meliloti. Stagonospora meliloti is associated mainly with the leaf spot phase during the summer.
The fungi overwinter only in residue as mycelia and pycnidia of S. meliloti and possibly P. meliloti and as perithecia of L. pratensis, although little is known about the
role of the perithecial stage in the epidemiology of Stagonospora root rot. During wet spring weather, conidia are extruded from pycnidia and disseminated to host
plants by rain or irrigation water and infrequently by wind. Secondary spread is also by conidia during wet conditions. The root rot phase develops slowly, over 2 to 3
years at 15° to 25°C, from stem and crown infections. Pycnidia of P. meliloti are produced on stems during low autumn temperatures; pycnidia of S. meliloti are
produced on residue later in the growing season.
Distribution.
Symptoms.
A brown to black rot of the taproot and crown are common symptoms. Lesions on the taproot are reported to occur 7.2512.50 cm below the crown. Lesions on
roots and crowns are cracked and irregular in shape. Lengthwise sections through rotted areas show affected bark and xylem tissue with bright, reddishbrown flecks.

Page 27
Management
1. Rotate with a resistant plant host for 2 to 3 years.
Stemphylium Leaf Spot
Stemphylium leaf spot is also called target spot.
Cause.
Stemphylium alfalfae, teleomorph Pleospora alfalfae; S. botryosum, teleomorph P. tarda; S. globuliferum, teleomorph Pleospora sp.; S. herbarum, teleomorph
P. herbarum; and S. vesicarium, teleomorph Pleospora spp.
Overwintering is by mycelia in infested residue and on seed, and as perithecia in residue. Spores are produced during moist weather at any time of the growing season
and are disseminated by wind to leaves of host plants. Stemphylium botryosum is divided into two biotypes: A warmtemperature (WT) biotype and a cool
temperature (CT) biotype. Temperature requirements for disease development depend upon the fungal biotype. Disease caused by the WT biotype occurs at
temperatures of 23° to 27°C, while disease caused by the CT biotype is most severe at temperatures of 8° to 16°C. Under greenhouse conditions, disease also is
severe when plants are exposed to light before and after inoculation, followed by alternating dark and light periods and extended free moisture for several days.
Disease is most severe on dense foliage during late summer and autumn but can occur throughout the growing season.
A Stemphyliumincited disease in Australia and South Africa has been attributed to a fungus that more closely resembles S. vesicarium than S. botryosum.
Stemphylium vesicarium is seedborne; seed becomes infected in either wet or dry climates. Disease caused by this Stemphylium is more common during cooler
weather.
Distribution.
Africa, Australia, Europe, New Zealand, and the United States, particularly the southeastern United States. The warmtemperature (WT) biotype occurs in central
and eastern North America during warm, wet periods; the cooltemperature (CT) biotype occurs in California during cool, wet springs.
Symptoms.
The WT biotype produces oval or circular, slightly sunken, light brown leaf spots with dark brown borders that are surrounded by a pale yellow halo. Spots enlarge
and form concentric light and dark brown zones to somewhat resemble a target. During wet weather, older lesions appear sooty from the abundant production of large
spores within the lesion. Severe defoliation may occur. A single large lesion may cause a leaf to become chlorotic and defoliate prematurely.
Black areas may appear on peduncles, petioles, and stems. Girdling of stems and petioles in wet weather causes foliage to wilt and die.
Symptoms of the CT biotype are common in the interior valleys of Cal

Page 28
ifornia but occur throughout the year along the coast. The CT biotype produces elongate lesions, of various sizes but seldom exceeding 3 to 4 mm, that cease to
expand once the border is formed. Lesions have irregular outlines and light tan, almost white, centers with dark brown borders. Premature defoliation is unusual.
Stemphylium vesicarium is reported to cause symptoms similar to the CT biotype during cooler weather in Queensland, Australia. Only leaflets on actively growing
shoots are affected. The Australian S. vesicarium causes circular to irregularshaped leaf lesions with white to cream centers surrounded by a sharply defined dark
brown margin. On susceptible cultivars, spots coalesce to cause a leaf blight.
Symptoms caused by S. vesicarium reported from South Africa also differ with temperature. In warm areas under overhead irrigation, lesions are irregular or circular
to ovalshaped (0.13.0 mm in diameter); are light to dark brown and often are lighter in the center, which sometimes results in a concentrically zonate or target effect;
and have diffuse margins that are frequently surrounded by lightercolored halos. In cooler areas, lesions are circular to oval (0.12.0 mm in diameter) but uniformly
white or tan with a distinct black margin. Elongated black lesions up to 2 mm long occur on petioles and stems. Under both temperature regimes, lesions are usually
distinct but may later coalesce. Defoliation may occur.
Symptoms on annual Medicago vary from black specks to spots (1.02.0 mm in diameter) with tan centers and irregular brown margins.
Management
1. Grow the most resistant cultivar. No cultivar is highly resistant. In Australia the nondormant cultivars are most susceptible.
2. Harvest stands early to save foliage and allow plants to dry out.
Summer Black Stem
Summer black stem is also called Cercospora leaf spot and Cercospora black stem.
Cause.
Cercospora medicaginis overwinters as mycelia in infested residue and is seedborne in warm and humid alfalfagrowing areas but not under other conditions. During
warm, moist weather later in the growing season, spores are produced that are disseminated by wind and rain to host plants. Secondary spread of conidia occurs as
plants grow taller and form a natural humidity chamber that prevents conidia from drying out.
Distribution.
Africa, Asia, Europe, South America, and the central and eastern United States.
Symptoms.
Summer black stem symptoms appear during hot, moist periods late in the growing season. Initially, small, brown spots that occur on both leaf surfaces enlarge to
circular lesions (36 mm in diameter) and turn a

Page 29
reddish to smoky brown color. Frequently, only one or two lesions will develop on a leaflet. During moist weather, lesions appear ashy gray due to sporulation on the
lesion surface. During severe disease, entire leaflets die and defoliation occurs.
The leaf spot phase is followed by the appearance of reddish to chocolate brown, elliptical or linear lesions on diseased petioles and stems. These lesions eventually
enlarge and coalesce. Under moist conditions, the entire stem may be discolored. Smaller peduncles, petioles, and stems may die, resulting in further defoliation and
loss of seed.
Summer black stem is most damaging when harvesting is delayed.
Management
1. Grow the most resistant cultivar.
2. Harvest hay when plants are in early bloom stage to reduce defoliation and allow foliage to dry out.
3. Do not allow cattle to graze on fields late in season since disease is more severe in second year stands that do not complete growth before dormancy.
Verticillium Wilt
Cause.
Verticillium alboatrum (dark mycelial species) overwinters as thickwalled mycelia in soil, live alfalfa plants, infested residue, and parasitized weeds, and is internally
seedborne. Verticillium alboatrum has a limited saprophytic ability and does not survive well in dead plant tissue that becomes colonized by more aggressive
saprophytes. Under humid conditions, the fungus will colonize the pod and seed coat, but it does not survive long on the outside of seed. Pollen can be infected in
vitro.
During cool, moist weather, conidia are initially produced on diseased leaflets, petioles, stipules, and stubble remaining from last seasons harvest. Eventually, conidial
sporulation also occurs on diseased stems. Stubble is an effective source of inoculum only before it decomposes.
Dissemination is by any means that moves infested plant residue. A unique means of dissemination between fields utilizes the sclerotia of Sclerotinia sclerotiorum,
which are colonized by V. alboatrum. Because sclerotia are approximately the same size as alfalfa seed, they are present in cleaned and sized alfalfa seed lots and
disseminate V. alboatrum from seed fields to other fields. Secondary spread during the growing season is by harvest machinery, windborne conidia, and plant debris.
A combination of wet conditions and ideal air currents results in significant dispersal of conidia for a short time after harvest and before healing of the cut stem occurs.
Some evidence suggests, however, that airborne conidia do not cause systemic infections through penetration of uninjured leaf and stem tissues. Further evidence
suggests that inoculum carried on the cutter bar, rather than airborne conidia, is the most important means of dispersal within and be

Page 30
tween fields. Longrange dissemination of V. alboatrum may be by internal seedborne inoculum.
Under laboratory conditions, several insects have been implicated in dissemination. Grasshoppers, Melanophus sanquinipes and M. bivittatus; alfalfa weevils,
Hypera postica; and woolly bears, Apantesis blakei, were fed diseased alfalfa leaves. The fungus was able to safely pass through their digestive systems and was
detected in feces about 1 day after feeding. Fungus gnats, Bradysia impatiens, disseminate V. alboatrum in the greenhouse, and the leafcutter bee, Megachile
rotundata, disseminates the fungus in the field. The pea aphid, Acyrthosiphon pisum, is a vector by carrying spores as a surface contaminant on its legs and
antennae. Verticillium alboatrum has been reported to pass through the digestive tract of sheep, which affords another means of spread.
Plants are infected through the roots. Mycelia grow into the xylem tissues, where conidia are produced that spread upward within the xylem tissue of the plant. The
fungus is present only in xylem elements of diseased stems. Fungus and vascular occlusions eventually plug the xylem tissue, preventing movement of water up the plant
and causing wilt symptoms. Optimum growth of V. alboatrum occurs at temperatures of 19° to 25°C.
The alfalfa strain V. alboatrum is known to only infect alfalfa. Verticillium dahliae (microsclerotial species) occasionally causes similar symptoms on alfalfa in
England, but it is less virulent.
Distribution.
Canada, Europe, and the United States, primarily the Pacific Northwest.
Symptoms.
Fewer symptoms are present during drought stress than during nondroughtstressed conditions. The first symptom is a "flagging" or wilting of the upper leaves on
warm days. Initially, Vshaped, pinkishorange to brown areas occur on leaflets. Leaflets on severely diseased shoots become necrotic and twisted, forming spirals.
Lower leaves eventually wilt, become yellow to white, and die.
New shoots develop from the crown, but they also become diseased and die. Entire plants become stunted and have dead, yellow stems. Frequently, stems remain
green but attached leaves are bleached and dead. Conidiophores cover the bases of infected stems and give them a grayish appearance. When the stem dies, the
infected area becomes black.
In advanced stages of the disease, plants are stunted and have yellow and desiccated shoots and leaves. Xylem tissue is brown and frequently the discoloration can be
traced from the taproot up into the stems. This symptom can be confused with both bacterial and Fusarium wilts. Flowering may be suppressed.
A high percentage of plants in some resistant cultivars are symptomless carriers of the pathogen, but plant height, dry weight, and flowering are affected. Stem dry
weight is less affected by V. alboatrum. Up to 50% re

Page 31
duction in yield can occur in susceptible plants by the end of the second year.
Verticillium alboatrum is often confined only to the midrib and lateral veins of infected leaflets. This pattern prevails even after browning and death of an entire
leaflet because the fungus is confined to xylem tissue. There is often a discontinuous pattern in the midrib of symptomed and symptomless leaflets due to the movement
of spores within the xylem and their eventual germination within the xylem tissue.
Management
2. Sow seed that is free of plant debris and has been treated with a fungicide seed protectant.
3. Harvest the youngest stands first.
4. Clean equipment before leaving an infested field.
5. Seedlings inoculated with vesiculararbuscular mycorrhizal fungi are reported to have a lower incidence of wilt than nonmycorrhizal seedlings.
Violet Root Rot
Cause.
Rhizoctonia crocorum (syn. R. violaceae), teleomorph Helicobasidium brebissonii, survives in soil as sclerotia or as a saprophyte in infested residue. Infection is
most common when moisture is present in low organic matter soils, but disease may also occur in high organic soils.
Distribution.
Europe and infrequently in the United States.
Symptoms.
Symptoms occur in midsummer as circular patterns associated with low, flooded areas within a field and as individual plants in older stands that have other root
injuries. Diseased plants in an area are brown, in contrast to surrounding green plants. Diseased roots are brown on the inside and covered with thick mats of violet to
cinnamon mycelia that extend 20 or more cm below the soil surface. Later, roots are rotted and shredded and have a brown to dark violet discoloration. Barely
visible, tiny, black sclerotia are seen on diseased roots.
Management
1. Grow alfalfa in welldrained soil.
2. Harvest hay in prebloom stage.
3. Rotate alfalfa with resistant crops, such as small grains and corn.
Winter Crown Rot
Winter crown rot is also called Coprinus snow mold and snow mold.
Cause.
Coprinus psychromorbidus. However, in some reports C. urticicola has been tentatively identified as the causal organism. If two organisms are involved, this may
account for the differences in temperature for optimum

Page 32
growth in cultures: 12°C according to some reports, and 13° to 15°C according to others.
In the autumn, during conditions favorable for disease development, the fungus grows in close association with alfalfa crowns and produces hydrogen cyanide (HCN),
which is absorbed by crown tissue at temperatures near 0°C. Mycelia invade crown buds in March and destroy the diseased tissue. When temperatures rise above
freezing, alfalfa is no longer susceptible.
Distribution.
Canada (Alberta, British Columbia, Manitoba, and Saskatchewan) and the United States (Alaska).
Symptoms.
Differentsized areas of dead plants occur in a field. Dark brown, rotted areas occur on crowns and infrequently on roots. Often only the crown bud and underlying
tissue is diseased. The taproot may be unaffected even though the crown is dead, but it will eventually be rotted by secondary organisms. Mycelia may grow on the
soil surface in early spring.
Management
1. Grow cultivars that have Medicago falcata parentage.
2. Grow small grains instead of alfalfa in infested soil for a minimum of 3 years.
3. Application of borax to plants in the fall prevents HCN production. However, this treatment is sometimes phytotoxic.
Yellow Leaf Blotch
Cause.
Leptotrochila medicaginis (syn. Pseudopeziza jonesii and Pyrenopeziza medicaginis) overwinters as stromata in residue on the soil surface. During cool, wet
weather in late spring, stromata give rise to apothecia in which ascospores are produced. Ascospores are disseminated by wind to host plants.
Distribution.
Wherever alfalfa is grown in temperate climates.
Symptoms.
Yellow leaf blotch is most severe on the lower diseased leaves in stands of rank, tall plants. Young lesions appear as yellow stripes and blotches that are elongated
parallel to the leaflet veins. As lesions enlarge, they become "fanshaped" or circular and their color changes from yellow to orangeyellow or brown.
Small, dark pycnidia develop mostly on the upper surface of the blotches. Eventually, pseudostromata, and later stromata, form in the center of the blotch, giving it a
dark brown to black color. Stromata are uncommon on the under surface of the leaf until after leaf defoliation. Dead leaves frequently remain attached to the stem for
an extended time, curling downward as they dry. Similar yellow blotches, which later become dark brown, may occur on the stems.

Page 33
Management
1. Cut plants before leaf defoliation becomes severe.
2. Do not leave a high stubble or allow weeds to become a problem.
3. Rotate alfalfa with a resistant host, such as soybean, maize, or a small grain, for at least 2 years.
Alfalfa Stem
Alfalfa stem nematode is sometimes called the bulb and stem nematode.
Cause.
Ditylenchus dipsaci survives for years as larvae in dry hay stems, alfalfa crowns, soil, and other plant hosts. Larvae, which feed and reproduce in shoots near the
crown, move over the plant surface in a film of water and infect plants through stomates. A female nematode lays 75 to 100 eggs; optimum reproduction and infection
are in heavy, wet soils at soil temperatures of 15° to 21° C. Dissemination is by machinery, rain, and irrigation water.
Distribution.
Worldwide.
Symptoms.
Diseased plants are stunted and have a bushy appearance because swollen nodes and shortened internodes result in abnormal proliferation and swollen, short stems.
White stems are scattered throughout a field.
Alfalfa plants growing in weedy, lowlying areas of the field have increased severity of fungal and bacterial rots. Shoots from diseased buds are severely dwarfed and
have buds that are swollen, spongy, and easily detached. A ruined stand and considerable yield loss may occur with 2 to 3 years of disease.
Management
2. Plow under infested stands.
3. Use nematicides where feasible.
4. Rotate alfalfa with other crops for 2 to 3 years.
Cyst
Cause.
Heterodera trifolii.
Distribution.
Not known.
Symptoms.
Lightcolored immature females may be visible on roots. Roots tend to be smaller and have reduced nodulation.
Management.
Not known.

Page 34
Dagger
Cause.
Xiphinema americanum is an ectoparasite.
Distribution.
Widely distributed.
Symptoms.
Root growth is reduced. Necrotic areas occur where feeding has occurred. Cells next to necrotic tissue may enlarge and cause a galllike growth.
Management.
Not known.
Pin
Cause.
Paratylenchus hamatus.
Distribution.
Thought to be widespread.
Symptoms.
Necrotic areas occur on roots.
Management.
Not known.
Reniform
Cause.
Rotylenchulus spp.
Distribution.
Tropical and semitropical areas.
Symptoms.
Enlarged cells occur at the site of nematode feeding. Feeding sites provide entrance for secondary microorganisms, specifically fungi, that may cause necrotic areas.
Management
1. Practice clean tillage.
2. Nematicides are effective where it is practical to use them.
Root Knot
Cause.
Root knot nematodes Meloidogyne arenaria, M. chitwood, (primarily race 2), M. hapla, M. incognita, and M. javanica infect alfalfa that grows in sandy soils. The
second stage, or newly hatched larvae, infect the root tip. Meloidogyne arenaria, M. incognita, and M. javanica do not survive if the temperature averages below
3°C during the coldest month. Meloidogyne hapla is limited by temperatures greater than 27°C.
Distribution.
Widely distributed.
Symptoms.
The top growth of diseased plants is chlorotic and stunted. Roots branch excessively and have galls or knots that vary in size. Bacterial wilt severity may increase.

Page 35
Management
1. Use nematicides in areas of high nematode infestation.
Root Lesion
Cause.
Pratylenchus penetrans is the most important root lesion nematode on alfalfa. Other root lesion nematodes associated with alfalfa are P. crenatus, P. neglectus, P.
coffeae, P. pratensis, and P. vulnus. All life stages except the firststage larva invade roots. The preferred area of infection is root hairs on feeder roots, where
nematodes force their way through or between epidermal and cortical cells. Maximum invasion by males and larvae occurs at temperatures of 10° to 30°C, while
females invade roots at temperatures of 5° to 35°C.
Gravid females deposit eggs in infected root tissue or soil. The second stage larvae emerge. Generation time is 4 to 8 weeks depending upon species.
Distribution.
Wherever alfalfa is grown in the tropical and temperate areas.
Symptoms.
Injury is most severe in sandy and sandy loam soils. Initially, a lesion appears on the root as a watersoaked area that becomes yellow and elliptical. Dark brown cells
later appear in the center of the lesion. Yields and cold tolerance of diseased plants are decreased and infection by Fusarium species is increased.
Management.
Nematicides are effective but impractical.
Spiral
Cause.
Helicotylenchus spp. are ectoparasites.
Distribution.
Widely distributed.
Symptoms.
Necrotic spots occur at feeding sites. Roots may be severely damaged when high nematode populations are present.
Management.
Nematicides control nematodes on some crops.
Stubby Root
Cause.
Paratrichodorus spp.
Distribution.
Not known for certain, but it is presumed Paratrichodorus species are widely spread on alfalfa.
Symptoms.
Symptoms on alfalfa are not well known, but a primary symptom is reduced root growth.
Management.
Not known.

Page 36
Stunt
Cause.
Tylenchorhynchus spp.
Distribution.
Widely distributed.
Symptoms.
The growth of foliage and roots is reduced. Diseased plants may be chlorotic.
Management.
Nematicides have been effective on some crops.
Aster Yellows
Cause.
A phytoplasma transmitted by leafhoppers.
Distribution.
Wherever alfalfa is grown, but aster yellows is not a serious disease of alfalfa.
Symptoms.
Diseased plants are stunted and excessively branched. Flowers are chlorotic and sterile, develop leaflike structures, and remain on the plant rather than being shed at
normal senescence.
Management.
Not reported.
Witches' Broom
Cause.
A phytoplasmalike organism that overwinters in several perennial plants, such as Astragalus, Hedysarum, Lathyrus, Lotus, Medicago, Melilotus, and Trifolium. It
is transmitted by grafting, dodder, and the leafhoppers Orosius argentatus, Scaphytopius actus, and S. dubius.
Distribution.
Australia, North America, Russia, Saudi Arabia, and possibly other semiarid areas where alfalfa is grown.
Symptoms.
An abnormal number of crown buds develop that form thin, short, pale green stems, which give a ''broomlike" appearance to a diseased plant. Leaflets are small and
have a yellowing and crinkling around their edges that give plants a yellowish cast. Flower buds develop slowly and may be green on some plants.
Diseased plants are shortlived and may appear to recover during cool weather in the winter and spring, but recurrent symptoms develop during warm weather and
moisture stress in summer.
Management.
Not reported.
Unknown Phytoplasma Causing a Witches' Broom
This may possibly be the same organism described in the previous Witches' Broom description.

Page 37
Cause.
A phytoplasmalike organism. Pleomorphic bodies, spherical to filamentous in shape and 60 to 650 nm in diameter, were observed in phloem tissue and roots. The
causal organism is transmitted by leafhoppers and sometimes by dodder but is not transmitted mechanically.
Distribution.
South Africa.
Symptoms.
Diseased plants are stunted and have an abnormal proliferation of stems. Leaves are abnormally small and chlorotic. Phyllody and negative geotropism occur.
Management.
Not reported.
Alfalfa Enation
Cause.
Alfalfa enation virus (AEV). AEV is a rhabdovirus that is transmitted in the field by the cowpea aphid, Aphis craccivora, and in the laboratory by grafts.
Distribution.
Eastern and southern Europe and Morocco.
Symptoms.
Diseased leaflets are "crinkled." Enations several millimeters long occur on the underside of the midvein of the crinkled leaflets. Diseased plants may be of normal size
but become "bushy."
Management.
Not reported.
Alfalfa Latent
Alfalfa latent virus is also called pea streak virus.
Cause.
Alfalfa latent virus (ALV) is in the carlavirus group. ALV is transmitted in a nonpersistent manner by the pea aphid, Acyrthosiphon pisum. ALV is also seed
transmitted at a low rate and sap transmitted by machinery during harvesting.
Distribution.
Hungary and the United States (Arizona, Nebraska, and the northwestern United States); however, ALV is presumed to be widespread in most alfalfagrowing areas.
Symptoms.
Diseased plants are apparently symptomless.
Management.
Grow alfalfa cultivars resistant to the pea aphid to prevent spread of ALV to food legume crops.
Alfalfa Mosaic
Cause.
Alfalfa mosaic virus, (AMV), overwinters in alfalfa and other perennial host plants. AMV is disseminated from diseased to healthy plants pri

Page 38
marily by the pea aphid, Acyrthosiphon pisum, although other aphids may also be involved. AMV is also seedborne and is transmitted through pollen and
occasionally the ovules. Infected seed is the most likely source of inoculum in new alfalfagrowing areas.
The AMV complex is composed of many strains that differ in infectivity and other characteristics. It is similar to ilarviruses and is comprised of four elongate forms (18
× 3159 nm). Three forms of the virus are bacilliform; the fourth is spheroidal.
Distribution.
Symptoms.
Older stands have the highest number of diseased plants. Symptoms are most obvious during cool weather in the spring and autumn. The most common symptoms are
yellow streaks parallel to the leaf veins and yellow or light green mottling that is often accompanied by a distortion of the leaves. Stunting often occurs, and,
infrequently, plants die. Infected plants may also be symptomless.
Management
1. Sow virusfree seed.
2. Control aphids where possible.
Bean Leaf Roll
Bean leaf roll was named legume yellows virus and pea leaf roll virus.
Cause.
Bean leaf roll virus (BLRV) is in the luteovirus group and consists of isometric particles 28 nm in diameter. BLRV is confined to phloem and phloem parenchyma cells.
BLRV is persistently transmitted by the pea aphid, Acyrthosiphon pisum, from midJune to midJuly, but it is not mechanically transmitted.
Distribution.
North America.
Symptoms.
Diseased plants have a mild, transient yellowing of older leaves.
Management.
Management measures are not necessary since BLRV has not been demonstrated to cause a yield loss in alfalfa.
Lucerne Transient Streak
Cause.
Lucerne transient streak virus (LTSV) is in the sobemovirus group. The virus consists of isometric particles 30 nm in diameter. The method of transmission in the field
is not known, but in the laboratory LTSV is readily transmitted by sap.
Distribution.
Australia, Canada, and New Zealand.
Symptoms.
Symptoms are most obvious on newly expanded leaflets and fade as leaflets age. No symptoms occur during high temperatures in the sum

Page 39
mer. Chlorotic streaks that vary in size from small spots to streaks 1 to 2 mm wide occur on the main lateral veins of leaflets. Leaflets are often distorted around the
streaks. Yield losses of up to 18% have occurred in the field.
Management.
Not reported.
Red Clover Vein Mosaic
Cause.
Red clover vein mosaic virus (RCVMV) is in the carlavirus group and has straight to slightly flexuous, rodshaped particles (13 × 650 nm). RCVMV is sap
transmitted in an inefficient, nonpersistent manner by several aphid species, including the pea aphid, Acyrthosiphon pisum, and the green peach aphid, Myzus
persicae.
Distribution.
Canada (Alberta) in breeding lines maintained in the greenhouse and field and in Trifolium species in Europe, North America, and South America.
Symptoms.
There is a general reduction in the winter hardiness of diseased plants. Initially, a yellow vein mosaic and chlorosis occur at the leaflet edges. Necrosis that occurs in
interveinal areas results in premature plant death.
Management.
Not known.
Selected References
Alcorn, J. L., and Irwin, J. A. G. 1987. Acrocalymma medicaginis gen. et sp. nov. causing root and crown rot of Medicago sativa in Australia. Trans. Br. Mycol.
Soc. 88:163167.
Allen, S. J., Barnes, G. L., and Caddel, J. L. 1982. A new race of Colletotrichum trifolii on alfalfa in Oklahoma. Plant Dis. 66:922924.
Basu, P. K. 1981. Existence of chlamydospores as soil survival and primary infective propagules. (Abstr.) Phytopathology 71:202.
Blackstock, J. McK. 1978. Lucerne transient streak and lucerne latent: Two new viruses of Lucerne. Aust. J. Agric. Res. 29:291304.
Carroll, R. B., Jones, E. R., and Swain, R. H. 1977. Winter survival of Colletotrichum trifolii in Delaware. Plant Dis. Rptr. 61:1215.
Christen, A. A. 1982. Demonstrations of Verticillium alboatrum within alfalfa seed. Phytopathology 72:412414.
Christen, A. A. 1983. Incidence of external seedborne Verticillium alboatrum in commercial seed lots of alfalfa. Plant Dis. 67:1718.
Claflin, L. E., and Stuteville, D. L. 1973. Survival of Xanthomonas alfalfae in alfalfa debris and soil. Plant Dis. Rptr. 57:5253.
Claflin, L. E., Stuteville, D. L., and Armbrust, D. V. 1973. Windblown soil in the epidemiology of bacterial leaf spot of alfalfa and common blight of bean.
Phytopathology 63:14171419.
Cowling, W. A., and Gilchrist, D. G. 1981. Distinction between the "Californian" and

Page 40
"Eastern" forms of Stemphylium leaf spot of alfalfa in North America. (Abstr.) Phytopathology 71:211.
Cowling, W. A., and Gilchrist, D. G. 1982. Effect of light and moisture on severity of Stemphylium leaf spot of alfalfa. Plant Dis. 66:291294.
Cowling, W. A., Gilchrist, D. G., and Graham, J. H. 1981. Biotypes of Stemphylium botryosum on alfalfa in North America. Phytopathology 71:679684.
Emberger, G., and Welty, R. E. 1981. Relationship of Fusarium wilt resistance and soil moisture to yield and persistence of alfalfa. (Abstr.) Phytopathology 71: 766.
Farr, D. F., Bills, G. R., Chamuris, G. P., and Rossman, A. Y. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society,
St. Paul, MN. 1252 pp.
Gilbert, R. G. 1985. Sclerotinia sclerotiorum causing crown and stem rot of alfalfa. (Abstr.) Phytopathology 75:1333.
Gilbert, R. G. 1988. Verticillium wilt of alfalfa: Dissemination via sclerotia of Sclerotinia. (Abstr.) Phytopathology 78:1514.
Gilbert, R. G. 1991. Burning to reduce sclerotia of Sclerotinia sclerotiorum in alfalfa seed fields of southeastern Washington. Plant Dis. 75:141142.
Gilbert, R. G., and Peaden, R. N. 1988. Dissemination of Verticillium alboatrum in alfalfa by internal seed inoculum. Can. J. Plant Pathol. 10:7377.
Gossen, B. D. 1987. Initiation of crown bud rot of alfalfa. (Abstr.)Can. J. Plant Pathol. 9:277.
Gotlieb, A. R., Pellett, N. E., and Parker, B. 1987. Sitona/Fusarium/cold hardiness interaction in alfalfa. (Abstr.) Phytopathology 77:1615.
Graham, J. H. (Coordinator). 1979. A Compendium of Alfalfa Diseases. American Phytopathological Society, St. Paul, MN. 65 pp.
Graham J. H., Kreitlow K. W., and Falkner, L. R. 1972. Diseases, pp. 497526. In Alfalfa Science and Technology. C. H. Hanson (Ed.). American Society of
Agronomy, Madison, WI.
Graham, J. H., Devine, T. E., and Hanson, C. H. 1976. Occurrence and interaction of three species of Colletotrichum on alfalfa in the midAtlantic United States.
Griffin, G. D. 1968. The pathogenicity of Ditylenchus dipsaci to alfalfa and the relationship of temperature to plant infection and susceptibility. Phytopathology
58:929932.
Griffin, G. D., and Thyr, B. D. 1988. Interaction of Meloidogyne hapla and Fusarium oxysporum f. sp. medicaginis on alfalfa. Phytopathology 78:421425.
Hancock, J. G. 1983. Seedling diseases of alfalfa in California. Plant Dis. 67:12031208.
Hancock, J. G. 1984. Prevalence and pathogenicity of Pythium paroecandrum on alfalfa in California. (Abstr.) Phytopathology 74:855.
Hemmati, K., and McClean, D. L. 1977. Gameteseed transmission of alfalfa mosaic virus and its effect on seed germination and yield in alfalfa plants.
Hiruki, C., and Miczynski, K. 1987. Severe isolate of alfalfa mosaic virus and its impact on alfalfa cultivars grown in Alberta. Plant Dis. 71:10141018.
Holub, E. B., and Grau, C. R. 1987. Root disease of alfalfa caused by Aphanomyces euteiches in Wisconsin. (Abstr.) Can. J. Plant Pathol. 9:278.
Huang, H. C. 1989. Distribution of Verticillium alboatrum in symptomed and symptomless leaflets of alfalfa. Can. J. Plant Pathol. 11:235241.
Huang, H. C., and Hyvr, A. M. 1984. Transmission of Verticillium alboatrum to alfalfa via

Page 41
feces of leafchewing insects. (Abstr.) Phytopathology 74:797.
Huang, H. C., Hironaka, R., and Howard, R. J. 1986. Survival of Verticillium alboatrum in alfalfa tissue buried in manure or fed to sheep. Plant Dis. 70:218221.
Huang, H. C., Kokko, E. G., and Erickson, R. S. 1997. Infection of alfalfa pollen by Sclerotinia sclerotiorum. (Abstr.). Can. J. Plant Pathol. 19:111.
Irwin, J. A. G. 1984. Etiology of a new Stemphyliumincited leaf disease of alfalfa in Australia. Plant Dis. 68:531532.
Jimenez Diaz, R. M., and Millar, R. L. 1988. Sporulation on infected tissues and presence of airborne Verticillium alboatrum in alfalfa fields in New York. Plant
Pathol. 37:6470.
Koch, S. H., KnoxDavies, P. S., and Lamprecht, S. C. 1988. Colletotrichum trifolii causing root rot of lucerne in South Africa. Phytophylactica 20d:305309.
Kuan, T. L., and Erwin, D. C. 1980. Predisposition effect of water saturation of soil on Phytophthora root rot of alfalfa. Phytopathology 70:981986.
Laemmlen, F. F., Cooksey, D. A., and Erwin, D. C. 1990. Naturally occurring crown gall of alfalfa. (Abstr.) Phytopathology 80:890
Leath, K. T., and Hill, R. R., Jr. 1974. Leptosphaerulina briosiana on alfalfa: Relation of lesion size to leaf age and light intensity. Phytopathology 64:243245.
Leath, K. T., and Hower, A. A. 1993. Interaction of Fusarium oxysporum f. sp. medicaginis with feeding activity of clover root curculio larvae in alfalfa. Plant Dis.
77:799802.
Leath, K.T., and Kendall, W. A. 1983. Myrothecium roridum and M. verrucaria pathogenic to roots of red clover and alfalfa. Plant Dis. 67:11541155.
Lukezic, F. L. 1974. Dissemination and survival of Colletotrichum trifolii under field conditions. Phytopathology 64:5759.
Lukezic, F. L., and Leath, K. T. 1983. Pseudomonas viridifiava associated with root and crown rot of alfalfa and wilt of birdsfoot trefoil. Plant Dis. 67:808811.
Marks, G. C., and Mitchell, J. E. 1970. Penetration and infection of alfalfa roots by Phytophthora megasperma and the pathological anatomy of infected roots. Can.
J. Bot. 49:6367.
McVey, D. V., and Gerdemann, J. W. 1960. Hostparasite relations of Leptodiscus terrestris on alfalfa, red clover and birdsfoot trefoil. Phytopathology 50:416
421.
O'Neill, N. R. 1996. Pathogenic variability and host resistance in the Colletotrichum trifolii/Medicago sativa pathosystem. Plant Dis. 80:450457.
Ooka, J. J., and Vchida, J. Y. 1982. Cylindrocladium root and crown rot of alfalfa in Hawaii. (Abstr.) Phytopathology 72:955.
Pennypacker, B. W. 1983. Dispersal of Verticillium alboatrum in the xylem of alfalfa. Plant Dis. 67:12261228..
Pennypacker, B. W., Leath, K. T., and Hill, R. R., Jr. 1985. Resistant alfalfa plants as symptomless carriers of Verticillium alboatrum. Plant Dis. 69:510511.
Pennypacker, B. W., Leath, K. T., and Hill, R. R., Jr. 1988. Growth and flowering of resistant alfalfa infected by Verticillium alboatrum. Plant Dis. 72:397400.
Pennypacker, B. W., Leath, K. T., and Hill, R. R., Jr. 1991. Impact of drought stress on the expression of resistance to Verticillium alboatrum in alfalfa.
Pesic, Z., and Hiruki, C. 1987. Occurrence of red clover vein mosaic virus (RCVMV) in alfalfa breeding lines. (Abstr.) Phytopathology 77:1732.
Pfender, W. F., Hine, R. B., and Stanghellini, M. E. 1977. Production of sporangia and release of zoospores by Phytophthora megasperma in soil. Phytopathology
67: 657663.

Page 42
Pierce, L., and McCain, A. H. 1987. Alfalfa sprout rot caused by Erwinia chrysanthemi. Plant Dis. 71:786788.
Pratt, R. G., and Rowe, D. E. 1991. Differential responses of alfalfa genotypes to stem inoculations with Sclerotinia sclerotiorum and S. trifoliorum. Plant Dis.
75:188191.
Pratt, R. G., and Rowe, D. E. 1995. Comparative pathogenicity of isolates of Sclerotinia trifoliorum and S. sclerotiorum on alfalfa cultivars. Plant Dis. 79:474477.
Ribeiro, O. K., Erwin, D. C., and Khan, R. A. 1978. A new hightemperature Phytophthora pathogenic to roots of alfalfa. Phytopathology 68:155161.
Rodriguez, R., and Leath, K. T. 1987. Phoma medicaginis var. medicaginis: A primary root pathogen of alfalfa. (Abstr.) Phytopathology 77:1618.
Rodriguez, R., and Leath, K. T. 1992. Pathogenicity of Phoma medicaginis var. medicaginis to crowns of alfalfa. Plant Dis. 76:12371240.
Rodriguez, R., Leath, K. T., and Hill, R. R., Jr. 1990. Pathogenicity of Phoma medicaginis var. medicaginis to roots of alfalfa. Plant Dis. 74:680683.
Seif ElNasr, H. I., AbdelAzim, O. F., and Leath, K. T. 1983. Crown and root fungal disease of alfalfa in Egypt. Plant Dis. 67:509511.
Seif ElNasr, H. I., AbdelAzim, O. F., and Leath, K. T. 1984. Marasmius root rot of alfalfa and khella in Egypt. Plant Dis. 68:906907.
ShyhJane Lu, N., Barnes, D. K., and Frosheiser, F. I. 1973. Inheritance of Phytophthora root rot resistance in alfalfa. Crop Sci. 13: 714717.
Simmons, E. G. 1985. Perfect states of Stemphylium. II. Sydowia 38:284293.
Skinner, D. Z., and Stuteville, D. L. 1995. Host range expansion of the alfalfa rust pathogen. Plant Dis. 79:456460.
Smith, O. F. 1940. Stemphylium leaf spot of red clover and alfalfa. J. Agric. Res. 61:831846.
Stack, J. P., and Millar, R. L. 1985. Competitive colonization of organic matter in soil by Phytophthora megasperma f. sp. medicaginis. Phytopathology 75:1020
1025.
Stack, J. P., and Millar, R. L. 1985. Relative survival potential of propagules of Phytophthora megasperma f. sp. medicaginis. Phytopathology 75:10251031.
Streets, R. B., and Bloss, H. E. 1973. Phymatotrichum root rot. American Phytopathology Society, Monograph No. 8.38 pp.
Stuteville, D. L., and Erwin, D. C. (Ed.). 1990. A Compendium of Alfalfa Diseases, Second Edition. American Phytopathological Society, St. Paul, MN. 84 pp.
Stutz, J. C., Leath, K. T., and Kendall, W. A. 1985. Woundrelated modifications of penetration, development, and root rot by Fusarium roseum in forage legumes.
Sundheim, L., and Wilcoxson, R. D. 1965. Leptosphaerulina briosiana on alfalfa: Infection and disease development, hostparasite relationships, ascospore
germination and dissemination. Phytopathology 55:546553.
Thompson, A. H. 1987. Phytophthora root rot of lucerne in Transvaal, South Africa. Phytophylactica 19:319322.
Thompson, A. H., and Pietersen, G. 1988. Witches' broom of lucerne associated with a mycoplasmalike organism in South Africa. Phytophylactica 20:297303.
Turner, V., and Van Allen, N. K. 1983. Crown rot of alfalfa in Utah. Phytopathology 73:13331337
Veerisetty, V., and Brakke, M. K. 1977. Alfalfa latent virus: A naturally occurring carlavirus in alfalfa. Phytopathology 67:12021206.
Vincelli, P. C. 1992. Two diseases of alfalfa caused by Rhizoctonia solani AG1 and AG4. Plant Dis. 76:1283.

Page 43
Vincelli, P. C., Nesmith, W. C., and Doney, J. 1991. Seedling disease of alfalfa in Kentucky caused by Aphanomyces euteiches. (Abstr.) Phytopathology 81:1136.
Webb, D. H., and Nutter, F. W., Jr. 1997. Effects of leaf wetness duration and temperature on infection efficiency, latent period, and rate of pustule appearance of
rust in alfalfa. Phytopathology 87:946950.
Welty, R. E., and Rawlings, J. O. 1980. Effects of temperature and light on development of anthracnose on alfalfa. Plant Dis. 64:476478.
Wick, R. L., and Jeschke, N. 1987. Deterioration of alfalfa sprouts by Pseudomonas species during production. (Abstr.) Phytopathology 77:1620.

Page 45
2.
Diseases of Barley (Hordeum Vulgare)
Bacterial Blight
Bacterial blight is also called bacterial leaf blight, bacterial leaf streak, bacterial streak, black chaff, black chaff and bacterial streak, and Xanthomonas streak.
Cause.
Xanthomonas translucens pv. translucens (syn. X. campestris pv. translucens) is seedborne and overwinters in infested residue. Some researchers have reported
X. campestris pv. undulosa as a causal bacterium.
The taxonomy of the causal organism(s) continues to be a subject in flux. Bacterial blight, which is called bacterial streak, bacterial leaf streak or black chaff on other
small grains, is considered to be caused by five of the former X. campestris pathovars: pv. cerealis, pv. hordei, pv. secalis, pv. translucens, and pv. undulosa. The
pathovars are often grouped together under the name "translucens" or are considered a single species or a pathovar named X. translucens and X. campestris pv.
translucens, respectively. Bragard et al. (1997) agree that X. translucens pv. translucens and X. translucens pv. hordei are true synonyms. They further report that
using restriction fragmentlength polymorphism and fatty acid methyl esters analysis, the pathovars X. translucens pv. cerealis, X. translucens pv. translucens, and
X. translucens pv. undulosa cluster in different groups and correspond to true biological entities.
Inoculum is spread to new locations primarily by infested seed. However, bacteria are also disseminated by the physical contact of a diseased leaf rubbing against a
healthy one, splashing rain, and insects. Bacteria enter the plant through natural openings such as stomata and wounds.
Distribution.
Wherever barley is grown.
Symptoms.
Black chaff is seldom serious, and symptoms are confined mainly to leaves. Small, watersoaked spots occur on tender green leaves and

Page 46
sheaths of older plants, and sometimes on seedlings. Occasionally, a spot may become large and blotchy, causing the leaf to die, shrivel, and turn light brown in color.
The spots enlarge and coalesce to become glossy, yellow or brown, translucent, narrow stripes that are limited by leaf veins but frequently extend the length of a
diseased leaf blade. When a newly developed stripe is cut laterally, a milky "ooze" consisting of bacteria will exude from the cut edges. Severely diseased leaves die
back from the tips. If a flag leaf is infected, the head may not emerge from the boot but may break through the side of the sheath and be distorted and blighted. Under
humid, early morning conditions, droplets of milky bacterial exudate may be seen on the surface of spots and stripes. Bacterial exudate eventually dries into hard,
yellowish flakes that can be easily removed from the leaf surface.
Chaff may also be affected after several days of damp or rainy weather. Watersoaked areas may occur on glumes but bacterial exudate will not be evident. Seed is
not destroyed but may become brown, shrunken, and carry bacteria that, potentially, can infect next year's crop. Diseased plants grow slowly and are stunted, but
disease symptoms are not noticed until plants are about twothirds grown.
Management
1. Sow diseasefree seed.
2. Treat seed with a seedprotectant fungicide.
3. Rotate barley with other crops. Xanthomonas translucens pv. translucens also infects wheat.
4. After dry heat treatments of heavily infested seed at 71°, 75° or 84°C for 11 days, the reduction in germination was negligible and X. translucens pv. translucens
was not detected.
Bacterial Leaf Blight
Cause.
Pseudomonas syringae pv. syringae. Bacteria infect leaves through stomates or wounds during cold, wet, and windy weather.
Distribution.
North America.
Symptoms.
Normally, only upper leaves, particularly the flag leaves, are diseased. Initially, small, watersoaked, graygreen lesions form, often where the leaf bends. Later, these
coalesce to form larger tan or white lesions that cover the entire leaf. Eventually, the whole leaf may die, become necrotic, and curl inward from the edges.
Other symptoms caused by P. syringae in south central Colorado have been described as typical halo blight.
Management.
Not necessary.
Bacterial Stripe
Bacterial stripe is also called bacterial stripe blight.

Page 47
Cause.
Pseudomonas syringae pv. striafaciens (syn. P. striafaciens) is seedborne and survives in infested crop refuse for at least 2 years. Bacteria are splashed or blown
onto leaves during cool, wet weather. Warm, dry weather stops the spread of the bacteria.
Distribution.
Australia, Europe, North America, and South America. Bacterial stripe occurs infrequently.
Symptoms.
Initially, sunken, watersoaked dots appear on diseased leaves and, if dots are numerous, the leaf may die. The dots enlarge into watersoaked stripes or blotches
with narrow yellowish margins that extend the length of the leaf blade. Stripes become a translucent rusty brown as they age. Droplets of bacteria exude from stripes in
moist weather and later dry up and form white scales on the stripe surfaces.
Management
1. Plow under infected residue.
Barley Basal Kernel Blight
Barley basal kernel blight is also called bacterial kernel blight.
Cause.
Pseudomonas syringae pv. syringae survives on infested residue and leaf surfaces of nonhost plants and is seedborne. Kernel infection occurs before the milky
dough stage. The infection process starts with an epiphytic inoculum buildup on the kernel surface. Bacteria enter kernels primarily through stomates located on the
inner epidermis of the barley lemma before the lemma becomes attached to the caryopsis. At soft dough stage, P. syringae might enter kernels through pits or wounds
in the external epidermis.
Distribution.
North America.
Symptoms.
Infected kernels have tan to dark brown spots (approximately 2 mm in diameter) with distinct margins that develop at the embryo end on the posterior surface of the
kernel. A lemma spot symptom caused by P. syringae pv. syringae, but possibly also by other P. syringae pathovars, is a welldefined tan to dark brown
discoloration of the kernel lemma. Bacteria are found in intercellular spaces of the aleurone layer, within amyloplast cells, and in vascular bundles.
Management.
Not known.
Basal Glume Rot
Basal glume rot may be the same disease as basal bacteriosis.
Cause.
Pseudomonas syringae pv. atrofaciens (syn. P. atrofaciens and Phy

Page 48
tomonas atrofaciens) survives epiphytically on seed and in infested soil residue. Bacterial spores on dust particles are disseminated by wind and become entrapped in
the water in grooves and small spaces of the spikelets. Bacteria are also disseminated by insects and splashing water. Bacteria multiply near glume joints in the
presence of moisture but remain dormant when conditions are dry.
Distribution.
Symptoms.
Symptoms occur during wet weather, particularly at heading time. The main symptom is a brown, discolored area at the base of the glumes that cover a kernel. This
discoloration is darker on the inside than the outside of the glume. Usually only onethird of the glume is discolored but sometimes the entire glume may be affected.
Infrequently, the only sign of disease is a dark line at the attachment of the glume to the spike.
Severely diseased spikelets are slightly dwarfed and lighter in color than healthy ones. The base of a diseased kernel has a light brown to black discoloration.
Infected leaves have small, dark, watersoaked spots. Spots eventually elongate and become yellow, then necrotic as the tissue dies.
Management
1. Seed should be thoroughly cleaned and treated with a seedprotectant fungicide.
2. Rotate barley with resistant crops, such as legumes.
3. Plow under residue.
Anthracnose
Cause.
Colletotrichum graminicola is seedborne and overwinters as mycelia and conidia in infested residue, cereals, and wild grasses. Optimum conidia production is
during wet weather at a temperature of 25°C; conidia are disseminated primarily by wind to barley and other host plants.
Anthracnose is most severe when barley is grown on sandy soils that are low in fertility.
Distribution.
Symptoms.
Seedling infection may occur under severe disease conditions. Symptoms generally become apparent toward plant maturity as premature ripening or whitening of
diseased plants, a general reduction in plant vigor, and plant death. Ellipticalshaped, watersoaked lesions (12 cm long) that later become bleached and necrotic
occur on the lower part of the diseased plant. The entire crown and bases of stems become bleached

Page 49
and then turn brown. Later, acervuli, which appear as small, black, raised spots to the unaided eye and as clumps of dark spines under magnification, develop on the
lesion surfaces of diseased lower leaf sheaths and culms. Acervuli may also develop on moist leaf blades of dead plants. Kernels may be shriveled and light in weight if
plants are infected early.
Management
1. Rotate barley with a noncereal crop.
2. Improve soil fertility.
3. Treat seed with a fungicide.
Arthrinium arundinis Kernel Blight
Cause.
Arthrinium arundinis is a saprophyte of decaying grasses, but barley grown in highly humid environments may be susceptible.
Distribution.
The United States (Montana).
Symptom.
A brown discoloration occurs on the basal portion of the diseased kernel.
Management.
Not reported.
Ascochyta Leaf Spot
Cause.
Ascochyta hordei vat. americana is generally accepted as the cause of Ascochyta leaf spot; however, A. graminea, A. sorghi, and A. tritici have also been
reported to cause leaf spot diseases of barley.
Ascochyta hordei var. americana survives as mycelia and pycnidia in infested residue. Pycnidiospores are liberated during wet weather and are disseminated by
splashing rain and wind. Disease is associated with dense foliage, leaves in contact with soil, and high humidity.
Distribution.
Japan and the United States, primarily the northwestern states and New York.
Symptoms.
Spots, which are round (4 mm in diameter), oval (24 × 812 mm), or irregular in shape and sometimes have several rings, occur primarily on approximately onethird
of the lower leaf blades nearest the tip end. Initially, spots are brown but fade to pale yellow, ashy gray, or tan necrotic centers that are surrounded by a narrow
brown band.
Lesions at leaf tips often coalesce to cause dieback but without the brown margin. The latter symptom is often masked by frost injury. Pycnidia, which appear as tiny
black specks, are present in diseased tissue but are absent from frostdamaged tissue.
Management.
Disease management is not necessary since Ascochyta leaf spot is generally considered to be of minor importance.

Page 50
Barley Stripe
Barley stripe is also called barley leaf stripe, barley stripe disease, Helminthosporium stripe, leaf stripe, Pyrenophora leaf stripe, and stripe disease.
Cause.
Pyrenophora graminea, anamorph Drechslera graminea (syn. Helminthosporium gramineum) is seedborne and survives up to 5 years as mycelia in hulls,
pericarps, and seed coats. At seed germination, mycelia, primarily from the pericarp but also from the seed coat over the pericarp, grow into the sheath that surrounds
the leaves of the seedling. The critical stage for infection of the germinating embryo is when the coleoptile reaches the apex of the seed until the seedling emerges from
the soil. From the seedling leaves, mycelia grow into the first leaf and subsequently into succeeding leaves until eventually all leaves are infected. Infection is optimum at
soil temperatures of 12°C or less and is reduced or prevented at soil temperatures above 15°C.
Secondary infection is caused by conidia that are produced in stripes of infected barley leaves during high moisture conditions. The conidia mature in about 16 hours at
12°C and are disseminated by wind to the heads of healthy plants. Conidia lodge near the tips of glumes and germinate, with the resulting mycelia growing either
between hulls and kernels or into seed coats. Infection occurs at temperatures of 10° to 33°C. Seeds are most susceptible to infection in the early stages of plant
maturation; infection levels decrease from the boot stage to milk stage of plant growth. Free water, although beneficial, is not required because high relative humidity
provides adequate moisture for seed infection.
Disease spread is directly related to moisture. Compared with plants grown in a dry environment, irrigation or high relative humidity at heading will increase disease
incidence up to threefold. Barley stripe is more important on winter barley than on spring barley.
Distribution.
Wherever winter barley is grown.
Symptoms.
The first symptom occurs at the late tillering stage when small, yellow spots appear on seedling leaves. These minuscule spots could be easily overlooked by a casual
observer. Weeks before heading, one to several narrow, yellow to light tan, parallel stripes extend the length of leaf blades and sheaths. The alternate yellow and green
striping of diseased leaves contrasts with the uniform green of healthy ones. The margins of stripes turn reddish or dark brown but the stripe centers remain tan or light
brown. Diseased tissue dies, then splits within the stripes, causing the entire leaf to become shredded. Stripes eventually become gray to olive gray due to sporulation
by D. graminea. The culm dies if the growing point is infected.

Page 51
Diseased plants are stunted. Heads either do not emerge or emerge twisted, compressed, brown, and standing erect, in contrast to mature healthy heads that bend
over slightly. Grain in diseased heads is undeveloped or shriveled and brown.
Management
Blast
Cause.
Pyricularia oryzae. However, some isolates obtained from tworowed barley are not pathogenic to rice and have been tentatively identified as P. grisea. Rice likely
provides an inoculum source for P. oryzae, and ryegrass may provide a source for P. grisea. See blast in the chapter on rice diseases.
Distribution.
Reported in tworowed barley, Hordeum distichum, from Japan; however, blast likely occurs where barley and rice or other hosts are grown in the same vicinity.
Symptoms.
Spots on leaves begin as small, watersoaked, white, gray, or blue dots that quickly enlarge under moist conditions (0.30.5 × 10.015.0 mm). Mature leaf spots are
elliptical and pointed at both ends and have gray to white centers that are surrounded by brown to redbrown margins.
Spots may vary in shape and color depending on cultivar, environment, and age of the spot. Resistant cultivars have only brown specks; moderately resistant cultivars
have small, round lesions with necrotic centers and brown margins.
Later in the growing season, some cultivars become infected at the point where the flag leaf attaches to the sheath. The lesion continues to expand by enlarging
downward on the sheath and upward on the leaf and becomes gray at the point of attachment. The flag leaf may subsequently break off and become detached from
the plant.
Nodes may be diseased. The affected node itself eventually breaks apart and remains connected together only by a few vascular strands. The base of the leaf sheath,
which is connected to the node, turns black due to the sporulation of conidia. The portion of the plant above the diseased node dies.
Any portion of the panicle, panicle branches, and glumes may become diseased and have brown lesions on the diseased plant part. If the base of the panicle is
diseased, rotten neck or neck rot symptoms cause the stem below the panicle to snap.
Management.
Grow resistant cultivars. In tworowed barley, resistance has been found to be conditioned by a single dominant gene.

Page 52
Cephalosporium Stripe
Cause.
Hymenula cerealis (syn. Cephalosporium gramineum) survives as conidia, and as mycelia in residue in the top 8 cm of soil for at least 5 years. Soilborne conidia
serve as primary inoculum and infect roots during winter and early spring through mechanical injuries caused by soil heaving and insects. Infection is most severe in
wet, acid soils (pH 5.0) because of a combination of increased fungal sporulation and root growth. The subcrown internode can also be infected just as the seed is
germinating.
After infection, conidia enter xylem vessels and are carried upward in the plant's xylem tissue, where they lodge and multiply at nodes and leaves, subsequently
preventing water from moving up the plant. Hymenula cerealis also produces metabolites that are harmful to the plant. At harvest time, H. cerealis is returned to the
soil in infested residue, where it is a successful saprophytic competitor against other soilborne microorganisms.
Distribution.
Great Britain, Japan, and in most winter barleygrowing areas of North America.
Symptoms.
Stunted plants are scattered throughout a field but are more numerous in the lower and wetter areas of the field. During jointing and heading, one or two, and rarely up
to four, distinct yellow stripes, in which infected veins appear as thin brown lines, develop the length of the plant on leaf blades, sheaths, and stems. Stripes eventually
become brown and are highly visible in contrast to the rest of the green leaf. After harvest, stripes remain visible on the yellow straw. At plant maturity, culms at or
below nodes become darkened because of sporulation by H. cerealis. Heads are white and do not contain seed, or if seed is present, it is usually shriveled.
Management
1. Rotate barley for at least 2 years with a noncereal crop.
2. Sow winter barley later in the autumn or when the soil temperature at the 10cm level in the soil is below 13°C. The plants will have limited root growth, which
reduces the number of potential infection sites.
3. Plow residue deeper than 8 cm.
Ceratobasidium gramineum Snow Mold
Cause.
Ceratobasidium gramineum (syn. Corticium gramineum). Snow mold occurs in welldrained, upland paddy fields.
Distribution.
Japan. Ceratobasidium gramineum snow mold is most common on barley but also occurs on wheat.
Symptoms.
As the snow melts, leaves on diseased plants are rotted and dark green. After leaves dry, they turn pale gray to pale yellow. Lesions on sur

Page 53
viving leaves are ellipsoidal and have pale gray mycelial mats in their centers and narrow brown margins. Leaf sheaths frequently are brown.
Symptom development ceases after snowmelt and the plants are exposed to light and drying wind. However, later in the growing season, ellipsoidal lesions are found
on leaf sheaths near the soil level.
Management.
Not reported.
Common Root Rot
Cause.
Several fungi, including Bipolaris sorokiniana, teleomorph Cochliobolus sativus, Fusarium culmorum, and F. graminearum. Conidia of B. sorokiniana and
chlamydospores of Fusarium spp. survive for several years in soil. These fungi also are excellent saprophytes and colonize plant material added to the soil.
Microdochium bolleyi also is a secondary invader of roots and is sometimes isolated together with B. sorokiniana and Fusarium spp. In Finland, M. bolleyi is
reported to commonly be isolated together with B. sorokiniana and Fusarium spp.
Plants under stress from drought, warm temperatures, lack of nutrition, and Hessian fly injury are most subject to infection. Moisture is required for infection, but once
disease is initiated, further development requires warm temperatures and moisture stress. Disease initiation by B. sorokiniana begins 25 to 30 days following sowing
and reaches maximum levels at about 60 days after sowing.
Sites for secondary sporulation of fungi vary, presumably because of the different sporulation requirements for different fungi. The most abundant sporulation for some
fungi, especially B. sorokiniana, is on crowns, with the remainder occurring on crown roots and on subcrown internodes, seed pieces, and seminal roots. Other
sporulation by Fusarium spp. occurs on mature plants; the highest numbers of conidia are present on necrotic or senescent tissues, such as coleoptiles, and the lower
outside leaf sheaths.
Disease incidence increases under continuous cultivation. Isolates of C. sativus from fields in continuous barley are more pathogenic to barley than isolates from fields
in firstyear barley. Isolates of C. sativus from diseased wheat and barley are highly virulent to their original host species but are weakly virulent to alternate host
species.
An increase in root rot levels causes an increase in net blotch severity on winter barley.
Distribution.
Generally distributed wherever barley is grown, but common root rot is more frequent where plants are under moisture stress during the growing season.
Symptoms.
Common root rot is usually noticed after plant heading, when it resembles drought damage. Lesions develop on the subcrown internode in 7 to 9 weeks after
emergence and cause the lower leaves to die. Brown le

Page 54
sions of variable size may develop on the leaf base nearest the soil surface and extend partially or completely around the stem. Later in the growing season, the lower
parts of leaves, tiller buds, crown roots, and internodes below and above crowns have brown lesions.
Rotted crown and crown roots can be seen when dead leaves and tillers are removed from the crown. Diseased plants are shorter, and survival of winter barley is
reduced, particularly when infected by B. sorokiniana.
Management.
The following aid in managing disease:
1. Rotate barley with noncereal crops.
2. Plow under infested residue where feasible.
3. Experimental seed treatment with the fungicide imazalil lowered disease severity in the subcrown internode, increased grain yield by 6%, and increased test weight
compared to the control.
Covered Smut
Cause.
Ustilago hordei. Smutted heads emerge at the same time as heads of healthy plants. When the semipersistent membrane covering the teliospores is ruptured by wind,
rain, and harvest machinery, the teliospores are liberated and become windborne for a considerable distance. They come to rest on or under the hulls of healthy
kernels and on the soil surface. Spores on the kernel surface remain dormant until the kernel is sown the following spring or autumn. Spores deposited under hulls may
germinate and infect just the outer layers of the seed, where the resultant mycelia remain dormant until sowing time the following spring or autumn. Spores also
overwinter in soil.
Seedlings become infected between germination and emergence by seedborne spores and mycelia or by soilborne spores. Mycelia then grow internally just behind the
growing point of the infected plant. At the boot stage, mycelia grow into the flower ovary, eventually converting it into masses of spores.
The amount of infection depends on the percentage of infested kernels that are sown. Acid or neutral soils, soil temperatures of 14° to 25°C, and high soil moisture are
favorable conditions for disease development.
Physiologic races of U. hordei are present.
Distribution.
Symptoms.
A somewhat persistent grayishwhite membrane that encloses millions of black teliospores emerges from the boot instead of a normal green head. From a distance,
smutted heads will appear grayish and are easily noticed throughout a field. Each smutted seed is now a dark, powdery mass of teliospores that crushes easily and
colors fingers a dark brown or black. After the membrane ruptures and teliospores are released, the remaining naked rachis contrasts with the surrounding healthy
heads.

Page 55
Management.
1. Treat seed with a systemic seedprotectant fungicide.
Crown Rust
Cause.
Puccinia coronata. The rust is highly virulent on winter barley and is pathogenic to spring barley; foxtail barley, Hordeum jubatum; quackgrass, Elytrigia repens;
common buckthorn, Rhamnus carthartica; Secale spp.; and many gramineous species. This form of P. coronata differs from P. coronata var. avenae by having
low pathogenicity on Avena spp., darker urediniospores, and longer telial appendages.
Distribution.
The United States (Minnesota, Nebraska, North Dakota, and South Dakota).
Symptoms.
Infection occurs on leaves, leaf sheaths, awns, and peduncles. Uredinia are elongate and light orange. When viewed under magnification, the teliospore apical cell has
four to six appendages that are up to 46 M long.
Management.
Not reported.
Downy Mildew
Cause.
Sclerophthora rayssiae is an obligate parasite that survives for several years as oospores that are in residue or are released into soil when residue decays. Oospores
are seedborne and are also disseminated in water and windborne residue and soil.
Leaves of newly emerged seedlings in contact with water 24 hours or longer are most susceptible to infection. Oospores germinate in watersaturated soil to produce
sporangia. Zoospores are then produced within sporangia and, upon their release from the sporangium, ''swim" through water to the leaves of developing seedlings,
where they germinate to produce a germ tube. Oospores may also survive for months in dry soil and germinate to form a single germ tube that directly penetrates a
host. Infection occurs over a wide temperature range (7° to 31°C). Sclerophthora rayssiae then develops systemically in the plant, particularly in meristematic tissue.
Eventually, during the growing season, oospores are produced within diseased tissue to complete the life cycle of the fungus.
Distribution.
Wherever winter barley is grown.
Symptoms.
Diseased plants are scattered in areas where excess water was present in low areas of a field, usually after excessive rainfall. Diseased plants are dwarfed and
deformed, tiller excessively, and may be "flagged" with prominent yellowed leaves. Leaves are leathery, stiff, "warty" and thickened.

Page 56
Affected heads are twisted in various ways and distorted. Seed is normally not formed in severely diseased plants. Severely diseased plants may die before jointing.
In less severely diseased plants, dwarfing may be slight, with one or more of the upper leaves stiff, upright, or curled, and twisted. Heads and stems may not be
deformed.
In diseased tissue, numerous round, yellow to brown oospores may be observed under magnification.
Management
1. Provide proper soil drainage.
2. Control grassy weeds that may serve as hosts.
3. Sow cleaned seed from diseasefree plants.
Dwarf Bunt
Cause.
Tilletia controversa survives as teliospores in soil or on seed. When seed is sown, teliospores on or close to the seed germinate in the presence of moisture to
produce a promycelium on which 8 to 16 basidiospores are formed. A basidiospore then fuses in the middle with a compatible basidiospore to form an Hshaped
structure that germinates to form yet other structures called secondary sporidia. The secondary sporidia germinate to produce mycelia that infect seedlings.
The infection process takes 35 to 105 days, depending on temperature. The optimum temperature for spore germination is 1° to 5°C, a condition that occurs under
heavy snow cover over unfrozen ground. The mycelium grows internally in meristematic tissue of the plant, invades the developing head, and replaces seed with
teliospores. At harvest, diseased seed is broken and teliospores are windborne and contaminate healthy kernels or soil. Isolates of T. controversa from barley can
infect wheat and vice versa.
Distribution.
Winter barley in the United States (Utah). Dwarf bunt has never been a serious disease problem on barley and is rarely or infrequently observed.
Symptoms.
Dwarf bunt is restricted to areas where winter barley grows under snow cover for a long time. Infected tillers are stunted and grow to about onefourth to onehalf the
height of a normal plant. Diseased heads are more compact than healthy plant heads, and sori fill the seed coat to form bunt "balls" that are rounder and shorter than
normal barley seed. A foul odor, similar to rotten fish, occurs when bunt balls are broken and teliospores are moistened.
Management.
Not necessary because of the low incidence of disease.

Page 57
Ergot
Cause.
Claviceps purpurea, anamorph Sphacelia segetum, survives for approximately 1 year as sclerotia in soil. Prior to plant blossoming, sclerotia germinate to produce
stromatic heads at the end of stipes in which perithecia are formed. Ascospores form in perithecia and are primarily windborne but occasionally are splashed by rain to
florets, where they germinate. The resulting mycelium grows into the young ovary and eventually produces conidia along with a sweet, sticky liquid called honeydew.
Insects are attracted to honeydew and, in the process of feeding on the sweet liquid, inadvertently become contaminated with conidia. Insects disseminate the conidia
to healthy flowers, where the conidia germinate and cause a secondary infection.
Eventually, the diseased ovaries enlarge and are converted into sclerotia, which are composed of hardened mycelium, from the kernel base to the kernel tip. Since
infection of flowers does not occur after pollination, infection is favored by prolonged flowering, which tends to occur during cool, wet weather.
Plants infected with the barley stripe mosaic virus are more susceptible to infection by C. purpurea than healthy plants. Several grasses and other cereals are
susceptible to infection by C. purpurea.
Distribution.
Wherever barley is grown. However, ergot is normally not a severe disease of barley.
Symptoms.
The only plant part affected is the head. Initially, infected flowers ooze droplets of a yellowish, sticky liquid called honeydew that attracts insects. Insects may be
observed clustered about a diseased flower. Also, dust adheres to the sticky liquid to give it a "dirty" or dusty appearance. At maturity, diseased kernels are replaced
by larger, hard, black to bluishblack sclerotia that protrude from the flume.
Management
1. Plow residue deep into the soil so sclerotia will be placed in the soil profile, where they cannot release ascospores into the air. Sclerotia are normally decomposed
by soil microorganisms in about 1 year.
2. Control grassy weeds around fields that may be collateral hosts for C. purpurea and increase inoculum that will infect cereal crops, including barley.
3. Rotate barley with resistant hosts.
4. Separate sclerotia from seed. Sclerotia may be harmful when fed to livestock because of the potential for production of mycotoxins.
Eyespot
Eyespot is also called culm rot, foot rot, straw breaker, and straw breaker foot rot.

Page 58
Cause.
Pseudocercosporella herpotrichoides (syn. Cercosporella herpotrichoides), teleomorph Tapesia yallundae. Two varieties of the fungus are recognized.
Pseudocercosporella herpotrichoides var. herpotrichoides produces fourseptate conidia measuring 35.080.0 × 1.52.5 M; P. herpotrichoides var. acuformis
produces four to sixseptate conidia measuring 43.0120.0 × 1.22.3 M. Races have not been reported, but pathogenic specialization to host species does occur.
There are two main pathogenic types: Wtype (wheattype) isolates are most virulent on wheat and less virulent on barley and rye. Rtype (ryetype) isolates are
equally virulent on wheat, barley, and rye.
Pseudocercosporella herpotrichoides survives as mycelium in infested crop residue that was previously colonized during the parasitic stage of the fungus. Conidia
are produced during cool, damp weather in the autumn or spring and subsequently disseminated, primarily by rain, to crown and basal culm tissue of nearby plants.
Roots are normally not infected.
Infection is favored by high soil moisture, dense crop canopy, and high humidity near the soil surface. Winter barley is more likely to be infected than spring barley
because of predisposition by spring frosts and excessive nitrogen fertilization. Pseudocercosporella herpotrichoides has a wide host range and infects other cereals.
Distribution.
It is generally assumed that eyespot is widespread wherever barley is grown.
Symptoms.
Eyeshaped or ovate lesions with white to tan centers and brown margins develop first on the basal leaf sheath and darken with age. Similar spots form on the stem
directly beneath those on the sheath and cause lodging. Under moist conditions, lesions enlarge and a black stromalike mycelium develops over the crown surface
and base of the culms, giving them a charred appearance. The stems then shrivel and collapse, causing diseased plants to fall in all directions at maturity. Roots are not
affected but a necrosis occurs around roots in the upper crown nodes. Chlorotic plants with white heads or heads reduced in size and number are also present.
Management
1. Rotate barley with legumes.
2. Sow spring barley or delay sowing winter barley.
False Loose Smut
False loose smut is also called nigra loose smut, black smut, black loose smut, intermediate loose smut, and semiloose smut.
Cause.
Ustilago nigra (syn. U. avenae) is seedborne, surviving as teliospores (sometimes called chlamydospores) on the seed surface, under the hull,

Page 59
and in soil. Smutted heads emerge at approximately the same time as heads of healthy plants. A mass of teliospores that has replaced the kernels is covered by a
semipersistent membrane which may remain intact until harvest time unless it is ruptured by wind, rain, or other means. Teliospores are disseminated by wind and are
deposited on or under hulls of healthy kernels. Spores on the seed hull surfaces remain dormant until kernels are sown the following spring or autumn. Spores
deposited under seed hulls germinate immediately and the resultant mycelia grow into the kernel layers that are just under the hull. There, the mycelium remains
dormant until sowing time the following spring or autumn.
Seedlings become infected between germination and emergence by seedborne spores and mycelia or by soilborne spores. Soil temperatures of 15° to 21°C and dry
moisture conditions are most favorable for infection. Following infection, the mycelium grows just behind the growing point of the seedling. As diseased plants enter the
boot stage, the mycelium grows into the young flowers and converts them to masses of teliospores. The smutted head then emerges from the boot at approximately the
same time as a healthy head.
Physiologic races of U. nigra exist.
Distribution.
Africa, Asia, Australia, Europe, Central America, North America, and South America.
Symptoms.
Symptoms vary between those of loose smut and covered smut, but more closely resemble those of loose smut. False loose smut can be distinguished from true smut
with certainty only by observing smut spores and their germination under a microscope. The most reliable distinguishing feature is the sporidial germination type of U.
nigra compared to the mycelial germination type of U. nuda.
Ustilago nigra teliospores are spherical to subspherical, 59 M in diameter, and dark brown to black with echinulations varying from slight to pronounced.
Chlamydospores germinate to form a three or fourcelled basidium bearing sporidia from each cell.
Ustilago nuda teliospores are globose to subglobose or elongate, 57 M in diameter, olivaceous brown, lighter on one side, and minutely echinulate. Spores
germinate to form a slender germ tube that branches and rebranches to form mycelium.
Smutted heads appear at approximately the same time as healthy heads. The dark brown to black spore mass and variation in looseness of the mass are gross
characteristics. The membrane around the spore mass varies from easily broken to stronger persistent. When membranes break, spores are quickly washed or blown
away, leaving a bare rachis. Persistent membranes retain their spores until harvest.
Management.
Treat seed with a systemic seedprotectant fungicide.

Page 60
Fusarium Head Blight
Fusarium head blight is also called Fusarium blight, head blight, and scab.
Cause.
Fusarium graminearum, teleomorph Gibberella zeae, is generally considered to be the principal pathogen. Fusarium acuminatum, F. avenaceum, F. culmorum,
F. equiseti, and F. nivale are also reported to be pathogenic to barley.
Fusarium graminearum overwinters as mycelia and spores on seed, mycelia in infested residue, and perithecia on maize, wheat, and other crop residue infected the
previous season. Primary inoculum is a combination of ascospores that are produced in perithecia and conidia produced on mycelium during warm, moist weather and
disseminated by wind to flowers and developing seed. Secondary inoculum is primarily conidia produced on diseased heads. Disease severity is increased by wet,
warm weather during anthesis and ripening of kernels, and when grain is lodged or swathed.
Scabby grain is toxic, particularly to swine. Several toxins are produced: zearalenone (F2 toxin) is involved in causing hyperestrogenism, and vomitoxin is involved in
the refusal factor or vomiting syndrome. Feed containing 3% or more scabby kernels may be poisonous to dogs, humans, and swine. However, cattle and sheep are
normally not affected by ingesting scabby grain. The highest numbers of Fusarium propagules and mycotoxin concentrations occur in hulls.
Distribution.
Wherever barley is grown during warm, moist summer weather.
Symptoms.
The number of diseased kernels on a head may vary. Either only one or more spikelets or the entire head may be affected. Infection begins in flowers and spreads to
other parts of the head, causing it to be dwarfed and giving kernels the appearance of premature ripening. Initially, diseased spikelets are watersoaked, starting at the
base, then die and become light brown. Eventually, hulls change from a light to a dark brown color. When infection occurs late in kernel development, hulls may be
brown only at their bases. In severe cases, entire kernels become shrunken, brown, and lightweight and have a "floury" and discolored interior. During wet weather, a
pink mold consisting of mycelia and conidia grows on diseased spikelets. Later, small, black perithecia grow in the same area.
Sowing infected seed may result in seed and seedling damping off.
Management
1. Do not grow barley following barley, maize, or wheat.
2. Plow under infected residue where feasible.
3. Do not spread manure containing infested straw or maize stalks on soil in which barley is growing.
4. Sow early to allow grain to escape much of the warm, moist weather of summer.

Page 61
5. Treat seed with a fungicide seed protectant to reduce damping off.
6. Separate scabby kernels from healthy kernels with cleaning equipment.
7. Grow hullless cultivars as a means of managing mycotoxins.
Gibberella Seedling Blight
Cause.
Gibberella zeae, anamorph Fusarium graminearum, overwinters as mycelia and spores on seed, and as mycelia and perithecia on barley, maize, rye, and wheat
residue. Seedling infections are primarily from seedborne inoculum. Disease is favored by temperatures of 15°C and above and dry soil.
Distribution.
Symptoms.
Initially, seedlings are stunted, become chlorotic, and die. The root system has a reddishbrown rot and may be covered with white to pink mycelium.
Management
1. Treat seed with a fungicide seed protectant.
2. Sow certified seed.
3. Sow when the soil temperature is 15°C or below.
Gray Snow Mold
Typhula incarnata is considered one of the causal agents for speckled snow mold of wheat.
Cause.
Typhula incarnata (syn. T. itoana and T. graminum). Typhula incarnata survives as sclerotia under deep snow cover. Sclerotia germinate during wet weather in
the autumn to produce either basidiocarps on which basidiospores are borne or hyphae. Basidiospores are released in the Pacific Northwest of the United States in
mid to late October and are airborne to seedlings. Basidiospores may remain viable for up to 60 days. The optimum temperature range for disease development is 1°
to 5°C.
Distribution.
Canada (Quebec), central Europe, Japan, and the mountain valleys of the western United States. Gray snow mold is associated with snow cover.
Symptoms.
Winter barley plants are often infected without causing a reduction in survival or yield. However, if crowns become infected, plants normally die. Chlorotic plants are
observed to be scattered throughout a field after the snow melts in the spring. A few or many necrotic leaves are covered with a thick, graywhite mycelium. Diseased
leaves dry up and disintegrate easily when the snow cover disappears and temperatures rise. Sclerotia, which appear as hard, black structures of varying sizes, form
on lower leaf sheaths.

Page 62
Management.
Do not grow barley in areas where prolonged snow cover may occur.
Halo Spot
Cause.
Selenophoma donacis (syn. Phyllosticta stomaticola and Septoria donacis) and Selenophoma donacis var. stomaticola. Selenophoma donacis var.
stomaticola reportedly can be differentiated from S. donacis primarily by spore size. Selenophoma donacis var. stomaticola spores are falcate, aseptate, and
variable in size (13 × 1020 M but occasionally up to 25 M long). Selenophoma donacis spores are stoutly falcate to boomerangshaped and somewhat larger
(2.04.5 × 1835 M).
Selenophoma donacis overwinters as pycnidia, pycnidiospores, and mycelia in residue, seed, and cereals. During cool, moist weather, pycnidiospores are exuded
from pycnidia and disseminated by wind and splashing rain to host plants.
Distribution.
In cool, moist climates of Australia, Canada, Great Britain, northern Europe, New Zealand, South Africa, and the United States. Although halo spot rarely causes
severe damage, epiphytotics have been reported in southwest England and Norway.
Symptoms.
In the spring, spots appear on leaves and sometimes on culms of winter barley. Spots are less than 4 mm long, are elliptical, rectangular, or square, and have purple
brown margins that fade as the margins age. Centers of spots become gray and speckled with small, black pycnidia. Spots may become so numerous that much of the
leaf surface is destroyed.
Management.
Since halo spot does little damage to barley, disease management is not necessary.
Kernel Blight
Kernel blight is sometimes called black point and seed discoloration.
Cause.
Some reported causes of seed discoloration are Alternaria alternata, Arthrinium arundinis, Bipolaris sorokiniana, Cladosporium herbarum, Fusarium
culmorum, and F. graminearum. Discoloration is associated with excess rainfall between anthesis and harvest and is enhanced by late harvest.
Distribution.
Generally, wherever barley is grown.
Symptoms.
The embryo is dark brown to black. Germination is decreased if the embryo is invaded.
Management.
Treat seed with a seedtreatment fungicide.
Leaf Rust
Leaf rust is also called dwarf leaf rust and brown leaf rust.

Page 63
Cause.
Puccinia hordei (syn. P. anomala). The wheat leaf rust fungus, P. recondita f. sp. tritici, infects barley in some geographical areas but is generally considered a
weak pathogen to barley.
Puccinia hordei is a heteroecious rust fungus that overwinters as urediniospores on volunteer and winter barley in the southern United States. In the spring,
urediniospores are windborne to the northern United States and initiate infection just before heading. Leaf rust is most severe under warm, humid conditions where
plants mature later in the growing season.
StarofBethlehem, Ornithogalum spp., is the alternate host for P. hordei in Europe, Israel, and parts of Asia. In Israel, O. brachystachys and O. trichophyllum,
together with Dipcadi erythraeum and Leopoldia eburnea, have been reported to be alternate hosts of P. hordei. Basidiospores do not infect O. umbellatum and
O. nutans, and no pycnia or aecia have been found on these two Ornithogalum species in the United States except under experimental conditions.
Distribution.
Symptoms.
Symptoms are inconspicuous until uredinial development is abundant. Lower leaves are infected first, with disease subsequently progressing upward on plants during
warm, humid weather.
Uredinia are small, oval, light yellowbrown pustules scattered irregularly on both sides of diseased leaves. Severely diseased leaves eventually become chlorotic,
making it difficult to observe the tiny, yellowbrown uredinia.
Telia, which form as plants near maturity, are brown, oblong to round, and covered by plant epidermis. Telia tend to coalesce to form gray patches on leaves, but they
are less abundant than uredinia.
Seeds and their accompanying structures are normally not infected.
Management
1. Grow resistant cultivars. Most of the commercial barley cultivars grown in the United States are susceptible to P. hordei with the exception of those bred in
Virginia.
2. Apply foliar fungicides.
Leaf Speckle
Leaf speckle is also called Septoria blotch, Septoria leaf blotch, Septoria leaf spot, Septoria speckled leaf blotch, speckled blotch, and speckled leaf blotch. Speckled
blotch is sometimes considered a separate disease caused by Septoria passerinii. However, it is included in this discussion because of the similarity in the life cycles
of the two fungi and the disease symptoms they produce.
Cause.
Stagonospora avenae f. sp. triticea (syn. Septoria avenae f. sp. triticea), teleomorph Phaeosphaeria avenaria f. sp. triticea (syn. Leptosphaeria avenaria f. sp.
triticea), and Septoria passerinii.

Page 64
Stagonospora avenae f. sp. triticea and S. passerinii survive as mycelia for 2 to 3 years in live plants and as pycnidia on residue that is buried in soil or lying on the
soil surface. Pycnidiospores produced on the previous year's residue are the most important source of inoculum during the growing season. During temperatures of
15° to 25°C and 6 or more hours of moisture in the autumn or spring, pycnidiospores are exuded from pycnidia in a cirrhi and disseminated by splashing and blowing
rain to the lower leaves of poorly growing plants. Pycnidiospores then germinate immediately in the presence of moisture and infect leaves. The resulting mycelia in the
leaves of winter barley will become inactive during the winter but will resume growth during warm weather.
Ascospores produced in perithecia as plants mature may infrequently serve as primary inoculum when they are disseminated by wind in the spring or autumn. Pycnidia
are produced late in the growing season.
Distribution.
Wherever barley is produced, but disease is most severe in cool, wet climates.
Symptoms.
Yellow to light brown lesions of various sizes occur primarily on leaves and leaf sheaths. Septoria passerinii produces long linear lesions with definite margins parallel
to the leaf veins.
Symptoms produced by S. avenae f. sp. triticea have indefinite margins with the yellowishbrown area blending into the green of the leaf blade and sheath.
Eventually, lesions containing numerous small, black pycnidia merge and cover large areas of the diseased leaf. Leaf margins often pinch or roll and become dry.
Management
2. Apply foliar fungicides to susceptible cultivars when weather favors disease development.
3. Plow under or burn infested residue, where feasible.
4. Rotate barley with resistant crops, such as legumes.
Leaf Spot
Both fungi were isolated from leaf spots.
Cause.
Monographella nivalis (syn. M. nivalis var. mayor) and Fusarium culmorum. Both fungi are seedborne and are isolated from different plant parts during plant
development. Therefore, endophytic growth as a latent phase of the fungi is hypothesized.
Distribution.
Germany.
Symptoms.
Spots first appear on lower leaves early in the growing season. Later, spots do not occur on intermediate leaves but will reappear on upper

Page 65
leaves of plants in their late tillering stages. Spots are 3 to 5 mm long and grayish green but later become black on the upper leaves.
Management.
Not reported.
Leptosphaeria Leaf Spot
Cause.
Leptosphaeria herpotrichoides (syn. Phaeosphaeria herpotrichoides) overwinters as mycelia and as ascospores in pseudothecia on infested residue. Free water
must be present on leaves for 48 hours or more for infection to occur.
Distribution.
Canada, Europe, and the United States in areas that have long periods of wet weather. Leptosphaeria leaf spot is considered a minor disease.
Symptoms.
Irregular, diffuse, yellow to tan spots occur on diseased leaves. Under extended wet conditions, up to 50% of the leaf may be affected.
Management.
Grow the most resistant cultivars.
Loose Smut
Loose smut is also called true loose smut, nuda loose smut, and brown loose smut.
Cause.
Ustilago nuda. Farr et al. (1989) consider U. nuda to be a synonym of U. tritici. Ustilago nuda differs from other smut fungi on barley in that it infects flowers.
Ustilago nuda is seedborne, surviving as dormant mycelia in embryos. When diseased seed germinates, mycelia grow systemically within plants toward the shoot
apex and inhabit seed primordia. Eventually, smutted heads consisting of masses of teliospores are produced in place of healthy kernels.
Smutted heads emerge from boots a day or two earlier than the heads of healthy plants. Each smutted head is enclosed in a fragile membrane that soon disintegrates,
allowing the teliospores to be released. Teliospores are disseminated by wind to the flowers of healthy barley plants and germinate at temperatures of 16° to 22°C in
moisture provided by dews or light showers. The germ tube penetrates the flower ovary and possibly the stigma with subsequent mycelial growth occurring in the germ
or embryo of the developing seed. The mycelium, which is both intercellular and intracellular, develops within gall tissues derived mostly from the rachilla cortex and
becomes dormant in the embryo until the following season.
Several physiologic races of U. nuda exist.
Distribution.

Page 66
Symptoms.
Infected seed does not have obvious external symptoms and germination is ordinarily not affected. Before heading, diseased plants have dark green, erect leaves with
chlorotic or yellowish streaks. Smutted heads consist of a brown to dark brown mass of teliospores enclosed by a fragile, gray membrane consisting of plant
epidermis. The membrane soon ruptures, leaving an erect, naked rachis that protrudes slightly above the reclining heads of healthy plants.
Sori have been reported in flag leaves of greenhousegrown 'Larker' barley, where they appeared prior to or occasionally at the same time as the emergence of
smutted or healthy heads from leaf sheaths. Frequently, heads did not appear nor were any present in the leaf sheath. Infrequently, auricles, ligules, and sheaths were
also involved.
Losses are generally directly related to the percentage of infected heads: 10% infected heads normally yields a 10% yield loss.
Management
1. Treat seed with a systemic fungicide seed protectant.
Net Blotch
Cause.
Pyrenophora teres, anamorph Drechslera teres. Pyrenophora teres has been divided into two forms based on symptomology. Pyrenophora teres f. teres is the
name for the netcausing isolates, and P. teres f. maculata for the spotcausing isolates. Similarly, the anamorphs are identified as D. teres f. teres and D. teres f.
maculata. However, some workers do not utilize the taxonomic forms but refer to the organism either as D. teres or P. teres. Barley is the only known host.
The source of primary inoculum may vary with geographical area and form of the causal fungus. Some researchers have reported the causal fungus overwinters either
as seedborne mycelia or as pseudothecia in infested residue. Wild grass species may also be a potential source of primary inoculum. Crossinoculation experiments in
Israel have shown that isolates from Hordeum murinum, H. murinum subsp. leporinum, H. marinum, and H. vulgare subsp. spontaneum are capable of infecting
cultivated barley. In western Australia, P. teres f. teres has been isolated from Hordeum species and Bromus diandrus. In California, P. teres f. teres was found to
have a wide host range: susceptible species were found in 15 of 16 host genera that were artificially inoculated.
During temperatures of 10° to 15°C and 100% relative humidity, spores are produced on residue and disseminated by wind to healthy plants. It is not known for
certain if primary inoculum consists of conidia or ascospores. Later in the growing season, conidia produced in pycnidia on primary lesions cause secondary infections
during cool and moist weather

Page 67
conditions. Production of secondary conidia occurs only on senescent or dead host tissue and requires leaf surface wetness, high relative humidity, and appropriate
temperature regimes. The duration of leaf surface wetness required for secondary infection ranges from 3.0 to 8.5 hours at temperatures of 8° to 20°C. Moisture on
leaf surfaces in the form of dew is more conducive to infection than splashing rain.
As plants mature, P. teres will grow into sheath and culm tissue, where pseudothecia are eventually produced later in the growing season. Diseased winter barley is
more prone to freezing injury of crowns.
van den Berg and Rossnagel (1991) reported that spot blotch caused by P. teres f. maculata in Saskatchewan closely followed plant development and that each leaf
was infected shortly after its emergence. Only conidia produced on infested stubble were reported to be responsible for the infection of the lower leaves. Conidia
produced on both stubble and the lower leaves caused most of the infections on the upper leaves. They concluded that infested crop debris acts as an inoculum
reservoir for the lower leaves and that infested crop debris and the lower leaves act as an inoculum reservoir for the upper leaves.
In Pennsylvania, winter barley has the greatest disease severity in the earliest plantings; however, if the weather becomes warm and humid, previous differences in
disease severity attributable to dates of planting are eliminated. Net blotch severity of winter barley also increases as root rot levels increase.
Distribution.
Symptoms.
Leaves, stems, and seeds are affected. Disease severity is greatest on the oldest leaves of winter barley. The netlike symptoms caused by P. teres f. teres initially are
brown spots or blotches near the tips of seedling leaves. Dark brown, narrow lines that run longitudinally and transversely in the lighter brown area give spots a netted
or crosshatched appearance. This symptom is best seen when leaves are held up to a light source. Spots increase in length to form short, narrow streaks or they
coalesce to form long, brown stripes with irregular margins. On older spots, netting or crosshatching is visible only at the margins.
Small, brown streaks that develop on glumes and indistinct brown lesions that develop on kernel bases cause reduced yields and shriveled seed. Diseased stems are
light brown and lack strength.
Pyrenophora teres f. maculata causes a ''spot form" of net blotch that may be confused with symptoms caused by Cochliobolus sativus on leaves and leaf sheaths.
Symptoms, which may involve the entire leaf, consist of dark brown, elliptical or fusiform lesions (3 × 6 mm) that may be surrounded by a chlorotic zone of varying
width, depending upon the cultivar.

Page 68
Management
2. Rotate barley with resistant crops.
3. Grow resistant cultivars. Resistance is simply inherited and conditioned by one or two genes. It has been reported that mixing barley cultivars in a field reduces
severity of the net blotch/scald complex; however, disease is reduced because of moderately resistant genotypes in the mixture and no yield benefits are apparent.
4. Apply foliar fungicides to highyieldpotential maltquality or seedproduction fields when weather conditions favor disease development. A biological control
consisting of a bacterium applied to leaves has shown promise in experiments.
5. Increasing inrow seed spacing from 2 to 4 cm between plants and row spacing from 12 to 28 cm has been reported to decrease disease severity.
6. Application of nitrogen as ammonium nitrate at Zadok's growth stage 30 has been reported to decrease disease incidence.
Pink Snow Mold
Pink snow mold is also called Fusarium patch.
Cause.
Microdochium nivale (syn. Fusarium nivale, Microdochium nivalis, and Gerlachia nivalis). The teleomorph is Monographella nivalis (syn. Calonectria
nivalis, C. graminicola, Griphosphaeria nivalis, Micronectriella nivalis, and Monographella nivalis var. mayor). Overseasoning of the fungi is primarily by
mycelia within diseased live plants that are covered by snow.
Leaf sheaths and blades are infected near the soil line during cool, wet weather in the autumn by mycelia growing from residue and by ascospores and conidia
produced on infested residue and disseminated by wind to barley seedlings. Mycelia will then grow from these primary infections when plants are covered by snow.
Secondary infection is caused primarily by conidia produced in the spring and infrequently by ascospores. Perithecia develop in lower leaf sheaths in late spring and
early summer during cool, wet weather.
Distribution.
Canada (Quebec), central Europe, Japan, and the mountain valleys of the western United States.
Symptoms.
The most obvious symptom is observed after the snow melts, when infested residue, leaf sheaths, and leaf blades have a pinkish color caused by the fungal mycelia
and sporodochia. Leaves are chlorotic and necrotic but remain dry and intact when the snow cover disappears and temperatures rise. In contrast, diseased leaves that
crumble after snowmelt are a characteristic symptom of both gray snow mold and speckled snow mold.
Management.
Avoid growing barley where there is a persistent snow cover.

Page 69
Powdery Mildew
Cause.
Erysiphe graminis f. sp. hordei (syn. Blumeria graminis f. sp. hordei) overwinters as cleistothecia on residue and as mycelia and conidia in live leaves. Primary
inoculum is ascospores that form in cleistothecia in the spring and are disseminated by wind to plants. Secondary inoculum is conidia that are produced when mycelia
are established on leaf surfaces during temperatures of 15° to 22°C and 100% relative humidity but without free water. Cleistothecia are formed on leaf surfaces as
plants approach maturity.
Barley is very susceptible during periods of rapid growth. Such rapid growth is frequently aided by heavy nitrogen fertilization that results in a dense stand of tender,
rank plants.
Distribution.
Symptoms.
Superficial mycelia, conidia, and conidiophores appear as a light gray powder or white spots on the upper surfaces of leaf blades, leaf sheaths, and floral bracts. Most
fungal growth occurs on upper leaf surfaces and, infrequently, on lower surfaces. The powderyappearing leaf areas enlarge, eventually causing leaves to become
chlorotic, then necrotic. In some cultivars, leaf tissue adjacent to mycelia becomes brown and necrotic. Numerous small, round, dark cleistothecia develop on
diseased areas and can be readily observed with a hand lens. Powdery mildew ceases to be a problem when the weather becomes dry and warm later in the growing
season.
Management
2. Apply a foliar fungicide if economically feasible.
Pythium Root Rot
Pythium root rot is also called browning root rot.
Cause.
Pythium arrhenomanes (syn. P. arrhenomanes var. canadense), P. graminicola, P. heterothallicum, P. irregulare, P. tardicrescens, P. torulosum, and P.
ultimum have been reported to be pathogenic to barley. Pythium irregulare was reported to be the most pathogenic Pythium species to barley at temperatures of
10° to 25°C.
Most Pythium species survive as oospores in residue and soil for 5 or more years. Infection occurs in 3 to 5 hours, usually in the autumn or spring, when oospores
germinate to form sporangia in which zoospores are produced.
Zoospores are released into moist soil and swim a short distance to root tips. Optimum infection is in soils with a high water potential of1 bar or less and low
temperatures. At warmer soil temperatures, oospores may ger

Page 70
minate directly to form only one germ tube that penetrates roots. Oospores are produced in diseased tissue and are released into soil when residue decomposes, or
oospores may survive in tissue when it remains intact.
Distribution.
Wherever barley is grown. Disease is most common under wet soil conditions.
Symptoms.
Pythium root rot occurs throughout the season. Early infections may kill seed and seedlings before or after they have emerged, resulting in uneven stands. Later
infections reduce plant vigor, tillering, stem elongation, and head size. Heads of diseased plants also are unable to emerge from the boot.
Crown or basal stem tissues are ordinarily not infected. Lower leaves may become chlorotic, then necrotic, and dry up due to poor root growth caused by the fungi
pruning root tips. Rootlets may be soft and a light to dark yellow or brown color that occurs mainly in the stele. Brown lesions may be present on larger roots. If soils
become dry, new root growth may occur.
Management
2. Drain areas in fields that tend to remain wet after the rest of the field has dried up.
3. Apply the recommended amounts of phosphorous fertilizer in a band or broadcast at planting time.
Rhizoctonia Root Rot
Rhizoctonia root rot is also called bare patch, barley stunt disorder, purple patch, Rhizoctonia patch, and stunting disease.
Cause.
Rhizoctonia solani, teleomorph Thanatephorus cucumeris. Rhizoctonia solani isolates causing root rot may belong in AG3, while those causing sharp eyespot
belong primarily in AG4 and a few in AG1. In the United Kingdom, R. solani isolates were found to belong in AG8 instead of AG3. Rhizoctonia solani survives
as sclerotia in soil and as mycelia in residues of a large number of host plants.
In Scotland, disease is restricted to light, sandy soils within 40 km of Elgin, Scotland, and occurs on barley following heavily fertilized grass that has been grazed by
cattle. In Australia, the disease is found on calcareous mallee soils in regions around Salmon Gums. In the United States, disease occurs where barley was either direct
drilled into stubble, sown with a minimum of preparatory tillage, or sown the same day soil was tilled. The herbicide chlorsulfuron has been reported to increase
disease.
Distribution.
Australia, Canada, England, South Africa, and the United States (Oregon and Washington).

Page 71
Symptoms.
At 12°C, seedling emergence and growth are reduced. However, at 18°C and 26°C, only seedling growth is reduced after emergence, but not the emergence itself of
germinated seedlings. Symptoms start 6 weeks after sowing as circular patches with distinct borders that vary from 20 to 300 cm in diameter and persist in the same
location for up to 4 years. Plants inside the circular patch are stunted and chlorotic, but those outside the patch are a normal green. Plant shoots tend to be spindly,
stunted, and abnormally erect. Leaf development is retarded, and after leaves form, they senesce prematurely and become chlorotic, starting at the leaf tip. Basal leaf
sheaths near the soil surface are often discolored brown.
Lesions on diseased primary and secondary roots and subcrown internodes are brown and often girdle the root. Cortices collapse and roots have pinchedoff
pointed tips or are frequently rotted back to brown stumps. Surviving roots often produce large numbers of lateral roots, which results in a heavily branched root
system with a large amount of cortical tissues and root tips that have sloughed off.
A number of plants die prematurely. Those that survive are poorly developed and yield little grain.
Management.
The disease apparently does not occur in the northwestern United States if some time has elapsed between tillage and sowing. The disease is more common in barley
grown in minimumtillage systems. Compared with notill or minimumtillage systems, cultivation prior to sowing reduces disease incidence in Australia. Under zero
tillage conditions, nitrogen in the form of ammonium sulfate, sodium nitrate, or urea reduces disease.
Scald
Scald is also called barley scald, leaf scald, and Rhynchosporium scald.
Cause.
Rhynchosporium secalis (syn. Marsonia secalis) overwinters primarily as stroma either in lesions on winter barley that was infected in the autumn or in residue on the
soil surface. Primary inoculum is conidia that are produced in the spring on stroma during cool temperatures (10°18°C optimal) and humid weather. Conidia are
disseminated primarily by splashing water and, for a short distance, by wind. Moisture in the form of rain is more conducive to infection than dew. Secondary inoculum
consists of conidia produced in both new and old lesions during cool and humid weather.
Rhynchosporium secalis can be seedborne as mycelia in the pericarp and hull. Greenhouse tests demonstrated the transmission of the fungus from the seed to the
seedling: at a soil temperature of 16°C, hyphae invaded the coleoptile as it emerged from the embryo. However, the importance of seedborne inoculum in the field is
not well known.
Scald is more severe under reduced tillage conditions and irrigation. Different races have been identified.

Page 72
Distribution.
Symptoms.
Lesions occur on coleoptiles, leaves, leaf sheaths, glumes, floral bracts, and awns. Young lesions occur as oval to irregularshaped blotches that are a dark to pale
gray or bluishgray color. Later, lesions become watersoaked and, as tissues die, change to brown, then to light tan bordered by a brown margin that is sometimes
surrounded by a chlorotic area. Often, lesions have a zonate appearance. Inconspicuous brown spots may occur on the tips of glumes.
An unusual symptom developed on Ethiopian barley cultivars inoculated with an R. secalis isolate from Montana. Leaf blades were free of symptoms but brown
discoloration and subsequent wilting of leaf sheaths occurred.
Management
1. Rotate barley with other crops. Barley is the only known host to R. secalis.
2. Plow under infected crop residues.
3. Grow resistant cultivars. It has been reported that mixing barley cultivars in a field reduces severity of the net blotch/scald complex. Disease is reduced because of
moderately resistant genotypes in the mixture, however, and no yield benefits are apparent.
Sclerotinia Snow Mold
Cause.
Sclerotinia borealis (syn. Myriosclerotinia borealis) overseasons as sclerotia in residue. In the autumn, sclerotia germinate to produce apothecia on which
ascospores are formed. Ascospores are disseminated by wind to healthy plants. Sclerotinia borealis has been identified on cocksfoot, Dactylis glomerata.
Distribution.
Canada (Quebec), central Europe, Japan, and the mountain valleys of the western United States.
Symptoms.
Symptoms are observed in isolated patches throughout a field after the snow melts. Dead leaves on plants are gray and appear "thready" or decomposed with only the
vascular tissue remaining. Numerous black sclerotia (24 mm long) are produced in diseased tissue during late spring and summer.
Management.
Do not grow barley in areas of prolonged snow cover.
Septoria Speckled Leaf Blotch
Cause.
Stagonospora avenae f. sp. triticea (syn. Septoria avenae f. sp. triticea), teleomorph Phaeosphaeria avenaria f. sp. triticea (syn. Leptosphaeria avenaria f. sp.
triticea). Septoria passerinii is also reported to be a causal fungus.
Survival, for at least 2 years, is by pycnidia and pseudothecia in infested

Page 73
residue. Primary inoculum is either pycnidiospores or ascospores that are disseminated by splashing water to host plants. Pycnidiospores from overwintering pycnidia
also are suspected to provide continuous inoculum throughout the growing season.
Extended periods of moisture at 97% relative humidity and above, together with day temperatures of 16° to 23°C and night temperatures of 10° to 20°C, are optimal
for pycnidiospore germination. Optimum temperatures for infection are 16° to 18°C during the day and 11° to 14°C at night. Pycnidia form on diseased tissue later in
the growing season.
Distribution.
Worldwide.
Symptoms.
Grayishgreen lesions of variable sizes and shapes occur on leaves and leaf sheaths. Later in the growing season, the lesions turn light tan. Stagonospora avenae f. sp.
triticea causes lesions with indefinite margins, whereas S. passerinii causes linear lesions with definite margins that are parallel to the leaf veins.
Young lesions are generally lensshaped but later may expand, merge, and cover much of the leaf. Leaf margins roll and become dry. Pycnidia begin to appear later in
the growing season as small, black dots within lesions. Later, large blotches occur as leaves and leaf sheaths senesce, and numerous pycnidia are produced.
Management
2. Rotate barley with nonhosts.
Sharp Eyespot
Sharp eyespot is also called Rhizoctonia root rot in some literature.
Cause.
Rhizoctonia cerealis. However, R. solani is still reported in some literature as a causal fungus although R. cerealis and R. solani were separated into two species in
1977. Where R. solani is attributed as a cause, isolates are reported to belong in the AG4 group and a few in AG1.
Rhizoctonia cerealis survives as sclerotia in soil or as mycelia in residues of a large number of plant hosts. Sclerotia germinate or mycelia grow from residue to infect
roots and culms, particularly in cool soils with 20% or less moisture. Barley may be infected any time during the growing season, but damage is most severe when
seedlings are infected. Barley is not as susceptible as oat, rye, and wheat.
Distribution.
Symptoms.
Serious losses rarely occur. Diamondshaped lesions that resemble those of eyespot, but are more superficial, occur on lower leaf sheaths. Lesions are light tan with
dark brown margins and frequently have dark mycelium on them. Sclerotia may develop in lesions and between culms and leaf sheaths.

Page 74
Seedlings may be killed, but when roots are infected, new ones may be produced. Plants are stiff and grayish; they are delayed in maturity, lodge, and produce white
heads.
Management.
No management is effective. Vigorous plants growing in wellfertilized soil are not as likely to become as severely diseased as plants growing in nutrientdeficient soil.
Southern Blight
Southern blight is also called foot rot and white rot.
Cause.
Sclerotium rolfsii, teleomorph Athelia rolfsii, presumably overseasons as sclerotia and mycelial strands that also function as the main infective propagules.
Dissemination is by any means that moves infested soil. Disease is favored by high temperatures of around 30°C and periods of high relative humidity and moisture.
Distribution.
Brazil, India, Puerto Rico, and the United States (California). Southern blight is a rare disease on barley.
Symptoms.
Groups of plants wilt and appear chlorotic or "blighted." Small, irregularshaped or elongated, necrotic spots develop on the base of the stem near the soil surface.
Spots eventually develop into lesions that further enlarge, coalesce, become sunken, and ultimately girdle the plant. Subsequently, stem tissues become soft and
necrotic for approximately 2.50 to 3.75 cm above and below the soil line. The entire plant becomes chlorotic and, eventually, white or "bleached" in appearance.
Diseased plants are stunted, and tillering and root length are reduced. Eventually, sclerotia develop on necrotic tissues near the soil line.
Similar symptoms have been reported from Brazil. White mycelium and sclerotia occur on necrotic areas of roots, crowns, and lower portions of stems. Plants
become white in appearance and die.
Management
1. Treat seed with a seedtreatment fungicide.
2. Do not grow barley in fields in which susceptible crops have grown.
4. Maintain proper plant population to prevent spread of the pathogen from plant to plant.
Speckled Snow Mold
Cause.
Typhula ishikariensis (syn. T. ishikariensis var. idahoensis, T. ishikariensis var. ishikariensis, and T. ishikariensis var. canadensis). Typhula ishikariensis
survives as sclerotia under a thick snow cover. Sclerotia germinate during wet weather in the autumn to produce either basidiocarps on which basidiospores are borne,
or hyphae. Basidiospores are released in early to

Page 75
midNovember in the northwestern United States and are disseminated by wind to seedlings. The optimum temperature for infection is 1°C. Typhula ishikariensis
has been identified on cocksfoot, Dactylis glomerata.
Distribution.
Canada (Quebec), central Europe, Japan, and the mountain valleys of the western United States. Speckled snow mold is associated with snow cover.
Symptoms.
A few or many necrotic leaves, which are covered with a thick, graywhite mycelium, dry up and disintegrate when the snow cover has melted and temperatures rise.
The numerous dark sclerotia (0.22.0 mm in diameter) produced under leaf sheaths, within plant tissue, or scattered throughout the mycelium give a "speckled"
appearance to diseased plants. Plants die when crowns become diseased.
Management.
Do not grow barley in areas of prolonged snow cover.
Spot Blotch and Associated Seedling and Crown Rots
This disease syndrome is also called black point, head blight, Helminthosporium blight, Helminthosporium head blight, and kernel blight. Spot blotch and associated
seedling and crown rots also may be considered part of the common root rot syndrome.
Cause.
Bipolaris sorokiniana (syn. Helminthosporium sativum and H. sorokinianum), teleomorph Cochliobolus sativus. Bipolaris sorokiniana is seedborne and
overwinters as mycelia and conidia on residue and seedling leaves of winter barley, and as conidia in soil. Conidia are produced in spring on either infested residue or
wild grasses and are disseminated by wind to seedlings. Seedborne inoculum results in seedling blight and in root and crown rot in dry, warm soils.
Leaf spots will begin to develop at temperatures lower than 20°C, but optimal symptoms, including a pronounced chlorosis, develop at temperatures of 20°C and
above during wet conditions or high relative humidity. High light intensities favor leaf spot development, but incubation of diseased plants under temporary low light
conditions results in chlorosis and accelerated senescence of leaves.
Based on their virulence to barley cultivars, three pathotypes of B. sorokiniana (labeled 0, 1, and 2) currently have been identified.
Distribution.
Wherever barley is grown in warm, humid conditions.
Symptoms.
Seedlings may be killed after they have emerged or, less frequently, before emergence from the soil. Leaves of diseased seedlings are dark green. At their bases near
the soil line, leaf sheaths have dark brown to black lesions that eventually extend into the leaf blades. Crowns and roots are dark brown and rotted, and seedlings are
dwarfed, chlorotic, and excessively tillered. Later, head emergence and kernel filling of the dis

Page 76
eased plant may be affected, depending upon how severe the disease was when the plant was a seedling.
Round to oblong (15 × 225 mm), dark brown spots with definite margins appear on lower leaves following warm, moist weather favorable for disease development.
The spots may eventually coalesce to form lesions that cover large areas of the leaf. Older lesions are olivecolored due to sporulation of B. sorokiniana. Severely
diseased leaves will completely dry up.
Lesions on floral bracts and kernels vary from small black spots to an overall dark brown discoloration of the kernel end. Browning or blackening of lemma and palea
is due to discoloration of the pericarp layer and underlying embryo region. Early head blight causes sterility or killing of individual kernels soon after pollination.
Infected kernels may result in seedling blight if the kernels are sown, and they are normally discounted as unacceptable for malting purposes.
Management
3. Apply a foliar fungicide if weather conditions favor the spread of the disease.
4. Rotate with resistant crops, such as legumes.
Stagonospora Blotch
Stagonospora blotch is also called glume blotch, and leaf and glume blotch.
Cause.
Stagonospora nodorum (syn. Septoria nodorum), teleomorph Phaeosphaeria nodorum (syn. Leptosphaeria nodorum). Stagonospora nodorum survives for up
to 3 years as mycelium in live plants and seed, and for an indefinite time as pycnidia on residue. During temperatures of 20° to 27°C and wet weather in the autumn or
spring, pycnidiospores are exuded from pycnidia in a cirrhi and disseminated by splashing and blowing rain to the lower leaves of plants. Spore germination and
infection are optimum at temperatures of 15° to 25°C and 6 or more hours of wetness between flowering and grain harvest.
Secondary pycnidia and pycnidiospores are produced 10 to 20 days after infection. In Denmark, ascospores, which reportedly are produced in pseudothecia as
barley matures in late summer or early autumn, are disseminated by wind to other plants. However, ascospores are not known to be produced in North America.
Stagonospora nodorum infects both wheat and barley.
Distribution.
Symptoms.
Glumes, culms, leaf sheaths, and leaves are infected; however, little damage occurs until plants approach maturity. The first symptoms ap

Page 77
pear in the spring as brown or gray spots on the leaves and sheaths or at the junction of the leaf and sheath. Later, oval, redbrown spots (12 cm long) that develop
on leaf veins have chlorotic margins that may extend to the leaf tip. Irregularshaped lesions that develop at the junction of the leaves and sheaths affect the entire leaf.
Diseased leaves senesce earlier than healthy leaves.
As lesions on leaves begin to age, portions of their necrotic centers fade to light brown or gray but longitudinal brownpigmented streaks remain in the lesion.
Eventually, dark pycnidia become readily visible as black specks throughout the lesions. Diseased stem nodes, which turn brown and shrivel, are speckled with dark
pycnidia, as are leaf lesions. Stem infections cause straw to lodge and bend over above the nodes.
Two to 3 weeks after the head emerges, small gray to brown spots can be observed on the top third of glumes. Eventually, these spots enlarge and become a darker
chocolate brown. Later, the centers of spots become gray with numerous pycnidia that resemble tiny black specks similar to those in leaf and stem lesions. Seed may
become diseased with both the attached lemma and palea, and the caryopsis becoming discolored. Pycnidia also develop on diseased seed surfaces. These symptoms
may be confused with those of black chaff or basal glume rot. However, Stagonospora blotch spots do not form streaks and are not as sharply defined or as dark
brown as those of black chaff. Stagonospora blotch also does not have the watersoaked appearance of basal glume rot.
A Septoria sp. that is different pathologically from S. nodorum has been reported to cause oval leaf spots with a buff center that contains numerous pycnidia. This
Septoria sp. was also isolated from glumes.
Management
1. Sow certified, diseasefree seed that has been cleaned and treated with a seedprotectant fungicide.
2. Grow the most tolerant barley cultivar. Several winter barley cultivars have been reported to have some resistance.
3. Plow under or burn infested residue where feasible.
4. Apply a foliar fungicide if conditions warrant it.
5. Rotate barley every 3 or 4 years with a nonsusceptible crop.
6. Sow winter barley after Hessian flyfree date.
Stem Rust
Cause.
Puccinia graminis f. sp. tritici and P. graminis f. sp. secalis are heteroecious rust fungi that have the barberries Berberis vulgaris, B. canadensis, B. fendleri and
some species of Mahonia as the alternate host. Japanese barberry, B. thunbergii, is thought to be immune.
Puccinia graminis overwinters as teliospores on barley and wheat residue and as urediniospores on winter wheat and barley in the southern Great

Page 78
Plains. Severity of stem rust on barley in the northern Great Plains depends on the amount of inoculum, in the form of urediniospores, that overwinters in the southern
United States and northern Mexico and is disseminated north by wind.
The full life cycle is as follows. The teliospore, or overwintering stage, is produced on barley as the plants mature. Teliospores germinate in spring to produce a hyaline
basidium on which four hyaline basidiospores, or sporidia, develop on sterigmata. Basidiospores are then disseminated by wind to barberry plants, where infections
result in pycnia. Pycnia exude slender pycniospores and receptive hyphae in sticky drops of liquid that are attractive to insects. Pycniospores are transferred, primarily
by insects, from one pycnia to another, where pycniospores germinate and exchange genetic material with receptive hyphae. The result is the formation of aecia,
normally on the bottom of the leaf. Aeciospores are then produced in aecia formed on the underside of barberry leaves and disseminated by wind to barley. The result
of the aeciospore infection is the formation of uredinia. Urediniospores are produced in uredinia to serve as the secondary inoculum during the growing season.
Urediniospores are disseminated by wind to barley plants to cause secondary infections throughout the growing season until plants reach maturity. The optimum
temperature for disease development is 20°C.
Several races are known to exist. A new race called QCC has developed that is capable of attacking barleys that possess the T gene source of resistance to stem rust.
At present, all barley varieties and some winter wheat varieties are susceptible, but durum wheat and hard red spring wheat are resistant to P. graminis f. sp. tritici
and P. graminis f. sp. secalis.
Distribution.
Symptoms.
Stem rust occurs on stems, leaf sheaths, leaf blades, glumes, and beards. Uredinia are characteristic brickred pustules with ragged edges that were created as the
urediniospores broke through the leaf epidermis. Dark brown to black teliospores form in old uredinial pustules. Basidia and basidiospores are colorless and
microscopic and cannot be readily observed without the aid of magnification. Pycnia are small orange spots on upper barberry leaves with a drop of liquid in the
center of the spot. Aecia and aeciospores are orange ''belllike" structures on the underside of barberry leaves. During severe disease development, kernels are
shriveled and stems become brown, dry, and brittle and often break over.
Management
2. Eliminate the common barberry bushes from the vicinity of any barley fields.
3. Apply fungicides in emergency situations.

Page 79
Stripe Rust
Stripe rust is also called barley stripe rust, barley yellow rust, glume rust, and yellow rust.
Cause.
Puccinia striiformis f. sp. hordei (syn. P. glumarum) is a rust fungus whose alternate host is not known. The fungus oversummers as urediniospores that are
disseminated by wind to other plants, such as rye, wheat, barley, and grasses. Optimum disease development is at temperatures of 10° to 15°C with periodic rain or
dew. Little or no infection occurs during warm weather in the summer. Teliospores are formed but are not known to function as overwintering spores.
Distribution.
In North America, stripe rust occurs at the higher elevations and cooler climates along the Pacific Coast and intermountain areas from Canada to Mexico. It also
occurs under the same environmental circumstances in South America and in the mountainous areas of central and western Europe, South Asia, and Africa.
Symptoms.
Stripe rust symptoms occur on leaves and heads during cool weather in the spring before the symptoms of other rusts are apparent. Yellow uredinia appear on barley
foliage formed in the autumn and on new foliage produced early in the spring. Eventually, uredinia coalesce to form long stripes between veins of leaves and sheaths.
Small, linear lesions also occur on floral bracts. Telia develop as narrow linear dark brown pustules covered by the epidermis.
Management
TakeAll
Takeall is also called dead head and white head.
Cause.
Gaeumannomyces graminis var. tritici survives as mycelia in live overwintering plants, mycelia and perithecia in infested residue for about 10 months, mycelia in
soil outside of residue for about 5 months, and, parasitically, on the roots of a number of different grasses. Maize roots can also become infected and serve as a
source of inoculum to infect subsequent barley crops.
Dissemination of the fungus is by any means that moves residue. Planttoplant spread occurs by hyphae growing through the soil from root to root or directly by root
to root contact. Ascospores are produced in perithecia during wet weather but apparently are not disseminated either by splashing water or wind a great distance.
Therefore, ascospores are not considered important in either the dissemination of the disease or the infection of susceptible plants.

Page 80
Seedlings become infected in the autumn or spring when roots grow in the vicinity of residue precolonized by G. graminis var. tritici. Plants infected early in the
growing season become the most severely diseased. Disease is favored by high pH soils that are deficient in nitrogen and phosphorous and that remain cool and wet (
1.2 to 1.5 bars) for prolonged periods of time.
Takeall is more severe on wheat than barley; however, barley is usually more severely affected than rye.
Distribution.
Symptoms.
Takeall symptoms become most obvious at heading as patches or circular areas of plants in a field are uneven in height and appear to be in different stages of
maturity. The first symptom on a diseased plant is light brown to dark brown necrotic lesions on roots. At the jointing stage, most roots are brown to black, sparse,
dead, and brittle. Plants eventually die, or if they are still alive, they are stunted, leaves are chlorotic, and the whole plant is easily broken free of crowns when pulled
from the soil.
A dark discoloration, which is a good diagnostic characteristic, occurs on the stem above the soil line, together with a mat of dark brown mycelium that grows under
the lower sheath between the stem and the inner leaf sheaths. Plants have few tillers and heads are bleached (white heads), sterile, and ripen prematurely.
Management
1. Rotate barley with a resistant crop.
2. Sow winter barley as late as feasible.
Verticillium Disease
Cause.
Verticillium dahliae. Oat and wheat are also susceptible but do not develop severe symptoms.
Distribution.
United States (Idaho).
Symptoms.
Leaves, usually along the leaf margin, have longitudinal chlorotic stripes in which the vascular bundles have become discolored brown. Chlorotic leaves are often
flaccid and eventually become necrotic. Symptoms are similar to those associated with Cephalosporium stripe.
Management.
Resistance is reported to exist among present cultivars.
Wirrega Blotch
Cause.
Drechslera wirreganensis. Six other grasses are hosts. Disease is favored by reduced tillage practices.
Distribution.
Australia, in areas with rainfall exceeding 350 ram.

Page 81
Symptoms.
Two symptoms occur on leaves: a blotch and a spot. Blotches are large, medium brown, oval lesions, sometimes with chlorotic margins. Depending on the cultivar,
blotches may remain small or extend along the full length of the leaf to give the appearance of a toxin spreading from the lesion. At the center of a blotch, tissue
becomes necrotic and dry until it eventually tears apart.
Spots are small and dark brown with lightcolored centers, usually without a chlorotic margin. There is often a hole at the center of a spot.
Management
1. Some barley cultivars are resistant.
2. Change tillage practices from reduced tillage to conventional tillage.
Yellow Leaf Spot
Yellow leaf spot is also called blight, leaf spot, and tan spot.
Cause.
Pyrenophora triticirepentis (syn. P. trichostoma), anamorph Drechslera triticirepentis (syn. Helminthosporium triticirepentis).
Pyrenophora triticirepentis overwinters as pseudothecia on infested residue. During frequent rains and cool, cloudy, humid weather early in the growing season,
primary inoculum is ascospores that are released and disseminated by wind to plants. Later in the growing season, under similar conditions, secondary inoculum is
provided by conidia produced in older lesions and disseminated by wind to plants. In the autumn, pseudothecia are produced on diseased culms and leaf sheaths.
Distribution.
Worldwide; however, barley is rarely affected.
Symptoms.
Initially, tan flecks appear on both sides of lower leaves and progress upward to upper leaves during the growing season. Flecks eventually become tan, diamond
shaped lesions up to 12 mm long, with a yellow border and a dark brown spot in the center that is caused by sporulation of P. triticirepentis. Lesions eventually
coalesce to cause large areas of leaf to die from the tip inward. Pseudothecia will eventually develop on residue and appear as small, dark, raised bumps.
Management
1. Apply a foliar fungicide before the disease becomes severe and if weather conditions favor spread of the disease.
3. Grow resistant barley cultivars.

Page 82
Cereal Cyst
The cereal cyst nematode is sometimes called the oat cyst nematode.
Cause.
Heterodera avenae, H. hordecalis, and H. latipons survive as eggs and as larvae within cysts in soil for several years. Dissemination is by any means that moves soil.
The optimum emergence of larvae from eggs from midwinter until spring occurs at a temperature of 10°C and moist soil; larvae then migrate to nearby plant roots.
Optimum infection occurs behind the growing point at 20°C. As nematodes mature, they swell and erupt through root tissues. Males return to a vermiform shape, but
females become lemonshaped as egg production begins. Within 2 months of infection, the female dies and the body hardens into a cyst that protects eggs and larvae
from growing season to growing season. One generation is completed each growing season.
Distribution.
Australia, Canada (Ontario), Middle East, northern Europe, India, Japan, New Zealand, and the United States (Idaho, Oregon, Washington).
Symptoms.
The cereal cyst nematode is the most important nematode pathogen of barley; yield reductions up to 22% have been reported. Symptoms are most pronounced on
plants growing in light, sandy soils. A severe infestation causes patches of weeds to overgrow stunted barley plants whose leaves have a chlorotic discoloration similar
to a nitrogen or phosphorous deficiency. Head emergence is delayed and the number of spikelets is reduced.
Roots are stunted and knotted and have a pronounced proliferation. Immature, white cysts that are approximately the size of pinheads or smaller start to appear on
roots at heading.
Management
2. Rotate barley with a nongrass crop.
Root Gall
The disease caused by the root gall nematode is known as "krok" in Scandinavia.
Cause.
Subanguina radicicola (syn. Ditylenchus radicicola and Anguillulina radicicola) survives by continuous habitation in host roots. Larvae penetrate roots and
develop in cortical tissue, forming a gall in 2 weeks. Mature females begin egg production within galls. Eventually, galls disintegrate and release into the soil larvae,
which cause secondary infections. A generation of nematodes is completed in about 60 days.

Page 83
Distribution.
Canada, Europe, Russia, and the United States.
Symptoms.
Top growth of seedlings is reduced, and the tips of outer leaves are chlorotic. Roots are branched, twisted, and bent at the sites of the numerous inconspicuous galls
that vary in diameter from 0.5 to 6.0 mm. The centers of the larger galls have a cavity that is usually filled with nematode larvae.
Management.
Rotate barley with noncereal crops.
Root Knot
The root knot nematode is also called the cereal root knot nematode.
Cause.
Meloidogyne naasi is an endoparasitic nematode that overwinters as eggs in soil. In the spring, larvae hatch from eggs and infect roots. By the middle of summer,
females inside root knot tissue release their eggs into the soil.
Distribution.
Northern Europe, Iran, the United States, and Yugoslavia.
Symptoms.
Stunted, chlorotic plants occur in patches that range in size from a few square meters to large areas within a field. Diseased plants have short heads with no spikelets
or are completely lacking a seed head. Swellings or thickenings comprised of swollen cortical cells and bodies of nematodes containing egg masses can be found on
roots, especially near the root tips in the sprirng and summer. When root knots are cut open, egg masses within the knot will turn dark when exposed to the air.
Management
1. Sow barley in autumn.
2. Rotate barley with root crops such as sugar beet.
Root Lesion
Cause.
Pratylenchus crenatus, P. fallax, P. neglectus, and P. thornei overwinter as eggs, larvae, or adults in host tissue and soil. At temperatures of 13°C and above,
both larvae and adults penetrate roots, where they move through cortical cells. The females deposit eggs as they migrate through tissue. Older roots are eventually
abandoned by nematodes and new roots sought as sites for further penetration and feeding.
Distribution.
Wherever barley is grown. Pratylenchus thornei is found in the dry regions of Australia and Israel; P. crenatus and P. thornei are common in the United States; and
P. crenatus, P. fallax, and P. neglectus are common in lighter soils in Europe.
Symptoms.
Plants will be stunted, chlorotic, and under moisture stress. Rhizoctonia solani often infects through nematode wounds and eventually

Page 84
rots roots and crowns. New roots may also become dark and stunted, with resultant loss in yield.
Management
1. Sow in autumn.
2. Use soil nematicides where high costs warrant them.
Stunt
Cause.
Merlinius brevidens, Tylenchorhynchus dubious, and T. maximus are ectoparasites that feed on external cells and are favored by wet soils.
Distribution.
Peru and the United States.
Symptoms.
Damage has been reported only on winter barley. Plants in areas throughout a field of approximately 1 m in diameter have short, stubby roots, are stunted and
chlorotic, and have fewer tillers and kernels than healthy plants.
Management.
Not reported.
Aster Yellows
Cause.
The aster yellows phytoplasma (AYPLO) survives in several plants and leafhoppers. AYPLO is transmitted primarily by the aster leafhopper, Macrosteles
fascifrons, as it feeds on diseased plants. Transmission of AYPLO is less common by Endria inimica and M. laevis.
Two strains of AYPLO exist: the eastern strain (NAYPLO) and the western strain (CAYPLO). Disease development occurs at temperatures of 25° to 32°C, with
the most severe symptoms occurring at the higher temperatures.
Distribution.
Generally throughout eastern Europe, Japan, and North America. Aster yellows is rarely severe on barley.
Symptoms.
Seedlings will either die 2 to 3 weeks after infection or, if they survive, plants will be stunted, leaves will be entirely chlorotic or have yellow blotches, and heads will be
sterile with distorted awns.
Infection of older plants causes leaves to become stiff and yellow, red, or purple inward from the leaf tip or margin. Root systems may not be well developed.
Management.
Not reported.

Page 85
African Cereal Streak
Cause.
African cereal streak virus (ACSV) is limited to the phloem. ACSV is transmitted only by the delphacid leafhopper, Toya catilina. The natural virus reservoir is
presumably native grasses. Disease development occurs at temperatures of 20°C and above.
Distribution.
East Africa.
Symptoms.
Initially, faint broken chlorotic streaks begin near the leaf base and extend upward. Eventually, definite alternate yellow and green streaks develop along the entire leaf
blade, which eventually becomes completely chlorotic. Leaves formed after infection develop a "shoestring" habit and die.
Young plants become chlorotic, severely stunted, and die. Older plants become soft, flaccid, and velvety to the touch and have yellow, distorted heads that yield little
seed. A phloem necrosis develops.
Management.
Not reported.
American Wheat Striate Mosaic
Cause.
American wheat striate mosaic virus (AWSMV) is in the rhabdovirus group. AWSMV is transmitted by the leafhoppers Endria inimica and Elymana virenscens.
Distribution.
Canada and the central United States.
Symptoms.
Plants are stunted and have slight to moderate leaf striations that consist of yellow to white parallel streaks.
Management.
Not reported.
Australian Wheat Striate
Cause.
Australian wheat striate virus (AWSV) is also known as chloris striate mosaic virus (CSMV). AWSV is transmitted by the leafhoppers Nesoclutha obscura and N.
pallida but is not saptransmissible.
Distribution.
Australia. The disease is of little importance in barley.
Symptoms.
Plants are dwarfed and have fine, broken yellow to gray streaks or stripes on leaves.
Management.
No management measures are necessary.

Page 86
Barley Mosaic
Cause.
Barley mosaic virus (BMV) is seedborne and is transmitted both by the corn leaf aphid, Rhopalosiphum maidis, and mechanically. Oat and wheat are also hosts.
Distribution.
India.
Symptoms.
Diseased plants are generally stunted. Initially, leaves are chlorotic but later develop mosaic symptoms. Diseased seeds, which are small and shriveled, have poor
germination.
Management.
Barley Stripe Mosaic
Barley stripe mosaic is also known as barley false stripe, false stripe, lantern head, and stripe mosaic.
Cause.
Barley stripe mosaic virus (BSMV) can remain viable in seed for up to 8 years and overwinters in wild oat, Avena fatua. When infected seed germinates, the highest
numbers of resulting seedlings become diseased at temperatures of 20° to 24°C. BSMV is spread when injured leaves rub against each other and by infected pollen,
but it is not known to be transmitted by insects or other means. BSMV is spread further in barley sown in the spring than in the autumn.
Distribution.
Southern Asia, Australia, Europe, Japan, Mexico, western North America, and Russia.
Symptoms.
Symptoms vary with the mode of infection and temperature. Leaf symptoms that result from seedborne infection are a mottling or spots that are either narrow or wide,
numerous or few, and continuous or broken. The color of the mottling or spots may be light green, tan, yellowish, or bleached white, which contrasts to the rest of the
green leaf. Infrequently, entire diseased leaves may be nearly white.
Virulent strains of BSMV cause brown stripes, which are continuous or broken and have irregular margins, often form a V or chevronshape on leaves. Sometimes
plants are severely stunted, and florets, which are sterile, may have no heads or poorly developed heads and kernels. Protein synthesis is affected.
Management
3. Rotate barley with nongrass crops.

Page 87
Barley Yellow Dwarf
Barley yellow dwarf is also called yellow dwarf.
Cause.
Several luteoviruses are grouped under the name barley yellow dwarf virus (BYDV). The viruses share the characteristic of infecting gramineous plants, but differ in
various other properties, such as virulence, host range, serological behavior, and transmissibility by aphid vectors.
BYDV survives or is reservoired in perennial grasses and grains sown in the autumn. Perennial grasses are a large reservoir of BYDV but may not serve as the most
important source of inoculum. In Canada, inoculum carried by aphids from elsewhere was considered to be the main source of infection rather than grasses, winter
wheat, or maize. In the United States and possibly within North America, most overwintering is reported to occur in warmer barleygrowing areas. In areas where
oversummering is a factor, maize is a reservoir for both aphids and some isolates of BYDV.
BYDV is transmitted by several species of aphids, including the corn leaf aphid, Rhopalosiphum maidis; oat birdcherry aphid, R. padi; rice root aphid, R.
rufiabdominelis; Russian wheat aphid, Diuraphis noxia; early instars of greenbug, Schizaphis graminum; and the English grain aphid, Sitobion avenae.
Based on transmission by different insects, five types of BYDV are recognized. MAV is transmitted specifically by S. avenae; RMV by R. maidis; RPV by R. padi;
SGV by S. graminum; and PAV nonspecifically by R. padi and S. avenae and infrequently by D. noxia. However, some BYDV isolates obtained from cereal plants
in Victoria, Australia were serologically similar to MAV but distinct in being readily transmissible by the aphid R. padi. Some RMV isolates from Montana were
transmitted efficiently by both R. maidis and S. graminum, and two RMV isolates were occasionally transmitted by R. padi. After virus acquisition, an aphid may
transmit BYDV for the rest of its life.
Subsequent investigations of serological relationships showed a parallel separation into serotypes. Vector specificities, serotyping, and other characteristics have been
used to group MAV, PAV, and SGV serotypes into BYDV subgroup 1 and RPV and RMV serotypes into BYDV subgroup 2.
BYDV is not transmitted through eggs, newborn aphids, seed, or soil, or by mechanical means. Disease development occurs during temperatures of 10° to 18°C and
moist conditions that favor grass and cereal growth, and aphid reproduction and migration. Storm fronts aid flights of aphids, which may cover hundreds of kilometers
from southern areas, where most overwintering is reported to occur, to Canada and the Upper Midwest in the United States.
Distribution.
Africa, Asia, Australia, Europe, New Zealand, North America, and South America.

Page 88
Symptoms.
Symptom expression is greatest at low temperatures of around 16°C. Plant stands appear uneven due to stunting of plants that were infected early in the growing
season. This latter symptom is confused with nutrient deficiency and other unfavorable growing conditions.
Initially, faint yellowishgreen blotches occur near the leaf tip, the leaf margin, or on the leaf blade itself, a characteristic that helps to distinguish yellow dwarf from
other maladies. Discolored areas enlarge and coalesce at the leaf base, but tissue next to the midrib remains green longer than the rest of the leaf. Eventually, diseased
plants are dwarfed and leaf color becomes a bright yellow or occasionally red or purple. The bright yellow discoloration occurs on older leaves but not the youngest
leaves except in late infections when only flag leaves show symptoms.
In the laboratory, root dry weight, length, and numbers were reduced the most when plants were infected early. Root development stops when shoots display
symptoms and is not correlated to the degree of BYDV resistance.
Infection by BYDV increases freezing injury to crowns of winter barley. There is also a reduction in malt quality and yield.
Management
1. Grow resistant or tolerant cultivars.
2. Avoid sowing in early autumn or late spring.
Barley Yellow Mosaic
Cause.
Barley yellow mosaic virus (BYMV) survives up to 5 years in airdried soil. The soil fungus Polymyxa graminis is thought to be the vector. Dissemination is by any
means that will move soil, particularly machinery, wind, and water. Two types of BYMV have been reported from Germany. One type is disseminated both by soil
and mechanically, while the other type is disseminated only by soil.
Distribution.
Belgium, England, France, Germany, and Japan.
Symptoms.
Symptoms are most prominent in spring and disappear as temperatures rise above 18°C. Plants in areas throughout a field are stunted and yellow. Initially, diseased
leaves have yellow spots and short streaks, then become totally yellow, beginning at the leaf tip. Necrotic spots sometimes appear on older leaves, which may die
prematurely.
Management
2. Sow barley in spring.
Barley Yellow Streak Mosaic
Cause.
Barley yellow streak mosaic virus (Ba YSMV) is a novel virus transmitted by the brown wheat mite, Petrobia latens, a nonwebspinning spider

Page 89
mite that is generally believed to reproduce parthenogenetically. The mite deposits eggs on debris in surface soil layers near its host plant. BaYSMV particles are
extremely large for a plant virus (64 by 1000 nm on average) and appear to be enveloped and contain ssRNA. BaYSMV has been transmitted mechanically to
Nicotiana benthamiana and Chenopodium quinoa.
Distribution.
Canada (Alberta) and the United States (Idaho and north central Montana).
Symptoms.
Diseased leaf symptoms consist of yellowgreen mosaic, streaking, color banding, and severe necrosis.
Management.
Resistant genotypes have been identified.
Barley Yellow Striate Mosaic
Cause.
Barley yellow striate mosaic virus (BYSMV) is transmitted by planthoppers. Wheat is also a host of BYSMV.
Distribution.
France, Italy, and Morocco.
Symptoms.
Diseased leaves are stunted and chlorotic and have a mosaic pattern.
Management.
Not reported.
Barley Yellow Stripe
Cause.
The causal agent has not been identified, but it is thought to be a virus or viruslike entity. It is transmitted by the leafhopper Euscelis plebejus but not by sap.
Distribution.
Turkey.
Symptoms.
Symptoms commonly occur along field borders and other grassy areas infested by E. plebejus. Fine continuous stripes that occur on leaves sometimes are followed
by leaf yellowing and death.
Management.
Not reported.
Brome Mosaic
Cause.
Brome mosaic virus (BMV) is in the bromovirus group and is transmitted primarily by sap. The Russian aphid, Diuraphis noxia, has been reported as a vector. The
nematodes Xiphinema coxi and X. paraelongatum are inefficient vectors, and the cereal leaf beetle has transmitted BMV under controlled conditions. Transmission
by nymphs and adults of red spider mites, Tetranychus cinnabarinus, has also been reported.
Distribution.
North central Europe, Russia, South Africa, the United States, and Yugoslavia.

Page 90
Symptoms.
Diseased plants are dwarfed and have shriveled heads. Leaf symptoms are most obvious on young plants and fade as plants mature, often disappearing by heading.
Initially, light yellow or white spots and streaks occur that spread rapidly, giving leaves a bright yellow mosaic pattern.
Management.
Not considered necessary.
Cereal Chlorotic Mottle
Cause.
Cereal chlorotic mottle virus (CeCMV) is in the rhabdovirus group and is transmitted by cicadellids.
Distribution.
Northern Africa and Australia.
Symptom.
Severe necrotic and chlorotic streaks occur on leaves.
Management.
Not Reported.
Cereal Tillering
Cause.
Cereal tillering disease virus (CTDV) is circulative in the planthoppers Laodelphax striatellus and Dicranotropis hamata but is not passed through eggs.
Distribution.
Finland, Italy, and Sweden.
Symptoms.
Plants are dwarfed and have excessive tillering. Leaves are dark green and sometimes malformed with serrated margins. Grain yields are reduced.
Management.
Not reported.
Eastern Wheat Striate
Cause.
Eastern wheat striate virus (EWSV) is transmitted by the leafhopper Cicadulina mbila but not by seed, soil, aphids, or mechanically. EMSV overseasons in the
perennial Narenga grass.
Distribution.
India.
Symptoms.
Plants infected while very young have the most severe symptoms and usually die. Diseased leaves and leaf sheaths develop thin, chlorotic stripes that become necrotic
as diseased plants mature. Heads are partially filled with shriveled, poorquality grain. Plants are stunted.
Management.
Not reported.
Enanismo
Enanismo is also called cereal dwarf.
Cause.
The causal agent has not been described, but one or more viruses and a toxin produced by the leafhopper Cicadulina pastusae may be responsi

Page 91
ble. Leafhopper adults and nymphs transmit the causal agent in a circulative fashion; females are more efficient vectors than males.
Distribution.
Colombia and Ecuador.
Symptoms.
Seedlings are killed or stunted. Later infections cause less stunting, but yellow leaf blotches with dark green stripes appear. Galllike enations develop on new leaves 1
to 3 weeks after insects have fed on older leaves. Plants infected just before heading develop distorted heads with poorly filled kernels, which reduces yields in
localized areas.
Management.
Sow later in the spring after vector activity declines.
Flame Chlorosis
Cause.
Doublestranded RNAs ranging in size from 900 to 2800 base pairs are present in vesicles and are likely the disease agent or its replicative intermediate, rather than
virions. The causal agent is considered to be soiltransmitted and has been transmitted by sowing seed or planting seedlings in soil where diseased plants had grown.
There may be an association with infection by Pythium spp.
The grassy weeds green foxtail, Setaria viridis, and barnyard grass, Echinochloa crusgalli, are also hosts.
Distribution.
Canada (Manitoba), in springsown barley.
Symptoms.
A striking flamelike pattern of leaf chlorosis and severe stunting occurs in spring barley. Chloroplasts and mitochondria of affected cells are hypertrophied and contain
an extensive proliferation of fibrilcontaining vesicles that form within the organellar envelope. Affected plants continue to produce leaves with symptoms after transfer
to sterile potting medium.
Management.
Not reported.
High Plains Virus
Cause.
Since High Plains virus (HPV) is transmitted by the wheat leaf curl mite, Aceria tosichella, which also transmits wheat streak mosaic virus (WSMV), mixed infections
by these two viruses can occur. HPV is associated with a 32kDa protein that resembles tenuiviruses. However, it is also suggested by some researchers that HPV
has some resemblance to tospoviruses.
HPV is also transmitted to maize and wheat.
Distribution.
The United States (Colorado, Idaho, Kansas, Nebraska, Texas, and Utah).
Symptoms.
The first symptom is small, chlorotic spots on leaves. These spots rapidly expand into a mosaic pattern and then into a general yellowing of

Page 92
the plant. Severely diseased plants eventually become necrotic. Field infections very often are mixed infections of WSMV and HPV.
Management.
Not reported.
Hordeurn Mosaic
Cause.
Hordeum mosaic virus.
Distribution.
Canada (Alberta).
Symptoms.
Symptoms develop at temperatures of 10° to 30°C. Streaks develop near the base of young leaves and a diffuse chlorotic mottle develops on all leaves.
Management.
Not reported.
Maize Yellow Stripe
Cause.
Maize yellow stripe virus (MYSV) is associated with tenuiviruslike filaments. MYSV is transmitted in a persistent manner by both nymphs and adults of the
leafhopper Cicadulina chinai. Acquisition and inoculation threshold times are each 30 minutes, with a latent period of 4.5 to 8.0 days, depending on temperature.
Acquisition and inoculation occur at a minimum temperature of 14°C and a maximum temperature of 25°C. The maximum retention period is 27 days.
Wheat, sorghum, and graminaceous weeds are winter hosts. Different strains of MYSV exist.
Distribution.
Egypt.
Symptoms.
Symptoms on barley are not well known. Three symptom types exist on maize: a fine stripe, coarse stripe, and chlorotic stunt. Each type may represent different
MYSV strains. Experimentally, fine stripes appear on the first leaves, followed by coarse stripes on younger leaves; however, some leaves have both symptom types.
Management.
Not reported.
Northern Cereal Mosaic
Cause.
Northern cereal mosaic virus (NCMV) is in the rhabdovirus group and is transmitted by the planthopper Laodelphax striatellus. Other insects that have been
implicated as vectors for NCMV are Unkanodes sapporonus and species of Delphacodes.
Distribution.
Japan, Korea, and Siberia.
Symptoms.
Initially, yellowishwhite or whitishgreen specks occur on young and newly emerged leaves and leaf sheaths. Later, leaf blades are short and

Page 93
narrow with yellowishwhite stripes parallel to veins. Plants are stunted, have increased tillering, and have a few untilled panicles or no panicles at all.
Management.
Not reported.
Oat Blue Dwarf
Oat blue dwarf is possibly the same disease as moderate barley dwarf.
Cause.
The oat blue dwarf virus (OBDV) is in the marafivirus group and is transmitted primarily by the adult aster leafhopper, Macrosteles fascifrons, with occasional
transmission by immature leafhoppers. OBDV cannot be transmitted by seed, mechanically, or soil.
Distribution.
Czechoslovakia, Finland, North America, and Sweden.
Symptoms.
Symptom development is greater at temperatures of 16° to 18°C than at higher temperatures. Plants are bluegreen and stunted, tiller excessively, and either do not
produce heads or have sterile spikes. Leaves are short and stiff and have enations along veins of the leaves and leaf sheaths.
Management.
Not reported.
Oat Pseudorosette
Cause.
Oat pseudorosette virus (OPV) is transmitted by the leafhopper Laodelphax striatellus.
Distribution.
Russia.
Symptoms.
Plants are stunted and tiller excessively.
Management.
Grow the least susceptible cultivars.
Oat Sterile Dwarf
Oat sterile dwarf is called oat base tillering disease in Finland and oat dwarf tillering disease in Sweden.
Cause.
Oat sterile dwarf virus (OSDV) is in the fijivirus group and is transmitted by delphacid planthoppers, especially Javesella pellucida and Dicranotropis hamata.
OSDV is transmitted after 1 month incubation in vectors, but the virus is rarely passed through eggs.
Distribution.
England and eastern and northern Europe.
Symptoms.
Plants are slightly stunted and have few juvenile tillers. Leaves are darker green than normal.
Management.
Control grassy weeds and oat cover crops.

Page 94
Rice BlackStreaked Dwarf
Cause.
Rice blackstreaked dwarf virus (RBSDV) is in the fijivirus group and is transmitted by the planthoppers Laodelphax striatellus, Unkanodes sapporonus, and U.
albifascia but not by seed or sap. RBSDV overwinters in winter wheat and is retained from season to season in all stages of planthoppers. Nymphs are more efficient
vectors than adults, but the virus is not transmitted through eggs. Plants acquire RBSDV after 30 minutes feeding by planthoppers in which the virus has incubated 7 to
35 days.
Distribution.
China, Japan, Korea, and Russia.
Symptoms.
Diseased plants are severely stunted and have twisted leaves. Waxy swellings are present on veins, the under surfaces of leaves, and culms.
Management
1. Grow resistant rice cultivars to lessen the chance of virus transmission to barley.
2. Do not grow barley close to rice.
Rice Stripe
Cause.
Rice stripe virus is in the tenuivirus group and is transmitted by the planthopper Laodelphax striatellus.
Distribution.
Japan, Korea, and Taiwan.
Symptoms.
Plants are dwarfed and have yellowgreen to yellowwhite stripes that are parallel to midribs of leaves.
Management.
It is not necessary to manage rice stripe in barley since the extensive use of resistant rice cultivars has reduced the vector population.
Russian Winter Wheat Mosaic
Cause.
Winter wheat mosaic virus is disseminated by the leafhoppers Psammotettix striatus and Macrosteles laevis.
Distribution.
Eastern Europe and Russia.
Symptoms.
Seedlings are stunted and have excessive tillering and necrosis. Surviving seedlings are rosettes without leaf mosaic symptoms. Older plants are slightly stunted, and
leaves have a typical mosaic and streakmosaic pattern with chlorotic dashes and streaks parallel to veins.
Management.
Not reported.
Soilborne Wheat Mosaic
Soilborne wheat mosaic is also called wheat soilborne mosaic.

Page 95
Cause.
Soilborne wheat mosaic virus (SBWMV) is in the furovirus group and survives in the soilborne fungus Polymyxa graminis. SBWMV is spread by any method that
disseminates soil containing P. graminis. Motile zoospores infect root hairs and epidermal cells in the autumn and infrequently in the spring during wet soil conditions
and soil temperatures of 10° to 20°C. Two to 4 weeks after infection, P. graminis replaces plant cell contents with plasmodial bodies that either segment into
additional zoospores or develop into thickwalled resting spores.
Disease is most severe on barley sown in the autumn in low, wet areas. Soils may remain infected for years. There are different strains of SBWMV.
Distribution.
Argentina, Brazil, Canada, Egypt, Italy, Japan, and the eastern and central United States. Soilborne wheat mosaic is not considered an important disease of barley.
Symptoms.
Symptoms, which are most prominent in spring on the youngest or lowest leaves, range from light green to yellow leaf mosaics or mottling that later develops into
parallel streaks. Plants may be slightly or severely stunted and rosetted by some strains of SBWMV. Warm weather prevents disease development, thus confining
symptoms to lower leaves.
Management
1. Rotate barley with noncereal crops.
2. Sow barley late in the autumn.
3. Grow tolerant cultivars.
Wheat Dwarf
Cause.
The causal agent is suspected to be a virus that is transmitted by several leafhoppers, primarily Psammotettix alienus and Macrosteles laevis, but not by sap, seed,
or soil.
Distribution.
Bulgaria, Czechoslovakia, Russia, and Sweden.
Symptoms.
Plants infected as seedlings are severely stunted and do not form heads, but plants infected later are less stunted. Leaves have small, light green to yellowbrown spots
and blotches that may coalesce to cause yellowing and necrosis.
Management.
Not reported.
Wheat Streak
Wheat streak is also called wheat streak mosaic.
Cause.
Wheat streak mosaic virus (WSMV) is in the potyvirus group and survives in infected plants. No active virus has been detected in dead plants or in seed. WSMV is
transmitted primarily by windborne wheat curl mites, Aceria tulipae, for up to 2.4 km but also is transmitted mechanically.

Page 96
Mites overwinter on live plants. Only young mites acquire WSMV after feeding 15 or more minutes on diseased plants. They carry the virus internally for several
weeks, but neither the mite nor the virus can survive longer than 1 or 2 days in the absence of a living plant.
As winter barley plants mature during late summer or early autumn, WSMV is disseminated by mites to volunteer grasses and cereals and eventually to earlysown
barley. However, wheat streak mosaic is a problem on barley only when mite populations build to extremely high levels in nearby wheat fields. WSMV has a wide
host range, but some grasses are hosts for the mites but not for the virus, and vice versa, and some are susceptible or resistant to both.
Distribution.
Eastern Europe, western and central North America, and Russia.
Symptoms.
The most severe symptoms occur in plants sown early in the autumn but do not appear until the following spring. Initially, light green to light yellow blotches, dashes, or
streaks occur parallel to leaf veins and turn brown as plants mature. Feeding mites often cause leaf edges to curl tightly in toward the upper midvein. Plants become
stunted, display a general yellow mottling, and develop large numbers of tillers that vary in height. Plants may die before maturity or have sterile or partially sterile
heads with shriveled kernels. At harvest, stunted plants, some with sterile heads, remain that are the same height or shorter than stubble.
Synergistic effects are suspected between WSMV and other viruses, such as barley yellow dwarf virus, making field identification difficult.
Management
1. Destroy volunteer cereals and grasses in adjoining fields 2 weeks before sowing and 3 to 4 weeks before sowing in the same field.
2. Sow after Hessian flyfree date.
Wheat Yellow Leaf
Cause.
Wheat yellow leaf virus is in the closterovirus group and is transmitted by the corn leaf aphid, Rhopalosiphum maidis.
Distribution.
Japan.
Symptoms.
Leaves become yellow and blight. Plants die or ripen prematurely.
Management.
Not reported.

Page 97
Selected References
Anikster, Y. 1981. Alternate hosts of Puccinia hordei. Phytopathology 72:733735.
Bockelman, H. E., Sharp, E. L., and Bjarko, M. E. 1983. Isolates of Pyrenophora teres from Montana and the Mediterranean region that produce spottype lesions
on barley. Plant Dis. 67:696697.
Boosalis, M. G. 1952. The epidemiology of Xanthomonas translucens (J.J. & R) Dowson on cereals and grasses. Phytopathology 42:387395.
Bragard, C., Singer, E., Alizadeh, A., Vauterin, L., Maraite, H., and Swings, J. 1997. Xanthomonas translucens from small grains: Diversity and phytopathological
relevance. Phytopathology 87:11111117.
Braun, A., Brumfield, S., Hamacher, J., and Sands, D.C. 1997. Ultrastructural localization of Pseudomonas syringae in barley kernel tissue. (Abstr.) Phytopatholgy
87:S11.
Brown, J. K., and Wyatt, S. D. 1981. Corn as an oversummering host of barley yellow dwarf virus and aphid vector in eastern Washington. (Abstr.) Phytopathology
71:863.
Brown, M. P., Steffenson, B. J., and Webster, R. K. 1993. Host range of Pyrenophora teres f. teres isolates from California. Plant Dis. 77:942947.
Brumfield, S. K. Z., Carroll, T. W., and Gray, S. M. 1992. Biological and serological characterization of three Montana RMVlike isolates of barley yellow dwarf
virus. Plant Dis. 76:3339.
Burton, R. J., ColeySmith, J. R., and Wareing, P. W. 1988. Rhizoctonia oryzae and R. solani associated with barley stunt disease in the United Kingdom. Trans.
Br. Mycol. Soc. 91:409417.
Chico, A. W. 1983. Reciprocal contact transmission of barley stripe mosaic virus between wild oats and barley. Plant Dis. 67:207208.
Conner, R. L., and Atkinson, T. G. 1989. Influence of continuous cropping on severity of common root rot in wheat and barley. Can. J. Plant Pathol. 11:127132.
Cook, R., and Williams, T. D. 1972. Pathotypes of Heterodera avenae. Ann. Appl. Biol. 71:267271.
Crosier, W. F., Nash, G. T., and Crosier, D.C. 1970. Ustilago nuda on leaves of 'Larker' barley. Plant Dis. Rptr. 54:927929.
Cunfer, B. M. 1981. Septoria sp. on barley and Hordeurn pusilium. (Abstr.) Phytopathology 71:869.
Damsteegt, V. D., Gildow, F. E., Hewings, A. D., and Carroll, T. W. 1992. A clone of the Russian wheat aphid (Diuraphis noxia) as a vector of the barley yellow
dwarf, barley stripe mosaic, and brome mosaic viruses. Plant Dis. 76:11551160.
Darlington, L. C., Carroll, T. W., and Mathre, D. E. 1976. Enhanced susceptibility of barley to ergot as a result of barley stripe mosaic virus infection. Plant Dis. Rptr.
60:584587.
Davies, K. A., and Fisher, J. M. 1976. Factors influencing the number of larvae of Heterodera avenae invading barley seedlings in vitro. Nematologica 22:153162.
Dehne, H. W., and Oerke, E. C. 1985. Investigations on the occurrence of Cochliobolus sativus on barley and wheat. I. Influence of pathogen, host plant and
environment on infection and damage. Zeitschrift fur Pflanzenkrankheiten und Pflanzenschutz 92:270280.
Delserone, L. M., and Cole, H., Jr. 1987. Effects of planting date on development of net blotch epidemics in winter barley in Pennsylvania. Plant Dis. 71:438441.
Delserone, L. M., Frank, J. A., and Cole, H., Jr. 1983. Net blotch epidemics on winter barley in the fall as influenced by planting date. (Abstr.) Phytopathology
73:965.

Page 98
Delserone, L. M., Cole, H., Jr., and Frank, J. A. 1987. The effects of infections by Pyrenophora teres and barley yellow dwarf virus on the freezing hardiness of
winter barley. Phytopathology 77:14351437.
Dewey, W. G., and Hoffmann, J. A. 1975. Susceptibility of barley to Tilletia controversa. Phytopathology 65:654657.
Dubin, H.J., and Stubbs, R. W. 1986. Epidemic spread of barley stripe rust in South America. Plant Dis. 70:141144.
Duczek, L.J. 1990. Sporulation of Cochliobolus sativus on crowns and underground parts of spring cereals in relation to weather and host species, cultivar, and
phenology. Can. J. Plant Pathol. 12:273278.
Esnard, J., and Hepperly, P. R. 1995. First report of southern blight of common barley in Puerto Rico. Eur. J. Plant Pathol. 101:497501.
Fargette, D., Lister, R. M., and Hood, E. L. 1982. Grasses as a reservoir of barley yellow dwarf virus in Indiana. Plant Dis. 66:10411045.
Fart, D. F., Bills, G. R., Chamuris, G. P., and Rossman, A. Y. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society,
Frank, J. A., and Cole, H., Jr. 1987. The influence of common root rot on net blotch of winter barley. Phytopathology 77:14541457.
Gill, C. C., and Westdal, P. H. 1966. Effect of temperature on symptom expression of barley infected with aster yellows or barley yellow dwarf viruses.
Haber, S., and Chong, J. 1993. Flame chlorosis induces vesiculations in chloroplasts and mitochondria: What does it mean? (Abstr.) Can J. Plant Pathol. 15:57.
Haber, S., and Hardener, D. E. 1992. Green foxtail (Setaria viridis) and barnyard grass (Echinochloa crusgalli): New hosts of the viruslike agent causing flame
chlorosis in cereals. Can. J. Plant Pathol. 14:278280.
Haber, S., and Kim, W. 1989. Flame chlorosis: A new viruslike disease of barley in Manitoba. (Abstr.) Can. J. Plant Pathol. 11:189.
Hannukkala, A., and Koponen, H. 1988. Microdochium bolleyi, a common inhabitant of barley and wheat roots in Finland. Karstenia 27:3136.
Harder, D. E., and Bakker, W. 1973. African cereal streak, a new disease of cereals in East Africa. Phytopathology 63:14071411.
Hosford, R. M., Jr. 1978. Effects of wetting period on resistance to leaf spotting of wheat, barley, and rye by Leptosphaeria herpotrichoides. Phytopathology
68:591594.
Huftalen, C. S., and Bergstrom, G. C. 1986. First report of Ascochyta leaf spot caused by Ascochyta hordei var. americana on barley in New York. Plant Dis.
70:1074.
Hyung, L. S., and Skikata, E. 1977. Occurrence of northern cereal mosaic virus in Korea. Kor. J. Plant Prot. 16:8792.
Ingram, D. M., and Cook, R.J. 1987. Influence of temperature and plant residues on pathogenicity of Pythium spp. on wheat, barley, peas and lentils. (Abstr.)
Inouye, T. 1976. Wheat yellow leaf virus. Descriptions of Plant Viruses, No. 157. Commonw. Mycol. Inst., Assoc. Appl. Biol., Kew, Surrey, England.
Jenkins, J. E. E. 1974. New or uncommon plant diseases and pests: Botrytis diseases in barley. Plant Pathol. 23:8384.
Jin, Y., and Steffenson, B.J. 1992. Puccinia coronata on barley. Plant Dis. 76:1283.
Johnson, D. A., Tew, T. L., and Banttari, E. E. 1977. Factors affecting symptoms in barley infected with the oat blue dwarf virus. Plant Dis. Rptr. 61:280283.

Page 99
Kainz, M., and Hendrix, J. W. 1981. Response of cereal roots to barley yellow dwarf virus infection in a mist culture system. (Abstr.) Phytopathology 71:229.
Kelemu, S., and Sharp, E. L. 1986. Unique symptoms induced in Ethiopian barley cultivars by Rhynchosporium secalis. Plant Dis. 70:800.
Lister, R. M., and Sward, R.J. 1988. Anomalies in serological and vector relationships of MAVlike isolates of barley yellow dwarf virus from Australia and the
U.S.A. Phytopathology 78:766770.
Lockhart, B. E. L. 1986. Occurrence of cereal chlorotic mottle virus in northern Africa. Plant Dis. 70:912915.
Luzzardi, G. C., Luz, W. C., and Pierobom, C. R. 1983. Podridao branca dos cereais causada pot Sclerotium rolfsii no Brazil. Fitpathologia Brasileira 8:371375
(in Portugese).
MacNish, G. C. 1985. Methods of reducing Rhizoctonia patch of cereals in Western Australia. Plant Pathol. 34:175181.
Martin, R. A. 1985. Influence of seeding rate and nitrogen top dressing on net blotch development in barley. (Abstr.) Can. J. Plant Pathol. 7:446.
MartinezCano, C., Grey, W. E., and Sands, D.C. 1992. First report of Arthrinium arundinis causing kernel blight on barley. Plant Dis. 76:1077.
MartinezEspinoza, A.D., Bjarko, M. E., and Riesselman, J. H. 1990. Studies on Rhynchosporium secalis as a seedborne pathogen. (Abstr.). Phytopathology
80:1006.
Mathre, D. E. (Ed.). 1982. Compendium of Barley Diseases, First edition. The American Phytopathological Society, St. Paul, MN. 78 pp.
Mathre, D. E. 1986. Occurrence of Verticillium dahliae on barley. Plant Dis. 70:981.
Mathre, D. E. 1989. Pathogenicity of an isolate of Verticillium dahliae from barley. Plant Dis. 73:164167.
Mathre, D. E. (Ed.). 1997. Compendium of Barley Diseases, Second Edition. The American Phytopathological Society, St. Paul, MN. 90 pp.
Metz, S. A., and Scharen, A. L. 1979, Potential for the development of Pyrenophora graminea on barley in a semiarid environment. Plant Dis. Rptr. 63:671675.
MihutaGrimm, L., and Forster, R. L. 1989. Scab of wheat and barley in southern Idaho and evaluation of seed treatments for eradication of Fusarium spp. Plant
Dis. 73:769771.
Murray, D. I. L., and Nicholson, T. H. 1979. Barley stunt disorder in Scotland. Plant Pathol. 28:200201.
Nagaich, B. B., and Sinha, R. C. 1974. Eastern wheat striate: A new viral disease. Plant Dis. Rptr. 58:968970.
Nutter, R. W., Jr., Pederson, V. D., and Timian, R. G. 1984. Relationship between seed infection by barley stripe mosaic virus and yield loss. Phytopathology
74:363366.
O'Brien, P. C., and Fisher, J. M. 1978. Factors influencing the number of larvae of Heterodera avenae within susceptible wheat and barley seedlings. Nematologica
24:295304.
Palival, Y. C. 1982. Role of perennial grasses, winter wheat and aphid vectors in the disease cycle and epidemiology of barley yellow dwarf virus. Can. J. Plant
Pathol. 4:367374.
Peters, R. A., Timian, R. G., and Wesenberg, D. 1983. A bacterial kernel spot of barley caused by Pseudomonas syringae pv. syringae. Plant Dis. 67:435438.
Piening, L.J., and Orr, D. 1988. Effects of crop rotation in common root rot of barley. Can. J. Plant Pathol. 10:6165.
Raemaekers, R. H., and Tinline, R. D. 1981. Epidemic of diseases caused by Cochliobolus sativus on rainfed wheat in Zambia. Can. J. Plant Pathol. 3:211214.
Richardson, M.J., and Noble, M. 1970. Septoria species on cereals: A note to aid their identification. Plant Pathol. 19:159163.

Page 100
Roane, C. W., Roane, M. K., and Starling, T. M. 1974. Ascochyta species on barley and wheat in Virginia. Plant Dis. Rptr. 58:455456.
Robertson, N. L., and Carroll, T. W. 1991. Mechanical transmission, partial purification, and preliminary chemical analysis of barley yellow streak mosaic virus. Plant
Dis. 75:839843.
Rovira, A.D., and McDonald, H.J. 1986. Effects of the herbicide chlorsulfuron on Rhizoctonia bare patch and takeall of barley and wheat. Plant Dis. 70:879882.
Sampson, G., and Cloug, K. S. 1979. A Selenophoma leaf spot on cereals in the Maritimes. Can. Plant Dis. Surv. 59:3.
Seifers, D. L., Harvey, T. L., Martin, T.J., and Jensen, S. G. 1997. Identification of the wheat curl mite as the vector of the High Plains virus of corn and wheat. Plant
Dis. 81:11611166.
Shane, W. W., Baumer, J. S., and Teng, P.S. 1987. Crop losses caused by Xanthomonas streak on spring wheat and barley. Plant Dis. 71:927930
Sinha, R. C., and Benki, R. M. 1972. American wheat striate mosaic virus. CMI/A.A.B. Descriptions of Plant Viruses. Set 6., No. 99.
Skaf, J. S., Brumfield, S. K., and Carroll, T. W. 1992. Barley yellow streak mosaic virus infection of barley in Idaho. Plant Dis. 76:861.
Slack, S. A., Shepherd, R.J., and Hall, D. H. 1975. Spread of seedborne barley stripe mosaic virus and effects of the virus on barley in California. Phytopathology
65:12181223.
Steffenson, B. J., Grasmick, D. L., and Webster, R. K. 1988. Comparative epidemiology of net blotch and leaf scald of barley. (Abstr.) Phytopathology 78:1538.
Takamatsu, S. 1989. A new snow mold of wheat and barley caused by foot rot fungus, Ceratobasidium gramineum. Ann. Phytopathol. Soc. Japan 55:233237.
Tekauz, A., and Chico, A. W. 1980. Leaf stripe of barley caused by Pyrenophora graminea: Occurrence in Canada and comparison with barley stripe mosaic.
Can. J. Plant Pathol. 2:152158.
Teviotdale, B. L., and Hall, D. H. 1976. Factors affecting inoculum development and seed transmission of Helminthosporium gramineum. Phytopathology 66:295
301.
Thomas, P. L. 1981. Distinguishing between the loose smuts of barley. Plant Dis. 65:834.
van den Berg, C. G.J., and Rossnagel, B. G. 1991. Epidemiology of spottype net blotch on spring barley in Saskatchewan. Phytopathology 81:14461452.
Velasco, V. R., Ishimaru, C. A., and Brown, W. M., Jr. 1991. Halo blight of spring wheat caused by Pseudomonas syringae. (Abstr.) Phytopathology 81:1159.
VeljavecGratian, M., and Steffenson, B.J. 1997. Pathotypes of Cochliobolus sativus on barley in North Dakota. Plant Dis. 81:12751278.
Walker, J. 1975. Takeall disease of Graminae: A review of recent work. Rev. of Plant Pathol. 54:113144.
Weller, D. M., Cook, R. J., MacNish, G., Bassett, E. N., Powelson, R. L., and Peterson, R. R. 1986. Rhizoctonia root rot of small grains favored by reduced tillage
in the Pacific Northwest. Plant Dis. 70:7073.
Westphal, A., Tidemann, A. V., and Fehrmann, H. 1995. Occurrence of Monographella nivalis var. mayor and Fusarium culmorum on barley in Germany in
1992. (Abstr.). Phytopathology 85:1169.
Yaegashi, H. 1988. Inheritance of blast resistance in tworowed barley. Plant Dis. 72:608610.
Zamora, M. R., Burnett, P. A., Vivar, H. E., Rodriguez, R., and Navarro, M. 1988. Barley mosaic virus in Mexico. Plant Dis. 72:546.

Page 101
3.
Diseases of Buckwheat (Fagopyrurn Esculentum)
Diseases Caused By Fungi
Ascochyta Leaf Blight
Cause.
Ascochyta fagopyri (syn. A. bresadolae) overwinters as pycnidia in infested residue. Disease is favored by wet weather.
Distribution.
Widespread.
Symptoms.
Round to irregularshaped leaf spots have light tan to dark brown centers and darker margins. Spots may coalesce to form brownishpurple blotches. Pycnidia,
resembling black specks, may be scattered throughout the spots.
Management.
Not reported.
Blight
Cause.
Phytophthora parasitica (syn. P. nicotianae var. parasitica).
Distribution.
Russia.
Symptoms.
Cotyledons are infected first. Brown spots spread in concentric circles on diseased stems. Disease results either in reduction of plant growth or plant death.
Management.
Not reported.
Botrytis Rot
Cause.
Botrytis cinerea is externally seedborne and overwinters in infested residue and soil. Disease is favored by warm, wet weather.
Distribution.
Russia.

Page 102
Symptoms.
''Powdery" spots that are covered with a gray mold or a black film form on diseased leaves and stems. Spots on diseased lower stems cause them to break off.
Management.
Apply a fungicide seed treatment.
Chlorotic Leaf Spot and Stipple Spot
Cause.
Possibly Bipolaris sorokiniana and Alternaria alternata. Although A. alternata was isolated from lesions, it was not pathogenic alone when inoculated to
buckwheat.
Distribution.
Canada (Manitoba).
Symptoms.
Chlorotic, circular lesions (1226 mm in diameter) are randomly scattered on leaves on the upper half of diseased plants. Lesions are of three types: spreading and
uniformly chlorotic; spreading with concentric, chlorotic bands that alternate with normal dark green tissue; and small, restricted, tan lesions with sharply defined
borders. This latter symptom is referred to as stipple spot. Necrosis occurs in the older lesions and in the older chlorotic rings.
Management.
Not reported.
Collar Rot
Cause.
Sclerotinia sp. is presumed to overwinter as sclerotia.
Distribution.
Not known for certain but presumed to be widespread.
Symptoms.
The first symptom is the presence of prematurely ripened plants that are easily pulled from the soil and are either scattered or grouped among healthyappearing green
plants. Pale gray stem lesions develop at the soil line. Initially, lesions are watersoaked and eventually expand to girdle stems and kill plants. Stems are bleached, have
a chalkywhite appearance, and tend to shred longitudinally. Sclerotia appear as hard, black, grainsized bodies inside stems near the bases of killed plants.
Management.
Not reported.
Downy Mildew
Cause.
Peronospora ducometi (syn. P. fagopyri) is seedborne and causes systemic infection. Seed infested with oospores gives rise either to symptomless or stunted plants,
depending on which of two types of hyphae occurs in diseased plants. Type A hyphae are found in stems, leaves, flowers, and seeds but not in roots; are narrow (8.6
µm in diameter) and branched; and produce haustoria. Sexual and asexual reproductive structures originate from

Page 103
type A hyphae. Type B hyphae are wide (27 µm in diameter) and unbranched and do not form haustoria. Type B hyphae often grow along the outside of xylem
vessels but are rarely found inside xylem tissue.
Distribution.
Canada, Europe, and Japan.
Symptoms.
Type A hyphae are associated with stunting, leaf mottling, and rugosity. Type B hyphae are common in petioles and flowers of symptomless plants but occasionally
are found in stunted plants. Large, circular, chlorotic lesions appear first on the leaves below the top of the diseased plant and eventually cover most or all of the leaf.
Lesions sometimes have concentric chlorotic bands that alternate with normal, dark green tissue. Some badly diseased leaves have a mosaiclike appearance.
Systemic symptoms occur on the tops of plants as shortened internodes, epinasty of leaves, and a reduced number of seeds. Sparse conidia and conidiophores occur
on the under surfaces of diseased leaves. Conidia that are "clumped" together are purplish and can be seen without magnification.
Symptoms of seedborne infection include stunted seedlings and seedlings with a small stem diameter. Leaves of diseased seedlings are rugose and mottled.
Management.
Not reported.
Fusarium Wilt
Cause.
Fusarium sp. is externally seedborne and soilborne.
Distribution.
Russia.
Symptoms.
Wilting symptoms occur first at the top of diseased plants, then proceed to involve the entire plant. Lower stems become discolored, necrotic, and eventually covered
with "pinkish" conidia, conidiophores, and mycelia. Smallsized seed may be formed. Roots are necrotic and easily pulled from soil.
Management.
Not known.
Leaf Spot
Cause.
Phyllosticta polyconorum.
Distribution.
Not known for certain but presumed to occur under warmer buckwheatgrowing conditions.
Symptoms.
Brownish, irregularshaped leaf spots sometimes have a dark brown to purplish margin. The center of the spot frequently falls out, giving the diseased leaf a ragged
appearance.
Management.
Not reported.

Page 104
Powdery Mildew
Cause.
Erysiphe commonis f. sp. fagopyri is thought to overwinter as cleistothecia.
Distribution.
Not know for certain but thought to be widespread.
Symptoms.
The upper surfaces of diseased leaves have a "typical" white, powdery appearance due to mycelia, conidiophores, and conidia. Eventually, cleistothecia form and
appear as dark specks within the mycelium.
Management.
Not reported.
Pythium Palingenes Disease
Cause.
Pythium palingenes. Disease is favored by midday air temperatures exceeding 30°C and watersaturated soils.
Distribution.
The United States (Missouri).
Symptoms.
Diseased plants wilt during the warmest portion of the day. Sunken, tan lesions occur on stems at the soil line. Mats of white mycelia grow on the surface of the
taproot.
Management.
Not reported.
Ring Spot
Cause.
Cercospora fagopyri. Disease is favored by extended periods of high humidity and warm temperatures.
Distribution.
Ring spot is presumed to occur in the warmer buckwheatgrowing areas.
Symptoms.
Reddish, circular to irregularshaped lesions occur on diseased leaves. Lesions vary in size from a pinpoint to large necrotic areas formed by the growth and
coalescing of lesions. Circular lesions may have a dark purplish margin.
Management.
Not reported.
Broad Bean Wilt
Cause.
Broad bean wilt virus (BBWV) serotype 1 is in the fabavirus group. BBWV is transmitted mechanically and by aphids.
Distribution.
Italy.

Page 105
Symptoms.
In a mixed infection with turnip mosaic potyvirus, diseased plants displayed a yellow or chlorotic mottle on the leaves.
Management.
Not reported.
Turnip Mosaic
Cause.
Turnip mosaic virus (TuMV) is in the potyvirus group. TuMV is likely transmitted by aphids.
Distribution.
Italy.
Symptoms.
In a mixed infection with broad bean wilt fabavirus, infected plants displayed a yellow or chlorotic mottle on the leaves.
Management.
Not reported.
Selected References
Bellardi, M. G., and RubiesAutonell, C. 1997. First report of broad bean wilt fabavirus on Polygonum fagopyrum. Plant Dis. 81:959.
Conners, I. L. 1967. An Annotated Index of Plant Diseases in Canada. Canada Dept. Agric. Res. Branch. Pub. No. 1251.
Mihail, J. D. 1993. Diseases of alternative crops in Missouri. Can. J. Plant Pathol. 15:119122.
Savitskiy, K. A. 1970. Getchika (Buckwheat). Moscow: 'Kolos'. 312 pp.
Zimmer, R. C. 1974. Chlorotic leaf spot and stipple spot, newly described diseases of buckwheat in Manitoba. Canada Plant Disease Survey 54:5556.
Zimmer, R. C. 1978. Downy mildew, a new disease of buckwheat (Fagopyrum esculentum) in Manitoba, Canada. Plant Dis. Rptr. 62:471473.
Zimmer, R. C. 1984. A possible new downy mildew syndrome on buckwheat seedlings. Canada Plant Disease Survey 64:79
Zimmer, R. C., McKeen, W. E., and Campbell, C. G. 1990. Development of Peronospora ducometi in buckwheat. Can. J. Plant Pathol. 12:247254.

Page 107
4.
Diseases of Canola (Rapeseed) and Mustard (Brassica campestris, B. juncea, B. napus, B. nigra, and B. rapa)
Bacterial Black Rot
Bacterial black rot is also called black rot.
Cause.
Xanthomonas campestris pv. campestris is seedborne and overwinters in soil residue. Bacteria are disseminated by splashing water and enter plants through
stomates. Little is known of the life cycle of X. campestris as it relates to disease development on canola.
Distribution.
Canada; however, bacterial black rot is not a common disease.
Symptoms.
Diseased leaves become chlorotic and have dark veins in the chlorotic areas.
Management.
Bacterial black rot is not important enough to warrant management.
Bacterial Pod Rot
Cause.
Pseudomonas syringae pv. maculicola.
Distribution.
The United States.
Symptoms.
Diseased pods become watersoaked and necrotic and eventually dry up.
Management.
Not reported.
Bacterial Soft Rot
Bacterial soft rot is also called bacterial stalk rot.
Cause.
Erwinia carotovora and Pseudomonas marginalis pv. marginalis. Disease is most severe on vigorously growing plants that have become more suc

Page 108
culent due to excessive nitrogen fertilization and on plants growing in poorly drained soil.
Distribution.
India.
Symptoms.
Watersoaked lesions that are frequently accompanied by a white "frothing" occur at the collar region of diseased plants. Tender branches are also affected as the
lesions advance upward on the plant. Leaves are waterstressed and eventually wither. Diseased stems and branches, particularly in the pith tissues, become soft and
pulpy and produce dirty, white ooze with a foul odor. The diseased collar region becomes sunken and turns buff white to pale brown. Within a short time, severely
diseased plants topple down at the basal region.
Management.
Not reported.
Bacterial Wilt and Rot
Cause.
Erwinia carotovora subsp. atroseptica (syn. E. atroseptica).
Distribution.
Mexico.
Symptoms.
Rot starts where larvae of the insect Hylemyia sp. damage stems at the soil level or where branching occurs. At or before flowering time, the centers of stems may be
partially or completely rotted, causing diseased plants to wilt. Wilting is associated with a mottled leaf appearance.
Management.
Not reported.
Crown Gall
Cause.
Agrobacterium tumefaciens. Bacteria enter the root system and stem near the soil line through wounds. Once inside the infected plant, the bacterium invades
intercellularly and stimulates the surrounding cells to divide.
Distribution.
Widely distributed, but the disease rarely occurs on canola and mustard.
Symptoms.
Initially, small swellings occur on diseased stems or roots, particularly near the soil line. These swellings later turn into galls that become dark brown to black. Galls
have no definite size and shape. Diseased plants, in general, are stunted and have small, chlorotic leaves.
Management.
No practical disease management strategy is available. Most canola and mustard cultivars appear to have a high degree of resistance or tolerance. However, disease
may be more severe if canola and mustard follow sunflower, another host of A. tumefaciens, in a rotation.

Page 109
Unnamed Seedling Root Rot
Cause.
A fluorescent pseudomonad designated Pseudomonas rp2. This is an opportunistic pathogen that infects immature roots. Surface microcolonies penetrate tissue of
immature host roots by intrusion along epidermal cell anticlinal walls.
Distribution.
Canada (Alberta).
Symptoms.
Diseased roots are inhibited in growth and development. Brown, watersoaked lesions also occur on roots.
Management.
Not reported.
Xanthomonas Leaf Spot
Cause.
Xanthomonas campestris pv. armoraciae.
Distribution.
India, Turkey, and the United States.
Symptoms.
Light brown spots occur on diseased leaves and veins.
Management.
Not reported.
Alternaria Black Spot
Alternaria black spot is also called gray leaf spot, pod drop, and dark leaf spot.
Cause.
Alternaria brassicae, A. brassicicola, and A. raphani survive as mycelia in infested residue, and are seedborne as conidia and mycelia on the outside of seed coats.
Primary inoculum is conidia produced on residue and disseminated by wind to host plants. Secondary inoculum is conidia that are produced on leaf spots. Black spot
is favored by humid, warm conditions that occur at midseason.
Distribution.
Canada, Europe, Mexico, and the United States.
Symptoms.
Infected seed may cause preemergence or postemergence damping off. Hypocotyls and cotyledons of surviving seedlings may be infected by secondary conidia
produced on dampedoff seedlings. Initially, brown to black dots occur on diseased leaves, stems, and pods.
Under humid conditions, dots enlarge on diseased leaves to form gray, circular spots containing concentric rings with purple or black borders. However, under dry
conditions, spots remain small and black or become gray with black borders. Tissue surrounding spots becomes chlorotic. Severe disease may result in defoliation.

Page 110
On stems and pods, dots enlarge into lesions that are either completely black or black with gray centers. Pods with diseased pedicels fail to develop and drop from
plants. Severely spotted pods dry, shrink, and may split open prematurely to drop shrunken, diseased seed on the soil surface.
Specific symptoms caused by A. brassicae on Japanese mustard, Brassica campestris subsp. nipposinica, are small (24 mm in diameter), circular to oblong, brown
leaf spots that contain concentric rings. Elongated brown spots develop on petioles. Symptoms on tah tsai, B. campestris subsp. narinosa, are circular (36 mm in
diameter), tan to brown leaf spots that contain concentric rings and are surrounded by yellow borders. These leaf spots are slightly larger than on Japanese mustard.
Elongated brown spots develop on petioles.
Management
1. Sow clean, diseasefree seed.
2. Rotate canola and mustard with noncrucifers for a minimum of 3 years.
4. Control volunteer mustard, canola, and cruciferous weeds.
Alternaria Leaf Spot
Cause.
Alternaria alternata.
Distribution.
Canada on Polishtype canola.
Symptoms.
The symptoms described here were on artificially inoculated plants. Grayish to brownish necrotic spots develop on diseased leaves. Spots eventually enlarge, resulting
in drying and dropping out of affected areas. Flowers are frequently blighted.
Management:
Not reported.
Anthracnose
Cause.
Colletotrichum gloeosporioides, teleomorph Glomerella cingulata, and C. higginsianum.
Distribution.
India, Nigeria, and Uganda.
Symptoms.
Oval, elliptical, watersoaked lesions appear on stems or leaf axis. The spots do not encircle the stem completely, but longitudinal streaks of dead tissue are formed.
The cortical tissue of diseased stem and branches cracks open and exposes inner tissue.
Management.
Not reported.

Page 111
Ascochyta Leaf Spot
Cause.
Ascochyta spp. The pathogens survive in infested residue and are probably seedborne. Dissemination is by splashing rain and movement of infected seed. The fungus
may also be windborne.
Distribution.
Wherever canola is grown.
Symptoms.
Diseased seed is discolored.
Management.
Not reported.
Blackleg
Blackleg is also called root and collar rot and stem canker.
Cause.
Leptosphaeria maculans, anamorph Phoma lingam. Formerly, four different strains, or pathogenicity groups, of L. maculans were recognized that varied
considerably in virulence and symptoms to a set of B. napus differentials as follows: A common strain, PG1, is weakly virulent, produces ascospores late in the
growing season, and infects plants as they approach maturity, thereby causing little injury and few symptoms. The second strain, PG2, is highly virulent and sporulates
early in the spring. A third strain, PG3, has been found on stinkweed, Thlaspi arvense, in Canada but does not seem to be important in causing blackleg on canola
or mustard. Another strain from Australia and Europe, labeled PG4, also differs in pathogenicity.
Based on pathogenicity and a number of correlated cultural, chemical, and genetic phenotypes, P. lingam currently is classified broadly into aggressive (virulent) and
nonagressive (avirulent) strains. Increasing evidence suggests the two strains represent different species. Variation in pathogenicity exists within the aggressive strain:
isolates have been classified into three groups, PG2, PG3, and PG4, based on differential pathogenicity on Brassica napus cultivars. Pathogenicity of L. maculans
to canola has been reported to be related to the production of the phytotoxin sirodesmin PL.
Leptosphaeria maculans and P. lingam survive up to 2 years in residue as pseudothecia and pycnidia, respectively. Phoma lingam is also seedborne as mycelia in
seed, which constitutes an important means of introducing the fungus into new areas.
During wet weather or high relative humidity and cool temperatures of 8° to 15°C in the spring or autumn, ascospores are produced in pseudothecia after a few hours
and disseminated by wind for several miles. Pycnidiospores are produced in pycnidia and are disseminated by splashing rain to host plants. Pycnidiospores are also
disseminated by adhering to seed after harvest and by being disseminated by wind to neighboring fields during harvesting.

Page 112
Pycnidia are produced on diseased plants throughout the growing season, while perithecia develop only as diseased plants mature. Stems and crowns from the current
season's spring canola crop may serve as a source of ascospores that are able to infect the winter canola crop in the autumn.
Canola is most susceptible to infection during the first few weeks of growth, while the plant is in the rosette stage. While young plant tissue is susceptible to infection,
all plant parts, including leaves, stems, and roots, can be infected. Infection of petioles and stems usually occurs through an injury. Subsequent disease development is
favored more by a higher temperature of 18° than a lower temperature of 12°C.
Distribution.
Australia, Canada, Europe, and the United States (Kentucky and North Dakota).
Symptoms.
In the spring, inconspicuous pallid areas form on diseased leaves. Eventually, the areas become irregularshaped, gray lesions dotted with pycnidia that appear as
small, black specks. Occasionally, lesions or cankers are associated with axils of leaves.
The stem canker phase can originate from injuries and leaf lesions by systemic growth of L. maculans through the laminae and petioles into the main stem. The first
noticeable symptom may be patches of lodged plants caused by diseased stems breaking at the soil line. Stems have poorly defined white to ashgray, brown, or
black lesions, often with purplish borders, that commonly develop near the soil line. Long, black transverse streaks occur in the cortex. Pycnidia are numerous and
appear as tiny, black specks on the lesions. During wet weather, conidia are extruded in a pinkish exudate from pycnidia. Severely diseased stems eventually become
girdled by large cankers that cause plants to ripen prematurely and produce light, shriveled seed, and that break over the entire plant.
Lesions near the base of stems extend downward into the root system, where black cankers are formed. Diseased roots subsequently disintegrate, further weakening
plants and frequently causing them to break off just below the soil line.
Management
1. Rotate canola and mustard with resistant crops, such as cereals, every 3 years.
2. Do not grow canola and mustard near fields in which the disease occurred the previous season.
3. Plow under infested residue because L. maculans is relatively shortlived and does not survive longer than 2 years in the soil.
4. New canola and mustard varieties are tolerant. Analyses of F1 and F2 progeny suggest resistance is determined by two dominant, independently segregating genes.
In Canada, cultivars with partial resistance have been released.

Page 113
5. Fungicides have been reported to be effective in managing disease when they were applied on a 7weekold crop.
6. Treat seed with a fungicide seed treatment.
7. Sow seed certified to be free of L. maculans.
Black Mold Rot
Cause.
Rhizopus stolonifer.
Distribution.
Canada.
Symptoms.
Seed rot and preemergence seedling blight occur. Postemergence seedling blight is scattered throughout a field and losses are usually negligible.
A hard, brown to black lesion (12 cm long) may be seen at the base of the diseased stem. Such diseased stems are sometimes girdled near the soil line. The taproot
may be discolored.
Management.
Black Root
Cause.
Aphanomyces raphani presumably survives as oospores in infested residue or soil. Zoosporangia, in which zoospores are produced, are likely formed from
oospores. Oospores are eventually produced in diseased roots. Disease is most severe under wet soil conditions.
Distribution.
Not known.
Symptoms.
Seedlings are stunted, and roots and hypocotyls are blackened. Aphanomyces raphani moves up the hypocotyl into the cotyledons, causing chlorosis and blackening
of the diseased tissues. Under magnification, oospores are evident in diseased root cortex.
Management.
Not reported.
Brown Girdling Root Rot
Brown girdling root rot is likely similar to foot rot because of the mutual pathogens involved. However, brown girdling root rot is treated as a separate disease from
foot rot because of its separate treatment in the literature and apparent dissimilarity of symptoms, which suggests the possibility of different pathovars. Brown girdling
root rot is also called Rhizoctonia root rot. The postemergence seedling blight phase is called wirestem.
Cause.
The most frequently isolated fungi are Fusarium roseum, Pythium ultimum, and Rhizoctonia solani; however, R. solani is considered the primary cause of the root
rot syndrome. The following anastomosis groups of R. solani are known to be involved: AG2, AG21, and AG4.

Page 114
Isolates of AG2 and AG21 are more virulent than AG4 to plants sown early in the growing season and to plants of all ages during periods of high soil moisture.
Early sowing, in general, results in significantly greater seedling infection by F. roseum, P. ultimum, and R. solani, regardless of what anastomosis groups may be
involved.
Distribution.
Canada (Alberta and British Columbia).
Symptoms.
Preemergence and postemergence damping off may occur. Later, distinct brown to redbrown lesions occur on diseased taproots. Several lesions may coalesce and
girdle taproots or a single large lesion may girdle a taproot.
Management
1. Rotate canola and mustard with cereals; however, it is not certain if cereals have the same disease that occurs on canola and mustard.
2. Sow cleaned, healthy seed early in the growing season.
3. Rhizoctonia solani is most destructive in a loose, wellworked soil; therefore, the seedbed should have firm soil.
4. Control cruciferous weeds and volunteer plants in and adjacent to fields.
Cercospora Leaf Spot
Cause.
Cercospora brassicicola. Disease is favored by extended periods of high humidity and temperatures of 28° to 30°C.
Distribution.
Sri Lanka.
Symptoms.
Redpurple, angular to irregularshaped lesions occur on diseased leaves. Lesions vary in size and originate from a pinpoint that enlarges and coalesces to form large,
necrotic areas. Veinal necrosis may also occur. Severe disease may cause rapid chlorosis and necrosis, resulting in defoliation that begins with the upper diseased
leaves and progresses down the plant.
Redpurple, slightly sunken lesions may occur on petioles and stems.
Management.
Not reported.
Charcoal Rot
Cause.
Macrophomina phaseolina. Optimum infection and resulting disease symptoms occur during high temperatures (32° to 36°C).
Distribution.
The United States (Kentucky and Indiana).
Symptoms.
Diseased plants prematurely senesce or die. Microsclerotia are present in taproots as multiple specks that somewhat resemble charcoal. Diseased tissue is shredded.
Management.
Not reported.

Page 115
Clubroot
Cause.
Plasmodiophora brassicae overwinters as resting spores, called hypnospores, that form within an infected cell. Hypnospores are liberated into soil when roots
disintegrate after the growing season. The following spring, when the soil warms up and moisture is present, a hypnospore germinates to form a single biflagellate
zoospore that ''swims" to a root hair. The zoospore loses its flagella, becomes amoeboid, and enters the epidermal cell, presumably with the aid of enzymes. Inside the
plant, the fungus produces an amoeboid thallus that soon gives rise to zoosporangia from which zoospores are liberated and move out of the diseased root. Cells of
infected roots contain naked fungal plasmodium that is able to move from cell to cell. Eventually, naked protoplasm breaks into multiple cells around which walls form
to become hypnospores.
Clubroot may occur at any soil temperature between 9° and 30°C but is most severe at the cooler temperatures. Hypnospores do not germinate when the soil pH is
higher than 7.2. In Canada, disease incidence and severity is greater in regions with severe winters.
Many physiological races of P. brassicae exist.
Distribution.
In cool, canolagrowing areas of the world.
Symptoms.
Diseased plants are stunted and chlorotic. The roots contain the typical galls symptomatic of clubroot. Galls are often spindleshaped and may involve the entire
diameter of the diseased root. Multiple branch roots frequently grow from galls to give them a hairy appearance.
Management.
Resistance is common in canola cultivars, especially in Sweden.
Damping Off
Damping off is also called seedling blight.
Cause.
Several fungi, including Pythium spp., Phytophthora spp., Fusarium spp., and Rhizoctonia solani. Some Pythium species involved in the preemergence phase of
seedling blight are P. paroecandrum and P. sylvaticum.
Disease severity and incidence are greater in heavy, wet soils that are common in the lowlying areas of a field, and during cool, wet weather. The causal fungi are
relatively weak pathogens that infect young, succulent tissue.
Distribution.
Wherever canola is grown.
Symptoms.
Seeds fail to germinate or seedlings are killed either preemergence or postemergence. Postemergence damping off is characterized by constriction and tapering of the
hypocotyl and brown lesions on the diseased hypocotyl and cotyledons. Seedlings rot at the soil line, causing them to fall over. Seedlings may emerge and not grow
larger then the one to fourleaf stage for a period of time, then they either die or resume growth.

Page 116
Management
1. Sow seed when the soil temperature has warmed up.
2. Seed should be sown at a depth of 1 to 25 mm in a firm seedbed.
Downy Mildew
When downy mildew occurs together with white rust caused by Albugo candida, it is called staghead.
Cause.
Peronospora parasitica overwinters primarily as systemic mycelia in perennial or overwintering plants and as oospores in soil and infested residue. Conidia
(sporangia) are produced on diseased leaves of systemically infected plants and disseminated by wind to other hosts.
Zoospores are not commonly formed; therefore, infection occurs by conidia germinating directly to form either germ tubes that penetrate hosts or a conidiophore on
which a large conidium is formed. Secondary inoculum is provided by conidia produced on leaves. Different races of P. parasitica exist.
When downy mildew occurs together with white rust to cause staghead, the effect is synergistic since disease development caused by both fungi together is greater
than either fungus alone. Cool, moist weather favors staghead development.
Distribution.
Wherever canola is grown; however, downy mildew is usually more severe in northern canolagrowing areas.
Symptoms.
Spots appear on diseased leaves, stems, and seedpods as small purple, irregularshaped areas. Leaf spots enlarge to form yellow areas in which a white, downy
growth occurs on diseased upper leaf surfaces, while conidia and conidiophores form on lower leaf surfaces. The downy growth also occurs on blisters and stagheads.
Management
1. Grow resistant cultivars, such as Argentinetype cultivars. Resistant cultivars of turnip canola are available. The oilseed canola cultivar 'Cresor' is resistant to 14
isolates of P. parasitica.
2. Control volunteer turnip canola and wild mustard.
3. Sow only cleaned seed.
4. Rotate canola with resistant crops.
Foot Rot
Cause.
Rhizoctonia solani AG4 and Fusarium roseum. Rhizoctonia solani is considered the primary pathogen. Rhizoctonia solani survives as sclerotia and mycelia in
infested residue. Fusarium roseum survives as chlamydospores in soil, mycelia in residue, and perithecia on infested residue. Both fungi have a wide host range.

Page 117
Other fungi associated with this disease complex are Alternaria alternata, F. solani, F. tricinctum, Leptosphaeria maculans, Pythium debaryanum, and P.
polymastum. The Fusarium spp. are sometimes seedborne.
Distribution.
Wherever canola and mustard are grown; however, disease incidence is usually sporadic.
Symptoms.
Prematurely ripened plants are found singly or in patches throughout a field during the summer. Hard, clearly defined, brown lesions with rough surfaces, sometimes
with a black border, are present on diseased stem bases. During wet conditions, salmonpink spore masses may be present on lesions. A white, mycelial growth may
be present on discolored root tissue. Severe disease will girdle stems and kill plants.
Management
1. Rotate canola and mustard with cereals; however, it is not certain if cereals have the same disease that occurs on canola and mustard.
2. Sow cleaned, healthy seed early in the growing season.
3. Rhizoctonia solani is most destructive in a loose, wellworked soil; therefore, the seedbed should have firm soil.
4. Control cruciferous weeds and volunteer plants in and adjacent to fields.
Fusarium Seed Infection
Cause.
Fusarium moniliforme, F. oxysporum, and F. semitectum.
Distribution.
Not known for certain, but Fusarium seed infection is presumably widespread.
Symptoms.
Qualitative and quantitative changes occur in the amino acid and sugar content of diseased seeds, and protein content declines.
Management.
Not reported.
Fusarium Wilt
Fusarium wilt is also called yellows.
Cause.
Fusarium oxysporum f. sp. conglutinans survives as chlamydospores in residue and soil. Different races are reported to exist.
Distribution.
Widespread.
Symptoms.
Symptom expression varies with plant age. Foliar symptoms progress from the base of the diseased plant upward. Leaves droop, display veinclearing and chlorosis,
followed by wilting and drying, a symptom that often precedes death of the entire plant.
Plants infected during preflowering and early flowering become defoli

Page 118
ated. Stems of such plants develop external longitudinal ridges and furrows, a symptom that generally is not observed when older plants are infected. Plants infected
early in their growth are often stunted, but plants infected later generally do not have this symptom. Frequently only one side of the plant displays symptoms. Xylem or
vascular tissue is discolored brown, a symptom caused by the plugging of the tissue by a dark gummy substance.
Management
1. Do not grow canola and mustard following cabbage or other Brassicae spp.
2. Canola and mustard may not be susceptible to all races of Fusarium wilt.
Gray Mold
Cause.
Botrytis cinerea. Disease is favored by rainy weather.
Distribution.
Germany, Sweden, Great Britain, and the former USSR.
Symptoms.
Mycelium that varies from a "dirty white" or gray to black in color occurs on diseased flowers and pods.
Management.
Not reported.
Leaf Spot
Cause.
Myrothecium roridum and Phyllosticta brassicae.
Distribution.
India.
Symptoms.
Brownish spots occur on diseased leaves. Sometimes the center of the spot falls out and gives the leaf a ragged appearance.
Management.
Not reported.
Light Leaf Spot
Light leaf spot is also called leaf scorch.
Cause.
Pyrenopeziza brassicae (syn. Cylindrosporium concentricum). Pyrenopeziza brassicae is seedborne and presumably overwinters in canola stubble and on wild
crucifers and brassicas. Primary inoculum is conidia that are splashed from the overwintering sites onto nearby host plants. Disease is favored by excess moisture and
temperatures of 5° to 15°C.
Distribution.
France, Germany, Great Britain, and Sweden.
Symptoms.
Rarely, severe infection may kill seedlings. Blanched, "papery" lesions first appear on older diseased leaves, which eventually wither. During the stem extension growth
stage of the plant, infection may spread to

Page 119
the upper leaves and bracts to cause severe leaf scorch, gross plant distortion, and stunting. Stunted, diseased winter canola plants that survive through the winter
regenerate new shoots in the spring. Siliquae of diseased plants may mature prematurely and split.
Management
1. Cultivars vary in tolerance or resistance. The more resistant cultivars are high erucic acid types.
2. Foliar fungicides have been effective in field trials.
Pod Drop
Cause.
Alternaria alternata and Cladosporium sp. Dead or dying petals are infected and provide a food base for fungi to grow into the pedicels.
Distribution.
Canada.
Symptoms.
Pedicels are blackened and weakened at, or below, their point of attachment to pods, which sometimes causes pods to drop. Pedicel tips then display a typical black
discoloration. Pods on diseased pedicels do not fill normally.
Management.
Summer turnip canola is more resistant than Argentine types.
Powdery Mildew
Cause.
Erysiphe polygoni and E. cruciferarum overwinter as cleistothecia or mycelia in volunteer host plants. Disease is favored by relatively dry weather conditions and
moderate temperatures of 7.1° to 25.0°C.
Distribution.
Worldwide, but powdery mildew is usually not considered serious on canola and mustard.
Symptoms.
Dirty white, circular, floury patches occur on both sides of lower diseased leaves. These powdery mildew patches increase in size and coalesce to cover the entire
stem and leaves. Severely diseased plants grow poorly and produce less siliquae. Green siliquae also show white patches in the initial stage of infection. Later, such
siliquae become covered with a white mass of mycelium and conidia. Severely diseased siliquae remain small in size and produce seeds that are also small and
shriveled. Such siliquae produce a few seeds at the base that have twisted sterile tips. Later in the season, cleistothecia may be formed on both sides of diseased
leaves, stems, and siliquae as scattered small, black bodies visible to the unaided eye.
Management
1. Limited resistance has been identified in some canola and mustard cultivars.
2. Foliar fungicides have been effective in field trials.

Page 120
Rhizoctonia Crown Rot
Rhizoctonia crown rot may be a similar disease to foot rot and brown girdling root rot. However, symptoms are sufficiently different to currently treat them as separate
diseases.
Cause.
Rhizoctonia solani AG21 and AG4. Crown rot is most prevalent in wet or poorly drained areas of fields, but the disease is also reported to be severe on early
sown canola growing on sandy soils in Indiana. Earlysown plants, which make extensive growth in the autumn, are more severely diseased than smaller plants that
were sown later in the growing season. By early winter, crown tissues near the soil surface are infected through direct penetration of mycelia and through leaf scars,
but root tissues below the crown generally are not infected until midwinter and spring.
Distribution.
The United States (Indiana). However, crown rot is probably distributed wherever canola is grown.
Symptoms.
Severe crown rot occurs with varying degrees of cortical necrosis. Root tissues below the crown are not diseased. The bases of diseased leaves frequently have dark
brown to black, necrotic lesions that result in leaf death.
Management.
Sowing date and cultivar selection may reduce severity of crown rot.
Ring Spot
This disease is also called black blight, black stem ring spot, and white leaf spot and gray stem.
Cause.
Mycosphaerella brassicicola overwinters as thickwalled mycelia and perithecia in infested residue. The fungus is not seedborne to any extent. In the spring, conidia,
produced from mycelia that overwintered in residue, become disseminated by wind to host plants. Most secondary inoculum and spread are by conidia produced in
spots during cool, wet environmental conditions.
Perithecia form on diseased plant tissue later in the growing season during periods of low night temperatures and heavy dews. Ascospores are thought to be a means
of spread of M. brassicicola in Europe and the United States but not in Canada.
Distribution.
Canada, Europe, and the United States.
Symptoms.
Circular (12 cm in diameter), whitish leaf spots are produced on diseased leaves. Later in the season, large, elongate, purple to gray lesions with lighter centers that
are speckled with numerous perithecia occur on diseased stems and pods. Lesions may coalesce and completely blacken large portions of affected plants.

Page 121
Management.
Although ring spot is not considered important because it develops too late in the life of the plant, the following are aids to management:
1. Rotate canola and mustard with noncruciferous crops.
2. Control weeds.
3. Sow healthy, cleaned seed.
Sclerotinia Stem Rot
Cause.
Sclerotinia sclerotiorum overwinters as sclerotia either in the soil or as a contaminant of seed lots. Infrequently, seed itself may be infected. Mycelia do not survive
well enough in infested stems to be significant sources of pathogenic inoculum.
Sclerotia have a dormancy mechanism that requires certain physical factors to occur before germination. Sclerotia from Saskatchewan required 2 to 6 weeks
incubation at 10°C, followed by 4 to 6 weeks at 20°C in diffuse light, for initiation of stipes and cap expansion. Sclerotia have a higher germination at high soil
moisture than at low soil moisture before plant flowering. However, after flowering, germination is higher at lower soil moisture because of the large number of viable
sclerotia.
After physical factors have been satisfied, sclerotia germinate in one of two ways. First, in the spring, sclerotia germinate to produce mycelia that grow a short distance
across moist soil and infect plants at the soil line. Carpogenic germination, reported to be the most common method of sclerotia germination, occurs later in the
growing season, at flowering time, when sclerotia germinate to produce one to several cupshaped apothecia. Ascospores are borne in asci on the apothecium surface
and are disseminated by wind, pollen, and insects to host plants, where infection occurs in leaf axils and, more commonly, in the dead or dying petals of blossoms that
have fallen onto leaves and stems. Although most ascospores are dispersed within 5 m of their source, some may be transferred up to 200 m. Sclerotia are eventually
formed from mycelium in diseased stems.
In a slight derivation from the previous method of infection, ascospores first infest canola blossoms; infection is initiated when infested petals dehisce, fall, and adhere
to the stem. Ascospores germinate, penetrate the stem, and form lesions in which sclerotia develop. Sclerotia fall out of these lesions into the soil and, after
physiological conditioning, including overwintering, germinate to form apothecia.
Sclerotinia stem rot is reported to be most severe under warm, wet weather conditions. Two weeks of wet weather before and during flowering favors disease
development. Lodged mustard and canola provide conditions conducive to disease. In North Dakota, Sclerotinia stem rot is reported to be more prevalent during
rainy seasons when sclerotiainfested

Page 122
field soils are wet for approximately 10 to 14 days at the beginning of blossoming and when blossoms remain wet for several days.
Distribution.
Wherever canola and mustard are grown.
Symptoms.
The first symptom is the presence of prematurely ripened plants that are scattered or are grouped among green, healthyappearing plants in a field. These diseased
plants are easily pulled from the soil.
The pale gray lesions with faint concentric markings that are on stems develop from the soil line or from the axils of branches or leaves. At first, lesions are water
soaked, then eventually expand to girdle stems, which kills the diseased plants. Such stems are bleached, have a chalky white appearance, and tend to shred
longitudinally. Sclerotia appear as hard, black, grainsized bodies inside stems near the bases of dead plants. Under moist conditions, sclerotia occur in all parts of
stems and pods.
Management
1. Rotate canola and mustard with cereals and grasses every 4 years.
2. Sow only cleaned seed with all sclerotia removed.
4. Control volunteer canola, mustard, and susceptible weeds.
Smut, Root Gall
Cause.
Urocystis brassicae. Galls from roots contain spore balls of the fungus. When galls decay, the spores that are liberated into the soil constitute the primary source of
inoculum. Disease does not spread but remains in the same general area within a field.
Distribution.
India.
Symptoms.
Galllike bodies that occur on roots may be as large as 2.5 to 3.5 cm in diameter. Galls may be observed in all parts of the root system. Initially, galls are small and
whitish but become grayish black as they mature. Diseased plants remain stunted and branch freely. Diseased mustard plants produce flowers earlier than healthy
plants but have poor seed production.
Management.
Not reported.
Southern Blight
Cause.
Sclerotium rolfsii.
Distribution.
Malaya.
Symptoms.
A general leaf blight occurs.
Management.
Not reported.

Page 123
Storage Molds
Cause.
Penicillium spp., primarily P. verrucosum var. cyclopium; and Aspergillus spp., primarily A. amstelodami, A. repens, and A. sejunctus. Other reported fungi are
Alternaria spp., Aspergillus candidus, A. fumigatus, A. versicolor, A. wentii, Cephalosporium acremonium (syn. Acremonium strictum), Cladosporium
cladosporioides, and Wallemia sebi.
Verticillium Wilt
Cause.
Verticillium alboatrum and V. dahliae.
Distribution.
Sweden.
Symptoms.
A general wilting of diseased plants occurs.
Management.
Not reported.
White Blight
Cause.
Rhizoctonia solani. Disease is favored by high temperatures and excess moisture.
Distribution.
India.
Symptoms.
A general blighting of diseased leaves occurs. Blighted leaves are covered with the white to grayish mycelium of R. solani.
Management.
Not reported.
White Leaf Spot
Cause.
Pseudocercosporella capsellae (syn. Cercosporella brassicae).
Distribution.
The United States (California). However, white leaf spot is likely to be wherever canola and mustard are grown.
Symptoms.
Circular, light tan to offwhite spots measuring 2 to 8 mm in diameter occur on diseased leaves. White downy or "fuzzy" sporulation that consists of conidia,
conidiophores, and mycelium occurs in the leaf spots.
Management.
Not reported.
White Rust
White rust is also called staghead, either as a synonym only for white rust or to refer to the white rustdowny mildew complex. White rust is usually associated with
downy mildew caused by Peronospora parasitica.
Cause.
Albugo candida (syn. A. cruciferarum) overwinters as oospores in residue and soil and as a contaminate of seed lots. In the spring, oospores

Page 124
germinate to produce sessile vesicles or short exit tubes that terminate in a vesicle. Zoospores are released from vesicles and "swim" to host tissue, where they encyst
and germinate to form infective mycelium that penetrates plant tissue. The resulting mycelium growing inside the infected plant then becomes systemic.
Secondary infection is by sporangia produced in leaf blisters and disseminated by wind to other hosts. Sporangia germinate by producing zoospores that first encyst,
then germinate to form infective mycelium that penetrates the host and causes localized infections. Oospores eventually develop within diseased swollen or
hypertrophied tissue.
White rust is most severe during wet weather conditions. Day and night temperatures of 22°C and 17°C, respectively, are more favorable to fungal growth than 15°C
and 10°C, respectively.
Different races exist. Collections from radish, Raphanus sativus; brown and oriental mustard, Brassica juncea; shepherd's purse, Capsella bursapastoris; and
turnip rape, B. campestris subsp. eucampestris represent different races. Race 7 infects B. campestris but not B. napus. Differences in susceptibility exist between
Brassica napus and B. rapa.
Distribution.
Wherever canola and mustard are grown.
Symptoms.
The most obvious symptom is a swelling and deformation of terminal parts of flower stalks which results in the "spiny" staghead symptom that accounts for most of the
yield losses. Initially, stagheads are green but later become brown and hard as they dry up.
Raised green or brown blisters occur on the undersides of diseased leaves, stems, and pods. Initially, blisters are smooth but later rupture to release white to cream
colored masses of sporangia. Similar blisters may appear on surfaces of green stagheads. Portions of individual flowers may also become distorted with sterile
inflorescences.
Management
1. Grow resistant Argentinetype cultivars. Resistant cultivars of turnip canola may be available.
2. Control volunteer turnip canola and wild mustard.
4. Rotate canola with resistant crops.
5. Under experimental conditions, metalaxyl applied as a foliar, seed, and soil application reduced disease incidence.
Winter Decline Syndrome
Cause.
Physical damage on roots, crowns, or stems caused by sublethal low temperatures occurs on plants that have bolted prematurely, are not adequately coldhardened,
or have undergone plant heaving and/or depletion of soil oxygen from waterlogged soils. The physical damage provides ports of entry for invasion by a variety of
secondary organisms. Clavibacter sp.,

Page 125
Fusarium sp., Rhizoctonia sp., and Xanthomonas sp. have been inconsistently isolated from affected tissue.
Distribution.
The southeastern and midsouthern states of the United States.
Symptoms.
Taproots and crowns of diseased plants deteriorate and often become hollow. Diseased plants may die before or during bolting, may bolt normally but later lodge and
fall down because of weakened crown tissue, or remain upright but die prematurely and reduce the seed yield. Stands may be reduced by over 90%.
Management.
Not reported.
Wirestem
Wirestem is a form of Rhizoctonia root rot.
Cause.
Rhizoctonia solani.
Distribution.
Widespread.
Symptoms.
A narrow, rotted root comprised primarily of the stele begins below apparently healthy tissue. Diseased tissue is a light brown lesion on the taproot and the bases of
larger lateral roots. Eventually, the taproot may be girdled. Eventually, the diseased portion of the root somewhat resembles a ''wire" that hangs below the healthy
appearing root tissue. Root regeneration may occur above the rotted area.
Management.
Not reported.
Yeast Infection of Seed
Cause.
Nematospora sinecauda is transmitted by the false chinch bug, Nysius niger. Flixweed, Descurainia sophia, is the overwintering host.
Distribution.
Canada (Prairie Provinces) and the United States (Montana and North Dakota).
Symptoms.
An undesirably high plate count of microorganisms occurs in condiment flours ground from diseased seed.
Management.
Not reported.
Root Knot
Cause.
Meloidogyne arenaria and M. incognita. Meloidogyne arenaria and M. incognita do not survive if the temperature averages below 3°C during the coldest month.

Page 126
Distribution.
The United States (Georgia).
Symptoms.
Typical root galls form on diseased roots.
Management.
Sources of resistance are available in advanced germplasms.
Aster Yellows
Cause.
Aster yellows phytoplasma survives in several dicotyledonous plants and in leafhoppers. The phytoplasma is disseminated from collateral hosts to canola and mustard
primarily by the aster leafhopper, Macrosteles fascifrons, and less commonly by the leafhoppers Endria inimica and M. laevis.
Distribution.
Wherever canola and mustard are grown. Aster yellows is not an important disease of canola or mustard.
Symptoms.
Diseased plants are infected systemically but symptoms usually occur only on inflorescences. Flowers and pods become distorted and sterile and frequently form
small, bluegreen, hollow, bladderlike structures instead of normal seedpods.
Management.
Not reported.
Green Petal Disease
Cause.
A phytoplasma that is transmitted by the insect Euscelis plebejus and by grafting.
Distribution.
Germany and Hungary.
Symptoms.
Internodes are shortened and diseased plants are stunted. Virescence, flower proliferation and deformation, and vein clearing of the leaves are prominent symptoms.
Management.
Not reported.
Cauliflower Mosaic
Cause.
Cauliflower mosaic virus is transmitted by the aphids Myzus persicae and Brevi coryne.
Distribution.
Bulgaria, New Zealand, and the United States.
Symptoms.
Diseased leaves display a general mosaic.
Management.
Not reported.

Page 127
Crinkle
Cause.
Turnip crinkle virus (TCV) is a singlestranded RNA virus in the carmovirus group. TCV supports the replication of at least three satellite RNAs. One satellite RNA
(satRNA C) intensifies symptoms on a turnip cultivar, but it does not have any intensifying effect on canola.
Distribution.
Not known.
Symptoms.
Diseased plants are stunted. Leaves are mildly to severely crinkled and have vein clearing.
Management.
Not reported.
Mosaic
Cause.
Turnip mosaic virus (TuMV) is in the potyvirus group. TuMV is transmitted mechanically and, frequently, by the green peach aphid, Myzus persicae. TuMV can also
be transmitted by several other species of aphids.
Distribution.
Widespread.
Symptoms.
A general mosaic pattern occurs on diseased leaves.
Management.
Not reported.
Phyllody
Cause.
Sesamum phyllody virus (SPV). SPV is transmitted by a jassid insect, Orosius albicinctus.
Distribution.
India.
Symptoms.
Diseased floral parts are transformed into leafy structures. The corolla becomes green and sepaloid, and stamens are green and become indehiscent. The gynoecium is
borne on a distinct gynophore and produces no ovules in the ovary. There also are some leafy structures attached to the false septum. The affected parts of the raceme
do not form siliquae. Some diseased plants may only have the terminal portions of branches affected; others may have entire branches that display symptoms.
Management.
Not reported.
Rai Mosaic
Cause.
Rai mosaic virus (RMV). RMV is saptransmissible and is transmitted in a nonpersistent manner by the aphids Myzus persicae and Lipaphis erysimi.
Distribution.
India.
Symptoms.
Characteristic mosaic symptoms occur on diseased leaves. Diseased plants are stunted and have deformed lamina.
Management.
Not reported.

Page 128
Yellows
Cause.
Beet western yellows virus (BWYV) and broccoli necrotic yellows virus. BWYV is transmitted in a nonpersistent manner by the aphids Myzus persicae and
Macrosiphum euphorbiae and possibly by other aphid vectors.
Distribution.
The United Kingdom.
Symptoms.
Interveinal chlorosis occurs on lower and intermediate diseased leaves. Leaves are frequently purple and plants ripen prematurely.
Management.
Not reported.
Brown Girdling Root Rot
Cause.
Unknown.
Distribution.
Western Canada.
Symptoms.
Symptoms are confined only to diseased roots. Light brown lesions occur on taproots and the bases of larger lateral roots 5 cm or more below the soil surface. Dark
brown, sunken lesions with vertical streaks may expand, coalesce, and girdle taproots. Lesions may expand up to the soil line but rarely beyond. If girdling occurs
more than 5 cm below the soil line, some root regeneration may occur if there is sufficient moisture.
Management.
Argentine cultivars have some field tolerance.
Pollen Necrosis
Cause.
Pollen shed from the plant. There are several possibilities as to what causes the symptom: (1) A chemical constituent of the pollen grain is perceived as an alien agent
by the leaf cells, which respond in a hypersensitive manner, or enzymes within the pollen grains may be responsible for the necrotic reaction. (2) The pollen grains may
promote some microbe(s) that are responsible for the browning reaction. (3) The necrotic areas may serve as points of entry for certain pathogens.
Distribution.
Canada, Germany, and India.
Symptoms.
Minute, necrotic spots develop under deposits of pollen grains. Eventually, a zone of chlorosis develops around the lesion.
Management.
Not known.

Page 129
Unknown
Cause.
Unknown, but probably of genetic or physiologic origin.
Distribution.
India.
Symptoms.
Diseased plants are stunted and have small, puckered, leatherlike, twisted leaves that are darker green than healthy leaves. Flowers are poorly developed and few
seeds are produced. Longitudinal fissures that ooze a watersoluble yellow gum are present on aerial plant parts.
Management.
Not reported.
Selected References
Anonymous. 1967. Diseases of field crops in the Prairie Provinces. Canada Dept. Agric. Res. Branch, Ottawa, Pub. 1008.
Assabqui, R., and Hall, R. 1990. In vitro production of sirodesmin PL correlated with pathogenicity of Leptosphaeria maculans to rapeseed. (Abstr.).
Baird, R. E., Hershman, E. E., and Christmas, E. P. 1994. Occurrence of Macrophomina phaseolina on canola in Indiana and Kentucky. Plant Dis. 78:316.
Berkenkamp, B., and Vaartnou, H. 1972. Fungi associated with rape root rot in Alberta. Can. J. Plant Sci. 52:973976.
Burgess, L., and McKenzie, D. L. 1991. Role of the insect Nysius niger and flixweed, Descurainia sophia, in infection of Saskatchewan mustard crops with a yeast,
Nematospora sinecauda. Can. Plant Dis. Surv. 71:3741.
Calman, A. I., and Tewari, J. P. 1987. Involvement of Pythium spp. in the preemergence phase of canola seedling blight. (Abstr.) Can. J. Plant Pathol. 9:274.
Calman, A. I., Tewari, J. P., and Mugala, M. 1986. Fusarium avenaceum as one of the causal agents of seedling blight of canola in Alberta. Phytopathology
70:694.
Campbell, J. N., Cass, D. D., and Peteya, D. J. 1987. Colonization and penetration of intact canola seedling roots by an opportunistic fluorescent Pseudomonas sp.
and the response of host tissue. Phytopathology 77:11661173.
Davidson, J. G. N. 1976. Plant Diseases in the Peace River Region in 1976. Agric. Can. Res. Sta., Beaverlodge, Alberta. Mimeo.
Davidson, J. G. N. (Undated). Disease Control in Rapeseed. Agric. Can. Res. Sta., Beaverlodge, Alberta. Mimeo.
Dueck, J. 1981. Dormancy in sclerotia of Sclerotinia sclerotiorum. (Abstr.) Phytopathology 71:214.
Fucikovsky, L. 1979. Bacterial disease of rape and carrot in Mexico. (Abstr.) Phytopathology 69:915.
Gladders, P., and Musa, T. M. 1980. Observations on the epidemiology of Leptosphaeria maculans stem canker in winter oilseed rape. Plant Pathol. 29:2837.
Gugel, R. K., and Petri, G. A. 1992. History, occurrence, impact, and control of blackleg of rapeseed. Can. J. Plant Pathol. 14:3645.

Page 130
Gugel, R. K., Yitbarek, S. M., Verma, P. R., Morrall, R. A. A., and Sadasivaiah, R. S. 1987. Etiology of the Rhizoctonia root rot complex of canola in the Peace
River region of Alberta. Can. J. Plant Pathol. 9:119128.
Hammond, K. E., Lewis, B. G., and Musa, T. M. 1985. A systemic pathway in the infection of oilseed rape plants by Leptosphaeria maculans. Plant Pathol.
34:557565.
Henry, A. W. 1974. Bacterial pod spot of rape in Alberta. Can. Plant Dis. Surv. 54:9194.
Hill, C. B., Phillips, D. V., and Hershman, D. E. 1992. Canola winter decline syndrome. Plant Dis. 76:861.
Huber, D. M., Herr, L. J., Christmas, E. P., and Roseman, T. S. 1991. Crown rot, a serious disease of canola in the Midwest. (Abstr.) Phytopathology 81:1186.
Huber, D. M., Christmas, E. P., Herr, L. J., McCayBuis, T. S., and Baird, R. 1992. Rhizoctonia crown rot of canola in Indiana. Plant Dis. 76:12511253.
HumphersonJones, F. M. 1985. The incidence of Alternaria spp. and Leptosphaeria maculans in commercial brassica seed in the United Kingdom. Plant Pathol.
34:385390.
Hwang, S. F., Swanson, T. A., and Evans, I. R. 1986. Characterization of Rhizoctonia solani isolates from canola in west central Alberta. Plant Dis. 70:681683.
Kohli, Y., Morrall, R. A. A., Anderson, J. B., and Kohn, L. M. 1992. Local and transCanadian clonal distribution of Sclerotinia sclerotiorum on canola.
Koike, S. T. 1996. Japanese mustard, tah tsai, and red mustard as hosts of Alternaria brassicae in California. Plant Dis. 80:822.
Koike, S. T. 1996. Red mustard, tah tsai, and Japanese mustard as hosts of Pseudocercosporella capsellae in California. Plant Dis. 80:960.
Kolte, S. J. 1985. Diseases of Annual Edible Oilseed Crops. Volume II: RapeseedMustard and Sesame Diseases. CRC Press Inc., Boca Raton, FL. 135 pp.
Kruger, W., and Wittern, I. 1985. Epidemiological investigations in the root and collar rot of soil seed rape caused by Phoma lingam. Phytopathol. Zeitschr.
113:125140.
Lamey, H. A. 1995. Survey of blackleg and Sclerotinia stem rot of canola in North Dakota in 1991 and 1993. Plant Dis. 79:322324.
Lamey, H. A., and Hershman, D. E. 1993. Blackleg of canola (Brassica napus) caused by Leptosphaeria maculans in North Dakota. Plant Dis. 77:1263.
Lefol, C., and Morrall, R. A. A. 1997. Dispersal of ascospores of Sclerotinia sclerotiorum in canopies of flowering canola. (Abstr.). Can. J. Plant Pathol. 19:113.
Li, X. H., and Simon, A. E. 1990. Symptom intensification on cruciferous hosts by the virulent satellite RNA of turnip crinkle virus. Phytopathology 80:238242.
Liu, Q., and Rimmer, S. R. 1990. Effect of host genotype, inoculum concentration, and incubation temperature on white rust development in oilseed rape. Can. J.
Plant Pathol. 12:389392.
Lucas, J. A., Crute, I. R., Sherriff, C., and Gordon, P. L. 1988. The identification of a gene for racespecific resistance to Peronospora parasitica (downy mildew)
in Brassica napus var. oleifer (oilseed rape). Plant Pathol. 37:538545.
Mathur, R. S., and Singh, B. R. 1975. A viruslike disorder of yellow mustard in India. Plant Dis. Rptr. 59:174175.
McGee, D. C. 1977. Blackleg (Leptosphaeria maculans (Desm.) Ces et de Not.) of rapeseed in Victoria: Sources of infection and relationships between inoculum,
environmental factors and disease severity. Aust. J. Agric. Res. 28:5362.
McGee, D. C., and Petrie, G. A. 1978. Variability of Leptosphaeria maculans in relation to blackleg of oilseed rape. Phytopathology 68:625630.
McGee, D. C., and Petrie, G. A. 1979. Season patterns of ascospore discharge by Lep

Page 131
tosphaeria maculans in relation to blackleg of oilseed rape. Phytopathology 69:586589.
Mengistu, A., Rimmer, S. R., Koch, E., and Williams, P. H. 1991. Pathogenicity grouping of isolates of Leptosphaeria maculans on Brassica napus cultivars and
their disease reaction profiles on rapidcycling brassicas. Plant Dis. 75:12791282.
Mills, J. T., and Sinha, R. N. 1980. Safe storage periods for farmstored rapeseed based on mycological and biochemical assessment. Phytopathology 70:541547.
Mithen, R. F., and Lewis, B. G. 1988. Resistance to Leptosphaeria maculans in hybrids of Brassica oleracea and Brassica insularis. J. Phytopathol. 123:253
258.
Petrie, G. A. 1974. Diseases in Rapeseed, Canada's "Cinderella" Crop, Third Edition. R. K. Downey, A. J. Klassen, and J. McAnsh (eds.). Pub. No. 33. Rapeseed
Association, Canada.
Petrie, G. A. 1975. Diseases of Rapeseed and Mustard. In Oilseed and Pulse Crops in Western Canada, J. T. Harapiak (ed.). Modern Press, Saskatoon,
Saskatchewan.
Petrie, G. A. 1988. Races of Albugo candida (white rust and staghead) on cultivated Cruciferae in Saskatchewan. Can. J. Plant Pathol. 10:142150.
Petrie, G. A., and Dueck, J. 1977. Diseases of Rape and Mustard. In Insect Pests and Diseases of Rape and Mustard, L. Burgess, J. Dueck, G. A. Petri, and L. G.
Putnam (eds.). Pub. No. 48. Rapeseed Association, Canada.
Ponce, F., and Mendoza, C. 1983. Fungal diseases and pests of the rapeseed Brassica napus L. and B. campestris L. in the high valleys of Mexico. (Abstr.)
Rao, D. V., Hiruki, C., and Chen, M. H. 1977. A mosaic disease of rape in Alberta caused by turnip mosaic virus. Plant Dis. Rptr. 61:10741076.
Rempel, C. B., and Hall, R. 1993. Dynamics of production of ascospores of Leptosphaeria maculans in autumn on stubble of the current year's crop of spring
rapeseed. Can. J. Plant Pathol. 15:182184.
Sippell, D. W., Davidson, J. G. N., and Sadasivaiah, R. S. 1985. Rhizoctonia root rot of rapeseed in the Peace River region of Alberta. Can. J. Plant Pathol. 7:184
186.
Stelfox, D., Williams, J. R., Soehngen, V., and Topping, R. C. 1978. Transport of Sclerotinia sclerotiorum ascospores by rapeseed pollen in Alberta. Plant Dis.
Rptr. 62:576579.
Stone, J. R., Verma, P. R., Dueck, J., and Spurr, D. T. 1987. Control of Albugo candida race 7 in Brassica campestris cv. Torch by foliar, seed, and soil
applications of metalaxyl. Can. J. Plant Pathol. 9:137145.
Teo, B. K., Yitbarek, S. M., Verma, P. R., and Morrall, R. A. A. 1988. Influence of soil moisture, seeding date, and Rhizoctonia solani isolates (AG 21 and AG
4) on disease incidence and yield in canola. Can. J. Plant Pathol. 10:151158.
Teo, B. K., Morrall, R. A. A., and Verma, P. R. 1989. Influence of soil moisture, seeding date, and canola cultivars ('Tobin' and 'Westar') on the germination and
rotting of sclerotia of Sclerotinia sclerotiorum. Can. J. Plant Pathol. 11:393399.
Tewari, J. P., Tewari, I., and Paul, V. H. 1994. Necrosis of Brassica leaves under deposits of pollen grains. (Abstr.) Can. J. Plant Pathol. 16:77.
Thomas, P. E., Hang, A. N., Reed, G. C., and Reisenauer, G. 1993. Potential role of winter rapeseed culture on the epidemiology of potato leaf roll disease. Plant
Dis. 77:420423.
Vaartnou, H., and Tewari, I. 1972. Alternaria alternata: Parasitic on rape in Alberta. Plant Dis. Rptr. 56:676677.
Vanterpool, T. C. 1974. Pythium polymastum: Pathogenic on oilseed rape and other crucifers. Can. J. Bot. 52:12051208.

Page 132
Vigier, B., Chiang, M. S., and Hume, D. J. 1989. Source of resistance to clubroot (Plasmodiophora brassicae Wor.) in triazineresistant spring canola (rapeseed).
Can. Plant Dis. Surv. 69:113115.
Walker, J. T., Phillips, D. V., Denmon, L., and Melin, J. 1997. Reaction of canola cultivars to rootknot nematodes Meloidogyne arenaria and Meloidogyne
incognita. (Abstr.). Phytopathology 87:S115.
Williams, J. R., and Stelfox, D. 1979. Dispersal of ascospores of Sclerotinia sclerotiorum in relation to Sclerotinia stem rot of rapeseed. Plant Dis. Rptr. 63:395
399.
Williams, P. H. 1992. Biology of Leptosphaeria maculans. Can. J. Plant Pathol. 14:3035.
Yitbarek, S. M., Verma, P. R., Gugel, R. K., and Morrall, R. A. A. 1988. Effect of soil temperature and inoculum density on preemergence dampingoff of canola
caused by Rhizoctonia solani. Can. J. Plant Pathol. 10:9398.

Page 133
5.
Diseases of Common Bean (Phaseolus vulgaris)
Bacterial Brown Spot
Bacterial brown spot is also called brown spot.
Cause.
Pseudomonas syringae pv. syringae is seedborne and overwinters in infested residue. Overwintering also occurs on hairy vetch, Vicia villosa; common vetch, V.
sativa; kudzu, Pueraria thunbergiana; and probably other weeds. In New York, bacteria overwintered on weeds primarily in areas where a severe incidence of
brown spot occurred the previous growing season. Otherwise the bacteria were not commonly isolated from weeds and residue was considered the primary source of
inoculum.
Epiphytic phytopathogenic bacteria provide inoculum for disease, with the probability of disease increasing as epiphyte populations increase. In Wisconsin, an
epiphytic population of approximately 10,000 bacteria per gram of snap bean leaf tissue was the minimum infection threshold required to produce brown spot
symptoms. Higher populations of bacteria occur on leaves of susceptible cultivars than on resistant cultivars.
Disease severity increases when leaves are moist for extended periods of time.
Distribution.
Wherever common bean is grown.
Symptoms.
Dark brown necrotic spots of various sizes occur on diseased leaves but without the initial watersoaking symptoms common to other foliar diseases caused by
bacteria. The marginal chlorosis or halos surrounding lesions also are absent. Pod symptoms are brown spots and, frequently, a pod twisting at the point of infection.
Management
1. Sow healthy seed treated with a seedprotectant fungicide.
2. Rotate common bean with resistant crops.

Page 134
3. Do not grow common bean adjacent to lima bean (Phaseolus limensis) fields since lima bean is very susceptible to P. syringae. Inoculum may be easily
disseminated from one field to the next.
4. Resistant germplasm in common bean has been identified.
Bacterial Wilt
Cause.
Curtobacterium flaccumfaciens pv. flaccumfaciens (syn. Corynebacterium flaccumfaciens) is seedborne. Some workers report the bacterium does not
overwinter in infested residue or soil but others state that it does, although poorly. Bacteria are disseminated by driving rain and hail, then enter plants through wounds
caused by mechanical injuries and storms.
Distribution.
Symptoms.
A few watersoaked lesions occur on leaves; however, these do not tend to be as numerous as lesions of bacterial blight or halo blight. Diseased plants eventually wilt.
Initially, leaves wilt when temperatures are high but become turgid again when temperatures are reduced. As the disease progresses, leaves eventually turn brown and
defoliate from the plant. Sutures of pods are discolored and pods become flaccid. Depending on the mode of infection, diseased seed will have two general symptoms:
When seed is invaded internally, white seed may appear yellowish due to bacteria that are visible through the seed coat. If seed is infected externally, bacterial crust
forms on the outside of the seed. Plants grown from diseased seed are frequently killed while still small.
Management.
Sow diseasefree seed.
Bean Wildfire
Bean wildfire is also called wildfire.
Cause.
Pseudomonas syringae pv. tabaci (syn. P. tabaci). This is a different strain from the P. tabaci that causes wildfire of tobacco.
Distribution.
Brazil.
Symptoms.
Symptoms of wildfire occur only on leaves. Lesions are watersoaked initially, then become light to dark brown and surrounded by a pronounced chlorotic halo.
These symptoms resemble those of halo blight but pods and seeds do not become diseased. Chlorotic halos of bean wildfire are produced at relatively "high"
temperatures, but halo blight bacteria induce the chlorotic effect only at "cooler" temperatures.
Management.
Not reported.

Page 135
Common Blight
Cause.
Xanthomonas campestris pv. phaseoli (syn. X. phaseoli and X. phaseoli var. fuscans) is seedborne in both resistant and susceptible genotypes and overwinters in
infested residue. Survival of bacteria occurs in conservation tillage systems but not in conventional tillage systems where residue is incorporated into the soil. The lack
of survival is presumably due to antagonism to X. campestris pv. phaseoli by soil microorganisms. Under tropical conditions, bacteria survive on the soil surface for 5
months but cannot be detected in buried infested residue after 30 days. Generally, infested bean residue is considered to be an important source of inoculum for X.
campestris pv. phaseoli. However, in Michigan, pathogenic bacteria were not isolated from residue for 10 years and did not constitute a source of primary inoculum.
Survival also occurs on kudzu leaves, Pueraria thunbergiana, and, to a lesser extent, on infested stems and pods of common bean in the southern United States.
Internally infected seed is the main source of primary inoculum, but externally infected seed is also a source. Bacteria have been reported to survive for up to 6 years
on seed. Infected seed gives rise to diseased plants and eventually bacteria are blown or splashed onto leaves, where they enter either through natural openings or
wounds caused by windblown soil or other means. Bacteria exude from the initial infections and are disseminated to other host plants by rain, wind, planttoplant
contact, and machinery. Disease development is favored by warm, humid conditions.
Distribution.
Wherever common bean is grown under warm, humid conditions.
Symptoms.
Seedlings that germinate but do not emerge through the soil have cotyledons with reddish lesions. Diseased plants that do emerge are stunted and the undersides of
leaves have small, watersoaked spots with dried bacterial ooze in the center. The spots or lesions turn brown and coalesce to form large dead areas, causing leaves
to defoliate and plants to die.
Small, watersoaked spots also occur on seedling stems. The spots eventually enlarge and become brown to reddish in color. On older plants, spots expand
lengthwise along the stem. Often a lesion may encircle the stem at a lower node when pods are half mature and cause the plant to fall over.
Watersoaked spots with concentric reddishbrown or brick red rings appear on diseased pods. These spots eventually become dry and sunken and have a crust of
dried, yellow bacterial ooze. Bacteria produced on pods may infect the seed through the pod hinges. Diseased seed has a discolored hilum and discolored tissue
surrounding the hilum, which give the seed a ''varnished" appearance. Diseased seed may sometimes appear healthy and symptomless.

Page 136
Management
2. Treat seed with a seedprotectant bactericide.
3. Do not cultivate when beans are wet because bacteria are spread by machinery.
4. Rotate common beans with cereals or other resistant crops every 3 to 4 years.
5. Apply copper fungicides in extraneous situations; however, fungicides are of limited value.
6. Plow under infested bean residue.
7. Disinfect seed equipment and storage facilities.
8. Grow the most tolerant cultivars. However, under tropical conditions, tolerant cultivars may become completely susceptible.
Erwinia nulandii Leaf Spot
Cause.
Erwinia nulandii.
Distribution.
The United States (Nebraska).
Symptoms.
Initially, diseased leaves have small, yellow spots that enlarge and coalesce to form irregularshaped, necrotic lesions. Eventually, diseased leaf tissue collapses. White
bean seed has a pink discoloration.
Management.
Not reported.
Fuscous Blight
Cause.
Xanthomonas campestris pv. phaseoli (syn. X. phaseoli var. fuscans). According to Fahy and Persley (1983), the causal bacterium for common blight and fuscous
blight are considered the same. However, because other researchers consider the causal organisms to be different, common blight and fuscous blight are discussed
here as two separate diseases.
Xanthomonas campestris pv. phaseoli survives up to 6 years on seed and overwinters in infested residue. Xanthomonas campestris pv. phaseoli also grows
epiphytically on the leaves of nonhost plants, which may be a significant factor in the epidemiology of fuscous blight. Disease development is favored by warm, wet
weather.
Distribution.
Wherever common bean is grown under warm, wet conditions.
Symptoms.
Symptoms of fuscous blight are identical to common blight. Positive identification of the disease is possible only when the causal organism is identified.
Seedlings that do not emerge through the soil have cotyledons with reddish lesions. Plants that do emerge are stunted and the undersides of leaves have small, water
soaked spots with dried bacterial ooze in the center. The spots or lesions turn brown and coalesce to form large dead areas, which

Page 137
cause diseased leaves to defoliate and plants to die. Small, watersoaked spots that occur on seedling stems enlarge and become brown to reddish in color.
On older plants, spots enlarge lengthwise along the stem. Often a lesion may encircle the stem at a lower node when pods are half mature and cause the plant to fall
over.
Watersoaked spots with concentric reddishbrown or brick red rings appear on pods. Spots eventually become dry and sunken and have a crust of dried yellow
bacterial ooze. Bacteria produced on pods may infect seed through pod hinges. Diseased seed has a discolored hilum and discolored tissue surrounding the hilum,
which give the seed a "varnished" appearance. Diseased seed may sometimes appear healthy and symptomless.
Management
2. Treat seed with a seedprotectant bactericide.
3. Do not cultivate when beans are wet because bacteria are spread by machinery.
4. Rotate common beans with cereals or other resistant crops every 3 to 4 years.
5. Apply copper fungicides in extraneous circumstances; however, fungicides are of limited value.
8. Grow the most tolerant cultivars. However, under tropical conditions, tolerant cultivars may become completely susceptible.
Halo Blight
Halo blight is also called bean halo blight.
Cause.
Pseudomonas syringae pv. phaseolicola (syn. P. phaseolicola) is primarily seedborne and overwinters in infested residue under dry conditions. Only race 1
survives in the weed Neonotonia wightii; however, inoculation with all three races causes disease symptoms in this weed. Race 2 strains are reported to survive in
dead standing plants in northern Tanzania and in the residue of the susceptible bean cultivar 'Canadian Wonder' that is buried 2 to 5 cm deep in the soil. Survival in
standing plants may bridge the gap between two beangrowing seasons in warmer parts of the world. Survival of both races 1 and 2 is generally longer in stems than in
leaves. Race 3 is presumed to survive in residue also.
Race 2 strains obtained from infested debris in northern Tanzania were reported to be consistently more aggressive than those from growing bean plants. It is
suggested that virulence of race 2 strains may increase during survival in bean residue under dry environmental conditions due either to a mutation or to a selection of a
subpopulation of bacteria whose increased

Page 138
virulence is associated with survival in residue.
Diseased seed gives rise to diseased cotyledons. Bacteria exude from these initial infections and are disseminated to other host plants by rain, wind, contact between
plants, and machinery. Residue from highly susceptible cultivars constitutes a source of primary inoculum under dry conditions. Bacteria are splashed or blown from
residue to leaves where they enter through natural openings or wounds caused by windblown soil or other means. Epiphytic phytopathogenic bacteria also provide
inoculum for disease; susceptible cultivars are more likely to serve as inoculum sources than are resistant cultivars.
Optimum disease development is at 21°C with wet weather. Some isolates reported to be strains of race 2 are known to have optimum growth at 34°C. In northern
Tanzania, bacterial populations are higher and disease severity is greater when beans are intercropped with maize than when bean is grown as a monoculture.
At least three races are known. Presumably other races also exist.
Distribution.
Where common bean is grown under cool, humid conditions.
Symptoms.
Plants growing from internally infected seed are stunted and gradually die. Seedlings may not emerge through the soil, and reddish lesions are normally present on
cotyledons.
Small, watersoaked spots occur on the undersides of diseased leaves and turn reddish brown; the surrounding tissue forms a large yellowgreen halo. Spots rapidly
enlarge and coalesce to form large, brown, dead areas on leaves that eventually cause defoliation. Dried bacterial ooze that is normally a light cream color is present in
the center of each spot. The upper trifoliate leaves on plants that are infected later in the growing season are chlorotic.
Reddish spots that become dry and sunken with concentric rings develop on pods. The pod hinge may become discolored also and may have bacterial exudate on it.
Seed may become infected through the hinge and become discolored; however, seed from symptomless pods also may be infected and display symptoms.
Young stems have reddish lesions that extend lengthwise. Infections at nodes may girdle the stems when pods are halfmature, causing stems to break at the diseased
node.
Race 3 from Africa causes a hypersensitive reaction in the cultivar 'Tendergreen,' which is susceptible to races 1 and 2. A race 2 strain isolated from residue in
northern Tanzania induced systemic chlorosis and stunting on the resistant bean cultivar 'Edmund.'
Management
1. Apply copper fungicides to foliage. Copper fungicides are more helpful in managing halo blight than common blight.

Page 139
3. Do not cultivate soil when beans are wet because machinery may disseminate bacteria from diseased to healthy plants.
4. Rotate common bean with cereals or other resistant crops every 3 to 4 years.
7. Grow the least susceptible cultivars.
Pseudomonas blatchfordae Leaf Spot
Cause.
Pseudomonas blatchfordae overwinters in infested bean straw on the soil surface. The oldest leaves are most susceptible to infection and subsequent disease
development and symptom expression. Symptom development is most rapid at 24°C.
Distribution.
Symptoms.
Initially, small yellow spots that are accompanied by watersoaking appear on the oldest leaves. Spots increase in size and become surrounded by a narrow chlorotic
halo. The middle areas of the spot turn orange to brown and give the spot a "sunscalded" appearance. Eventually, the diseased area becomes necrotic and causes
defoliation.
Management.
Not reported.
Alternaria leaf spot and black pod disease are both caused by Alternaria alternata but are treated as two separate diseases on the basis of symptoms.
Cause.
Alternaria alternata (syn. A. tenuis), A. brassicae f. phaseoli, and A. brassicicola. Disease development is most severe at high relative humidity and temperatures
of 16° to 24°C. Plants increase in susceptibility as they grow older and when they are grown in nitrogenand potassiumdeficient soils.
Distribution.
The United States.
Symptoms.
Small, brown, irregularshaped lesions occur on diseased leaves. Lesions expand, become graybrown to dark brown and ovalshaped, and have concentric zones.
The older portions of lesions sometimes fall out, giving a "shothole" appearance to diseased leaves. Lesions coalesce to form large necrotic areas and defoliation may
occur.
Management
1. Ensure adequate soil fertility.

Page 140
Angular Black Spot
Cause.
Erratomyces patelli. Protomycopsis patelii is reported to cause disease in India, and the agent of a similar disease is known as Entyloma vignae in North America.
However, Piepenbring and Bauer (1997) state E. vignae is a synonym of P. patelii. The fungus is related to smut fungi of the genus Tilletia because it produces
relatively large, opaque teliospores that have a partition in their wall and that germinate with holobasidia carrying needleshaped basidiospores. In contrast to species
of Tilletia and related genera, the teliospores are scattered in intercellular spaces in the mesophyll without rupturing it and develop mostly intercalaryly. A new genus,
Erratomyces, is proposed.
Spore germination occurs on water agar at 30°C or more.
Distribution.
India, Central and South America.
Symptoms.
Numerous polyangular, grayish, dark leaf spots (23 mm in diameter) occur predominantly on the lower leaves. Spots coalesce to form lesions that are 6 mm or larger
in size.
Management.
Not reported.
Angular Leaf Spot
Cause.
Phaeoisariopsis griseola (syn. Isariopsis griseola). Phaeoisariopsis griseola is divided into two major groups. Group 1 isolates are generally recovered from
Andean gene pool materials, whereas group 2 isolates are recovered from Mesoamerican materials. Group 1 isolates are more pathogenic on Andean beans, whereas
group 2 isolates are more pathogenic on Mesoamerican beans. Random Amplified Polymorphic DNA and pathogenicity data suggest groups 1 and 2 may have
originated in the Andes and Mesoamerica, respectively, and that coevolution of the P. griseola fungus and its common bean host has resulted in increased levels of
disease in this hostpathogen interaction.
Phaeoisariopsis griseola is seedborne but survives primarily in infested residue on the soil surface and in infested plant residue that remains upright after harvest.
Conidia are produced during wet weather and are disseminated by wind and rain to host plants. Secondary infection is by conidia produced in lesions on the
undersides of diseased leaves. These conidia are also wind or rain disseminated to other host plants. The optimum temperature for infection is 24°C. Disease severity
is higher in a monocultural system.
Distribution.
Africa, Central America, South America, and the eastern and southern United States. Angular leaf spot is of minor importance in the United States; however, sporadic
outbreaks have occurred and severe disease has been reported on dark red kidney bean in Michigan. Angular leaf

Page 141
spot is a major disease of dry edible bean in tropical and subtropical regions.
Symptoms.
Small, brownish spots first occur on diseased leaves and may eventually become numerous enough to cause defoliation. During moist weather, P. griseola sporulates
abundantly within a spot and gives it a grayish color.
Similar spots on pods are usually small but may enlarge and coalesce to involve a large area of the pod. There is no correlation between disease severity on pods and
percentage of seeds infected with the pathogen. Seed infection normally occurs at the hilum; therefore, seeds become infected when located directly under lesions
present at the pod suture.
Management
3. Apply foliar fungicide.
4. Grow the most resistant cultivar. Resistant germplasm has been identified.
Anthracnose
Cause.
Glomerella lindemuthiana, anamorph Colletotrichum lindemuthianum. Glomerella cingulata, anamorph C. gloeosporioides, is also reported to be a causal
fungus.
Several races of C. lindemuthianum occur. Previously, alpha, beta, delta, epsilon, gamma, and lambda races have been identified in Canada, while only alpha, beta,
and gamma races have been reported in the United States. A larger number of physiologic races have been reported in Africa, Europe, and Latin America.
Currently, Balardin et al. (1997) have characterized 41 races based on virulence to 12 differential cultivars of Phaseolus vulgaris. The 41 races are categorized into
two groups: those found over a wide geographic area and those restricted to a single country.
Glomerella spp. are seedborne and overwinter as perithecia in dry infested residue. Colletotrichum lindemuthianum also survives as mycelium under the seed coat
for at least 2 years if seed is dry and stored under cool conditions at an optimal temperature of 4°C. Colletotrichum lindemuthianum will also survive for at least 5
years in dry residue. An alternating wetdry cycle is detrimental to fungus survival and C. lindemuthianum will lose viability in several days.
In New York, C. lindemuthianum survived 4 months in infested bean residue placed 0, 10, and 20 cm deep in the soil, but the fungus was no longer detectable 22
months after placement at any soil depth. Bean residue infested with C. lindemuthianum that remains on the soil surface for only one winter may serve as an inoculum
reservoir the following

Page 142
growing season. Disease has been reported to be most severe when tillage practices leave infested residue on the soil surface.
Infected seed gives rise to diseased seedlings that have lesions on the cotyledons. Conidia are then produced in these lesions and disseminated by wind and rain.
Longdistance spread of 3 to 5 m during a rainstorm occurs when splashing raindrops are blown by gusting winds. Spores are covered by a sticky substance that
enables them to adhere to whatever they touch. Therefore, conidia are disseminated by insects, machinery, and several other means.
Disease is most severe during wet weather at temperatures of 14° to 18°C. Disease development is restricted at temperatures above 25°C.
Distribution.
Canada (Ontario); tropical and subtropical areas of Latin America, central and eastern Africa; and eastern, midwestern, and southern states in the United States.
Symptoms.
Symptoms may occur on any part of a susceptible plant. Diseased seed has dark, sunken lesions of various sizes that frequently extend through the seed coat into the
cotyledons. Initial symptoms may appear on cotyledonary leaves as small, dark brown to black lesions. Mature lesions have pinkish spore masses in their centers.
Numerous small rustcolored specks appear on hypocotyls. The specks gradually enlarge longitudinally and form sunken lesions or eyespots that cause the hypocotyls
to rot off.
On older stems, oval to eyeshaped lesions become sunken, brown cankers with purplish to brick red borders that are 5 to 7 mm long. These sunken cankers extend
up and down diseased stems. Cankers may eventually weaken stems enough to cause them to break over. Pods above symptomatic stems dry prematurely and
shrink, causing seed numbers and size to be reduced. Numerous pinpoint black dots, which are acervuli, develop in lesions on diseased stems and pods. Later in the
growing season, perithecia develop on diseased stems.
Lesions appear first on surfaces of diseased lower leaves and leaf veins as small, angular, brick red to purple spots that eventually become dark brown to black. Later,
lesions also appear on veinlets of diseased upper leaves. Brownish, angular, dead spots, which also may appear on upper leaf surfaces, give the diseased leaves a
ragged appearance.
Lesions on pods start as small, elongated reddishbrown spots that become somewhat circular (6 mm in diameter) and sunken with a rusty to brown border. Spots
may become numerous, and during moist weather, they become pinkish in color due to conidial sporulation.
Management
1. Grow a resistant cultivar.
2. Grow common bean in the same field every third or fourth year.
3. Sow diseasefree seed grown in areas where anthracnose normally does not occur and that have a seed inspection program.

Page 143
4. Apply foliar fungicides before anthracnose becomes severe.
5. Do not enter fields when plants are wet.
6. Apply a fungicide seed treatment to seed.
7. Quarantine pedigree inspection.
8. Incorporate residue in the autumn to hasten decomposition.
Aphanomyces Root and Hypocotyl Rot
Cause.
Aphanomyces euteiches f. sp. pisi infects both peas and beans. Aphanomyces euteiches f. sp. phaseoli infects alfalfa and beans.
Fungi survive in soil for several years as oospores, which presumably are the primary source of inoculum. Sporangia and zoospores are produced in roots and are
thought to be the source of secondary inoculum, although this has not been observed.
Aphanomyces euteiches f. sp. phaseoli has only been reported in sandy soils; however, it is not known if it is limited to this environment. Disease is most severe at
high soil moisture levels and temperatures of 20° to 28°C.
Distribution.
The United States (Minnesota, New York, Wisconsin, and possibly Michigan).
Symptoms.
Aphanomyces euteiches f. sp. phaseoli causes more injury on bean than A. euteiches f. sp. pisi does. Diseased plants are stunted, and roots and lower stems are
rotted. Necrosis of hypocotyls ranges from discolored streaks to complete destruction of the diseased hypocotyls. Infrequently, plant death occurs.
Management.
Grow the most tolerant cultivars. Resistant germplasm has been identified.
Ascochyta Blight
Ascochyta blight is also called Ascochyta leaf spot and blight, and speckle disease, although speckle disease is reported as a separate disease caused by
Stagonosporopsis hortensis (syn. Ascochyta boltshauseri). Ascochyta blight is basically the same disease as black node disease.
Cause.
Phoma exigua var. exigua (syn. Ascochyta phaseolorum). Survival is presumably as pycnidia in infested residue on the soil surface and as mycelia in seed. The
fungus is favored by a relative humidity greater than 80% and temperatures of 15° to 20°C.
Distribution.
Mid to highaltitude regions of eastern and central Africa, Central and Andean America, and western Europe.
Symptoms.
All aerial plant parts may be diseased. Leaves have brown to black lesions (1030 mm in diameter) that normally develop concentric zones and may contain numerous
small, black pycnidia.
Concentric dark gray to black lesions may appear on pods. Diseased

Page 144
seeds become brown to black. The fungus may spread systemically throughout the plant, and defoliation and pod drop may occur. Seed yield losses are more severe
following early infection and premature defoliation. Losses of about 40% have occurred under moderate disease pressure in an experimental trial in Colombia.
Management
1. Intermediate resistance has been identified in common bean germplasm. However, some researchers have reported that resistance is not available in common bean
but does occur in scarlet runner bean.
Ashy Stem Blight
Ashy stem blight is also called charcoal rot.
Cause.
Macrophomina phaseolina (syn. Botryodiplodia phaseoli, M. phaseoli, Rhizoctonia bataticola, and Sclerotium bataticola). Macrophomina phaseolina is
seedborne. Survival is primarily as microsclerotia in soil for 3 to 36 months, but M. phaseolina may also survive as pycnidia in residue.
Primary inoculum is presumably from direct germination of microsclerotia, seedborne mycelia, or conidia from pycnidia. Dissemination is by any means that moves
infested soil or seed. Sclerotia of M. phaseolina are reported to colonize beans under relatively dry conditions.
Airborne conidia, released from pycnidia, serve as one source of secondary inoculum for initiating infections on foliage of older plants. Another source of secondary
inoculum is the expansion of stem infections below the soil level. These infections occur later in the growing season when diseased plants start to senesce. Infection and
subsequent disease are favored by high humidity, temperatures of 27°C or higher for prolonged periods of time, and "normal" soil moisture conditions. The
microsclerotia are formed in host tissues and released into the soil as the diseased tissues decay.
Macrophomina phaseolina can grow and produce large quantities of microsclerotia under low water potentials. Radial growth on potato dextrose agar (PDA) was
maximum at osmotic water potential values of — 1220 to —1880 J/kg, but growth was reduced at lower values. Production of sclerotia on potato dextrose broth
was not affected by osmotic water potentials of —670 to —3920 J/kg but was completely inhibited from —8270 to —12,020 J/kg. Germination of sclerotia after 2
days on PDA is not significantly affected from —320 to —4760 J/kg, but germination is drastically reduced with further reductions in osmotic water potentials.
Distribution.
The Caribbean, Central and South America, and the eastern, southern, and western United States.

Page 145
Symptoms.
Initially, dark, sunken, irregularshaped lesions occur on seedling stems at the soil line and eventually kill the seedling. Sunken, reddishbrown lesions occur on stems at
the soil level or lower. Eventually, lesions enlarge and girdle the stem, extending down into the roots and up into the branches. Lesions become gray in the center and
numerous microsclerotia and pycnidia (about the size of a pinhead) appear as small, black objects that contrast with the gray centers of lesions. Young diseased plants
usually die before seed is produced.
Infection of older plants produces superficial lesions that are usually not sunken. Frequently, disease is more pronounced on one side of a plant, which causes the
primary leaf on that side to droop and die. Any remaining leaves turn yellow. Severely diseased plants are wilted, chlorotic, and defoliated, and mature early or die.
Management
1. Sow only healthy seed treated with a seedprotectant fungicide.
2. Rotate common bean with a resistant crop every 2 to 3 years.
3. Grow resistant cultivars. Choose droughttolerant cultivars. The mechanism for drought tolerance confers resistance to M. phaseolina under field conditions.
Aspergillus nidulans Disease
Cause.
Aspergillus nidulans (syn. A. nidulellus).
Distribution.
Unknown.
Symptoms.
Inoculation of excised tissue results in limited watersoaking and hostcell death. Sporulation occurs within several days.
Management.
Not reported.
Bipolaris sorokiniana Leaf and Pod Lesions
Cause.
Bipolaris sorokiniana.
Distribution.
Canada (New Brunswick and Nova Scotia) and the United States (Wisconsin), on snap bean.
Symptoms.
Small (1 mm in diameter), brown to black, round to irregularshaped lesions occur on diseased leaves and pods. Pod lesions pose a problem for processing beans
because blanching of fruit does not mask lesions.
Management.
Not reported.
Black Node Disease
Black node disease is basically the same disease as Ascochyta blight.
Cause.
Phoma exigua var. diversispora (syn. P. diversispora). Survival of P. exigua var. diversispora is presumably as pycnidia in infested residue on the soil

Page 146
surface and as mycelia in seed. Disease is favored by a relative humidity greater than 80% and temperatures of 15°to 20°C.
Distribution.
Eastern Africa and western Europe.
Symptoms.
Concentric dark gray to black lesions may appear on diseased branches, stems, and nodes, and cause stem girdling and plant death.
Management
1. Intermediate resistance has been identified in common bean germplasm. However, some researchers have reported that resistance is not available in common bean
but does occur in scarlet runner bean.
3. Rotate common bean with nonhost crops.
Black Pod Disease
Black pod disease is also called Alternaria pod flecking, and pod and seed coat discoloration of white bean. Alternaria leaf spot and black pod disease are both
caused by the same fungus but are treated as two separate diseases on the basis of symptoms.
Cause.
Alternaria alternata (syn. A. tenuis) overwinters in infested residue and seed and on leaf lesions of numerous weed species. Alternaria alternata is a weak parasite
that colonizes stomata cavities of growing plants. In the autumn, when plant senescence begins, A. alternata begins to grow rapidly. Disease is most severe during
cool, wet conditions that may occur in a closed foliage canopy. Autumn rains that delay harvest accentuate disease severity.
Distribution.
Canada (Ontario) and the United States (New York).
Symptoms.
Initially, small, irregularshaped, watersoaked flecks appear on pods. Later, flecks coalesce to produce long streaks or irregular, large, reddish to dark brown or
black discolored lesions. Lesions are either sunken or raised for just a few cells deep into the pod but have a corky layer below. Conidia are often produced in
lesions. Small, irregular, brownish spots are also produced on stem and leaf tissues.
Symptoms of pod and seed coat discoloration of white bean varies. Pod discoloration varies from dark gray flecks to stipples to dark gray patches that later coalesce.
Seeds, in discolored pods, have various degrees of discoloration that persists through processing.
Management

Page 147
Black Root Rot
Cause.
Thielaviopsis basicola survives as chlamydospores in infested residue and soil. Primary inoculum is chlamydospores that germinate to produce mycelia that penetrate
intact bean tissues, wounds, or lesions caused by other pathogens. Chlamydospores are produced throughout diseased tissue. Under wet conditions, hyphae grow on
the plant surface and produce endoconidia and chlamydospores. Sporulation of T. basicola is most prolific at temperatures of 25° to 28°C, but disease is most severe
at temperatures of 15° to 20°C. In New York, however, the disease is most severe during periods of high soil moisture and high temperatures.
Distribution.
Symptoms.
Elongated, narrow lesions occur on diseased hypocotyl and root tissues. Initially, the lesion color is reddish purple but becomes dark gray to black. Eventually, the
lesions coalesce and form large, dark areas on roots and stems. Lesions either are superficial and cause little injury or develop into deep lesions that cause plant
stunting, foliage wilting, and eventual defoliation and subsequent plant death.
Management
1. Resistance has been identified in some breeding lines.
2. Grow rye in alternate years. Populations of T. basicola and disease incidence decrease in soil sown to rye compared to fallow soil. Diseasesuppressing effects
occur during growth and subsequent decomposition and are associated with microbial antagonism and antibiotic production with rye as the substrate.
Cercospora Leaf Blotch
Cause.
Cercospora canescens and Pseudocercospora cruenta (syn. Cercospora cruenta), teleomorph Mycosphaerella cruenta. Cercospora caracallae and C.
phaseoli are also reported to be causal fungi. The fungi are seedborne and likely overseason in infested residue.
Distribution.
Latin America and the southern United States.
Symptoms.
Vigorously growing leaves infrequently display symptoms. Mature leaves have brown or reddishbrown lesions that vary in shape from circular to angular and in size
from 2 to 10 mm in diameter. Eventually, lesions may have a gray center, caused by fungal sporulation, with a reddish border that is the remainder of the original
lesion. Lesions may coalesce and dry up, and portions of them may fall out and give the diseased leaf a ragged appearance. Severely diseased leaves become
chlorotic.
Branches, stems, and pods may have lesions.

Page 148
Management
1. Resistant cultivars have been identified.
2. Apply copper fungicides early.
3. Rotate common bean with nonhost crops.
Chaetoseptoria Leaf Spot
Cause.
Chaetoseptoria wellmanii may be seedborne. Disease occurs in areas of moderately cool temperatures and moist environments.
Distribution.
Central America and South America.
Symptoms.
Circular to irregularshaped lesions (up to 10 mm in diameter) that consist of light tan centers surrounded by a reddishbrown border occur on diseased primary
leaves soon after plant emergence. Small, gray pycnidia, which appear as ''specks," form in lesions. Defoliation and yield reduction occur.
Management
1. Rotate common bean with other crops.
Floury Leaf Spot
Cause.
Mycovellosiella phaseoli (syn. Ramularia phaseoli) presumably survives in infested residue. Disease occurs in areas of moderate temperatures and moisture.
Distribution.
Africa, Asia, Europe, and Central and South America. In Colombia, floury leaf spot is more common at elevations of 1500 to 2000 m.
Symptoms.
Initially, white or "floury," angular lesions occur on older leaves and progress upward on the diseased plant to the newer leaves. The floury appearance is due to fungal
growth of mycelium and spores. These lesions may coalesce and appear irregularshaped. The upper leaf surface may have a light green discoloration but no floury
appearance of mycelium and spores. Defoliation may eventually occur.
Management
Fusarium Root Rot
Fusarium root rot is also called dry root rot.
Cause.
Fusarium solani f. sp. phaseoli survives saprophytically as mycelium in infested residue and as chlamydospores in soil. Conidia, and some mycelial cells growing on
residue, are eventually converted to chla

Page 149
mydospores. Chlamydospores are stimulated to germinate by root excretions of susceptible plant hosts. The chlamydospores germinate to form germ tubes that enter
roots directly or through wounds and grow in the outer layers of tissue, especially the cortex. Fusarium solani f. sp. phaseoli is disseminated in dust and plant debris
mixed with seed, in soil on machinery, and by any means that transports soil.
Beans sown into cold soils or subjected to low temperatures after emergence tend to have severe root rot, while beans sown into warm soils with adequate moisture
tend to escape serious root rot. Root growth is restricted in cold soil, and herbicide and decomposing organic matter may also be toxicogenic. Preconditioning
stresses, such as soil compaction by tractor wheels, subsurface pans, and intermittent drought, especially in coarsetextured soils of low waterholding capacity,
restrict root growth and precondition roots to infection and disease development.
Root rot and postemergence damping off is greater in soils that have been subsoiled or disked rather than plowed. In 1 of 3 years, postemergence damping off is
greater when nitrogen is broadcast prior to sowing than when nitrogen is applied through overhead irrigation.
High disease incidence and severity are associated with high populations of F. solani f. sp. phaseoli in soil. Infection may be great at lower inoculum levels when the
lesion nematode, Pratylenchus penetrans, is present; however, there is no effect on final disease severity.
Distribution.
Symptoms.
Initially, slightly red to brown areas or streaks occur on diseased taproots and hypocotyls, often around the points of secondary root emergence. This reddish
discoloration increases in intensity and may eventually cover the taproot and hypocotyl. Later in the season, the red color is replaced by a brown discoloration and
roots become hollow and dry. The pith area in the taproot is often a bright red. Lateral roots are often destroyed and plants develop a secondary root system near the
soil line. Most diseased roots do not extend beyond the plowed layer of soil and penetrate no deeper into the soil than 7.6 to 15.2 cm.
Aboveground symptoms do not appear until roots are seriously decayed. Symptoms are similar to those caused by low soilmoisture conditions or lack of nitrogen.
Young plants will be stunted and have chlorotic leaves. Older plants will have chlorotic leaves and some defoliation. Yield is reduced by a reduction of seed weight;
however, the number of pods per plant is normally not reduced. Root rot has been reported to be more severe on bean grown in soil infested with both F. solani f.
sp. phaseoli and Pythium ultimum.
Management
2. Rotate common bean with resistant crop plants every 3 to 4 years.

Page 150
3. Sow seed that is free of any debris.
4. Use practices that condition soil for good moisture distribution and root penetration.
5. Sow seed rates that are high enough to ensure a good stand.
6. Do not feed infested bean straw to animals because the fungus may be spread in the manure.
7. Plow under common bean refuse.
8. Do not cut off newly formed roots during cultivation.
9. Practice subsoiling or other practices that increase root volume and depth.
10. Sow seeds into warm soil.
11. Irrigate when necessary.
12. Test soil to determine fungus population and identify fields at high risk from Fusarium root rot.
Fusarium Yellows
Fusarium yellows is also called Fusarium wilt.
Cause.
Fusarium oxysporum f. sp. phaseoli survives as mycelia in infested residue and as chlamydospores in soil. Spores and chlamydospores may also be externally
seedborne. Infection of bean plants is through root and hypocotyl wounds. Optimum disease development is at 20°C.
Wilt severity in common bean increases proportionally to inoculum concentration in the soil, especially chlamydospores. Disease has been reported severe where
plants were stressed by high temperatures, poor water drainage, and soil compaction. Fusarium yellows affects most commercial pinto, greatnorthern, and navy bean
cultivars of common beans.
At least two physiologic races exist. One race is in Europe and North America, and the second race is in Brazil.
Distribution.
Symptoms.
Initially, chlorosis and senescence occur on the lower leaves and progress to the upper leaves of the diseased plant. Leaves become increasingly chlorotic and, in some
cases, eventually defoliate. A reddishpurple to reddishorange discoloration of the vascular system of roots, stem, petioles, and peduncles occurs. Early infection
results in plant stunting.
Management
1. Grow tolerant or resistant cultivars.

Page 151
Gray Leaf Spot
Gray leaf spot is also called gray spot and mancha gris (gray blotch).
Cause.
Cercospora vanderysti and C. castellanii. Disease development is favored by cool, wet weather at elevations greater than 1500 m.
Distribution.
Colombia.
Symptoms.
Initially, numerous slightly chlorotic, angular spots (25 mm in diameter) occur on diseased upper leaf surfaces. Spots may be so numerous that diseased leaves have a
mosaiclike appearance. Spots eventually coalesce and cause leaves to defoliate. Eventually, a grayishwhite, powdery growth consisting of conidia and conidiophores
occurs in these spots. The most distinguishing symptom of mancha gris occurs in spots on the surfaces of lower leaves, where a gray mat or cushionlike fungal growth
consisting of a dense growth of flexuous conidiophores and their conidia completely covers the spots.
Management
3. Some breeding lines show resistance.
Gray Mold
Cause.
Botrytis cinerea, teleomorph Botryotinia fuckeliana, overwinters as stroma and sclerotia on infested residue and other hosts, including weeds. Survival for extended
periods may also occur as mycelia and conidia. Conidia are produced early in the spring and throughout the summer when wet conditions occur and are disseminated
by wind and splashing rain to plant hosts. Also, ascospores of B. fuckeliana are produced on apothecia that develop from stroma or sclerotia and are disseminated
by wind.
Disease development is most severe under cool, humid conditions. Common bean is infected at different stages of growth but senescing cotyledons are colonized first.
Young stem and leaf tissues can become diseased before plant bloom and serve as inoculum sources within a field. Infection frequently occurs where old blossoms
have fallen onto the plant or have been retained at the tips of pods. Diseased stems may continuously produce inoculum into the bloom period.
Distribution.
Symptoms.
All aboveground plant parts may show symptoms, but pods are most commonly diseased. Economic loss is due primarily to pod rot, which reduces quality and
increases processing costs. Initially, watersoaked lesions occur and, under humid conditions, a white mold develops, followed by a gray fungal growth consisting of
conidia and conidiophores. Tip wilt and decay of shoots may occur.

Page 152
Management
1. Sow certified diseasefree seed.
3. Apply foliar fungicides if weather conditions favor disease development.
4. Do not sow common bean too thickly because a thick canopy retards air circulation and favors disease development.
Phyllosticta Leaf Spot
Cause.
Phyllosticta phaseolina survives as pycnidia in infested residue. Disease is favored by high humidity and rainfall at moderate temperatures.
Distribution.
Europe, Japan, Latin America, South Africa, and the United States.
Symptoms.
Mature leaves display small, angular, watersoaked spots that may coalesce and enlarge to 7 to 10 mm in diameter. Spots have a lightcolored, necrotic center
surrounded by a reddishbrown margin. Centers of older lesions may fall out and give diseased leaves a tattered appearance. Small, black specks, which are the
pycnidia, develop throughout the lesion. Petioles and stems may also become infected and flower buds may become necrotic. Small lesions (1 mm in diameter) with
dark centers and reddish margins infrequently develop on pods.
Management
2. Rotate common bean with a resistant crop.
Phymatotrichum root rot is also called cotton root rot.
Cause.
Phymatotrichopsis omnivora (syn. Phymatotrichum omnivorum) survives as sclerotia in soil or infested residue. Fungal strands grow from sclerotia until they
contact a host root. The fungal strand then encompasses the root and grows upward to the soil surface, where it grows around the upper root system and eventually
penetrates the plant.
Disease is favored by alkaline, calcareous soils and moist, warm soils at temperatures of 15° to 35° C.
Distribution.
Northern Mexico and the southwestern United States.
Symptoms.
An initial slight yellowing or bronzing of leaves is followed by a sudden wilting as plants begin to flower. Cortical tissue sloughs easily and is covered by a visible
network of hyphal strands. A few days after wilting, plants die in circular patterns corresponding to the radial growth of the fungus originating from dying plants.
Following rains, a cottony growth or

Page 153
spore mat of the fungus may occur on the soil surface around the stems of dead plants.
Management
1. Rotate common bean with a resistant crop for at least 4 years.
2. Control susceptible weeds.
3. Deep chisel or deep plow green manure crops, manure, or composts.
Pink Pod Rot
Cause.
Trichothecium roseum is a common soil fungus that is saprophytic on residue or is weakly parasitic to common bean. In Canada, T. roseum is frequently isolated
from seeds of soybean, pea, faba bean, kidney bean, and scarlet runner bean.
Distribution.
The United States (Red River Valley of North Dakota). Trichothecium roseum has been occasionally isolated from common bean roots showing root rot symptoms
in Canada (southwestern Ontario).
Symptoms.
A white, powdery mold that later turns pink occurs on senescent and mature pods. Mold occurs infrequently on stems, petioles, and dead leaves. Seeds from
diseased pods are shriveled and yellow or pinkish yellow.
At first, inoculated pods have watersoaked areas that develop into a lesion whose center becomes chocolate brown. Later, a white, powdery mold develops in the
lesion, then spreads outward and becomes pink, similar to field symptoms. Seeds from infected pods do not germinate.
Management.
Not reported.
Pod Rot, Seed Rot, and Root Rot
Cause.
Fusarium pallidoroseum (syn. F. semitectum) causes disease under humid conditions.
Distribution.
Brazil.
Symptoms.
Initially, pinpointsized, watersoaked lesions that occur on diseased pods become necrotic and rusty brown and vary in shape from circular to elongated, depending
on the diseased cultivar. Under humid conditions, pods become soft and covered with fungal mycelia. Under less humid conditions, pods become brittle and dry.
Whiteseeded snap bean seed becomes reddish brown, shriveled, and covered with mycelia. Light brown seed has blood red, circular lesions. Rotted roots are rusty
brown and "pulpy" and have a pruned appearance.
Management.
Not reported.

Page 154
Powdery Mildew
Cause.
Erysiphe polygoni overwinters as cleistothecia on residue. Ascospores are formed in cleistothecia and disseminated by wind to plant hosts. Conidia form on
superficial mycelia and function as secondary inoculum. Cleistothecia form later in the growing season on older infection sites or on mature diseased leaves. Mycelia on
infested residue may also function as a means of overwintering, especially in geographical areas with mild winters.
Distribution.
Worldwide.
Symptoms.
The most damage occurs to plants that mature late in the autumn in the southern United States. Typically, a white, powdery material consisting of conidia and
conidiophores is produced on all aboveground parts of plants. Diseased leaves become chlorotic and may defoliate. Pods and stems become purple. Pods are
malformed, small, and poorly filled, and fall from diseased plants before seed matures.
Management
1. Grow the most disease resistant cultivar adapted to an area.
2. Apply a foliar fungicide before disease becomes severe.
Pythium Root and Hypocotyl Rot
Cause.
Pythium aphanidermatum, P. aristosporum, P. catenulatum, P. dissotocum, P. irregulare, P. myriotylum, P. splendens, and P. ultimum have all been
reported to be pathogenic to beans. These fungi are most pathogenic in soils with high moisture. The optimum conditions for disease are a soil temperature of 15°C
and a soil water potential of 0 to lbar.
Distribution.
Not reported, but likely widespread.
Symptoms.
Damping off may occur. Symptoms, which occur on hypocotyls 16 to 22 days after sowing, initially appear as elongated, tan to brown, soft, watersoaked areas that
extend 3 to 5 cm above the soil line and onequarter to threequarters the distance around the hypocotyl circumference. These symptoms are also present below the
soil line. Although frequently roots are white and healthy, rot may begin at the tips of taproots and proceed upward on hypocotyls. Within 3 weeks, watersoaked
areas become dry and tan to reddish brown and have a slightly sunken surface. Later, after about 4 weeks, most of the belowground hypocotyl and fibrous roots die
and appear papery and reddishbrown. In advanced cases, roots may be a hollow tube. Root pruning that results in shortened roots may also occur. Adventitious
roots may be produced above or at the soil line.
Plants wilt and die, or if adventitious roots are produced, they may be stunted or chlorotic and produce smaller and fewer pods, although the seed weight is not
reduced. Secondary infection by Fusarium spp. may occur.

Page 155
Management
2. Apply systemic fungicides to seed.
3. Plowing to a depth of 20 to 25 cm increased plant stand, vine weight, and yield in research plots. Root rot and postemergence damping off is greater in soils that
have been subsoiled or disked rather than plowed.
4. Disease is suppressed by certain herbicides.
5. Throw soil up on the bases of plants during cultivation to promote the growth of adventitious roots.
6. Practice proper fertilizer application. In 1 of 3 years, postemergence damping off is more severe when nitrogen is broadcast before sowing than when nitrogen is
applied through overhead irrigation.
Pythium Wilt
Cause.
Pythium aphanidermatum (syn. P. butleri) survives as oospores in soil and infested residue.
Distribution.
Symptoms.
A watersoaked lesion occurs on the diseased stem near the soil line and progresses upward into the lower branches but rarely extends below the soil line. The outer
layer of stem and branch tissue becomes soft and watery and readily separates from fibrous tissue. Leaves wilt and plants quickly die. Death of plants is usually so
rapid that wilted leaves are green, then quickly turn brown.
Management.
Not necessary since Pythium wilt is infrequently a serious disease.
Rhizoctonia Root Rot and Damping Off
Cause.
Rhizoctonia solani. Several anastomosis groups occur, depending upon location. AG4 is the primary causal fungus isolated from dry bean hypocotyls and roots from
Zaire, and AG22 is the primary causal fungus from Ohio. AG1 has also been reported to be pathogenic. AG1 and AG22 are also pathogenic to common bean
and to sugar beet. Foliar isolates were AG1 IB from Zaire.
Rhizoctonia solani survives as sclerotia in soil and residue and is a vigorous saprophyte in infested residue. Roots or hypocotyls are infected by mycelium growing
from a precolonized substrate or by sclerotia germinating and forming infective hyphae. Infection occurs early in the growing season at a maximum temperature of 25°
and at low soil moisture. However, there are reports that R. solani is most active in warm, moist soil.
Distribution.
Symptoms.
Preemergence damping off may occur. Seedlings are infected during emergence and become twisted and stunted. Reddish, sunken cankers

Page 156
occur on diseased roots and main stems. If a canker girdles a stem, the seedling will die. Lesions enlarge and the taproot and the stem below ground may be
destroyed. Lesions then appear more brown than red. Diseased plants are stimulated to produce numerous adventitious roots near the soil surface. Older diseased
plants are stunted and chlorotic.
Management
1. Rotate common bean every 3 to 4 years but avoid rotations with sugar beet.
2. Ridge soil around the base of plants and irrigate soon thereafter to promote adventitious roots.
3. Avoid mechanical injury to seedlings.
4. Plow infested soil to a depth of 20 to 25 cm. This increases plant stand, vine weight, and yield. Root rot, hypocotyl rot, and postemergence damping off are greater
in soils that have been subsoiled or disked rather than plowed because plowing reduces the population of R. solani.
5. Apply nitrogen fertilizer properly. In 1 of 3 years, postemergence damping off is greater when nitrogen is broadcast before planting than when nitrogen is applied
through overhead irrigation.
6. Grow the most resistant bean. Blackseeded cultivars are more resistant than whiteseeded cultivars because seed coats of black seeds adhere tightly to cotyledons
and protect the germinating seed from infection. Black seed coats also contain phenolic compounds that inhibit growth of R. solani. Seed coats of white seeds crack
readily before emergence. The resistance of 3weekold red kidney bean plants to R. solani is associated with the inability of the fungus to form infection cushions and
penetrate the hypocotyl.
Rust
Cause.
Uromyces appendiculatus (syn. U. phaseoli) is a macrocyclic autoecious rust. In the spring, teliospores germinate to produce basidiospores that are disseminated by
wind to bean leaves. Following infection by basidiospores, pycnia are formed on the upper surfaces of diseased leaves and aecia are formed primarily on the under
leaf surfaces. Aeciospores form in aecia and infect bean leaves. Uredinia are formed in the aeciospore infections. Urediniospores are formed in uredinia and are
disseminated by wind to bean leaves, thereby providing secondary inoculum and functioning as a repeating cycle. The twospotted spider mite, Tetranychus urticae,
is attracted to uredinia on older diseased leaves. Populations of mites will be twofold to sixfold greater on diseased leaves than on healthy ones. Mites vector the
echinulate urediniospores to rustfree plants. Teliospores are eventually produced in the old uredinia as the diseased plant dies or matures.

Page 157
Disease development is optimum at temperatures of 17.5° to 22.5°C with 6 to 8 hours of leaf wetness. Several physiological races of U. appendiculatus exist.
Distribution.
Symptoms.
Usually symptoms become most conspicuous later in the growing season, but epiphytotics may occur earlier. Pycnia initially appear only on leaf upper surfaces as
chlorotic flecks that later become a slightly raised white bump. Aecia develop first on leaf lower surfaces as white rings or clusters of pustules; later, aecia may
occasionally develop on leaf upper surfaces. Uredinia begin as small white spots that enlarge and rupture in a few days to expose orangeyellow urediniospores.
Infected leaves become chlorotic, die, turn brown, and defoliate. Pods and stems may also become diseased. As tissue dies, black telia replace urediniospores in old
pustules.
Management
1. Destroy volunteer beans.
2. Rotate common bean with other crops every third year.
3. Do not grow common bean adjacent to previously infected fields.
4. Plow under common bean residue in the autumn.
5. Inspect fields during growing season to detect early symptoms of rust. Apply foliar fungicides if rust develops rapidly from early bloom to 4 weeks before harvest.
6. Grow resistant cultivars adapted to an area. Several pinto cultivars are resistant. Most black turtle and kidney beans are resistant to current rust races. Most navy
beans are moderately resistant. Adult resistance in some Jamaican varieties is correlated with mean hair density or leaf pubescence on both leaf surfaces.
Smut
Smut is also called leaf blister smut and Entyloma leaf spot. Although there are disparate reports of smut and Entyloma leaf spot in the literature, the symptom
descriptions appear to be similar enough to warrant them as the same disease.
Cause.
Entyloma petuniae survives in residue.
Distribution.
Dominican Republic, Guatemala, and Honduras.
Symptoms.
The first or second trifoliate leaves are normally infected first. Initially, spots are watersoaked but later are reported to become a grayishbrown to black discoloration
on the leaf upper surfaces and grayishblue on the leaf lower surfaces. What are described in the literature as grayishblack blisters occur on leaf upper surfaces and
contain subepidermal masses of black chlamydospores. Mature necrotic spots are dark brown,

Page 158
which gives leaves a burned appearance. Lesions are somewhat round or oval and sometimes are limited by leaf veins or veinlets but tend to coalesce.
Management
2. Destroy plant residue.
Southern Blight
Cause.
Sclerotium rolfsii.
Distribution.
Generally distributed in warm common beangrowing areas.
Symptoms.
Brown, watersoaked lesions occur on hypocotyls just beneath the soil line. Disease proceeds into the taproot and eventually destroys the cortex. Lower leaves
become chlorotic, followed by plant wilting and death. White mycelium develops around hypocotyls and on the surrounding soil. Spherical, white sclerotia (12 mm in
diameter) develop in the mycelium and eventually turn brown.
Management
Speckle Disease
Speckle disease is also called Ascochyta leaf spot. However, Ascochyta leaf spot is reported as a separate disease caused by Phoma exigua var. exigua (syn.
Ascochyta phaseolorum).
Cause.
Stagonosporopsis hortensis (syn. Ascochyta boltshauseri). The causal fungi are seedborne. Disease is favored by cool temperatures and abundant moisture at
elevations above 1500 m.
Distribution.
Higher elevations in Central and South America.
Symptoms.
Dark gray to black zonate lesions that contain small, black pycnidia occur on leaves. Defoliation occurs in severe cases. Lesions also occur on peduncles, petioles,
pods, and stems, where girdling can cause plant death.
Management

Page 159
Stem Rot
Cause.
An unknown Basidiomycete that resembles Athelia spp.
Distribution.
The United States (Florida).
Symptoms.
Stem lesions are dry, firm, and tan, and do not extend above the soil surface. Severity of stem rot will vary. Frequently, only small lesions or a single lesion will develop
on underground stems. However, dry rot may be present on the entire underground portions of stems of plants that wilted and quickly died or still remained alive.
Occasionally some plants will have only root rot symptoms but no stem lesions. Mycelial strands form on roots and underground stems of most diseased plants.
Management.
Not reported.
Web Blight
Cause.
Rhizoctonia solani, teleomorph Thanatephorus cucumeris. Most isolates causing web blight belong to the intraspecific groups AGIIB, including microsclerotial
and macrosclerotial types, and AG22. Isolates that cause damping off or root rot are mainly groups AG3, AG4, and AG5.
Fungus survival is by sclerotia in soil and infested residue and by being seedborne. Disease is spread by sclerotia disseminated by wind, rain, machinery, and other
means; airborne basidiospores; mycelial bridges between plants; and infested soil debris.
Sclerotia and infested debris splashed onto plant parts by rain serves as a primary inoculum source. Sclerotia germinate under favorable conditions to form mycelia
that infect host plants. Trifoliate leaves are infected by splashed inoculum but are infected more frequently by advancing hyphae from infested tissues.
Distribution.
Costa Rica and the southern United States; however, web blight is likely more widespread.
Symptoms.
Small, round, watersoaked spots are produced on diseased leaves. Spots on leaves are lighter in color than healthy tissue and appear scalded. Spots become tan and
are surrounded by a dark border.
Spots on young pods are light tan and irregularshaped, but spots on mature pods are dark brown and sunken and resemble those of anthracnose. Spots may
coalesce to cover the entire pod. Seeds are blemished and discolored. Seedborne fungi are pathogenic to bean seedlings and reduce seedling emergence and
establishment.
During moist, warm weather in the final stages of disease, mycelial growth, resembling spider webs, grows over all plant parts, binding leaves, petioles, flowers, and
pods together. Numerous small, brown sclerotia are imbedded or scattered throughout the mycelium.

Page 160
Management
1. Rotate common bean with resistant plants.
2. Diseased plants should be destroyed soon after harvest.
3. Apply a foliar fungicide when disease occurs.
4. Mulch soil. This helps to prevent dissemination by splashing.
5. Grow the most tolerant cultivar adapted to an area.
White Leaf Spot
White leaf spot is called mancha bianca in Spanish.
Cause.
Pseudocercosporella albida (syn. Cercospora albida) presumably survives in infested residue. Disease is most severe under cool and wet conditions.
Distribution.
Symptoms.
Initially, whitish, angular spots that are restricted by veins occur first on the undersides of diseased leaves, then on the upper sides of leaves. Spots enlarge, coalesce,
and cause defoliation in severe cases. All leaves of susceptible cultivars become diseased, but only the lower leaves of resistant cultivars become diseased.
Management.
Grow resistant common bean cultivars.
White Mold
White mold is also called Sclerotinia white mold.
Cause.
Sclerotinia sclerotiorum (syn. Whetzelinia sclerotiorum) survives 5 or more years as sclerotia in soil and up to 3 years as dormant mycelia in testae and cotyledons
of seeds. Survival of S. sclerotiorum in seed results in failure of most seed to germinate but provides a means of dissemination. Survival of mycelia in infested stems is
too low to be a significant source of pathogenic inoculum.
Sclerotia germinate either carpogenically or myceliogenically. Sclerotia germinate carpogenically to produce one or many apothecia, but will not do so until they have
been ''preconditioned." This preconditioning, or physiological maturation, occurs during the winter or noncrop season; however, freezing is not necessary.
In semiarid areas, carpogenic germination is initiated after the plant canopy covers the soil surface. Apothecia are produced from sclerotia in areas that stay moist for
relatively long periods of time, such as the sides of irrigation furrows or next to stems shaded by the plant canopy. Optimum apothecia production occurs at a soil
matric potential of0.25 bars and soil temperatures of 15° to 18°C for 10 to 14 days. Ascospores then are produced in a layer of asci on the surface of apothecia and
are disseminated by

Page 161
wind to old blossoms (which commonly serve as an energy source to support infection), stems, or leaves. Insects and splashing water also disseminate S.
sclerotiorum. Conformation of senescent blossoms may influence ascospore germination through availability of free moisture with nutrients leached from blossoms and
held within blossom convolutions. The most common means of disease spread after initial infection is by contact of healthy plant parts with diseased plants.
During moist, humid weather, sclerotia also germinate myceliogenically to produce mycelia that first colonize dead plant tissue, then, using dead tissue as a substrate,
invade living plant tissue. However, this is not considered an effective mode of infection.
The disease can occur early in the growing season but becomes most severe later in the season, with epiphytotics occurring only after flowering during wet, humid
conditions at an optimum temperature of 25°C. Disease severity is greatest under a dense plant canopy and is reduced early in the season if no plant canopy has
developed.
Severe epiphytotics of white bean have occurred in Ontario when the following conditions exist: Apothecia are present, the plant surface is wet longer than 39 hours,
the air temperature is 15° to 25°C, and there is a closed canopy containing petals.
Injury from Sclerotinia wilt increases with increasing irrigation in Fusariumfree soils but is negligible in Fusariuminfested soils. Sclerotinia sclerotiorum is a pathogen
of a large number of plant genera.
Distribution.
Symptoms.
Symptoms appear on stems, leaves, and pods. Soft, watery, irregularshaped areas first occur on stems just above the soil line, then on leaflet axils, leaves, and pods.
These areas rapidly enlarge and, in a short time, dense, white, cottony masses of mycelia containing small, brown droplets cover the infected spots. Small, hard, black
sclerotial bodies appear in the mycelium. Main stems and branches are often encircled by the infection, wilt, and die. The affected plant parts dry out and become
bleached and "punky." The white masses of mycelia turn light gray, or brown, and dry out, leaving the conspicuous sclerotia. Infected bean seed is orangecolored and
has a chalky texture. Sclerotia are often formed in place of seed.
Management
1. Grow resistant cultivars with open canopy structures.
3. Apply foliar fungicide at early bloom stage of growth.
4. Clean out harvesting equipment between fields.
5. Rotate common bean with small grains.

Page 162
6. Space rows 76 cm or wider to encourage air movement and dry out tissues.
7. Biological control with application of Coniothyrium minitans to soil in the spring reduced apothecial production from sclerotia buried in the soil and increased
parasitism on sclerotia produced on disease plants.
Awl
Cause.
Dolichodorus heterocephalus favors wet soils.
Distribution.
Widespread.
Symptoms.
Pitlike lesions occur on the sides of seedling hypocotyls. Diseased roots are stubby and discolored, often with some root destruction.
Management.
Not known.
Bulb and Stem
Cause.
Ditylenchus spp. are endoparasitic nematodes capable of surviving extended periods of time in dry tissue or soil. Ditylenchus spp. are reported to be seedborne on
other crops.
Distribution.
Widespread.
Symptoms.
Diseased plants are stunted and stems may be swollen and twisted.
Management.
Not known.
Cyst
Cause.
Heterodera glycines.
Distribution.
Widespread.
Symptoms.
Beans normally do not display symptoms, even at high nematode populations. Yields may be reduced.
Management.
Not reported.
Dagger
Cause.
Xiphinema americanum is an external parasite.
Distribution.
Widespread.
Symptoms.
Diseased roots have curly tips with galllike growths on the tips.
Management.
Not reported.

Page 163
Lance
Cause.
Hoplolaimus spp. are ectoparasites that feed a distance back from the root tips.
Distribution.
Widespread.
Symptoms.
Diseased plants are stunted and chlorotic. Necrotic areas occur on roots.
Management.
Nematicides are effective on other crops.
Lesion
Cause.
Pratylenchus penetrans and P. scribneri.
Distribution.
In warm common beangrowing areas.
Symptoms.
Diseased roots are greatly reduced and discolored.
Management
2. Apply nematicides.
Nematode Angular Leaf Spot
Cause.
Aphelenchoides ritzemabosi survives for up to 27 months in airdried bean leaf tissue stored at room temperature. In greenhouse inoculations, symptoms developed
in about 11 days at 22°C and became more pronounced in 14 to 20 days. Alfalfa is also affected and may provide a mechanism through which the nematode is able
to persist.
Distribution.
The United States (Wyoming).
Symptoms.
Numerous dark, angular lesions occur on leaves of the pinto bean cultivar 'Othello.' An occasional superficial necrosis occurs on the upper surface of petioles.
Management.
Do not rotate alfalfa with common beans.
Pin
Cause.
Paratylenchus spp. are reported to feed either on the outside or the inside of roots.
Distribution.
Widespread. Pin nematodes tend to be common in warmer climates.
Symptoms.
Plants are not seriously injured. Diseased plants may be stunted and chlorotic. Necrotic spots may occur on roots.
Management.
Not reported on bean, but nematicides have been effective on other crops.

Page 164
Reniform
Cause.
Rotylenchulus reniformis favors sandy soil. Only females are pathogenic.
Distribution.
The United States (Florida). However, R. reniformis is widespread on other crops.
Symptoms.
Yields are reduced.
Management.
Nematicides have been effective in increasing yields.
Ring
Cause.
Criconemoides ovantus is an ectoparasite.
Distribution.
Not known.
Symptoms.
Lesions occur on diseased roots.
Management.
Nematicides have been effective on other crops.
Root Knot
Cause.
Meloidogyne arenaria, M. hapla, M. incognita, and M. javanica. Infested soil contains eggs that hatch to produce larvae that move through soil to penetrate root
tips. Larvae migrate through roots to the vascular tissues, become sedentary, and commence feeding. Excretions of larvae stimulate cell proliferation, resulting in
development of syncythia, from which larvae derive food. Females lay eggs that are pushed out of roots into soil.
Distribution.
The southern United States and California, primarily on light, sandy soils.
Symptoms.
Fleshy, irregularshaped galls that are larger than nodules and more irregular in shape are produced on roots. Plants are stunted, chlorotic, and unthrifty. Root growth
is also suppressed; however, it has been reported that decreases in root and top growth are a temporary effect.
Nematode infestation has been reported to stimulate nodulation; however, nodules remain small and are not efficient in fixing nitrogen. Nitrogenase activity increases
but leghaemoglobin decreases. These effects are reported to be temporary, and a few days difference in infestation alters the severity of the effect.
Management
1. Do not grow common bean in infested soil for at least 3 years.
2. Apply a nematicide to soil if economic conditions warrant it.

Page 165
Spiral
Cause.
Helicotylenchus dihysteria is an ectoparasite.
Distribution.
Widespread, but reported to be more numerous under tropical and subtropical conditions.
Symptoms.
Root lesions are present but little decay occurs. Diseased plants are stunted.
Management.
Not known.
Sting
Cause.
Belonolaimus longicaudatus. Disease is favored by sandy soils.
Distribution.
Most prevalent in warm, sandy soils in the tropics and semitropics.
Symptoms.
Yields are reduced from reduced foliage growth. Diseased roots have necrotic lesions.
Management
2. Grow a summer cover crop of hairy indigo, Indigofera hirsuta.
Stubby Root
Cause.
Paratrichodorus christiei is an ectoparasite.
Distribution.
Not known for certain.
Symptoms.
Reduced root growth results in short and thickened roots. Diseased plants are stunted.
Management.
Stunt
Cause.
Tylenchorhynchus spp., Merlinius spp., and Quinisulcius acutus. Nematodes may be either internal or external parasites.
Distribution.
Most prevalent in warm soils. Likely widespread in warmer climates.
Symptoms.
Roots are shriveled and sparsely developed and do not elongate. Top growth is reduced.
Management.

Page 166
Machismo
Cause.
A phytoplasmalike organism that is disseminated by the leafhopper Scaphytopices fulginosus. The causal organism is also grafttransmitted but is not mechanically
or seedtransmitted. The average period of incubation until symptom expression is 37 days.
Distribution.
Colombia.
Symptoms.
Symptoms occur at flowering and pod formation. Diseased plants produce wrinkled, distorted pods with no seed. Plants may produce normalappearing pods, but
seeds germinate in the pod. In severe cases, buds proliferate, producing a witches' broom. Plants infected later in the season generally produce normal yields.
Management.
Not reported.
Witches' Broom
Cause.
A phytoplasmalike organism transmitted by the leafhopper Orosius orientalis.
Distribution.
Japan.
Symptoms.
Symptoms occur 1 month after leafhopper feeding. Plants are chlorotic and leaflet size is reduced. There is a shoot proliferation and phyllody of floral organs.
Management.
Not reported.
Bean Calico Mosaic
Cause.
Bean calico mosaic virus (BCMoV) is in the geminivirus group. BCMoV is transmitted by the white fly, Bemisia tabaci, and by mechanical means under greenhouse
conditions.
Distribution.
Mexico (Sonora).
Symptoms.
Diseased leaves attain a bright yellow and green mosaic that resembles a calico pattern. Plants are stunted.
Management.
Not reported.

Page 167
Bean Common Mosaic
Cause.
Bean common mosaic virus (BCMV) is in the potyvirus group. Several strains of BCMV are known to exist, and each strain may cause different symptoms. Two
serotypes are known and have been suggested as two distinct potyviruses. Serotype A induces a necrosis, and serotype B induces mosaic symptoms. It has further
been suggested that isolates of BCMV comprise two distinct potyviruses. On the basis of peptide profiles, McKern et al. (1992) propose that strains of one of the
potyviruses be named "bean necrosis mosaic virus" since these strains induce temperatureinsensitive necrosis in bean cultivars that carry the dominant I gene. The
strains of the other potyvirus would retain the name BCMV. Peptide profile data also suggest that isolates of adzuki bean mosaic virus, blackeye cowpea mosaic virus,
dendrobium mosaic virus, peanut stripe virus, and three potyvirus isolates from soybean are all strains of the second potyvirus, BCMV.
Some isolates of BCMV are seedborne, which constitutes the major means of overwintering. BCMV is transmitted mechanically and in a nonpersistent manner by
several species of insects, including 11 known species of aphids. BCMV also may be carried in pollen.
Distribution.
Symptoms.
Symptoms vary between plants and are influenced by cultivar, temperature, light, soil fertility, virus strains, and moisture conditions. General symptoms include
dwarfing, excessive branching, leaf cupping, and mottling.
The mosaic pattern may appear as dark bands along major veins with clearing of leaf areas along margins and between leaf veins. Also, the mosaic pattern may be
dark green areas varying in size from small granular flecks to large blisterlike areas in chlorotic leaves. The darker areas are raised and give leaves a warty, puckered
shape. Primary leaves of plants grown from infected seed rarely have a mosaic pattern. Diseased plants growing under low temperatures and low light intensity may
not have mosaic symptoms. Severe symptoms (local necrotic lesions on leaves) occur under high light intensity and at temperatures around 26.5°C. Leaves with only
granular mottling have little distortion and look normal. Leaves with less pronounced symptoms may be elongated, narrow, and cupped downward.
At high temperatures, a symptom occurs called black root, which is a lethal systemic vascular necrosis resulting from hypersensitivity of some dominant Igenebearing
resistant bean cultivars to some BCMV serotype A strains. Plants develop a systemic necrosis that causes the vascular system to be necrotic. Initially, young leaflets
wilt slightly, then turn brown to black and wilt, followed by the whole plant wilting and dying. The maturity of less severely diseased plants is delayed. Plants grown
from infected

Page 168
seed or infected early in plant growth may be spindly, have little growth, and rarely form pods.
Management
1. Sow only certified seed.
3. Rogue out infected plants if a small area is involved.
Bean Curly Dwarf
Cause.
Bean curly dwarf mosaic virus is in the comovirus group.
Distribution.
Central America, North America, and South America.
Symptoms.
Diseased leaves have chlorotic local lesions. Ring spots infrequently occur. Depending upon the virus/host combination, necrosis occurs on leaves and stems.
Management.
Not reported.
Bean Dwarf Mosaic
Bean dwarf mosaic was formerly called bean chlorotic mottle and infectious chlorosis of Malvaceae.
Cause.
Bean dwarf mosaic virus (BDMV) belongs to the geminivirus group and is serologically related to bean golden mosaic, tomato golden mosaic, mung bean yellow
mosaic, and African cassava mosaic viruses. BCMV is reservoired in several tropical weeds that serve as sources of inoculum. For example, two species of Sida are
known to be reservoirs of BDMV. BDMV is transmitted mechanically and by the whitefly, Bemisia tabaci.
Distribution.
Symptoms.
Plants infected at the seedling stage are stunted and have malformed or curled and deformed leaves that have a mosaic pattern and chlorotic or yellow patches. Later,
diseased plants may display only the variegated patches, which are irregularly distributed in the foliage. Diseased plants generally abort their flowers or produce
severely distorted pods. Witches' broom symptoms have often been described as part of the disease syndrome, but these malformations may be the result of mixed
virus infections.
Management.
Grow resistant or tolerant varieties.
Bean Golden Mosaic
Bean golden mosaic is also called bean golden yellow mosaic.
Cause.
Bean golden mosaic virus (BGMV) is in the geminivirus group. BGMV is transmitted mechanically and by the whitefly, Bemisia tabaci, but it is not seedborne.
BGMV may be reservoired in numerous weeds.

Page 169
Distribution.
Tropical countries in the Western Hemisphere and the United States (Florida). Bean golden mosaic is considered the most devastating disease of beans in Latin
America, particularly in Brazil, Mexico, Dominican Republic, and Guatemala.
Symptoms.
Diseased plants have an intense yellow appearance. Leaves generally curl downward, and newly emerged leaves have a bright yellow general mosaic pattern but older
leaves have a less distinct mosaic pattern. Plants of some cultivars are stunted and have severely malformed pods, which, together with a high incidence of flower
abortion, cause yield losses of 100%.
Management
1. Grow tolerant cultivars. No cultivar is immune to BGMV. Some blackseeded cultivars are not as severely affected under moderate BGMV disease pressure.
2. Control insects through application of insecticides.
Bean Mild Mosaic
Cause.
Bean mild mosaic virus.
Distribution.
Symptoms.
A mild mosaic occurs on diseased bean leaves.
Management.
Not reported.
Bean Pod Mottle
Cause.
Bean pod mottle virus is in the comovirus group.
Distribution.
The United States.
Symptoms.
Diseased leaves have chlorotic local lesions, and ring spots infrequently occur. Symptoms in very susceptible cultivars ranged from mild to severe mosaic and foliar
malformation. Depending upon the virus/host combination, necrosis occurs on leaves and stems.
Management.
Not reported.
Bean Red Node
Bean red node is also called red node.
Cause.
Tobacco streak virus (TSV) is in the ilarvirus group. Two pathotypes exist. Pathotypes I and II belong to distinct serotypes and cause different symptoms. TSV is
seedtransmitted and mechanically transmitted. TSV pathotype I is efficiently seedtransmitted and is also apparently transmitted by thrips (Frankliniella sp.). Other
insects also may be implicated in transmission.

Page 170
Seed transmission of TSV may depend on early movement into and replication in pollenassociated tissues.
Distribution.
The United States (Florida and Washington) and possibly other beangrowing areas.
Symptoms.
Pathotype I isolates induce reddening of nodes at the stem, necrosis of primary and trifoliate leaf veins, and sunken reddish lesions on bean pods. Pods are frequently
shriveled and deformed. Pathotype II isolates cause a green to yellow mosaic.
Management.
Avoid planting near adzuki bean, alfalfa, chickpea, fenugreek, and white sweet clover.
Bean Rugose Mosaic
Cause.
Bean rugose mosaic virus (BRMV) is in the comovirus group. BRMV is transmitted mechanically and by the beetles Cerotoma spp. and Diabrotica spp.
Distribution.
Symptoms.
Leaf symptoms include a light and dark green mosaic pattern that is often accompanied by severe leaf blistering, curling, and malformation that gives the leaf a
thickened or leathery appearance. Early infection results in severe stunting. Diseased pods may have a mosaic pattern and be malformed.
Management
Bean Southern Mosaic
Cause.
Bean southern mosaic virus (BSMV) is in the sobemovirus group. BSMV is transmitted by beetles.
Distribution.
Warm beangrowing areas.
Symptoms.
Diseased foliage has a green mosaic and is rugose.
Management.
Resistance has been identified.
Bean Yellow Mosaic
Cause.
Bean yellow mosaic virus (BYMV) is in the potyvirus group. BYMV overwinters in perennial plants, such as wild sweet clover; it is transmitted mechanically and by
several species of aphids, but the virus is not seedborne. Temperatures of 28°C and higher in the growth chamber inhibit development of tip necrosis. Several strains
of BYMV exist.

Page 171
Distribution.
Symptoms.
Symptoms of bean yellow mosaic are more prevalent along borders of fields. Initially, leaflets droop at the point of attachment to the stem, followed by development
of angular, pale spots (1.53.0 mm in diameter). In some bean cultivars, the pale, angular spots become more pronounced and are bright yellow. Spots may coalesce,
which results in general chlorosis. Leaves become thick, cupped, and brittle, which causes them to be malformed and distorted or to have a thickened granular
appearance. Some virus strains cause a purpling of the bases of lower leaves. Plants may be dwarfed and bunchy and have delayed maturity and reduced yield. Plants
may die.
The necrotic strain of BYMV causes tip necrosis and leaf abscission.
Management
1. Grow resistant cultivars that carry the ''I" gene.
2. Eliminate wild sweet clover from fence rows and ditch banks.
Bean Yellow Stipple
Cause.
Bean yellow stipple virus (BYSV) is in the bromovirus group and is considered a strain of cowpea chlorotic mottle virus. BYSV is transmitted by the chrysomelid
beetles Cerotoma ruficornis and Diabrotica balteata. BYSV is transferred after an acquisition period of less than 24 hours and is retained for 3 to 6 days by C.
ruficornis and 1 to 3 days by D. balteata.
Distribution.
Costa Rica, Cuba, and the United States (Arkansas and Illinois).
Symptoms.
Inoculated plants initially display a light yellow mottle that gradually develops into clearly distinct small spots which are unevenly distributed in the trifoliate leaves.
Spots may coalesce and form large, irregularshaped, bright yellow patches. The number and intensity of spots decrease in newer leaves as plants mature. A slight
stunting or vein necrosis occurs in some cultivars.
Management.
Not necessary since bean yellow stipple is of no economic importance.
Clover Yellow Vein
Cause.
Clover yellow vein virus (CYVV) overseasons in perennial clover hosts. CYVV is transmitted mechanically and in a nonpersistent manner by several aphids.
Distribution.
Europe and North America.
Symptoms.
Diseased foliage has a pronounced yellow mosaic and malformation, and plants have a pronounced stunting. Some cultivars develop api

Page 172
cal necrosis, premature defoliation, and wilting, and plants eventually die. Pods are severely distorted and mottled. Frequently, root rot caused by soilborne
pathogens develops.
Management.
Cowpea Mild Mottle
Cause.
Cowpea mild mottle virus is in the carlavirus group.
Distribution.
Tanzania.
Symptoms.
Diseased leaves are mottled with chlorotic spots.
Management.
Not reported.
Cowpea Severe Mosaic
Cause.
Cowpea severe mosaic virus is in the comovirus group.
Distribution.
Brazil.
Symptoms.
Leaves of diseased plants have vein clearing, mottling, and chlorotic spots. Pods are mottled and distorted.
Management.
Not reported.
Cucumber Mosaic
Cause.
Cucumber mosaic virus (CMV) is in the cucumovirus group. CMV is seedborne.
Distribution.
Europe and the United States.
Symptoms.
Leaves have a mosaic appearance.
Management.
Not reported.
Curly Dwarf Mosaic Disease
Cause.
Bean curly dwarf mosaic virus (BCDMV) is transmitted mechanically, and by the Mexican bean beetle and the spotted cucumber beetle. Fifteen other species of
legumes are also susceptible to BCDMV.
Distribution.
El Salvador.
Symptoms.
Diseased plants are dwarfed. Leaves have a mosaic pattern, are rugose, and curl downward. Inoculated plants have symptoms that range from mild mosaic to lethal
top necrosis.
Management.
Not reported.

Page 173
Curly Top
Cause.
The curly top virus overwinters in a large number of perennial plants and is transmitted by the leafhopper Circulifer tenellus.
Distribution.
The western United States.
Symptoms.
Plants usually die of curly top if infected in the crookneck stage. If a plant has developed only primary leaves at the time of infection, the growing point will die without
further production of trifoliate leaves, followed by yellowing and drying of the whole plant.
Plants infected in early blossom stage drop blooms, become chlorotic and die. If a plant is infected in pod set, new pods will not be set but lightweight and poorly
developed seed will mature.
When older plants become infected, the first symptom is a downward cupping of the youngest trifoliate leaf. The growing point then dies or subsequent internodes are
shortened, causing plants to be stunted and bushy. Trifoliate leaves formed before infection become chlorotic, thickened, and cup downward. The whole plant
becomes brittle, and leaves and the growing point are easily broken off.
Management.
Dwarfing Disease
Cause.
Soybean dwarf virus (SDV) is transmitted by the aphids Aulacorthum solani and Acyrthosiphon pisum. Subterranean clover red leaf virus is considered a strain of
SDV.
Distribution.
Australia (Tasmania), Japan, and New Zealand.
Symptoms.
Symptoms are similar to those on soybean. Plants are severely stunted. Leaves are rugose, curl down, and may have interveinal yellowing.
Management.
Not reported.
Peanut Mottle
Cause.
Peanut mottle virus (PMV) is in the potyvirus group. PMV is transmitted mechanically and in a nonpersistent manner by several species of aphids. Infected peanut
seed provides primary inoculum.
Distribution.
Australia and the United States (New York and Texas).
Symptoms
Three types of symptoms occur: one in susceptible genotypes and the other two in resistant genotypes. Susceptible genotypes display necrotic lesions and vein
necrosis of inoculated unifoliate leaves. Uninoculated trifoliate leaves in the field develop a mosaic, followed by chlorosis and necrosis of veins, petioles, and stems.
Plants frequently die.

Page 174
Resistant genotypes react with necrotic lesions and vein necrosis or with chlorotic lesions that eventually coalesce. In both reactions, the virus remains localized in
inoculated leaves.
Few or no seeds are produced on diseased plants.
Management
2. Separate bean fields from peanut fields.
Peanut Stunt
Cause.
Peanut stunt virus is in the cucumovirus group. For further information, see Chapter 12, "Diseases of Peanut."
Distribution.
The United States (North Carolina, Tennessee, and Washington).
Symptoms.
Diseased plants are stunted, and there is necrosis of growing tips or branches in some cultivars. Leaves are malformed, mottled, and crinkled. Pods are few, small, and
malformed and have a few small seeds.
Management.
Not reported.
Southern Bean Mosaic
Cause.
Southern bean mosaic virus (SBMV), which is in the sobemovirus group, consists of different strains. SBMV is seedborne; the incidence of infection is higher in seeds
with cracked coats than in seeds with intact coats. SBMV is also transmitted mechanically, by growing plants in virusinfested soil, and by several beetles.
Accumulation of the cowpea strain of southern bean mosaic virus in bean is facilitated by coinfection with sunnhemp mosaic, a tobamovirus.
Distribution.
South America.
Symptoms.
Either circular (13 mm in diameter), brownishred local lesions or systemic mottling and vein banding symptoms occur on diseased leaves. Leaves also may be
blistered and malformed or crumpled.
Pods have dark green, watersoaked, irregularshaped blotches. The number and weight of seed may be reduced; however, the number of pods may be greater in
diseased than in healthy plants.
Management
Soybean Yellow Shoot
Cause.
Soybean yellow shoot virus (VABS) is in the potyvirus group. VABS is mechanically transmitted.

Page 175
Distribution.
Brazil.
Symptoms.
Symptoms on inoculated plants vary from interveinal mosaic, severe mosaic, and systemic or vein necrosis to top necrosis, followed by plant death.
Management.
Not reported.
Stipple Streak
Cause.
Tobacco necrosis virus (TNV) is transmitted in a nonpersistent manner by attachment to the surface of zoospores of the fungus Olpidium brassicae. Olpidium
brassicae is disseminated primarily by splashing rain and irrigation water. Disease is most common on wet soils, particularly soils high in organic matter or peat soils.
Dissemination of TNV is by planttoplant contact during windy weather and by man. The virus has several strains and may have a satellite virus.
Distribution.
Australia, Europe, New Zealand, and the United States (New York).
Symptoms.
Symptoms are most severe during warm, cloudy weather but may not occur on leaves developed during hot, sunny weather. Scattered reddish, dark brown, or black
spots and streaks or bands occur on stems, petioles, and veins. Variously sized and shaped reticulate necroses of veins may develop on leaves in isolated patches.
Such leaves are malformed and often wither and drop. However, tip leaves may remain normal.
Pods of plants may be symptomless or display rusty brown, irregularshaped, sometimes concentric necrotic lesions. If plants are infected when young, they may
become distorted and shrivel. Necrotic lesions may develop on pods after harvest.
Management.
Not reported.
Selected References
Abawi, G. S., Potlach, F. J., and Molin, W. T. 1975. Infection of bean by ascospores of Whetzelinia sclerotiorum. Phytopathology 65:673678.
Abawi, G. S., Crosier, D. C., and Cobb, A. C. 1977. Pod flecking of snap beans caused by Alternaria alternata. Plant Dis. Rptr. 61:901905.
Acosta, L. O., Alegria, A., Lastra, R., and Morales, F. 1991. Partial characterization of a Colombian isolate of bean mild mosaic virus from Phaseolus vulgaris.
(Abstr.). Phytopathology 81:690.
Adegbola, M. O. K., and Hagedom, D. J. 1969. Symptomatology and epidemiology of Pythium bean blight. Phytopathology 59:11131118.
Anderson, F. N., Steadman, J. R., Coyne, D. P., and Schwartz, H. F. 1974. Tolerance to white mold in Phaseolus vulgaris dry edible bean types. Plant Dis. Rptr.
58:782784.
Balardin, R. S., Jarosz, A. M., and Kelly, J. D. 1997. Virulence and molecular diversity of

Page 176
Colletotrichum lindemuthianum from South, Central, and North America. Phytopathology 87:11841191.
Batra, L. R., and Stavely, J. R. 1994. Attraction of twospotted spider mite to bean rust uredinia. Plant Dis. 78: 282284.
Bernier, C. 1975. Diseases of pulse crops and their control. In Oilseed and Pulse Crops in Western Canada, J. T. Harapick (ed.). Modern Press, Saskatoon, Sask.
Blad, B. L., Steadman, J. R., and Weiss, A. 1978. Canopy structure and irrigation influence white mold disease and microclimate of dry edible beans. Phytopathology
68:14311437.
Boland, G. J., and Hall, R. 1987. Epidemiology of white mold of white bean in Ontario. Can. J. Plant Pathol. 9:218224.
Brown, J. K., JimenezGarcia, E., and Nelson, M. R. 1988. Bean calico mosaic virus, a newly described geminivirus of bean. (Abstr.) Phytopathology 78:1579.
Burke, D. W., and Miller, D. E. 1983. Control of Fusarium root rot with resistant beans and cultural management. Plant Dis. 67:13121317.
Burke, D. W., Miller, D. E., Holmes, L. D., and Barker, A. W. 1972. Counteracting bean root rot by loosening the soil. Phytopathology 62:306309.
Caesar, A. J., and Pearson, R. C. 1983. Environmental factors affecting survival of ascospores of Sclerotinia sclerotiorum. Phytopathology 73:10241030.
Cafati, C. R., and Saettler, A. W. 1980. Transmission of Xanthomonas phaseoli in seed of resistant and susceptible Phaseolus genotypes. Phytopathology 70:638
640.
Campbell, C. L., and Steadman, J. R. 1985. The relationship of Sclerotinia sclerotiorum ascospore germination on bean blossoms to disease development in a bean
canopy microclimate. (Abstr.) Phytopathology 75:1369.
Claflin, L. E., Stuteville, D. L., and Armbrust, D. V. 1973. Windblown soil in the epidemiology of bacterial leaf spot of alfalfa and common blight of bean.
Cook, G. F., Steadman, J. R., and Boosalis, M. G. 1975. Survival of Whetzelinia sclerotiorum and initial infection of dry edible beans in western Nebraska.
Correa, F. J., and Saettler, A. W. 1987. Angular leaf spot of red kidney beans in Michigan. Plant Dis. 71:915918.
Coyne, D. P., and Schuster, M. L. 1970. 'Jules,' a great northern dry bean variety tolerant to common blight bacterium (Xanthomonas phaseoli). Plant Dis. Rptr.
54:557559.
Cupertino, F. P., Costa, C. L., Lin, M. T., and Kitajimi, E. W. 1982. Infeccas natural do feyoeiro (Phaseolus vulgaris L.) Pelo virus do mosaico severs do feijao
macassar. Fitopatologia Brasileria 7:275283 (in Portugese).
Daub, M. E., and Hagedorn, D. J. 1981. Epiphytic populations of Pseudomonas syringae on susceptible and resistant bean lines. Phytopathology 71:547550.
Dean, R. A., and Timberlake, W. E. 1977. Aspergillus nidulans: A potential plant pathogen? (Abstr.) Phytopathology 77:1692.
Dhingra, O. D. 1978. Internally seedborne Fusarium semitectum and Phomopsis sp. affecting dry and snap bean seed quality. Plant Dis. Rptr. 62:509512.
Dhingra, O. D., and Kushalappa, A. C. 1980. No correlation between angular leaf spot intensity and seed infection in beans by Isariopsis griseola. Fitopaathologia
Brasileria 5:149152.
Dickson, M. H., and Abawi, G. S. 1974. Resistance to Pythium ultimum in whiteseeded beans (Phaseolus vulgaris). Plant Dis. Rptr. 58:774776.

Page 177
Dillard, H. R., and Cobb, A. C. 1993. Survival of Colletotrichum lindemuthianum in bean debris in New York State. Plant Dis. 77:12331238.
Echandi, E., and Hebert, T. T. 1970. An epiphytotic of stunt in beans incited by the peanut stunt virus in North Carolina. Plant Dis. Rptr. 54:183184.
Echandi, E., and Hebert, T. T. 1971. Stunt of beans incited by peanut stunt virus. Phytopathology 61:328330.
Engelkes, C. A., and Windels, C. E. 1996. Susceptibility of sugar beet and beans to Rhizoctonia solani AG22 IIIB and AG22 IV. Plant Dis. 80:14131417.
Fahy, P. C., and Persley, G. J. 1983. Plant Bacterial Diseases: A Diagnostic Guide. Academic Press, Inc. New York, NY.
Franc, G. D., and Beaupre, C. M.S. 1993. A new disease of pinto bean caused by Aphelenchoides ritzemabosi in Wyoming. Plant Dis. 77:1168.
Franc, G. D., Beaupre, C. M.S, Gray, F. A., and Hall, R. D. 1996. Nematode angular leaf spot of dry bean in Wyoming. Plant Dis. 80:476477.
Fuentes, A. L., and Hamilton, R. I. 1991. Sunnhemp mosaic virus facilitates celltocell spread of southern bean mosaic virus in a nonpermissive host.
Galindo, J. J., Abawi, G. S., and Thurston, H. D. 1982. Variability among isolates of Rhizoctonia solani associated with snap bean hypocotyls and soils in New
York. Plant Dis. 66:390394.
Galindo, J. J., Abawi, G. S., Thurston, H. D., and Galvez, G. E. 1982. Source of inoculum and development of webblight of beans in Costa Rica. (Abstr.)
Galvez, G. E., Mora, B., and Alfaro, R. 1984. Integrated control of web blight of beans (Phaseolus vulgaris). (Abstr.) Phytopathology 74:1015.
Gilbertson, R. L., Carlson, E., Rand, R. E., Hagedom, D. J., and Maxwell, D. P. 1986. Survival of Xanthomonas campestris pv. phaseoli in bean stubble and
debris with three tillage systems. (Abstr.) Phytopathology 76:1078.
Gilbertson, R. L., Rand, R. E., and Hagedorn, D. J. 1990. Survival of Xanthomonas campestris pv. phaseoli and pectoytic strains of X. campestris in bean debris.
Plant Dis. 74:322327.
GodoyLutz, G., Arias, J, Steadman, J. R., and Eskridge, K. M. 1996. Role of natural seed infection by the web blight pathogen in common bean seed damage,
seedling emergence, and early disease development. Plant Dis. 80:887890.
Goode, M. J., Hagedorn, D. J., and Cross, J. E. 1985. Occurrence of snap bean bacterial blight pathogens on wild legumes. (Abstr.) Phytopathology 75:1287.
Granada, G. A. 1979. Machismo, a new disease of beans in Colombia. (Abstr.) Phytopathology 69:1029.
Groth, J. V., and Mogen, B. D. 1978. Completing the life cycle of Uromyces phaseoli var. typica on bean plants. Phytopathology 68:16741677.
Hagedorn, D. J., and Binning, L. K. 1982. Herbicide suppression of bean root and hypocotyl rot in Wisconsin. Plant Dis. 66:11871188.
Hagedorn, D. J., and Rand, R. E. 1979. Development of processing type beans (Phaseolus vulgaris) resistant to bacterial brown spot (Pseudomonas syringae).
(Abstr.) Phytopathology 69:1030.

Page 178
Hagedorn, D. J., and Rand, R. E. 1986. Development and release of WIS (MDR) 147 bean breeding line. (Abstr.) Phytopathology 76:1067.
Hagedom, D. J., Rand, R. E., and Saad, S. M. 1972. Phaseolus vulgaris reaction to Pseudomonas syringae. Plant Dis. Rptr. 56:325328.
Hall, R. 1991. Compendium of Bean Diseases. American Phytopathological Society, St. Paul, MN. 73 pp.
Hampton, R. O., Silbernagel, M. J., and Burke, D. W. 1983. Bean common mosaic virus strains associated with bean mosaic epidemics in the northwestern United
States. Plant Dis. 67:658661.
Hanson, P. M., PastorCorrales, M. A., and Kornegay, J. L. 1993. Heritability and sources of Ascochyta blight resistance in common bean. Plant Dis. 77:711714.
Heimann, M. G., Stevenson, W. R., and Rand, R. E. 1989. Bipolaris sorokiniana found causing lesions on snap bean in Wisconsin. Plant Dis. 73:701.
Hoch, H. C., Hagedorn, D. J., Pinnow, D. L., and Mitchell, J. E. 1975. Role of Pythium spp. as incitants of bean root and hypocotyl rot in Wisconsin. Plant Dis.
Rptr. 59:443447.
Howard, C. M., Conway, K. E., and Albregts, E. E. 1977. A stem rot of bean seedlings caused by a sterile fungus in Florida. Phytopathology 67:430433.
Hunter, J. E., Dickson, M. H., Boettger, M. A., and Cigna, J. A. 1982. Evaluation of plant introductions of Phaseolus spp. for resistance to white mold. Plant Dis.
66:320322.
Hutton, D. G., Wilkinson, R. E., and Mai, W. F. 1973. Effect of two plant parasitic nematodes on Fusarium dry root rot of beans. Phytopathology 63:749751.
Johnson, K. B., and Powelson, M. L. 1983. Influence of prebloom disease establishment by Botrytis cinerea and environmental and host factors on gray mold pod
rot of snap bean. Plant Dis. 67:11981202.
Kaiser, W. J., Wyatt, S. D., and Klein, R. E. 1991. Epidemiology and seed transmission of two tobacco streak virus pathotypes associated with seed increases of
legume germplasm in eastern Washington. Plant Dis. 75:258264.
Katherman, M. J., Wilkinson, R. E., and Beer, S. V. 1980. The potential of four dry bean cultivars to serve as sources of Pseudomonas phaseolicola inoculum.
Plant Dis. 64:7274.
Kelly, J. D., Afanador, L., and Cameron, L. S. 1994. New races of Colletotrichum lindemuthianum in Michigan and implications in dry bean resistance breeding.
Plant Dis. 78:892894.
Kobriger, K., and Hagedom, D. J. 1984. Additional Pythium species associated with bean rot complex in Wisconsin's Central Sands. Plant Dis. 68:595596.
Lanter, J. M., Pastor Corrales, M. A., and Hancock, J. G. 1977. Progress of angular leaf spot of bean grown in monocultures and in beanmaize intercrops. (Abstr.)
Legard, D. E., and Schwartz, H. F. 1987. Sources and management of Pseudomonas syringae pv. phaseolicola and Pseudomonas syringae pv. syringae
epiphytes on dry beans in Colorado. Phytopathology 77:15031509.
Lewis, J. A., Lumsden, R. D., Papavizas, G. C., and Kantzes, J. G. 1983. Integrated control of snap bean disease caused by Pythium spp. and Rhizoctonia solani.
Plant Dis. 67:12411244.
Mabagala, R. B., and Saettler, A. W. 1992. Pseudomonas syringae pv. phaseolicola populations and halo blight severity in beans grown alone or intercropped with
maize in northern Tanzania. Plant Dis. 76:687692.

Page 179
Mabagala, R. B., and Saettler, A. W. 1992. Races and survival of Pseudomonas syringae pv. phaseolicola in northern Tanzania. Plant Dis. 76:678682.
Mabagala, R. B., and Saettler, A. W. 1992. The role of weeds in survival of Pseudomonas syringae pv. phaseolicola in northern Tanzania. Plant Dis. 76:683687.
McFadden, W. R., Hall, R., and Phillips, L. G. 1989. Relation of initial inoculum density to severity of Fusarium root rot of white bean in commercial fields. Can. J.
McKern, N. M., Mink, G. I., Barnett, O. W., Mishra, A., Whittaker, L. A., Silbernagel, M. J., Ward, C. W., and Shukla, D. D. 1992. Isolates of bean common
mosaic virus comprising two distinct potyviruses. Phytopathology 82:923929.
McLaren, D. L., Huang, H. C., and Rimmer, S. R. 1996. Control of apothecial production of Sclerotinia sclerotiorum by Coniothyrium minitans and
Talaromyces flayus. Plant Dis. 80:13731378.
Meiners, J. P., Waterworth, H. E., Lawson, R. H., and Smith, F. F. 1977. Curly dwarf mosaic disease of beans from El Salvador. Phytopathology 67:163168.
Miller, D. E., and Burke, D. W. 1986. Reduction of Fusarium root rot and Sclerotinia wilt in beans with irrigation, tillage and bean genotype. Plant Dis. 70:163166.
Morales, F. J., and Castano, M. 1985. Effect of a Colombian isolate of bean southern mosaic virus on selected yield components of Phaseolus vulgaris. Plant Dis.
69:803804.
Morales, F. J., and Niessen, A. L 1988. Comparative responses of selected Phaseolus vulgaris germplasm inoculated artificially and naturally with bean golden
mosaic virus. Plant Dis. 72:10201023.
Morales, F. J., and Niessen, A. I. 1988. Isolation and partial characterization of bean dwarf mosaic virus. (Abstr.) Phytopathology 78: 858.
Morales, F., Niessen, A., Ramirez, B., and Castano, M. 1990. Isolation and partial characterization of a geminivirus causing bean dwarf mosaic. Phytopathology
80:96101.
Muckel, R. D., and Steadman, J. R. 1981. Dissemination and survival of Sclerotinia sclerotiorum in bean fields in western Nebraska. (Abstr.) Phytopathology
71:244.
Natti, J. J. 1971. Epidemiology and control of bean white mold. Phytopathology 61:669674.
Ntahimpera, N., Dillard, H. R., Cobb, A. C., and Seem, R. C. 1997. Influence of tillage practices on anthracnose development and distribution in dry bean fields.
Plant Dis. 81:7176.
Olaya, G., and Abawi, G. S. 1996. Effect of water potential on mycelial growth and on production and germination of sclerotia of Macrophomina phaseolina. Plant
Dis. 80:13471350.
PastorCorrales, M. A., and Abawi, G. S. 1988. Reactions of selected bean accessions to infection by Macrophomina phaseolina. Plant Dis. 72:3941.
Patel, P. N., et. al. 1964. Bacterial brown spot of bean in central Wisconsin. Plant Dis. Rptr. 48:335337.
Perry, V. G. 1953. The awl nematode, Dolichodorus heterocephalus, a devastating plant parasite. Proc. Helminth. Soc. Wash. 20:2127.
Pfender, W. F., and Hagedom, D. J. 1981. Aphanomyces root and stem rot of snap beans. (Abstr.) Phytopathology 71:250.
Pfender, W. F., and Hagedorn, D. J. 1982. Aphanomyces euteiches f. sp. phaseoli, a causal agent of bean root and hypocotyl rot. Phytopathology 72:306310.
Pieczarka, D. J., and Abawi, G. S. 1978. Effect of interaction between Fusarium, Pythium,

Page 180
and Rhizoctonia on severity of bean root rot. Phytopathology 68:403408.
Pieczarka, D. J., and Abawi, G. S. 1978. Influence of soil water potential and temperature on severity of Pythium root rot of snap beans. Phytopathology 68:766
772.
Piepenbring, M., and Bauer, R. 1997. Erratomyces, a new genus of Tilletiales with species on Leguminosae. Mycologia 89:924936.
Polach, F. J., and Abawi, G. S. 1975. The occurrence and biology of Botryotinia fuckeliana on beans in New York. Phytopathology 65:657660.
Prasad, K., and Weigle, J. L. 1976. Association of seed coat factors with resistance to Rhizoctonia solani in Phaseolus vulgaris. Phytopathology 66:342345.
Raid, R. N., McDaniel, L. L., Nuessly, G. S., and Scully, B. T. 1995. First report of bean red node in the eastern United States. Plant Dis. 79:539.
Reddy, M. S., and Patrick, Z. A. 1989. Effect of host, nonhost and fallow soil on populations of Thielaviopsis basicola and severity of black root rot. Can. J. Plant
Pathol. 11:6874.
Reeleder, R. D., and Hagedorn, D. J. 1981. Inheritance of resistance to Pythium myriotylum hypocotyl rot in Phaseolus vulgaris L. Plant Dis. 65:427429.
Ribeiro, R. De L. D., Hagedorn, D. J., Durbin, R. D., and Vchytil, T. F. 1979. Characterization of the bacterium inciting bean wildfire in Brazil. Phytopathology
69:208212.
Saad, S., and Hagedom, D. J. 1969. Symptomatology and epidemiology of Alternaria leaf spot of bean Phaseolus vulgaris. Phytopathology 59:15301533.
Saettler, A. W., and Correa, F. J. 1987. Transmission of Phaeoisariopsis griseola in bean seed. (Abstr.) Phytopathology 77:1707.
Saettler, A. W., and Stadt, S. J. 1981. Internal seed infection by Pseudomonas phaseolicola in susceptible and tolerant bean cultivars. (Abstr.) Phytopathology
71:252.
Saettler, A. W., Cafati, C. R., and Weller, D. M. 1986. Nonoverwintering of Xanthomonas bean blight bacteria in Michigan. Plant Dis. 70:285287.
Salgado, M. O., and Schwartz, H. F. 1993. Physiological specialization and effects of inoculum concentration of Fusarium oxysporum f. sp. phaseoli on common
beans. Plant Dis. 77:492496.
Schieber, E., and Zentmeyer, G. A. 1971. A new bean disease in the Caribbean area. Plant Dis. Rptr. 55:207208.
Schuster, M. L., Blatchford, G. J., and Schuster, A. M. 1980. A new bacterium, Pseudomonas blatchfordae nov. sp., pathogenic for bean. Fitopathologia Brasileria
5:283297.
Schuster, M. L., Schuster, A. M., and Nuland, D. S. 1981. A new bacterium pathogenic for beans (Phaseolus vulgaris L.). Fitopatologia Brasileria 6:345358.
Schwartz, H. F., and Steadman, J. R. 1978. Factors affecting sclerotium populations of, and apothecium production by, Sclerotinia sclerotiorum. Phytopathology
68:383388.
Schwartz, H. F., Galvez, G. E., Schoonhoven, A. Van, Howeler, R. H., Graham, P. H., and Flor, C. 1978. Field Problems of Beans in Latin America. Centro
Internacional de Agricultura Tropical, Cali, Colombia. 136 pp.
Schwartz, H. F., Katherman, M. J., and Thung, M. D. T. 1981. Yield response and resistance of dry beans to powdery mildew in Colombia. Plant Dis. 65:737738.
Shaik, M. 1985. Racenonspecific resistance in bean cultivars to races of Uromyces appendiculatus var. appendiculatus and its correlation with leaf epidermal
characteristic. Phytopathology 75:478481.
Shukla, D. D., McKern, N. M., Ward, C. W., and Ford, R. E. 1991. Molecular parameters suggest that cowpea aphidborne mosaic virus is a distinct potyvirus and
that bean

Page 181
common mosaic virus consists of at least three distinct potyviruses. (Abstr.) Phytopathology 81:1166.
Silbernagel, M. J., and Mills, L. J. 1990. Genetic and cultural control of Fusarium root rot in bush snap beans. Plant Dis. 74:6166.
Sippell, E. W., and Hall, R. 1981. Effects of Fusarium and Pythium on yield components of white bean. (Abstr.) Phytopathology 71:564.
Skiles, R. L., and CardonaAlvarez, C. 1959. Mancha gris, a new leaf disease of bean in Colombia. Phytopathology 49:133135.
Steadman, J. R. 1983. White mold, a serious yieldlimiting disease of bean. Plant Dis. 67:346350.
Steadman, J. R., Kerr, E. D., and Mumm, R. F. 1975. Root rot of bean in Nebraska: Primary pathogen and yield loss appraisal. Plant Dis. Rptr. 59:305308.
Stockwell, V., and Hanchey, P. 1984. The role of the cuticle in resistance of beans to Rhizoctonia solani. Phytopathology 74:16401642.
Sumner, D. R., Smittle, D. A., Threadgill, E. D., Johnson, A. W., and Chalfant, R. B. 1986. Interactions of tillage and soil fertility with root diseases in snap bean and
lima bean in irrigated multiplecropping systems. Plant Dis. 70:730735.
Teakle, D. S., and Moris, T. J. 1981. Transmission of southern bean mosaic virus from soil to bean seeds. Plant Dis. 65:599600.
Tu, J. C. 1981. Anthracnose (Colletotrichum lindemuthianum) on white bean (Phaseolus vulgaris L.) in southern Ontario: Spread of the disease from an infection
focus. Plant Dis. 65:477480.
Tu, J. C. 1981. Etiology of pod and seed coat discoloration of white beans. (Abstr.) Phytopathology 71:909.
Tu, J. C. 1983. Epidemiology of anthracnose caused by Colletotrichum lindemuthianum on white bean (Phaseolus vulgaris) in southern Ontario: Survival of the
pathogen. Plant Dis. 67:402404.
Tu, J. C. 1984. Biology of Alternaria alternata, the causal fungus of black pod disease of white beans in southwestern Ontario. (Abstr.) Phytopathology 74:820.
Tu, J. C. 1985. Pink pod rot of bean caused by Trichothecium roseum. Can. J. Plant Pathol. 7:5557.
Tu, J. C. 1988. Control of bean anthracnose caused by the delta and lambda races of Colletotrichum lindemuthianum in Canada. Plant Dis. 72:58.
Tu, J. C. 1988. The role of white moldinfected white bean (Sclerotinia sclerotiorum (Lib.) de Bary). J. Phytopathology 121:4050.
Tu, J. C. 1989. The role of temperature and inoculum concentration in the development of tip necrosis and seedling death of beans infected with bean yellow mosaic
Tu, J. C. 1990. First report of anthracnose caused by Glomerella cingulata on white beans in Ontario, Canada. Plant Dis. 74:394.
Tu, J. C., Sheppard, J. W., and Laidlaw, D. M. 1984. Occurrence and characterization of the epsilon race of bean anthracnose in Ontario. Plant Dis. 68:6970.
Van Bruggen, A. H. C., Arneson, P. A., and Whalen, C. H. 1983. Emergence of dry beans as affected by Rhizoctonia solani, soil moisture and temperature.
Van Bruggen, A. H. C., Whalen, C. H., and Arneson, P. A. 1986. Emergence, growth and development of dry bean seedlings in response to temperature, soil
moisture and Rhizoctonia solani. Phytopathology 76:568572.

Page 182
Verdejo, S., Green, C. D., and Podder, A. K. 1988. Influence of Meloidogyne incognita on nodulation and growth of pea and black bean. Nematologica 34:8897.
Walter, M. H., Kaiser, W. J., Klein, R. E., and Wyatt, S. D. 1992. Association between tobacco streak ilarvirus seed transmission and anther tissue infection in bean.
Webster, D. M., Atkin, J. D., and Cross, J. E. 1983. Bacterial blights of snap beans and their control. Plant Dis. 67:935940.
Webster, D. M., Temple, S. R., and Galvez, G. 1983. Expression of resistance to Xanthomonas campestris pv. phaseoli in Phaseolus vulgaris under tropical
conditions. Plant Dis. 67:394396.
Weller, D. M., and Saettler, A. W. 1980. Evaluation of seedborne Xanthomonas phaseoli and X. phaseoli var. fuscans as primary inocula in bean blights.

Page 183
6.
Diseases of Cotton (Gossypium barbadense and G. hirsutum)
Agrobacterium Root Rot and Wilt
Cause.
Agrobacterium biovar 1.
Distribution.
The United States (Arkansas, Louisiana, North Carolina, Tennessee, and Texas).
Symptoms.
Symptoms are characterized by ''copper top" and sudden wilt of diseased plants. Losses up to 50% have been reported.
Management.
Not reported.
Bacterial Blight
Bacterial blight is also called angular leaf spot, and black arm.
Cause.
Xanthomonas campestris pv. malvacearum (syn. Bacterium malvacearum, Phytomonas malvacearum, Pseudomonas malvacearum, X. campestris, and X.
malvacearum) survives on seed lint, in seed, in residue left in the field after harvest, and in buds of symptomless plants. In arid and semiarid areas, survival occurs in
soil residue consisting of stems and boils. Xanthomonas campestris pv. malvacearum is disseminated by wind, water, insects, animals, and machinery, and on seed.
Seed is the most important mode of longdistance spread. Volunteer plants that grow from infected seed often have infected cotyledons, which serve as a source of
inoculum.
The optimum conditions for the entry of bacteria into plants through stomata and wounds are temperatures of 30° to 36°C and abundant moisture, or relative
humidities of 85% or more. Boll rot frequently occurs during hot, humid weather when numerous insects may puncture or wound bolls. Seed becomes infected if
excess moisture is present at harvest time.
Different physiologic races of X. campestris pv. malvacearum are present in the field.

Page 184
Distribution.
Cosmopolitan; bacterial blight occurs wherever cotton is grown.
Symptoms.
Initially, green, round to elongate, watersoaked, translucent spots of different sizes appear on lower cotyledon surfaces 7 to 10 days after sowing. Eventually,
infections penetrate to the upper sides of leaves as angular or irregularshaped, brown to black lesions that are between veins and are along the main leaf veins and
petioles. Diseased areas dry up, become sunken, and are reddish brown with a brownish to purplish margin. Leaf defoliation may occur.
Lesions on seedling hypocotyls are black, elongated cankers that may girdle and kill the plant. This phase of the disease is called "black arm." Similar lesions may also
occur and girdle stems of older plants, causing death of the distal portion of the diseased plants.
Bolls have round to irregularshaped or angular, black, sunken spots. Bollrotting fungi may invade bacterial lesions and discolor or destroy bolls. A creamy, bacterial
exudate occurs on leaf lesions and bolls during high humidity or after rain. Dried exudate will appear as a sugarlike coating or film on a dark lesion.
Management
2. Acid delint seed.
3. Rotate cotton for at least 1 year with a resistant crop.
4. Plow under residue immediately after harvest.
5. Sow seed from diseasefree plants.
Bacterial Lint Discoloration
Cause.
Pseudomonas sp. survives in soil and is introduced into bolls by insects.
Distribution.
The United States.
Symptoms.
Fiber is discolored and fluoresces yellow to green under ultraviolet light (366 nm).
Management.
Not reported.
Crown Gall
Cause.
Agrobacterium radiobacter var. tumefaciens and new biotype 2. Infection is enhanced by the root knot nematode, Meloidogyne incognita, but bacteria can
penetrate root tissues without nematode involvement.
Distribution.
Israel and the United States. Crown gall on cotton is rare.
Symptoms.
Plants are generally stunted; the galls on stunted taproots are 1 to

Page 185
4 cm long, irregularshaped, and dark brown. Sometimes sphericalshaped galls approximately 1 cm in diameter are found on lateral roots.
Management.
Not practiced because of the infrequency of crown gall.
Erwinia Internal Necrosis
Cause.
Erwinia herbicola. Necrosis depends on development of a secondary internal boll that splits the placentae and causes an opening to the outside of the boll and
intertwining of fibers of affected locules. This allows the bacteria to enter the boll, where it spreads from the interplacentae space into locules. Erwinia herbicola may
have some association with the stinkbug Euschistus impictiventris.
Distribution.
Symptoms.
Immature cotton bolls have reddishbrown necrotic tissue. Diseased locules are soft and slimy. Affected seed coats are discolored and seed contents are completely
decayed. The lint of diseased mature open bolls is discolored tan, and the locules are compact.
Management.
Not reported.
Pantoea agglomerans Cotton Lint Rot
This disease had been associated with abnormal boll morphology previously described as supernumerary carpel syndrome (SCS).
Cause.
Pantoea agglomerans is a gramnegative bacterium with yellow pig mentation. Previously, P. agglomerans was reported to cause lint rot of cotton locules
associated with SCS and injury caused by the stinkbug Euschistus impictiventris.
Distribution.
The United States (California and Georgia).
Symptoms.
Cotton bolls contain internal lint rot within single or multiple locules. Internal lint damage occurs in the tips of bolls that have formed abnormal fissures or openings
nearest the sutures. Such bolls often contain an additional locule. Rotten lint within the locules, which is usually discolored a reddish brown, is mixed with diseased
yellow lint and olive to olivebrown lint.
Management.
Not reported.
Pseudomonas Leaf Spot
Cause.
Pseudomonas syringae. Disease is favored by wet weather.
Distribution.
The United States (Texas).

Page 186
Symptoms.
Symptoms occur on cotton seedlings. Circular spots (24 mm in diameter) consist of tan necrotic centers surrounded by dark brown to purple borders. Large,
irregularshaped, necrotic areas appear on severely diseased leaves. Symptoms are reported to be similar to those of Ascochyta blight.
Management.
Not reported.
Aerolate Mildew
Aerolate mildew is also called dahiya disease, false mildew, frosty mildew, gray mildew, moho blanco, and white mold.
Cause.
Mycosphaerella areola, anamorph Ramularia gossypii (syn. Cercosporella gossypii and R. areola). Mycosphaerella areola survives as mycelia, conidia, or
perithecia in infested residue. Maximum infection occurs at temperatures of 20° to 30°C, together with nightly wetting and daily drying of leaf tissues. Conidia are
produced in lesions and are disseminated through the air to provide secondary inoculum. Disease is most severe under wet, humid conditions.
Distribution.
Generally distributed, but gray mildew is most common in Africa and Asia.
Symptoms.
Symptoms normally appear toward the end of the growing season. Cotyledons initially have circular, watersoaked, dark green spots, which eventually become
chlorotic, wither, and turn reddish brown.
Typical symptoms on the upper leaf surfaces are small, light green to yellowish angular spots that are limited by the veins. During high humidity, the undersides of
diseased leaves are covered with a white growth consisting of mycelia, conidia, and conidiophores of M. areola. Severely diseased leaves become chlorotic, dry,
curly, and reddish brown, and defoliate prematurely. Bolls may open prematurely, resulting in loss of fiber quality.
Resistant cultivars have tiny, reddishbrown spots that are surrounded by a chlorotic area.
Management
Cause.
Alternaria gossypina survives as mycelium in infested residue. Conidia are produced from mycelium during moist conditions and are disseminated by wind to leaves.
Conidia produced in lesions on diseased leaves

Page 187
and disseminated to other host plants during the growing season are secondary inoculum. Alternaria gossypina may infect cotton after other pathogens have caused
disease, or plants are predisposed to infection by weak pathogens, such as A. gossypina, while under stress from low fertility or unfavorable environmental conditions.
Distribution.
Wherever cotton is grown under warm, moist conditions.
Symptoms.
Symptoms occur on young plant parts (such as cotyledons, seedlings, petioles, and stems) and on mature leaves. Spots are brown, have a "papery" consistency, and
are roughly circular (average diameter of 13 mm) with concentric rings that give them a targetlike appearance. During moist weather, spots become black because of
the production of fungal conidia. Severely diseased leaves shrivel and defoliate prematurely, especially during periods of moist weather later in the growing season.
Management
2. Maintain proper soil fertility.
3. Avoid insect and mechanical injury.
5. Grow latematuring cultivars. Earlymaturing cultivars that fruit heavily are more susceptible to Alternaria leaf spot than cultivars that mature later in the growing
season.
Alternaria Stem Blight and Leaf Spot
Alternaria stem blight and leaf spot is also called Alternaria leaf spot.
Cause.
Alternaria alternata and A. macrospora. Alternaria macrospora survives as mycelium in alternative hosts, seed, and infested leaf residue. Primary inoculum
consists of conidia produced from the overwintered mycelium and disseminated by wind to host plants.
Generally, cotton is relatively resistant to infection at the beginning of the growing season. At this stage of plant growth, the cotyledons are infected because they are
more susceptible than true leaves. Once flowering begins, host plants become progressively more susceptible to infection as the canopy closes over to create a
microclimate more favorable for disease development. Disease caused by A. alternata also increases with nutrient deficiency, presence of other diseases, moisture
stress, and leaf senescence. However, in Israel, A. alternata occurred on young leaves of the cultivar 'Acala' grown in wellfertilized fields in which trickle irrigation
was used to prevent moisture stress.
Exposure of both naturally infected and inoculated cotton (Gossypium hirsutum cv. Acala) to sunlight greatly increases expression of A. alternata symptoms.
Exposure for 8 hours was sufficient to produce this effect in plants of different ages and under a range of temperatures and wetness, in

Page 188
cluding marginal but recurrent dew periods interrupted by dryness.
Higher temperatures later in the growing season favor disease development. However, lesion formation may be influenced by extreme temperatures. In Arizona, a
40% to 100% reduction in the number of lesions occurred on plants grown at elevated temperatures compared to plants grown at 30°C.
Distribution.
Africa, China, South America, and the southeastern United States.
Symptoms.
Initially, tiny, dark brown, circular spots with deeply sunken centers appear on stems and leaf petioles of mature cotton. Spots develop into elliptical to ovalshaped
cankers that cause stems and petioles to split longitudinally or to crack into small pieces. Eventually, the diseased stem or petiole breaks off at the canker. Leaves are
frequently shed prematurely, resulting in yield losses of 20% to 40%.
Alternaria macrospora also infects bolls, bracts, and leaves of all but very young cotton plants under stress. At first, lesions on leaves are small, brown, and have
reddishpurple borders. Eventually, lesions enlarge to approximately 1 cm in diameter and coalesce, resulting in irregularshaped dead areas and premature defoliation.
Mature spots have dead, gray centers in which cracks develop, causing the center to fall out.
Management
1. Grow resistant cultivars. Pima cotton (G. barbadense) is highly susceptible to A. macrospora, but G. hirsutum is considered highly resistant. However, G.
hirsutum cv. Acala is susceptible to A. alternata.
2. Maintain cotton in a vigorous and wellfertilized condition.
3. In experimental plots, application of fungicides and removal of flowers reduced the effect of both pathogens. In Israel, the recommended spray program was to
initiate fungicide application at flowering rather than when an average of one lesion per 10m row of plants was detected on true leaves.
Anthracnose
Cause.
Glomerella gossypii, anamorph Colletotrichum gossypii, is seedborne as mycelium in or on seed and as conidia contaminating the outside of seeds. Glomerella
gossypii also survives as acervuli and perithecia in residue.
Colletotrichum capsici is also reported to be a pathogen of seedlings and bolls. Colletotrichum capsici reportedly survives on several weeds that serve as sources
of primary inoculum. These weed species include cocklebur, Xanthium strumarium; johnsongrass, Sorghum halepense; smooth pigweed, Amaranthus hybridus;
pitted morning glory, Ipomoea lacunosa; prickly sida, Sida spinosa; sicklepod, Cassia obtusifolia; smallflower morning glory, Jacquemontia tamnifolia; and
spotted spurge, Euphorbia maculata.

Page 189
Primary inoculum for G. gossypii and C. gossypii may originate from three different sources. The first source is from infected seed that gives rise to diseased
cotyledons on which conidia are produced and are disseminated by wind to host plants. The second primary inoculum originates from infested residue on which
perithecia produce ascospores that are disseminated by wind to host plants. A third source is from acervuli and mycelia that produce conidia, which are disseminated
by splashing rain and by wind.
Disease is favored by moist or humid conditions. Seedling blight is most severe at temperatures of 20° to 26°C.
Distribution.
Anthracnose occurs wherever cotton is grown; however, it is most prevalent under humid conditions.
Symptoms.
Symptoms occur on all aboveground plant parts. Seedling cotyledons have small, reddish to light brown spots or a brown necrosis of the margin. Oblong, dark brown
lesions, which occur on young hypocotyls and stems, become discolored pink in humid or wet weather because of the sporulation of conidia. Severe disease results in
stem girdling, yellowing of leaves, and lack of plant thriftiness. The greatest injury to diseased plants occurs on stems at the soil surface. Following inoculation, isolates
of C. capsici from weeds caused reddishbrown to black lesions on cotyledons, leaves, and stems of cotton seedlings.
Stems and, less frequently, leaves of mature or older plants become infected. Small, brown spots associated with injuries or angular leaf spots occur.
Diseased bolls initially have sunken, small, reddish or redbrown spots that become black to dark brown and have a reddish margin. During damp weather, the
centers of spots become pink due to formation of slimy masses of conidia. Infection through a dead pistil results in internal rot of the boll.
Acervuli, which look like "pin cushions" under magnification, develop on necrotic lesions. Perithecia may also develop in dead tissue, but they are difficult to observe,
even with magnification, as they appear only as tiny, dark bumps. These are the "beaks" of the perithecia that protrude above the plant epidermis; most of the
perithecial structure is submerged in the plant tissue.
Symptoms caused by C. capsici on inoculated seedlings first appear 6 days after inoculation as pinpoint, reddishbrown lesions that are generally distributed over both
surfaces of the cotyledons. Cotyledonary veins on the underside of cotyledons are conspicuously discolored. Two weeks after inoculation, cotyledonary symptoms
had progressed to sunken, localized necrotic lesions 1 to several millimeters in size, but there was no associated chlorosis. A general chlorosis of cotyledons eventually
occurs and is accompanied or followed by loss of turgidity. Seventeen days after inoc

Page 190
ulation, dark brown to black linear lesions up to several millimeters in length appear on cotyledonary petioles. Severely diseased cotyledons dehisce.
Management
2. Grow recommended cultivars.
3. Rotate cotton with other crops.
5. Control insects.
6. Fertilize properly.
7. Practice timely defoliation.
8. Skiprow planting provides an open stand and prevents buildup of high humidity around lower bolls.
Ascochyta Blight
Ascochyta blight is also called wet weather blight, and ashen spot.
Cause.
Ascochyta gossypii overwinters as pycnidia and mycelia in infested soil residue and as spores and mycelia on seed. Primary inoculum occurs during wet weather in
the spring as pycnidiospores are produced in the pycnidia and are disseminated by splashing rain or by wind to host plants. Spores from seedborne inoculum also
serve as an important source of primary inoculum. Ascochyta gossypii is most likely to infect young plants that are deficient in minerals and that are damaged by
insects and hail or have other wounds. Pycnidia are formed in mature lesions, and pycnidiospores serve as secondary inoculum. Disease is most severe under cool,
humid or moist conditions.
Distribution.
Higher elevations in Mexico, South America, Africa, and Asia. In the United States, Ascochyta blight is most important along the northern fringe of the eastern and
central cottongrowing areas.
Symptoms.
Either preemergence or postemergence seedling blight occurs. Later in the growing season, symptoms occur on bolls, leaves, stems, and branches of diseased plants.
Initially, round, brown spots approximately 2 mm in diameter occur on leaves. The spots rapidly enlarge during humid weather, become gray or light brown, and
sometimes have reddishbrown borders. As spots enlarge and age, their centers fall out and give diseased leaves a ragged appearance. During wet, cool weather,
spots coalesce and cause defoliation and blighting of younger plants.
At the bases of leaf petioles, stems and branches have dark brown, elongated lesions that enlarge rapidly and become sunken and light brown in the center. Lesion
centers decay early and tend to shred, break up, and fall out of the diseased tissue. Lesions eventually encircle stems, killing plants above the infections. Disease
symptoms on bolls are similar to those on stems and branches.

Page 191
Management
2. Rotate cotton with resistant crops. Ascochyta blight is more severe when cotton follows cotton.
4. Balance soil fertility.
Ashbya Fiber Stain
Cause.
Ashbya gossypii survives as mycelium in residue and enters the boll through feeding wounds of the cotton stainer bug. Asci are formed within mycelial strands.
Distribution.
Not reported.
Symptoms.
No external symptoms are visible on the boll. Fibers and seed have a tan to brown discoloration and eventually dry out.
Management.
Not reported.
Aspergillus Boll Rot
Cause.
Aspergillus flavus survives in soil and residue as spores and mycelia. Aspergillus flavus enters bolls through natural openings or wounds made by the pink bollworm
(Pectinophora gossypiella) and other insects. Infection is favored by high humidity and temperatures of 32°C and above. Aspergillus flavus moves from infected
locks to adjacent unwounded locks and contaminates seed produced there with low levels of aflatoxin. Certain pectolytic enzymes produced during host infection
contribute to fungal aggressiveness as it grows in locular tissues, through the lint, and into the cottonseed, where the aflatoxin is produced.
Drying is an important factor in fungal entry into seeds. The nucellus membrane surrounding the embryo forms a possible physical barrier to fungal entry. Upon drying,
the integrity of the nucellus membrane is affected, allowing the fungus to break through the membrane, enter the embryo, and form toxin. Diseased seed levels are also
affected by water potentials on the day of anthesis and infection, with the highest disease levels generally occurring in seed from plants with water potentials of1.6 to
1.9 bars. Aflatoxin is highest in seed from wounded locks and in seed harvested near the end, rather than at the beginning, of the harvest season.
Infection by A. flavus and subsequent aflatoxin production occurs primarily in green bolls close to maturity and has been reported to be most severe when carpels are
infected and separated by A. niger and Rhizopus sp. However, A. flavus grows into unwounded locks of young bolls more extensively than in older bolls. Maturation
of the intercarpellary membrane may hinder the interlock spread of A. flavus.

Page 192
Distribution.
Wherever cotton is grown.
Symptoms.
Lint is stained yellow and otherwise is discolored. Lint fluoresces greenish yellow under ultraviolet light. In the United States (Arizona and California), relatively little
aflatoxin is formed in bolls produced near the end of the season, and most toxin occurs in bolls borne near the soil.
Management.
Control insects such as pink bollworm on cotton.
Black Boll Rot
Cause.
Aspergillus niger survives saprophytically on several kinds of infested plant residue. Conidia are produced from mycelia and are disseminated by wind to host plants,
where they germinate and enter bolls through wounds. Black boll rot is more severe in rank cotton growth and during frequent rains that occur at boll development and
opening. In irrigated areas, boll rot is most severe when excessive moisture has occurred late in the growing season.
Distribution.
Symptoms.
Initially, a soft pinkish rot develops on the side or base of a boll. Eventually, the color of the rot changes from pink to brown and an abundant production of black
spores in the diseased area gives the boll a black sooty appearance.
Management
1. Avoid practices that promote rank growth, especially excessive nitrogen.
2. Use correct timing and control of irrigation.
3. Control insects after boll development.
4. Shield equipment to reduce mechanical injuries.
5. Use bottom defoliation and twostage harvesting to reduce exposure.
6. Keep cotton free of weeds.
7. Use skiprow plantings.
9. Plow under residues to prevent rotting bolls from being a source of inoculum.
Black Root Rot
Black root rot is also called internal collar rot.
Cause.
Thielaviopsis basicola, synamorph Chalara elegans, is a common soil inhabitant in both cultivated and noncultivated soils. However, Hood and Shew (1997) report
that T. basicola does not display significant saprophytic ability and should be classified ecologically as an obligate parasite. Thielaviopsis basicola does survive as
chlamydospores on and in roots; in

Page 193
ternally in the pith, phloem, and xylem; and in soil. Endoconidia are also produced, but their relevance to the survival of T. basicola is unknown.
Chlamydospores germinate to produce mycelia that infect roots through root hairs, then grow to the endodermis. Wet, alkaline soils at temperatures below 26°C
increase disease severity. Some reports state that soil temperatures of 15° to 20°C favor disease. These relatively low soil temperatures may stress plants and favor T.
basicola, although the optimum temperatures for pathogen growth in culture are 25° to 28°C. Internal colonization of root tissues is favored by high inoculum levels
and soil temperatures of 18° to 20°C. Seedling blight also occurs in cool, wet weather.
Thrips are reported to predispose seedlings to infection.
Distribution.
Egypt, Peru, Russia, and the United States.
Symptoms.
Seedlings are stunted and have small, cupped, chlorotic leaves that have purplish borders with brown margins. Leaves are shed from severely diseased plants.
Roots are brown and decayed and have taproots that are smaller in diameter than those of healthy plants, which allows diseased plants to be easily pulled from the
soil. There is a sharp line between diseased and healthy tissue. Cortical tissue at the stem base may appear healthy, but vascular tissue becomes black or purple. The
stem base and taproot are swollen; a black crust on the roots consists of chlamydospores. Within a few weeks, diseased tissue is sloughed off and no symptoms
remain.
An internal collar rot phase occurs on Gossypium barbadense from midseason to late season. Leaves and stems wilt and suddenly collapse. Reddish lenticels,
swelling, and brown to purpleblack discoloration of the stele occur in the crown.
Management
1. Sow into warm soils.
2. Rotate cotton with monocotyledons.
Botryodiplodia Seedling Blight and Boll Rot
Cause.
Botryodiplodia theobromae (syn. Lasiodiplodia theobromae) is seedborne and is considered a weak pathogen.
Distribution.
Brazil.
Symptoms.
Seedlings are killed, and diseased bolls rot.
Management.
Not reported.
Cause.
Cercospora gossypina, teleomorph Mycosphaerella gossypina, survives as conidia and mycelia on seed and in infested residue. Mycosphaerella gossypina may
survive as perithecia in infested residue. Primary infection occurs

Page 194
by conidia or by ascospores disseminated by wind to host plants. Secondary inoculum is provided by conidia produced in spots on diseased leaves. Because C.
gossypina is not a highly virulent pathogen, infection by C. gossypina may follow infections caused by other pathogens or may occur in cotton plants that are
predisposed to disease by being under various stresses. Examples of stresses are cotton growing on sandy soils, lack of soil moisture at the time of maximum boll set,
and lack of proper rates of nitrogen and potash throughout the growing season.
Distribution.
Worldwide in warm and humid cottongrowing areas.
Symptoms.
Symptoms are observed first on older upper leaves and eventually on younger leaves. Initially, leaf spots are barely visible reddish points, but eventually spots enlarge
to approximately 2 cm in diameter, are round to irregularshaped, and have white centers surrounded by a purple margin. Conidia growing on diseased areas give
both the diseased lower and upper leaf surfaces a dark appearance. The centers of lesions may drop out as they enlarge and give a ''shothole" effect to the lesion.
Diseased leaves turn brown and dry up, resulting in partial or complete defoliation. Young squares and bolls may fall from plants. The main terminal and upper fruiting
branches may die back under severe disease conditions. Other branches may be unaffected.
Management
2. Maintain proper soil fertility.
3. Avoid insect and mechanical injury.
5. Grow latermaturing cultivars rather than the more susceptible earlymaturing cultivars that fruit heavily.
CercosporaAlternaria Leaf Blight Complex
This disease has been called black rust, and the cotton leaf blight disease complex.
Cause.
Cercospora gossypina and Alternaria alternata (syn. A. tenuis). The disease complex occurs on plants under stress from moisture and mineral deficiencies or
following leaf infections caused by Xanthomonas campestris pv. malvacearum (syn. X. malvacearum).
Distribution.
The United States (Arizona, Arkansas, the upper San Joaquin Valley of California, Louisiana, Oklahoma, southern New Mexico, and southwestern Texas).
Symptoms.
The disease complex appears at "cutout," or approximately the time plants become dormant and cease setting bolls. Early symptoms

Page 195
somewhat resemble the beginning stages of potash deficiency or rust disease. Each pathogen causes circular, sometimes zonate, leaf spots late in the season.
Cercospora lesions are scattered over the entire leaf surface, while Alternaria lesions occur on leaf margins. A bluish color occurs where the different lesions overlap.
All lesions enlarge rapidly and coalesce; diseased leaves become necrotic and dry from the margins inward. Normally, the younger leaves, squares, and bolls die
prematurely and drop, but when they are killed rapidly, dropping does not occur. As symptoms of the disease complex become more severe, all leaves may desiccate
and defoliate prematurely.
Dieback of the main stem terminal and uppermost fruiting branches frequently occurs. Cutout of the upper third to half of the plant is initiated prematurely, and the
more mature bolls in this upper third of the plant open prematurely. Many plants have one or two unaffected lower vegetative branches whose leaves fail to defoliate
or defoliate poorly when treated with defoliants.
Management.
No disease management strategy is currently successful.
Charcoal Rot
Charcoal rot is also called ashy stem.
Cause.
Macrophomina phaseolina (syn. M. phaseoli, Macrophoma phaseolina, Macrophoma phaseoli, Rhizoctonia bataticola, and Sclerotium bataticola).
Macrophomina phaseolina survives as sclerotia in soil and infested residue and as saprophytic mycelia in soil residue. A pycnidial stage is formed; however, pycnidia
are rarely formed in the diseased stem. Sclerotia, which likely constitute the source of primary inoculum, germinate on root surfaces to produce one or multiple germ
tubes that directly penetrate roots. Wounds are not necessary for infection to occur. Infection occurs from the seedling to blossom stage.
Disease is most severe during high temperatures (35° to 39°C) and periods of moisture stress. It is generally thought that moisture is necessary for infection to occur
but that later moisture stress disposes the plant to disease development.
Distribution.
Throughout the world under hot, dry conditions.
Symptoms.
Diseased plants wilt and die rapidly. Leaves wilt, droop, become chlorotic, and are prematurely shed. Grayishwhite lesions develop on stems near the soil line and
extend for several centimeters up the diseased stem. Diseased plants have a "dry" rot with numerous tiny, black sclerotia distributed throughout the infected stem,
scattered through the lesion, and embedded in the cortex and wood that give tissue a grayish appearance, similar to charcoal.

Page 196
Roots may be partially or totally decayed. Subsequently, diseased plants may be stunted or may die but remain standing.
Management
1. Rotate cotton with other crops, preferably small grains.
2. Do not oversow. Crowded seedlings are more subject to infection.
3. Ensure that soils are well fertilized.
5. Manage water supply for irrigated cotton to reduce water stress during periods of high temperatures.
Choanephora Mold
Cause.
Choanephora cucurbitarum survives as mycelia, chlamydospores, and possibly spores in infested residue and soil. Blossoms become infected during wet, humid
conditions.
Distribution.
The United States.
Symptoms.
The corolla becomes covered with a white, fuzzy, fungal growth consisting of young mycelia and conidiophores. Later, the fungal growth becomes sprinkled with black
specks that are the conidial heads borne on the end of conidiophores.
Management.
General controls for other boll rots are presumed to be of benefit.
Cochliobolus Leaf Spot
Cause.
Cochliobolus spicifer, anamorph Curvularia spicifer, and C. lunatus.
Distribution.
India and possibly Malawi. Cochliobolus spicifer is the more important pathogen.
Symptoms.
Seed rot and preemergence damping off occurs. Leaf spots occur on seedling leaves as light yellow areas that eventually increase in size and become dark brown.
During wet weather, discoloration spreads from the leaf to the leaf stalk. Defoliation of older plants may occur.
Management
3. Apply a foliar fungicide.
Colletotrichum Boll Rot
Cause.
Colletotrichum capsici and C. indicum. The two fungi are considered synonymous by some researchers. Boll rot is reported to occur during exceptionally wet
conditions.

Page 197
Distribution.
The United States (Louisiana).
Symptoms.
Bolls initially have circular, dark lesions that are associated with sutures. Eventually the entire boll turns black. In advanced stages, the carpel wall is destroyed, leaving
the skeletonized remains of the wall. Severely rotted bolls often open, but the discolored lint usually does not fluff, leaving a "tightlocked" boll that dislodges and falls
to the ground.
Management.
Not reported.
Corynespora Leaf Spot
Cause.
Corynespora cassiicola overwinters as mycelia and chlamydospores in residue or as chlamydospores in soil. Corynespora cassiicola can also grow saprophytically
on different kinds of infested plant residue in the soil. Conidia are splashed or blown onto leaves and cause infection when free moisture is present or when the relative
humidity is 80% and above.
Distribution.
The United States (Mississippi) and possibly other cottongrowing areas of the world.
Symptoms.
Initially, brickred, pinpoint spots develop on diseased leaves. Later, the spots enlarge to become roughly circular (26 mm in diameter) with a dark brown margin and
a light brown center that falls out. Alternating light and dark brown areas give mature spots a zonate appearance. On severely diseased leaves, spots coalesce to form
large, irregularshaped, necrotic areas that cause leaves to become chlorotic, wilt, and defoliate from the plant. Reddish spots frequently girdle petioles.
Management.
Maintain plants in a vigorous growing condition.
Cylindrocladium Black Rot
Cause.
Cylindrocladium crotalariae survives as microsclerotia on infested residue and as mycelia in residue. Microsclerotia are disseminated by several factors that
transport soil. Microsclerotia also constitute the source of primary inoculum by germinating to form mycelia that penetrate roots.
Distribution.
The southeastern United States.
Symptoms.
Cylindrocladium black rot is considered a minor problem and ordinarily no aboveground symptoms are produced. Roots of susceptible cultivars are blackened and
reduced.
Management.
Not necessary. However, cotton maintains or increases levels of inoculum in soil that may harm other crops, such as peanut.

Page 198
Diplodia Boll Rot
Cause.
Lasiodiplodia theobromae (syn. Diplodia gossypina) survives as pycnidia in infested residue. Pycnidiospores are produced in pycnidia during wet weather and are
disseminated by splashing rain and by wind to bolls, where infection occurs through weevil punctures and wounds. Lower bolls in contact with soil are frequently
infected in this manner. Injured and uninjured bolls are infected at all stages of maturity but become the most severely diseased when they are infected at ages of 7 or
fewer days and at 40 or more days. Disease development is optimal during moist conditions and a temperature of 30°C.
Distribution.
Symptoms.
Initially, small, brown, watersoaked, and sunken lesions occur on capsules or bracts. Pycnidia appear as tiny, black specks on the boll surface. Black, sooty masses
of spores released from pycnidia under high humidity conditions cover the boll surface. Lesions may enlarge and cover the entire boll. Bolls eventually blacken
completely, dry up, and split to expose the blackened and matted lint.
Management.
In general, avoid practices that prevent plants from drying out.
1. Avoid practices that promote rank growth.
Escobilla
Escobilla is also known as "little broom," ramulose, superbrotamento, supersprouting, and witches' broom.
Cause.
Colletotrichum gossypii (syn. C. gossypii var. cephalosporioides), teleomorph Glomerella gossypii. Disease is most severe during periods of prolonged rainfall.
Plants of all ages may be diseased; however, those infected while young are most severely affected.
Distribution.
Brazil and Venezuela.
Symptoms.
Infected plants have both healthy and diseased branches and a dense shrublike appearance from numerous lateral branches and "tufts" caused by terminal buds being
killed. Swollen and twisted branches with shortened internodes and swollen nodes result in an excessive number of short twigs and leaves.
Leaves on diseased branches are small, dark green, wrinkled, and have reduced lobes and short petioles. Healthyappearing leaves may occur on affected branches
but have turnedup margins and swollen petioles with internal browning. Leaves and shoots have small, brown spots that later

Page 199
elongate along the veins, turn gray, and develop cracks in their centers. Gray mycelia in which black, dotlike acervuli occur eventually appear on lesions.
Bolls on diseased plants may remain green without opening. Seeds in unopened bolls may germinate abnormally.
Management.
Not practiced.
Fusarium Boll Rot
Cause.
Fusarium moniliforme, F. oxysporum, F. roseum, and F. solani. Fusarium oxysporum and F. roseum attack uninjured green bolls by initially infecting bracts,
then invading the capsule base through the receptacle. Production of vast numbers of spores on plant debris, such as flowers, bolls, and squares, apparently provides
the airborne inoculum necessary to initiate boll deterioration. Boll age is the most important factor in limiting rot. Bolls 33 or more days old are more susceptible than
younger fruits. Boll rot proceeds rapidly during moist conditions.
Distribution.
Symptoms.
Initially, small lesions occur along the bract margin, particularly at the apices of the toothed areas. Eventually, the entire bract becomes necrotic. The capsule becomes
invaded through the receptacle; tissues show a dark bluegreen discoloration. Decay is more rapid in dehiscing bolls.
Management.
Not reported, but development of resistant cultivars may be possible.
Fusarium Damping Off
Cause.
Fusarium spp., including F. equiseti, F. graminearum, F. moniliforme, F. oxysporum, and F. solani. Most Fusarium spp. survive as saprophytic mycelia in
infested residue and as chlamydospores in the soil. Seed and roots are infected under cool, wet soil conditions. Thrips predispose seedlings to infection.
Distribution.
Symptoms.
Seed may be rotted or seedlings may die before emergence. Roots and hypocotyls are tan to dark brown and are rotted. Frequently, the taproot dies.
Management
1. Sow highquality seed treated with a seedprotectant fungicide.
2. Apply fungicide as a spray or dust in the seed furrow.
3. Delay planting until soil temperature has warmed to 20°C or more for at least three or four mornings before sowing.

Page 200
4. Sow in bedded rows or slightly raised seedbeds, where the soil temperature normally warms up faster than in a furrow or level seedbed.
Fusarium nygami Root Colonization
Cause.
Fusarium nygami.
Distribution.
Widespread.
Symptoms.
Fungus was isolated from roots, but "infected" plants were symptomless.
Management.
Not necessary.
Fusarium Seed Infection
Cause.
Fusarium equiseti and F. semitectum were isolated from embryos of weathered cottonseed. Several isolates produced equisetin, a phytotoxin.
Distribution.
Symptoms.
Equisetin inhibits germination of various monocotyledonous and dicotyledonous seed when seed is germinated at 30°C under aqueous, shake conditions. Under
certain conditions, equisetin is highly toxic to rapidly growing plant tissues; therefore, seed and seedlings infected by F. equiseti and F. semitectum may be affected.
Necrotic lesions were produced on the cotyledons and radicles of young seedlings.
Management.
Not reported.
Fusarium Wilt
Cause.
Fusarium oxysporum f. sp. vasinfectum survives as chlamydospores and sclerotia in soil and as mycelia in infested residue. Fusarium oxysporum f. sp.
vasinfectum has also been isolated from seed and gin trash, which may also serve as means of dissemination. Conidia, chlamydospores, and sclerotia germinate and
infect roots through wounds made by nematodes, including Belonolaimus spp., Conemoides spp., Helicotylenchus spp., Meloidogyne spp., Pratylenchus spp.,
Rotylenchulus spp., Trichodorous spp., Tylenchorhynchus spp. and Xiphinema spp. Without nematode wounds, Fusarium wilt would not be a serious problem.
The mycelium then grows into xylem tissue and wilting occurs when water is prevented from moving up the plant. Sporulation occurs on the outside of dead plants,
and conidia are disseminated by wind to other areas. Dissemination is also by any means, including furrow irrigation water, that moves soil. Fusarium wilt is most
serious in an acid, sandy soil.
There are several races of F. oxysporum f. sp. vasinfectum.
Distribution.

Page 201
Symptoms.
Seedlings may damp off, but Fusarium wilt is normally observed at approximately blossom time. The general appearance of a field will be spotty or uneven. Areas that
range in size from a few scattered plants to several acres will be affected; the most severe symptoms occur on the sandiest soils.
Initially, diseased plants are stunted and unthrifty. Leaves turn yellow, beginning at the leaf margins and proceeding into interveinal areas, then brown, and eventually
are shed from the bottom of the plant upward. The entire plant eventually becomes leafless, dies, and turns black due to growth of saprophytic fungi.
If a diseased plant does not die, it remains stunted and the lateral branches outgrow the main stalk, but it flowers and matures earlier than healthy plants. The interior of
the main stem has a dark brown discoloration. Symptoms of nematode injury will be present on roots.
Management
2. Rotate cotton with crops, including millet, peanut, small grains, sorghum, and sudangrass, on which the cotton root knot nematode will not reproduce.
3. Mow and bury cotton stalks after harvest to reduce nematode populations. If erosion is a problem, plant a cover crop of rye.
4. Summerfallow and control weeds to reduce hosts on which nematodes reproduce.
5. Ensure adequate levels of potash.
6. Use a soil nematicide if the cost is warranted.
7. Avoid growing upland cotton in infested sandy, acid soils.
Helminthosporium Leaf Spot
Cause.
Helminthosporium gossypii overseasons in infested leaves. Leaves, flower bracts, and bolls are infected.
Distribution.
Asia.
Symptoms.
Spots on leaves and bracts are small (18 mm in diameter) and light red. In time, the spots turn dark purple and have a brown center that frequently falls out and gives
the spot a "shothole" effect. Spots may be numerous, causing diseased leaves to die and defoliate prematurely. Spots on bolls are small and purplish but usually cause
no damage to fiber.
Management.
Not reported.
Myrothecium Leaf Spot
Cause.
Myrothecium roridum is a common soil saprophyte. Primary inoculum

Page 202
is presumed to arise from infested soil and infected weeds. Optimum spore germination occurs at a temperature of 29°C.
Distribution.
India and the United States.
Symptoms.
Preemergence and postemergence damping off may occur. Initial symptoms appear on leaves of young plants 4 to 6 weeks old. The circular, tan leaf spots have
violetbrown margins. Eventually, spots may enlarge to 3 cm in diameter and become surrounded by translucent areas that are concentrically zoned and have black,
pinheadsized dots that are the sporodochia of the fungus. Spots increase in size and number and ultimately coalesce, affecting large areas of the leaf. Eventually, the
leaves defoliate.
Dark brown to black cankers on diseased stems occur relatively close to the soil line.
Management
1. Destroy infested residue.
2. Control susceptible weeds.
3. Fungicides have been used to manage disease.
Nematospora Boll Stain
Cause.
Nematospora coryli, N. gossypii, and N. nagpuri survive in infested residue and, probably, as parasites on nearby wild plants. Infection occurs through insect
wounds.
Distribution.
Nematospora coryli is reported from the United States (California), N. gossypii from West India and Africa, and N. nagpuri from India.
Symptoms.
Initially, diseased bolls do not display external symptoms except for tiny, inconspicuous wounds or scars. In time, lint becomes discolored tan, and seed is shriveled
and killed. Leaf sheaths are discolored, and diseased bolls are shed.
Management

Page 203
Nigrospora Lint Rot
Cause.
Nigrospora oryzae is disseminated and introduced into the boll by the mite Siteroptes reniformis. A mutualistic form of symbiosis exists between the two organisms.
Distribution.
Africa, Russia, and the United States.
Symptoms.
Lint is discolored by the presence of dark brown to black conidia on the lint surface and in the lumen. Lint also fails to fluff and the fibers are weakened.
Management.
Not reported.
Phomopsis Leaf Spot
Cause.
Phomopsis sp. survives as pycnidia in infested residue.
Distribution.
Symptoms.
All aboveground plant parts become diseased, but the principal damage is to flower buds, which then are not capable of opening. Gray, watersoaked, slightly sunken
areas occur on diseased leaves and stems. Later, the diseased areas are covered with numerous pycnidia, which resemble dark specks.
Management.
Not known.
Cause.
Phyllosticta gossypina and P. malkoffi. Although Phyllosticta species have been reported from Africa as the causal organisms, some researchers question the
identification of the fungi.
Distribution.
Tanzania and Zimbabwe.
Symptom.
Spotting occurs on diseased leaves.
Management.
Not reported.
Phymatotrichum root rot is also called cotton root rot and Texas root rot.
Cause.
Phymatotrichopsis omnivora (syn. Phymatotrichum omnivorum) survives in soil as sclerotia and hyphal strands. Survival may be facilitated by mycelial strands
from other diseased dicotyledonous plants and, possibly, by monocotyledonous plants in a rotation. However, unless they are attached to sclerotia, mycelial strands
will not infect taproots of cotton.
Early in the growing season, when soil temperatures have risen, sclerotia germinate to produce hyphal strands that contact roots of seedlings

Page 204
that have been emerged for 5 or more days. Strands grow ectotrophically on the taproot to the crown before penetrating and killing the plant. Root contact is not
necessary for planttoplant spread because fungal growth occurs through soil in advance of diseased roots; however, disease is inhibited when plants are spaced 20
to 69 cm apart. Planttoplant spread of P. omnivora in rows is more important than spread across rows.
Sclerotia are abundantly produced on rotted roots. When the soil is moist, conidia are produced on mycelial mats that form on the soil surface near dead plants, but
they are not known to germinate. Clay soils with high pH are especially conducive for disease caused by P. omnivora. High soil moisture during the early summer
months is favorable for disease development, but moisture levels of12 to16 bars reduces disease. Because of the increased inoculum resulting from the saprophytic
growth of P. omnivora on sorghum roots, disease incidence increases on ratoon sorghum that has preceded cotton in a rotation.
Almost 2000 species of dicotyledonous plants may be infected by P. omnivora.
Distribution.
Mexico and the United States (Arizona and Texas).
Symptoms.
Foliar symptoms do not develop until soil temperatures at the inoculum depth are 22°C and above. Leaves are chlorotic initially, then become a bronze color and wilt.
Later leaf symptoms are associated with cortical senescence in the roots: diseased leaves become brown and dry up but remain attached to plants.
Roots become watersoaked and discolored, and the cortex is sloughed 18 to 25 days after plant emergence, or at approximately the same time as foliar symptoms
occur. When taproots are girdled, plants rapidly wilt and die. Bark and cambial tissues of diseased roots turn brown and have light tan strands of mycelium growing on
the root surface. The root bark easily peels off and reveals a reddish stain along the white woody tissue.
When soils are moist, mycelial mats form on the soil surface near dead plants. Mats are white initially but later become tan and ''powdery" due to production of conidia
on the mat surface. Death of diseased plants normally occurs 27 to 50 days after emergence, regardless of the age of the plants when they were first exposed to
sclerotia.
The following atypical symptoms have been observed during periods of low soil moisture: The aboveground symptoms were a gradual wilting, followed by leaf
chlorosis and defoliation. Mature bolls and young leaves remained attached to stems, and plants remained alive. Roots had discolored, sunken lesions 10 to 20 cm
below the soil surface.
Management.
There are no economic cultural practices that can be routinely used to manage cotton root rot; however, the following are aids to management of disease:

Page 205
1. Plow under green manure crops. Residues can also be plowed under if nitrogen is applied to promote rapid decay.
2. Rotate cotton with cereals or grasses.
3. Plow deeply during hot, dry weather, thus exposing and killing the fungus.
4. Provide adequate fertility to ensure vigorous cotton growth.
5. Sow early and control insects and diseases to promote early maturation of bolls before P. omnivora becomes fully active.
6. When sorghum precedes cotton in a rotation, do not allow sorghum to regrow (ratoon) until killed by frost.
Phytophthora Boll Rot
Cause.
Phytophthora parasitica (syn. P. nicotianae var. parasitica). Infection occurs two ways: directly by sporangia forming a germ tube, or indirectly by the formation of
zoospores within sporangia. Zoospores are then liberated and "swim" for a few minutes, become rounded, and germinate to form germ tubes that penetrate the bolls.
Disease is most severe during conditions of high humidity.
Other species of Phytophthora reported to cause a boll rot are P. cactorum, P. capsici, and P. palmivora. Under conditions of high humidity, high rainfall, and
irrigation, Phytophthora capsici is reported to cause boll rot in Arizona.
Distribution.
The United States (Arizona and Louisiana).
Symptoms.
Boils are bluish black to black, and within a few days, the entire surface of an infected boll becomes black and spongy with a soft, watery rot. Eventually, a white,
mealy fungal growth consisting of sporangia and mycelium occurs on the boll surface. Bolls, particularly those approaching maturity, rot in 2 to 3 days.
Management.
Not reported.
Phytophthora boehmeriae Boll Rot
Cause.
Phytophthora boehmeriae survives as oospores in the soil. Inoculum is splashed from soil onto boils. Maximum temperature for fungal growth is 33°C.
Distribution.
China and Greece.
Symptoms.
Boll rot is restricted to the lower onehalf to twothirds of cotton plants. Diseased bolls are severely decayed; the subtending dried carpels are dark brown to black.
White patches of fungal mycelia bearing numerous sporangia are present on the surface of diseased bolls. Oospores are present on the cotton lint and internal carpel
surface.

Page 206
Management.
Not reported.
Powdery Mildew
Powdery mildew is also called manta blanca, or white mantle, when caused by Salmonia malachrae.
Cause.
Leveillula taurica (syn. E. taurica and Oidiopsis taurica) and Salmonia malachrae (syn. Erysiphe malachrae). The anamorph of L. taurica is Oidiopsis sicula
(syn. O. taurica), but the anamorph of S. malachrae is unknown. Oidiopsis gossypii is also reported to be a causal agent.
The fungi survive by continually infecting cotton or alternate hosts throughout the year. Infection is optimum at 85% to 100% relative humidity. The optimum
temperatures for L. taurica are 25° to 30°C; however, S. malachrae requires cooler temperatures to cause disease.
Distribution.
Leveillula taurica is found in India, Peru, Russia, Sudan, the United States (California), and the West Indies. Salmonia malachrae is found in the Antilles and South
America.
Symptoms.
Initial symptoms caused by Leveillula taurica depend on the diseased cultivar. Generally, symptoms are angular or rounded, powdery, white patches (1.52.0 mm in
size) on the undersides of diseased leaves. Later, the patches coalesce to cover the entire underside of the leaf. Sometimes no external symptoms occur until leaves
become chlorotic and defoliate. Cleistothecia are not present.
Scattered, circular areas of white mycelia of S. malachrae initially appear on the upper leaf surfaces and later coalesce to cover the entire leaf area. White to tan
cleistothecia are scattered throughout the mycelium. Eventually, diseased leaves become chlorotic, curl, and may defoliate. Later in the growing season, severe disease
gives a field the appearance of being covered with snow.
Management.
Not practiced.
Pythium Damping Off
Cause.
Pythium ultimum is the most prevalent species found on cotton. Other Pythium species associated with damping off include P. aphanidermatum, P. debaryanum,
P. heterothallicum, P. irregulare, P. polytylum, P. splendens, and P. sylvaticum. Pythium spp. generally survive as oospores in soil or residue and
saprophytically as mycelia in infested residue. Oospores germinate in wet soils at temperatures of 10° to 15°C and form sporangia in which zoospores are borne.
Zoospores are then liberated from sporangia and "swim" to a plant surface, where they encyst and germinate to form germ tubes that penetrate the plant. At higher
temperatures, oospores may germinate directly to form a single germ tube instead of a sporangium.

Page 207
Thrips predispose seedlings to infection.
Distribution.
Symptoms.
Seed is rotted and soft. Initially, hypocotyls and roots become watersoaked and pale green. Lesions on hypocotyls range from small, discolored spots to large
sunken, necrotic areas. Eventually, the diseased hypocotyls and roots become gray and dry up. The hypocotyl becomes constricted above the soil line, which causes
the seedling to fall over.
Severe root rot has not been observed under field conditions, although small, light brown lesions occur on taproots and secondary roots. Root rot caused by P.
splendens results in reduction of shoot growth.
Management
1. Sow highquality seed treated with a seedprotectant fungicide.
2. Apply fungicide as a spray or dust in the seed furrow.
3. Delay sowing until soil temperature has warmed to 20°C or more for at least three or four mornings before sowing.
4. Sow in bedded rows or slightly raised seedbeds, where the soil temperature warms up faster than in a furrow or a level seedbed.
Ramulose
Ramulose is also called witches' broom.
Cause.
Colletotrichum gossypii vat. cephalosporioides.
Distribution.
Brazil.
Symptoms.
Necrotic spots occur on diseased leaves. Growth abnormalities, or the witches' brooms, occur on the stem.
Management.
Rhizoctonia Leaf Spot
Cause.
Rhizoctonia solani survives as sclerotia in soil or infested residue and as mycelia growing saprophytically on residue of many different plants. Sclerotia germinate to
produce mycelia that infect hypocotyls near the soil surface, and in very humid weather, the fungus grows up the external surface of the stem.
The teleomorph Thanatephorus cucumeris produces basidiospores on a loose hyphal network growing on the stem; however, it is not certain what function
basidiospores have in the life cycle of the fungus. Leaves may be infected either by basidiospores or other soilborne propagules.
Disease is favored, particularly in thick foliage, by high rainfall and warm temperatures.
Distribution.
El Salvador and the United States (Louisiana).

Page 208
Symptoms.
The light brown, irregularshaped leaf spots have dark purple borders. As spots enlarge, centers become chlorotic, then necrotic; cracks develop and centers of older
spots drop out, giving a "shothole" effect and a general ragged appearance to diseased leaves. During periods of high humidity, the brownish growth of the fungus
may appear on the underside of the diseased leaves.
Management.
Not practiced.
Rhizopus Boll Rot
Cause.
Rhizopus nigricans (syn. R. stolonifer) survives as mycelia and spores in infested residue and soil. Under moist and warm weather conditions, spores infect bolls.
Distribution.
Symptoms.
Diseased areas of the boll are olive green initially but become black as they dry up. Fungal growth consisting of mycelium, sporangiophores, and sporangia forms a
dark gray mold over the boll.
Management
Rust
Cause.
Puccinia schedonnardi is a heteroecious longcycled rust whose alternate host consists of several grasses, including Muhlenbergia spp. and Sporobolus spp. The
pycnial and aecial stages occur on cotton, the uredinial and telial stages on grasses.
Distribution.
Mexico and southwestern United States.
Symptoms.
The inconspicuous pycnia are yellowish orange. Aecia develop around pycnia as large, orange, raised spots on leaves, bolls, and bracts. Uredinia are light cinnamon
brown; telia are dark brown.
Management.
Not reported.

Page 209
Sclerotium Boll Rot
Cause.
Sclerotium rolfsii, teleomorph Athelia rolfsii, overwinters as sclerotia in soil and as mycelia growing saprophytically in infested plant residue. Cool soil temperatures
kill both sclerotia and mycelia. Sclerotia germinate during high soil temperatures and in dry soil to form mycelia that infect plants of all ages. Usually, plant parts in
contact with soil or near the airsoil interface become infected. Disease is most common in neutral to acid sandy soils.
Distribution.
Wherever cotton is grown under warm conditions.
Symptoms.
Initially, light brown spots appear on carpels. Spots enlarge rapidly over whole carpels, peduncles, and leaf petioles, become brown, and cause all tissues to dry up.
Eventually, white, featherlike mycelium is produced on surfaces of bolls. Later, numerous round to irregularshaped, white to light brown sclerotia are produced in the
mycelium. When a diseased boll splits, white cottony mycelial growth and sclerotia are seen in locules, lint, and seeds. Inner tissues of bolls dry up and become brown,
and lint becomes discolored and eventually disintegrates. Frequently, seeds within a diseased boll decay.
Management
2. Rotate cotton with other crops, such as small grains.
3. Plow infected cotton residue 12 cm deep.
Sclerotium Stem and Root Rot
Sclerotium stem and root rot is also called Sclerotium rot and southern blight.
Cause.
Sclerotium rolfsii, teleomorph Athelia rolfsii, overwinters as sclerotia in soil and as mycelia growing saprophytically in infested plant residue. Cool soil temperatures
kill both sclerotia and mycelia. Sclerotia germinate during high soil temperatures and in dry soil to form mycelia that infect plants of all ages. Usually, plant parts in
contact with soil or near the airsoil interface become infected. Disease is most common in neutral to acid sandy soils.
Distribution.
Symptoms.
Initially, leaves wilt over time until plants become defoliated and blossoms or bolls drop. Eventually, diseased plants die. Plant wilting is caused by a canker that
develops on a stem at or just below the soil surface. The stem base and taproot may enlarge or swell. If soil moisture is present, a white, cottony growth composed of
mycelia grows up the stem for 3 or more centimeters. Dark brown to black sclerotia will eventually develop in and on the mycelium. Dense white mycelium, in which
successive con

Page 210
centric rings of sclerotia are formed, will grow out from the stem over moist soil for a distance up to 10 cm.
Management
2. Rotate cotton with other crops, such as small grains.
3. Plow infected cotton residue 12 cm deep.
Soreshin
Soreshin is also called damping off, postemergence damping off, and Rhizoctonia seedling blight.
Cause.
Rhizoctonia solani survives as sclerotia in soil or residue and as mycelia growing saprophytically on infested residue of many different plant species. Sclerotia
germinate to produce mycelia that infect hypocotyls near the soil line, and in very humid weather, the fungus grows up the external surface of the stem.
The teleomorph Thanatephorus cucumeris produces basidiospores on a loose hyphal network growing on the stem; however, it is not certain what function
basidiospores have in the life cycle of the fungus. Leaves may be infected either by basidiospores or other soilborne propagules.
Disease is favored, particularly in thick foliage, by high rainfall and warm temperatures.
Distribution.
Symptoms.
During cool, wet weather, seedlings may damp off either preemergence or postemergence. Hypocotyls are infected near the soil line and become necrotic, which
causes cotyledons to droop, then wilt. During warm, dry soil conditions, hypocotyl lesions become reddishbrown, sunken cankers that are superficial and grow
slightly into cortical tissue, or that may completely girdle stems near the soil line. If soil remains warm and dry, plants partially recover by producing new roots above
the diseased areas of the stem or hypocotyl. Infrequently, angular, brown leaf spots, whose centers may fall out and give leaves a shothole appearance, will occur
during moist weather. See Rhizoctonia leaf spot.
Management
1. Sow after soils have "warmed up." Temperatures warm up faster on a bed than in a furrow or on level soil.
2. Rotate cotton with other crops; however, R. solani has a wide host and exists saprophytically for several years in the absence of a host crop.
3. Adjust soil pH to 6.06.5.
4. Ensure that soil fertility is adequate.
5. Avoid chemical injury.
6. Sow only healthy, highquality seed treated with a seedprotectant fungicide.
7. Treat soil with an infurrow granule or spray fungicide.

Page 211
Southwestern Cotton Rust
Southwestern cotton rust is also called cotton rust.
Cause.
Puccinia cacabata (syn. P. stakmanii) is a heteroecious longcycle rust that has grama grass, Bouteloua spp., as the alternate host. Rust overwinters as teliospores
that form on grama grass in late summer. During wet summer weather and night temperatures below 28.5°C, teliospores germinate to produce basidiospores, which
are disseminated by wind to cotton. Pycnia are formed on the upper surface of diseased cotton leaves, and aecia are produced on the underside of cotton leaves,
bracts, green bolls, and stems. Aeciospores are released from aecia and are disseminated by wind to the alternate host, grama grass, which becomes infected during
wet conditions. Uredinia, in which urediniospores are produced, are formed on grama grass and are disseminated by wind to continually reinfect grama grass
throughout the growing season. Telia, in which teliospores are produced, appear on grama grass in late summer as the grass matures. High humidity and abundant
rainfall favor disease.
Distribution.
Mexico and the southeastern United States.
Symptoms.
Uredinia on grama grass leaves are small, pale brown, raised areas with the leaf epidermis turned back around the pustule in a ragged edge. Telia are formed either in
the uredinium or separately as dark brown to black raised pustules. Pycnia initially appear as small, inconspicuous yellowish spots, usually on the upper side of leaves;
however, they may occur on any aboveground plant part. Pycnia develop into bright yellow pustules that later turn brown. Aecia are large, slightly raised, circular,
orangeyellow lesions on the underside of cotton leaves that later fade to light yellow. In severe rust infestations, leaves curl and plants are defoliated. Stems and
branches become girdled and break, and bolls are smaller in size.
Management
2. Apply a foliar fungicide spray before rust becomes severe.
3. Destroy grama grass in the vicinity of cotton fields; however, this is of limited value since spores may be airborne a considerable distance.
Stemphylium Leaf Spot
Cause
Stemphylium sp.
Distribution.
Not know for certain but thought to be widespread.
Symptoms.
Small, roughly circular spots have concentric rings that give a targetlike appearance to the spot. Spots tend to be discrete and usually do not spread or coalesce. The
disease is of minor importance.
Management.
Not necessary.

Page 212
Tropical Cotton Rust
Cause.
Phakopsora gossypii (syn. Aecidium desmium, Cerotelium desmium, Doassansia gossypii, Kuehneola gossypii, and P. desmium). Only the uredinial stage is
known. Dissemination is by airborne urediniospores. High relative humidity favors disease.
Distribution.
India, South America, the South Pacific, the southeastern United States, and the West Indies.
Symptoms.
Leaves are primarily affected, but other aboveground plant parts may also become diseased. Initially, the upper leaf surface is marked by small, brown spots, which
are uredinia immersed in host tissue. Yellowbrown, circular (0.53.0 mm in diameter) uredinia occur in purple lesions (15 mm in diameter) on both leaf surfaces.
Lesions later become powdery. The spots coalesce into large patches and cause defoliation. Uredinia are elongated on pedicels and branches. Telia normally are not
present, but if present, they are found on lower leaf surfaces.
Management
2. Do not sow seed from diseased plants.
3. Remove infected residue.
Verticillium Wilt
Cause.
Verticillium dahliae; however, many researchers refer to the causal organism as V. alboatrum. The causal fungus will be referred to as V. dahliae in this description
because of the speciation criteria stated by Isaac (1967). Verticillium dahliae forms microsclerotia, whereas V. alboatrum forms oneand twocelled conidia and
sporophores with black bases. Verticillium tricorpus is also reported to colonize cotton.
Several strains of V. dahliae exist. Pathotypes of V. dahliae infecting cotton are differentiated mainly by whether or not they defoliate the diseased cotton plant. The
two strains most commonly found in the United States are the P1 and P2 strains, formerly designated as T1 and SS4, respectively. The P1 strain is considered
the defoliating strain, while the P2 strain is the nondefoliating strain.
Verticillium dahliae survives as microsclerotia, or dark resting hyphae, in soil or in infested residue. Dissemination is by seed lots contaminated with microsclerotia,
and by wind, surface water, and equipment that carry microsclerotia, hyphae, or conidia to host plants. Verticillium dahliae has a large host range; therefore,
inoculum may also originate from indigenous inoculum present on weeds in an area.
Infectious propagules are thought to originate from several sources. Microsclerotia may produce multiple germ tubes and conidia. Conidia and hyphae are also found
either free in the soil or in residue. Although both conidia and hyphae form hyphal germ tubes, those from hyphae infect

Page 213
roots and grow into the vascular system, while it is not known for certain what the role of conidia are in infection. Infectious propagules, primarily in the form of
microsclerotia, are stimulated to germinate by root exudates and establish colonies on the cotton root surfaces, usually 3 to 10 mm back from the root tip. Infectious
hyphae from the root colonies grow through the root cortex into the xylem tissue. In the xylem, mycelium colonize vessels and produce conidia that move upward in
the tissue. Eventually, hyphae penetrate from xylem cells into surrounding parenchyma cells and eventually throughout the necrotic tissue of dead leaves, stems, and
roots, where new microsclerotia are formed after several weeks or months. When tissue decays, the microsclerotia are released into the soil.
Seasonal changes in soil moisture and temperature are reported to have no influence on the colonization of roots by V. dahliae. However, colonization of roots by V.
tricorpus is affected by soil temperature: Colonization is greater at 20° to 23°C than at 28° to 31°C After infection, disease development is most severe during cool,
wet weather and ceases to occur during warm, dry weather. Foliar symptoms caused by strain P2 of Verticillium wilt decline at air temperatures of 25°C and above,
but vascular wilt symptoms continue to progress. Foliar symptoms caused by strain P1 occur at temperatures of 26°C and above.
Disease is also favored by alkaline soils. Verticillium dahliae grows, sporulates, and forms microsclerotia under relatively dry conditions. The only significant
saprophytic growth in soil occurs at the end of the growing season when infested dead plants are returned to soil. As a pioneer colonist, V. dahliae grows throughout
infested debris and forms numerous microsclerotia.
Distribution.
In most cottongrowing areas of the world except Egypt.
Symptoms.
The major effect of Verticillium wilt is a reduction of growth and development of plants that results in reduced height, lateral branching, and dry matter accumulation in
leaves, stems, roots, squares, and bolls. Cotton is susceptible at all stages of growth, but symptoms appear at a blossom time that follows rainy weather and vary
according to the fungus strain and soil temperature.
Cotyledons of young plants infected with strain P2 become chlorotic and dry up. Chlorotic areas that eventually become necrotic appear on leaf margins and between
veins of lower leaves. Chlorosis and necrosis of leaves, which proceed upward on the plant, result in defoliation of diseased plants.
Normally, the number of plants with foliar symptoms is fewer than the number of plants with vascular discoloration. Vascular discoloration by P2 is limited to the
lower half of diseased plants. If infection occurs later in the season, plants may only be stunted and have dark green leaves. Epinasty also may occur, but this is usually
a very mild symptom.
In susceptible plants infected by the P1 strain, symptoms in both

Page 214
young and old plants progress rapidly. Initially, the terminal leaf curls downward, followed by severe epinasty and general chlorosis of upper leaves, which soon
defoliate. Terminal dieback normally occurs. At temperatures of 26°C and above, leaf symptoms similar to those caused by P2 occur except that they are more
severe and progress to the top of the plant. Fruiting branches and bolls may be dropped. A high percentage of bolls on the top of diseased plants do not mature, and
dry up. If plants are not killed, branches may grow on lower plant portions and form bushy plants. Vascular discoloration may occur the length of the stem to the plant
top.
Another foliar symptom mimics potassium deficiency symptoms; it initially appears in younger leaves as a ''bronzing" at the leaf margins. The leaves eventually develop
a metallic sheen and become thick and brittle, which results in an extreme distortion of leaf tissues. Apparently, V. dahliae causes an impairment in the uptake and
translocation of potassium that is often associated with the development of potassium deficiency symptoms in leaves of plants with large boll loads.
Management
1. Grow tolerant cultivars. However, increases of inoculum of more aggressive strains occur when tolerant varieties are sown successive years in the same infested
soil.
2. Rotate cotton with resistant crops. Do not grow cotton in the same soil more than once every 3 years. Most shortterm rotations are of little value. Rotation with
perennial rye grass has been shown to reduce the population of propagules.
3. Avoid deep cultivation.
4. Use skiprow planting where possible.
5. Sow plant populations at higher than normal levels.
6. Do not apply gin trash to field in areas where Verticillium wilt is a problem.
7. Any cultural practice that increases soil temperature will partially aid in managing the disease.
Dagger
Cause.
Xiphinema americanum is an ectotrophic nematode.
Distribution.
Africa.
Symptoms.
Galls occur on root tips. Diseased plants are stunted.
Management.
Not reported.
Lance
Lance nematode is also called Columbia lance nematode.

Page 215
Cause.
Hoplolaimus columbus and H. galeatus. Hoplolaimus columbus feeds primarily in the cortex, but H. galeatus feeds as both an ectoparasite and an endoparasite.
Eggs are deposited in the cortex.
Distribution.
The United States. Hoplolaimus columbus is found mainly in Alabama, Georgia, and South Carolina, and H. galeatus in the southeastern Coastal Plains.
Symptoms.
Both nematodes cause plants to be stunted and chlorotic. Hoplolaimus columbus has been reported to cause defoliation during moisture stress conditions.
Management
1. Rotate cotton with nonhost plants.
3. Fumigate soil.
Lesion
Cause.
Pratylenchus spp.
Distribution.
Symptoms.
Little injury occurs, but root growth may be reduced. Diseased roots may be coarse and stubby and have some decay caused by secondary fungi.
Management.
Not necessary.
Needle
Cause.
Longidorus africans is an ectoparasite.
Distribution.
Africa.
Symptoms.
Diseased plants are stunted. Galls occur at root tips.
Management.
Not reported.
Pin
Cause.
Paratylenchus brachyurus, P. hamatus, and P. sudanensis are endoparasitic nematodes.
Distribution.
Africa and the United States.
Symptoms.
Cell breakdown and necrosis occur in diseased roots. Yields have been reported reduced; however, the nematodes are thought to be part of a disease complex rather
than a single causal agent.
Management.
Not reported.

Page 216
Reniform
Cause.
Rotylenchulus reniformis is a nematode where the female either is completely in the root or has just the posterior end protruding. Fifty to 80 eggs are laid outside
roots in a gelatinous matrix that encompasses the exposed portion of the female body. Eggs are resistant to drying and hatch under favorable conditions. Larvae molt
four times and develop into male and females; however, only females have been observed feeding. The life cycle is completed in 17 to 23 days.
Distribution.
The southeastern United States in localized areas in fields; however, reniform nematodes are a potential problem where cotton is grown in subtropical and tropical
areas.
Symptoms.
Diseased plants are severely stunted and chlorotic, and may wilt. Root growth is reduced; few large roots are produced, but numerous coarse and stubby lateral roots
are present. Decay caused by secondary fungi may occur. Weedy areas occur within a field where cotton has been affected.
Management
1. Rotate cotton with rice, sorghum, oat, mustard, turnip, corn, pepper, and grasses.
2. Fumigate soil.
Ring
Cause.
Criconemella spp. are ectoparasites.
Distribution.
Symptoms.
Symptoms on cotton are not well known. The aboveground symptom is a mild stunting. Belowground symptoms are lesions on roots and some decay caused by
secondary organisms.
Management.
Not reported.
Root Knot
Cause.
Meloidogyne incognita does not survive if the temperature averages below 3°C during the coldest month. Eggs in infested soil hatch to produce larvae that move
through soil to penetrate root tips; however, entry is not restricted only to this area of the root. Larvae migrate through the root to vascular tissues, become sedentary,
and commence feeding on undifferentiated provascular tissue. Excretions of larvae stimulate cell proliferation, which results in the development of syncythia from which
the larvae derive their food. Females lay 5001000 eggs in a gelatinous matrix that may be pushed out of roots into soil.
Distribution.
Wherever cotton is grown in sandy or sandy loam soil.

Page 217
Symptoms.
Diseased plants are less vigorous and shorter than healthy plants. Severely diseased plants are lighter green and quickly wilt when under moisture stress during the day,
but recover turgidity at night. Eventually, wilting becomes permanent.
The taproot is frequently missing or is greatly reduced in size. Lateral roots contain numerous spindleshaped galls or knots that become noticeable 3 to 4 weeks after
infection. Galls, which may be found in lesser numbers on the taproot, eventually grow up to 6 mm in diameter.
Management
1. Rotate cotton with alfalfa, oat, barley, and sorghum for 2 or more years.
2. Keep an infested field fallow for a "reasonable" time and control weeds.
3. Fumigate soil.
5. Apply nematicide.
Scutellonema spp.
Cause.
Scutellonema spp. are endoparasites.
Distribution.
Symptoms.
Symptoms are not well defined on cotton, but a yield loss has been reported with diseased plants.
Management.
Not reported.
Spiral
Cause.
Helicotylenchus spp. and Scutellonema spp. are endoparasites.
Distribution.
Symptoms.
The aboveground symptom for diseased plants is stunting. Belowground symptoms are a reduction in the number of feeder roots and some root rot caused primarily
by secondary fungi.
Management.
Not reported.
Sting
Cause.
Belonolaimus longicaudatus feeds mostly on the outside of root tips and along the sides of succulent roots without penetrating them or becoming attached to them.
Distribution.
Sandy soils in the Coastal Plains of the southeastern United States.
Symptoms.
Diseased plants are stunted and chlorotic; frequently, seedlings die. Roots are stubby and coarse and have necrotic lesions. Roots may end

Page 218
in enlargements caused by repeated forming and killing of new branches. Nematode injury may provide an entrance wound for the Fusarium wilt fungus, Fusarium
oxysporum f. sp. vasinfectum.
Management
1. Rotate cotton with tobacco, watermelons, and crotalaria.
2. Fumigate soil.
Stubby Root
Cause.
Paratrichodorus spp., P. minor (syn. Trichodorus christiei).
Distribution.
Symptoms.
Little injury generally occurs to diseased plants, but root growth is reduced. Roots may be coarse and stubby, and decay caused by secondary fungi may occur.
Management.
Not necessary.
Stunt
Cause.
Merlinius spp. and Tylenchorhynchus spp. are ectoparasites.
Distribution.
Thought to be widespread.
Symptoms.
Aboveground symptoms for diseased plants are moderate plant stunting and chlorosis. The belowground symptom is a reduction in root growth.
Management.
Not reported.
Phyllocly
Cause.
A phytoplasma disseminated by the leafhopper Orosius sp.
Distribution.
Ivory Coast, Mali, and Upper Volta.
Symptoms.
Diseased leaves are string or straplike. Diseased plants are sterile and have virescent, or green, floral parts.
Management.
Not reported.
Small Leaf
Cause.
A phytoplasma.

Page 219
Distribution.
Cuba and India.
Symptoms.
Diseased leaves are chlorotic, small, and malformed. Flowers tend to be small and may abort. Bolls are prematurely shed.
Management.
Not reported.
Abutilon Mosaic
Cause.
Abutilon mosaic virus (AbMV) is in the geminivirus III group. AbMV survives in a wide number of host plants, but Sida spp. are the most important. AbMV is
disseminated by the whitefly, Bemisia tabaci, and is grafttransmissible. AbMV is not transmitted by seed.
Distribution.
Symptoms.
Symptoms are most obvious on young diseased plants and become less pronounced on old plants. Diseased plants are dwarfed because of shortened internodes.
Leaves are crinkled, blistered, and malformed, and have a conspicuous mosaic of chlorotic and green areas. Chlorotic areas, which may be limited by veins, become
reddish and disappear in older leaves. Young leaves are smaller and wrinkled, and have fewer lobes than healthy leaves.
Management.
Abutilon mosaic is not a serious disease and management is not necessary.
Anthocyanosis
Cause.
Cotton anthocyanosis virus (CAV) survives in Gossypium barbadense, Sida spp., and ratoon cotton. CAV has been artificially inoculated into and recovered from
several other plants. CAV is disseminated by the aphid Aphis gossypii but not by seed or sap. A feeding period of 12 hours or longer is necessary for aphids to
become moderately infective. CAV is persistent within the aphid.
Distribution.
Brazil.
Symptoms.
Anthocyanosis is most severe on lower and middle leaves but may affect the upper leaves of older plants. Leaves develop chlorotic areas that turn reddish purple in
sunlight. Such purple areas are limited by veins, but the entire leaf, except for veins and a narrow band adjacent to the veins, may become purple.
Management.
Control insects on cotton throughout the growing season.

Page 220
Blue Disease
Cause.
An unknown virus that is transmitted by the aphid Aphis gossypii. Plants of various ages are affected.
Distribution.
Africa.
Symptoms.
Diseased plants are dwarfed, and stems have a "zigzag" pattern of growth. Apical leaves initially bulge between main veins and toward the base. Eventually, the entire
leaf is involved. Affected areas are light green but later turn a bluegreen.
Management
1. Grow resistant varieties.
2. Practice sanitation and destroy residue.
Cotton Leaf Crumple
Cause.
The cotton leaf crumple virus (CLCV) is in the geminivirus group. CLCV is transmitted by the white fly Bemisia tabaci at an optimum temperature of 32°C under
experimental conditions, and by grafting techniques. In Arizona, the causal organism overwinters in cheeseweed, Malva parviflora, and in cultivated beans,
Phaseolus vulgaris. Numerous plant species in the Malvaceae and Leguminosae are also hosts. Perennial cotton serves as an inoculum reservoir. Plants are infected
at all stages of development.
Distribution.
India, northern Mexico, and the southwestern United States.
Symptoms.
Symptoms are most severe in perennial cotton. Leaves curl downward due to hypertrophy of interveinal tissue. There is frequent vein distortion and clearing and a
mosaic appearance to leaves. Reddish spots sometimes occur in chlorotic, interveinal tissue of senescent leaves. Floral parts tend to be irregularshaped. Stunting
commonly occurs in perennial cotton. Although plants of all ages may become diseased, yield losses are most severe when plants are infected early in the growing
season.
Management.
Tolerance and resistance occurs in some cultivars; however, the following have been suggested as management measures:
2. Control weed hosts.
3. Eliminate diseased perennial cotton.
4. Sow clean seed.
Cotton Small Leaf
Cotton small leaf is also called cotton stenosis, and smalling. Cotton small leaf may be the same disease as small leaf, which is caused by a phytoplasma. However, the
descriptions of the symptoms in the literature are sufficiently different to discuss them here as two separate diseases.

Page 221
Cause.
Cotton small leaf virus (CSLV); however, CSLV may be a phytoplasma. It is not known how CSLV survives and is disseminated.
Distribution.
India and Pakistan.
Symptoms.
The aerial portions of diseased cotton plants are stunted. Leaves, which develop in clusters, are malformed, variously lobed, and of different sizes and shapes. Leaves
and epicalyx are mottled, and enations are produced on the lower surfaces of veins. Flowers remain small, and bolls do not form.
The taproot ends abruptly and gives rise to a large number of adventitious roots. Diseased plants can be easily pulled out of the ground.
Management.
Not reported.
Cotton Terminal Stunt
Cause.
Cotton terminal stunt virus (CTSV). It is not known how CTSV survives. CTSV is grafttransmissible, and insects are suspected of being vectors.
Distribution.
Mexico and the adjacent areas in the southern United States (Texas).
Symptoms.
Terminal growth of stems and branches is stunted. Young leaves are small, misshapen, and mottled and cup either upward or downward. Tan to brown streaks occur
in the xylem of the main stem. Immature bolls have a dark internal discoloration. Bolls, blooms, and squares are shed.
Management.
Not reported.
Leaf Curl
Leaf curl is also called cotton leaf curl and cotton leaf crinkle.
Cause.
Cotton leaf curl virus (CLCuV) is in the geminivirus group. CLCuV survives in several different hosts and is transmitted to cotton at all stages of growth by the
whitefly, Bemisia tabaci. CLCuV is not transmitted by sap, seed, or soil but has been transmitted by grafting. Different strains of CLCuV exist.
Distribution.
Africa and Pakistan.
Symptoms.
Only immature leaves develop disease symptoms. The lower surface of smaller veins has an intermittent thickening that eventually becomes continuous. When
backlighted, veins of a diseased leaf are darker green than the rest of the leaf.
Leaves formed after infection are shortened, small, and crinkled and curl either upward or downward at the edges. Enations are often formed on the thickened lower
sides of primary veins. Internodes are lengthened,

Page 222
twisted, and flattened. All parts of a diseased plant are brittle. Yield may be greatly reduced.
Management
2. Control whiteflies in the greenhouse.
Leaf Mottle
Cause.
Leaf mottle virus (LMV). It is not known how LMV survives and is disseminated.
Distribution.
Sudan.
Symptoms.
Younger diseased leaves have a pronounced mottling near the veins. Leaf lobes are distorted and elongated, and severely diseased leaves are a light green. The main
stem is stunted, and flowering is reduced.
Management.
Not reported.
Leaf Roll
Cause.
Leaf roll virus (LRV) is transmitted by aphids, including Aphis gossypii, A. laburni, Myzus persicae, and Epitetranychus althaeae.
Distribution.
Russia.
Symptoms.
Diseased plants are stunted, droop, and become prostrate and spreading. Leaves have chlorotic margins, are shiny and brittle, and curl upward at tips but downward
at the edges. Stems and petioles become reddish and sticky. Fruiting is reduced. Roots are poorly developed.
Management.
Some cultivars are less susceptible to infection by LRV in some geographic areas of Russia.
Mosaic
Cause.
An unknown virus transmitted by the whitefly, Bemisia tabaci.
Distribution.
Africa.
Symptoms.
Diseased leaves have a mosaic and are mottled.
Management.
Grow tolerant varieties.
Psylosis
Cause.
Virus that is transmitted by psyllids.
Distribution.
Africa.
Symptoms.
Diseased leaves are purple and have enations and thickened veins. There is a twisting and curving of internodes and petioles.

Page 223
Management.
Not reported.
Terminal Stunt
Terminal stunt is also called terminal.
Cause.
Possibly a virus, although the causal agent has been suspected to be a phytoplasma.
Distribution.
The United States.
Symptoms.
Terminal diseased leaves are puckered and twisted. Xylem tissue is frequently mottled and otherwise discolored.
Management.
Not reported.
Tobacco Streak
Cause.
Tobacco streak virus (TSV) is in the ilarvirus group. TSV survives in a wide number of host plants, but it is not known how it is disseminated to cotton, although
insects are suspected. Disease usually occurs too late in the season to do much damage.
Distribution.
TSV occurs on several other hosts around the world but is only known to infect cotton in Brazil.
Symptoms.
Diseased plants are slightly stunted and produce more axillary twigs than healthy plants. Initial infection of leaves results in necrotic rings or spots. Later, the leaf size is
reduced, and there are blisters along the veins and mosaic patterns between secondary veins.
Management.
Not necessary.
Vein Clearing
Cause.
Possibly a virus.
Distribution.
Symptoms.
Diseased leaves have a vein clearing initially, followed by a vein banding and, eventually, mottling. Young leaves cup downward, and plants are stunted.
Management.
Not reported.
Veinal Mosaic
Cause.
Veinal mosaic virus (VMV). It is not known how VMV survives or is disseminated, but it is grafttransmissible in inoculation studies.
Distribution.
Brazil.

Page 224
Symptoms.
Plants have shortened internodes and are slightly stunted, which gives them a compact and often bunchy appearance. Diseased leaves are dark green and have veinal
mosaic, roughening, and a downward curling of margins. Veinal mosaic may also occur on bracts. Severely diseased leaves may be rolled. Necrotic lesions of veins
sometimes occur.
Management.
Not reported.
Selected References
AlBeldawi, A. S., and Pinckard, J. A. 1970. Control of Rhizoctonia solani on cotton seedlings by means of benomyl. Plant Dis. Rptr. 54:7680.
Alderman, S.C., and Hine, R. B. 1981. Pathogenicity and occurrence of strands of Phymatotrichum omnivorum. (Abstr.) Phytopathology 71:198.
Arndt, C. H. 1944. Infection of cotton seedlings by Colletotrichum gossypii as affected by temperature. Phytopathology 34:861869.
Arndt, C. H. 1946. Effect of storage conditions on the survival of Colletotrichum gossypii. Phytopathology 36:2429.
Arndt, C. H. 1953. Survival of Colletotrichum gossypii on cotton seed in storage. Phytopathology 43:220.
Ashworth, L.J., Jr., Hildebrand, D.C., and Schroth, M. N. 1970. Erwiniainduced internal necrosis of immature cotton bolls. Phytopathology 60:602607.
Ashworth, L.J.,Jr., Rice, R. E., McMeans, J. L., and Brown, C. M. 1971. The relationship of insects to infection of cotton bolls by Aspergillus flavus.
Ashworth, L. J., Jr., Galanopoulos, N., and Galanopoulou, S. 1983. Selection of pathogenic strains of Verticillium dahliae and their influence on the useful life of
cotton cultivars in the field. Phytopathology 74:16371639.
Baehr, L. F., and Pinckard, J. A. 1970. Histological studies on the mode of penetration of bollrotting organisms into developing cotton bolls. (Abstr.) Phytopathology
60:581.
Bagga, H. S. 1970. Fungi associated with cotton boll rot in the YazooMississippi Delta, 19661968. Plant Dis. Rptr. 54:796798.
Baird, R. E., Gitaitis, R. D., and Herzog, G. A. 1997. First report of cotton lint rot by Pantoea agglomerans in Georgia. Plant Dis. 81:551.
Brown, J. K., and Nelson, M. R. 1984. Geminate particles associated with cotton leaf crumple disease in Arizona. Phytopathology 74:987990.
Brown, J. K., and Nelson, M. R. 1986. Cotton leaf crumple virus transmitted from naturally infected bean from Mexico. Plant Dis. 70:981.
Brown, J. K., and Nelson, M. R. 1987. Host range and vector relationships of cotton leaf crumple virus. Plant Dis. 71:522524.
Brown, J. K., Mihail, J. D., and Nelson, M. R. 1987. Effects of cotton leaf crumple virus on cotton inoculated at different growth stages. Plant Dis. 71:699703.
Calvert, O. H., Sappenfield, W. P., Hicks, R. D., and Wyllie, T. D. 1964. The CercosporaAlternaria leaf blight complex of cotton in Missouri. Plant Dis. Rptr.
48:466467.
Cleveland, T. E., and Cotty, P.J. 1991. Invasiveness of Aspergillus flavus isolates in wounded

Page 225
cotton bolls is associated with production of a specific fungal polygalacturonase. Phytopathology 81:155158.
Colyer, P.D. 1988. Frequency and pathogenicity of Fusarium spp. associated with seedling diseases of cotton in Louisiana. Plant Dis. 72:400402.
Colyer, P.D., Micinski, S., and Vernon, P.R. 1991. Effect of thrips infestation on the development of cotton seedling diseases. Plant Dis. 380382.
Correll, J.C. 1986. Powdery mildew of cotton caused by Oidiopsis taurica in California. Plant Dis. 70:259.
Cotty, P.J. 1987. Evaluation of cotton cultivar susceptibility to Alternaria leaf spot. Plant Dis. 71:10821084.
Cotty, P.J. 1987. Temperatureinduced suppression of Alternaria leaf spot of cotton in Arizona. Plant Dis. 71:11381140.
Cotty, P.J. 1989. Effects of cultivar and boll age on aflatoxin in cottonseed after inoculation with Aspergillus flavus at simulated exit holes of the pink bollworm. Plant
Dis. 73:489492.
Cotty, P.J. 1991. Effect of harvest date on aflatoxin contamination of cottonseed. Plant Dis. 75:312314.
DeVay, J. E., Forester, L., Garber, R. H., and Butterfield, E.J. 1974. Characteristics and concentrations of propagules of Verticillium dahliae in airdried field soils
in relation to the prevalence of Verticillium wilt in cotton. Phytopathology 64:2229.
DeVay, J. E., Weir, B. L., Wakeman, R. J., and Stapleton, J. J. 1997. Effects of Verticillium dahliae infection of cotton plants (Gossypium hirsutum) on potassium
levels in leaf petioles. Plant Dis. 81:10891092.
Dizon, T.O., and Reyes, T.T. 1986. Phytopathological note: Occurrence of Sclerotium boll rot of cotton in the Philippines. Philipp. Phytopathol. 22:6869.
Evans, G., Wilhelm, S., and Snyder, W. C. 1966. Dissemination of the Verticillium wilt fungus with cottonseed. Phytopathology 56:460461.
Garber, R. H., and Presley, J. T. 1971. Relation of air temperature to development of Verticillium wilt on cotton in the field. Phytopathology 61:204207.
Gergon. E. B. 1982. Diplodia boll rot of cotton: Pathogenicity and histopathology. (Abstr.) Philipp. Phytopathol. 18:6.
Grinstein, A., Fishler, G., Katan, J., and Hakohen, D. 1983. Dispersal of the Fusarium wilt pathogen in furrowirrigated cotton in Israel. Plant Dis. 67:742743.
Hancock, J. G. 1972. Root rot of cotton caused by Pythium splendens. Plant Dis. Rptr. 5:973975.
Hillocks, R. J. (Ed.). 1992. Cotton Diseases. C.A.B. International. Wallingford, United Kingdom. 415 pp.
Hood, M. E., and Shew, H. D. 1997. Reassessment of the role of saprophytic activity in the ecology of Thielaviopsis basicola. Phytopathology 87:12141219.
Hopkins, J. C. F. 1931. Alternaria gossypina (Thuem.) Comb. nov. causing a leaf spot and boll rot of cotton. Trans. Br. Mycol. Soc. 16:136144.
Huisman, O. C. 1988. Seasonal colonization of roots of fieldgrown cotton by Verticillium dahliae and V. tricorpus. Phytopathology 78:708716.
Huisman, O. C., and Ashworth, L.J.,Jr. 1976. Influence of crop rotation on survival of Verticillium alboatrum in soils. Phytopathology 66:978981.

Page 226
Isaac, I. 1967. Speciation in Verticillium. Ann. Rev. Plant Pathol. 5:201222.
Jeffers, D.P., Smith, S. N., Garber, R. H., and DeVay, J. E. 1984. The potential spread of the cotton Fusarium wilt pathogen in gin trash and planting seed. (Abstr.)
Joanne, N.R. W., Groan, R. G., and, Stapleton, J.J. 1977. Effect of water potential and temperature on growth, sporulation, and production of microsclerotia by
Verticillium dahliae. Phytopathology 67:637644.
Joaquin, T. R., and Owe, R. C. 1990. Reassessment of vegetative compatibility relationships among strains of Verticillium dahliae using nitratenonutilizing mutants.
Johnson, L. F., and Chambers, A. Y. 1973. Isolation and identity of three species of Pythium that cause cotton seedling blight. Plant Dis. Rptr. 57:848852.
Johnson, L. F., Baird, D. D., Chambers, A. Y., and, Shamiyeh, N. B. 1978. Fungi associated with postemergence seedling disease of cotton in three soils.
Johnson, W. M., Johnson, E. K., and, Brinkerhoff, L. A. 1980. Symptomatology and formation of microsclerotia in weeds inoculated with Verticillium dahliae from
cotton. Phytopathology 70:3135.
Jones, J.P. 1961. A leaf spot of cotton caused by Corynespora cassiicola. Phytopathology 51:305308.
King, C. J., and Presley, J. T. 1942. A root rot of cotton used by Thielaviopsis basicola. Phytopathology 32:752761.
Klich, M. A. 1987. Relation of plant water potential at flowering to subsequent cottonseed infection by Aspergillus flavus. Phytopathology 77:739741.
Koch, D. O., Jeger, M. J., Gerik, T. J., and Kenerly, C. M. 1987. Effects of plant density on progress of Phymatotrichum root rot in cotton. Phytopathology
77:16571662.
Lee, L. S., Lacey, P. E., and Goynes, W. R. 1987. Aflatoxin in Arizona cottonseed: A model study of insectvectored entry of cotton bolls by Aspergillus flavus.
Plant Dis. 71:9971001.
Ling,I., and Yang, J. Y., 1941. Stem blight of cotton caused by Alternaria macrospora. Phytopathology 32: 752761.
Mathre, D. E., Ravescroft, A. V., and Garber, R. H. 1966. The role of Thielaviopsis basicola as a primary cause of yield reduction in cotton in California.
Mauk, P. A., and Hine, R. B. 1987. Internal root colonization and chlamydospore production by Thielaviopsis basicola in mature Pima cotton. (Abstr.)
Mauk, P. A., and Hine, R. B. 1988. Infection, colonization of Gossypium hirsutum and G. Barbadense, and development of black root rot caused by Thielaviopsis
basicola. Phytopathology 78:16621667.
McCarter, S. M. 1972. Effect of temperature and boll injuries on development of Diplodia boll rot of cotton. Phytopathology 62:12231225.
McLean, K. S., and Roy, K. W. 1991. Weeds as a source of Colletotrichum capsici causing anthracnose on tomato fruit and cotton seedlings. Can. J. Plant Pathol.
13:131134.
Mertely, J., Gannaway, J., and Kaufman, H. 1994. A new disease of seedling cotton caused by Pseudomonas syringae. (Abstr.). Phytopathology 84:1094.
Nelson, M. R., and Stowell, L.J. 1989. Dispersion characteristics of a whiteflytransmitted geminivirus in the field. (Abstr.). Phytopathology 79:1219.

Page 227
Paplomatas, E. J., Elena, K., and Lascaris, D. 1995. First report of Phytophthora boehmeriae causing boll rot of cotton. Plant Dis. 79:860.
Pinckard, J. A., and Guidroz, G. F. 1973. A boll rot of cotton caused by Phytophthora parasitica. Phytopathology 63:896899.
Pizzinatto, M. A., Soave, J., and Cia, E. 1983. Patogenicidade de Botryodiplodia theobromae Pat. a plantas de diferentes idades e macao de algodoeiro
(Gossypium hirsutum L.). Fitopatologia Brasileira 8:223228 (in Portuguese).
Pullman, G. S., and DeVay, J. E. 1982. Effect of soil flooding and paddy rice culture on the survival of Verticillium dahliae and incidence of Verticillium wilt in
Pullman, G. S., and DeVay, J. E. 1982. Epidemiology of Verticillium wilt of cotton: A relationship between inoculum density and disease progression. Phytopathology
72:549554.
Pullman, G. S., and DeVay, J. E. 1982. Epidemiology of Verticillium wilt of cotton: Effects of disease development of plant phenology and lint yield. Phytopathology
72:554559.
Rane, M. S., and Patel, M. K. 1956. Diseases of cotton in Bombay. I. Alternaria leaf spot. Indian Phytopathol. 9:106113.
Rane, M. S., and Patel, M. K. 1956. Diseases of cotton in Bombay. II. Helminthosporium leaf spot. Indian Phytopathol. 9:169173.
Rathaiah, Y. 1976. Reaction of cotton species and cultivars to four isolates of Ramularia areola. Phytopathology 66:10071009.
Rathaiah, Y. 1977. Spore germination and mode of cotton infection by Ramularia areola. Phytopathology 67:351357.
Rotem, J., Eidt, J., Wendt, U., and Kranz, J. 1988. Relative effects of Alternaria alternata and A. macrospora on cotton crops in Israel. Plant Pathol. 37:1619.
Rotem, J., Wendt, U., and Kranz, J. 1988. The effect of sunlight on symptom expression of Alternaria alternata on cotton. Plant Pathol. 37:1215.
Rush, C. M., and Gerik, T.J. 1989. Relationship between postharvest management of grain sorghum and Phymatotrichum root rot in the subsequent cotton crop.
Plant Dis. 73: 304305.
Rush, C. M., Gerik, T. J., and Kenerley, C. M. 1985. Atypical disease symptoms associated with Phymatotrichum root rot of cotton. Plant Dis. 69:534537.
Rush, C. M., Gerik, T. J., and Lyda, S. D. 1984. Factors affecting symptom appearance and development of Phymatotrichum root rot of cotton. Phytopathology
74:14661469.
Rush, C. M., Lyda, S.D., and Gerik, T. J. 1984. The relationship between time of cortical senescence and foliar symptom development of Phymatotrichum root rot of
Schnathorst, W. C. 1973. Nomenclature and physiology of Verticillium spp. with emphasis on the V. alboatrum vs V. dahliae controversy, pp. 119. In
Verticillium Wilt of Cotton. ARSS19. Proceedings of a workshop conference held at the National Cotton Pathology Research Laboratory, College Station, Texas,
30 Aug.1 Sept. 1971. Published by U.S. Dept. Agric., Agric. Res. Serv., Publication Div., Beltsville, MD. 398 pp.
Sciumbato, G. L., and Pinckard, J. A. 1972. Alternaria macrospora leaf spot of cotton in Louisiana in 1974. Plant Dis. Rptr. 58:201202.
Shtienberg, D. 1992. Development and evaluation of guidelines for the initiation of

Page 228
chemical control of Alternaria leaf spot in Pima cotton in Israel. Plant Dis. 76:11641168.
Snow, J.P., and Mertley, J. C. 1979. A boll rot of cotton caused by Colletotrichum capsici. Plant Dis. Rptr. 63:626627.
Snow, J.P., and Sanders, D. E. 1979. Role of abscised cotton flowers, bolls and squares in production of inoculum by bollrotting Fusarium spp. Plant Dis. Rptr.
63:288289.
Sobers, E. K., and Littrell, R. H. 1974. Pathogenicity of three species of Cylindrocladium to select hosts. Plant Dis. Rptr. 58:10171019.
Sparnicht, R. H., and Roncadori, R. W. 1972. Fusarium boll rot of cotton: Pathogenicity and histopathology. Phytopathology 62:13811386.
Tarr, S. A. J. 1964. Virus diseases of cotton. Commonw. Mycol. Inst. Misc. Pub. No. 18.
Watkins, G. M. (Ed.). 1981. Compendium of Cotton Diseases. The American Phytopathological Society, St. Paul, MN. 85 pp.
Wheeler, J. E., and Hine, R. B. 1972. Influence of soil temperature and moisture on survival and growth of strands of Phymatotrichum omnivorum. Phytopathology
62:828832.
Wheeler, M. H., Stipanovic, R. D., and Puckhaber, L. S. 1996. Equisetin as a phytotoxin and its discovery in cultures of Fusarium equiseti and F. semitectum
isolated from cottonseed. (Abstr.). Phytopathology 86:S46.
Wilhelm, S., Sagen, J. E., and Tietz, H. 1974. Resistance to Verticillium wilt in cotton: Sources, techniques of identification, inheritance trends, and the resistance
potential of multiline cultivars. Phytopathology 64:924931.
Wilhelm, S., Sagen, J. E., and Tietz, H. 1985. Phenotype modification in cotton for control of Verticillium wilt through dense plant population culture. Plant Dis.
69:283288.
Wrather, J. A., Sappenfield, W. P., and Baldwin, C. H. 1986. Colonization of cotton buds by Xanthomonas campestris pv. malvacearum. Plant Dis. 70:551552.
Zutra, D., and Orion, D. 1982. Crown gall bacteria (Agrobacterium radiobacter var. tumefaciens) on cotton roots in Israel. Plant Dis. 66:12001201.

Page 229
7.
Diseases of Crambe (Crambe abyssinica)
Bacterial Blight
Cause.
Xanthomonas campestris is seedborne on the silicle and surface of the seed coat and possibly is systemic within the seed. The bacterium is yellowpigmented and
gramnegative.
Distribution.
Symptoms.
Diseased tissues are light tan, dry, and necrotic and often are bordered by a chlorotic halo. As the disease progresses, leaf symptoms are accompanied by stems with
black streaks that affect the vascular tissue.
Management.
Not reported.
Cause.
Alternaria circinans (syn. A. brassicicola) is seedborne.
Distribution.
Presumably wherever crambe is grown, but this is not known for certain.
Symptoms.
Inoculated plants have small, black, linear lesions on the petioles, stems, veins of lower leaf surfaces, and seedpods. Stem lesions (13 mm long) are discolored brown
to black and frequently coalesce or girdle diseased stems, which causes them to dry up. Seedpods are blackened and reduced in size, and seed maturation is
prevented. Leaf spots (15 mm) are brown to black and ovalshaped. Diseased leaves quickly become chlorotic and fall from the plant. Seedlings may damp off after
emergence through the soil.

Page 230
Management
1. Because some crambe cultivars have a low level of resistance to A. circinans, it is possible to screen for resistance.
Cause.
Aphanomyces raphani presumably survives as oospores in infested residue and soil. During the life cycle of A. raphani on other crops, zoosporangia, in which
zoospores are produced, are formed from oospores. Zoospores are released from the zoosporangia and ''swim" through soil moisture to the roots of host plants,
where they germinate to form a germ tube. Oospores are eventually produced in diseased roots. Disease is most severe under wet soil conditions.
Distribution.
Not known. Aphanomyces root rot has not been observed in the field but has been studied under greenhouse conditions.
Symptoms.
In inoculation studies, diseased seedlings were stunted; however, inoculated seedlings did not damp off. Roots and hypocotyls were discolored black. Aphanomyces
raphani moves up the hypocotyl into the cotyledons, causing a chlorosis and blackening of the diseased tissues. Under magnification, oospores are evident in the
diseased root cortex.
Management.
Not reported.
Fusarium Wilt
Cause.
Fusarium oxysporum f. sp. conglutinans race 2. Seedlings are susceptible to damping off until they grow to a height of approximately 6.5 cm.
Distribution.
Not known.
Symptoms.
Diseased plants are stunted. An early symptom of diseased leaves is an interveinal yellowing that is frequently followed by leaf abscission.
Management.
Not reported.
Cause.
Sclerotinia sclerotiorum.
Distribution.
The United States.
Symptoms.
The first symptom is the presence of prematurely ripened plants that are scattered or are grouped together among green plants in a field. Diseased plants are easily
pulled from the soil.
Diseased stems have pale gray lesions, with faint concentric markings, that develop from the soil line or from the axils of branches or leaves. Ini

Page 231
tially, lesions are watersoaked, then expand to girdle the stems and kill the plant. Diseased stems become bleached, have a chalky white appearance, and tend to
shred longitudinally. Sclerotia commonly appear as hard, black, grainsized bodies inside the bottom stems of dead plants. Under moist conditions, sclerotia occur in
all parts of diseased stems and pods.
Management.
Not reported.
Beet Western Yellows
Cause.
Beet western yellows virus (BWYV) is in the luteovirus group. BWYV overwinters in several weed hosts and in sugar beet. BWYV is transmitted primarily by the
green peach aphid, Myzus persicae, and infrequently by other aphid species. Known hosts for the virus are Brassica napus var. napobrassica, Capsella bursa
pastoris, Cardamine oligosperma, Cardaria draba, Erodium cicutarium, Lactuca scariola, Matricaria maritima, Polygonum lapathifolium, Raphanus
raphanistrum, Senecio vulgaris, Sisymbrium officinale, and Stellaria media.
Myzus persicae can acquire BWYV from a diseased plant after a 5minute feeding and can transmit the virus after a 10minute feeding on a healthy host plant. An
aphid can remain infective for several days. Different strains of BWYV exist.
An ST9associated RNA is a newly discovered type of plant infectious agent that depends on BWYV for encapsidation but not for replication. The agent is not a
satellite virus.
Distribution.
BWYV has been reported on sugar beet from Asia, Europe, and North America. It is not known what the distribution of BWYV on crambe is.
Symptoms.
Inoculated plants initially are generally a light green, followed by an interveinal reddening of diseased lower leaves. The reddening intensifies and involves more leaf
tissue as the disease progresses. Older diseased leaves become thickened, brittle, and discolored red except for green areas adjacent to the veins.
Young leaves inoculated with a severe virus strain develop black, necrotic, pinpointsized spots. Later, necrotic areas develop along diseased stems. Severely
diseased plants may be killed, and yield is reduced on plants that are not killed.
Management.
Not reported.

Page 232
Turnip Mosaic
Cause.
Turnip mosaic virus (TuMV) is in the potyvirus group. TuMV is transmitted mechanically and by the aphids Myzus persicae and Brevicoryne brassicae. TuMV is not
seedborne.
Distribution.
TuMV is distributed in Europe, Japan, North America, and South Africa on other hosts, but distribution on crambe is not reported.
Symptoms.
Inoculated plants have a systemic mottling that occurs in all diseased leaves. Stems are necrotic and inflorescences are stunted, distorted, and chlorotic. Seedpods do
not mature.
Management.
Not reported.
Selected References
Armstrong, G. M., and Armstrong, J. K. 1974. Wilt of Brassica carinata, Crambe abyssinica, and C. hispanica caused by Fusarium oxysporum f. sp.
conglutinans race 1 or 2. Plant Dis. Rptr. 58:479480.
Duffus, J. E. 1975. Effects of beet western yellows virus on crambe in the greenhouse. Plant Dis. Rptr. 59:886888.
Holcomb, G. E., and Newman B. E. 1970. Alternaria circinans and other fungal pathogens on Crambe abyssinica in Louisiana. Plant Dis. Rptr. 54:28.
Horvath, J. 1972. Reaction of crambe (family: Cruciferae) to certain plant viruses. Plant Dis. Rptr. 56:665666.
Humaydan, H. S., and Williams, P. H. 1975. Additional cruciferous hosts of Aphanomyces raphani. Plant Dis. Rptr. 59:113116.
Kilpatrick, R. A. 1976. Fungal flora of crambe seeds and virulence of Alternaria brassicicola. Phytopathology 66:945948.
Leppik, E. E. 1973. Diseases of crambe. Plant Dis. Rptr. 57:704708.
Mihail, J. D., Taylor, S. J., Verslues, P. E., and Hodge, N. C. 1993. Bacterial blight of Crambe abyssinica in Missouri caused by Xanthomonas campestris. Plant
Dis. 77:569574.
Thornberry, H. H., and Phillippe, M. R. 1965. Crambe: Susceptibility to some plant viruses. Plant Dis. Rptr. 49:7477.
White, G. A., and Higgins, J. J. 1966. Culture of crambe, a new industrial oilseed crop. USDA A. Res. Serv. Production Res. Rept. No. 95.

Page 233
8.
Diseases of Flax (Linum usitatissimum)
Alternaria Flower and Stem Blight
Alternaria flower and stem blight is sometimes called Alternaria blight.
Cause.
Alternaria lini is a good saprophyte that overwinters as mycelia and conidia in infested residue. During moist weather, conidia are produced from mycelia on residue
and disseminated by wind to host plants. Alternaria lini infects either moribund flowers or flowers that have died. Using the colonized flowers as an energy source,
the mycelium spreads to stems and leaves.
Distribution.
India.
Symptoms.
Initially, the flowers fail to open during the day. Minute, dark brown spots appear near the base of the calyx and gradually extend to the pedicel, causing the flower to
decay. Capsules formed at the time of infection may be similarly diseased.
When the growingpoint leaves are diseased, the fungus spreads from the bases of the leaves to the stem, which causes wilting and distortion. During severe disease,
all diseased plant parts become blackgreen in color due to the growth of mycelia and conidia on their surfaces.
Management.
Not reported.
Anthracnose
Cause.
Colletotrichum lini and C. linicola commonly survive as mycelium within seed and as conidia on seed coats. Colletotrichum lini also overwinters as mycelia,
acervuli, and possibly conidia in infested residue. Seedlings are infected primarily by conidia and mycelia during cool, wet weather.
After disease has progressed for a time, secondary inoculum, in the form of conidia, is produced in the following manner: Acervuli are formed

Page 234
subepidermally in cotyledon lesions caused by infections from the primary inoculum. The acervuli rupture the epidermis and release conidia that are disseminated by
wind to the foliage of host plants or are washed to the soil to infect stems. Conidial sporulation occurs throughout the growing season on plants that have died or on
stem cankers. Conidia from stem lesions infect flower sepals, which are a substrate, or energy source, from which C. lini infects bolls and seed.
Distribution.
Wherever flax is grown, but anthracnose is most common in cool, humid flaxgrowing areas.
Symptoms.
Symptoms are most noticeable when plants are 5 to 7 cm tall. Initially, small, circular, redbrown, zonate spots that occur on one or both cotyledons eventually cause
both cotyledons to become brown and shriveled. Seedlings may be killed if the growing points become diseased. A reddish canker develops on the stem at or below
the soil line, girdles the stem, and kills the plant. Diseased plants that are not killed may only be stunted.
Acervuli can be observed on leaf spots and stem cankers of diseased plants throughout the growing season. Acervuli appear in older lesions during moist weather as a
pink spore mass with dark hairlike objects that project stiffly upward. Lodged plants are likely to have diseased seed.
Management
1. Sow healthy seed that is treated with a seedprotectant fungicide.
3. Rotate flax with other crops.
Basal Stem Blight
Basal stem blight is also called foot rot.
Cause.
Phoma exigua var. linicola survives as pycnidia in infested residue, conidia on seed, and mycelium in seed coats. Primary infection occurs from conidia (produced
either in pycnidia or from mycelium) that are washed into soil or disseminated by wind to host plants. Foot rot becomes more severe under wet conditions when
numerous secondary infections are caused by conidia produced in pycnidia from lesions on recently killed plants.
Distribution.
Europe.
Symptoms.
The roots and stems at the soil level of diseased seedlings become discolored brown. The entire seedling then becomes chlorotic, wilts, and dies. Pycnidia, which look
like small, black "pinpoints," are produced in dead seedling tissue.
Symptoms on older plants are the most conspicuous at flowering time, when diseased plants become chlorotic and wilt. Similar to the earlier

Page 235
symptoms on diseased seedlings, the lower part of the stem and the roots are light brown. Later, numerous, small, black pycnidia form in the discolored area. The
epidermis is easily detached, causing the lower part of the diseased stem to appear "ragged." Eventually, plants are killed; their brown color contrasts with the normal
green color of healthy plants.
Management
1. Sow only healthy seed that is treated with a fungicide seed protectant.
3. Do not place flax straw or residue on soil in which flax will grow the following year.
4. Grow resistant or less susceptible cultivars.
Brown Stem Blight
Brown stem blight is also called Alternaria seedling blight.
Cause.
Alternaria linicola survives primarily as saprophytic mycelium in the residue of different plant species. Alternaria linicola may also be seedborne when conidia
contaminate the outside of seed coats. Only seedlings weakened by other causes become infected.
Distribution.
Canada and Europe.
Symptoms.
Infested seeds either do not germinate or produce stunted seedlings after germination. The root tips of diseased seedlings may have a reddish discoloration, and dark
red lesions on the hypocotyls and cotyledons develop into a moist, brown rot.
Dark spots and brown patches occur on diseased leaves, which soon become chlorotic and die. The larger lesions may have a margin or edge that is not typical of the
concentric ringssymptom caused by Alternaria spp. on other crops.
Management
1. Apply a fungicide seed treatment to seed.
2. Foliar fungicide treatments applied toward the end of flowering have been effective in managing disease.
Browning and Stem Break
Cause.
Aureobasidium lini (syn. Polyspora lini), teleomorph Guignardia fulvida, is primarily seedborne; it overwinters as conidia on and mycelium in seed coats.
Aureobasidium lini also overwinters as conidia and mycelium in acervuli on infested residue. When seeds germinate, conidia are produced during warm, wet weather
on seed coats that remain attached to cotyledons and are disseminated by wind to adjacent flax stems.
Distribution.
Wherever flax is grown.

Page 236
Symptoms.
Initially, watersoaked spots are produced on diseased cotyledons. Soon, cankers form approximately 2.5 cm above the soil line on diseased stems. Diseased plants
in the bud or flower stage may break over at the site of the stem canker but continue to live; however, any seed that is produced usually cannot be harvested.
Diseased areas on older plants appear brown, hence the name browning. The browning symptom occurs on upper stems as oval to elongated (6 mm long) brown
spots that are surrounded by narrow purple borders. Spots do not coalesce unless they are very numerous. Aureobasidium lini grows into bolls and kills young seed
but survives in the seed coats of mature seed that has not been killed.
Management
1. Sow healthy seed treated with a fungicide seed protectant.
4. If resistant cultivars are not grown, sow flax early in the growing season to attain sufficient growth before disease becomes severe.
Dieback
Cause.
Selenophoma linicola overwinters as pycnidia on infested residue. Pycnidia are formed in the late summer, primarily on earlymaturing varieties.
Distribution.
Canada (Saskatchewan) and the United States (California). Dieback is of no economic significance on flax.
Symptoms.
Selenophoma linicola was isolated from the upper third of plants that prematurely dried up or died back. In these cases it was observed that stems and bolls failed to
develop properly. Since the fungus has also been found on plants apparently killed by other causes, researchers conjectured the fungus may be more saprophytic that
pathogenic.
When fungus growing on agar disks was inoculated onto flaxseed that had germinated on filter paper, it caused a slight inhibition in the length of roots and a general
curling and increase in branch roots.
Management.
Not necessary.
Fusarium Secondary Rot
Cause.
Several Fusarium spp., of which F. roseum is the main incitant. The Fusarium spp. overwinter as perithecia, chlamydospores, or saprophytic mycelia in infested
residue. Fusarium spp. are secondary invaders of lesions caused by Aureobasidium lini or by the telia stage of Melampsora lini.
Distribution.
Northern Ireland and Russia.
Symptoms.
Diseased areas become light brown and extend up to 13 mm beyond a telial pustule of M. lini. Sporodochia, a mass of conidia supported

Page 237
on conidiophores and pseudoparenchyma, produced in the centers of diseased areas, give them a reddish to pinkish color. Under moist conditions, white mycelial
strands grow on the outside of diseased stems.
Management.
Not reported.
Gray Mold
Cause.
Botrytis cinerea survives as sclerotia in soil, saprophytic mycelia in infested residue, and mycelia in seed coats. Conidia are produced on mycelia and disseminated by
wind to plant hosts. Disease is favored by warm, wet conditions.
After the seedling stage, B. cinerea does not infect plants until the beginning of maturity. Fallen petals or pollen grains that adhere to the stem, leaves, and capsules
after rain are colonized by B. cinerea and used as an energy source from which to infect mature plants. Airborne spores usually enter through damaged plant tissues.
Lodged flax is more subject to infection.
Distribution.
Symptoms.
The first symptoms occur as cotyledonary leaves unfold. Initially, a barely visible, dark red neck rot occurs at the point the hypocotyl emerges from the seed coat.
Bright red lesions subsequently develop on the hypocotyl and cotyledons. These lesions either develop directly into infection sites or serve as an inoculum source for
disease of seedling stems at the soil level. Infections are observed as light brown spots that weaken the diseased stems and cause seedlings to wilt and fall over. The
fallen stem becomes overgrown with gray mycelial growth of B. cinerea, particularly during warm, wet weather.
Later in the growing season as plants begin to mature, portions (1.25 to 7.5 cm long) of the stems of diseased older plants become soft and discolored a light brown
with yellow margins. The stem, leaves, and petioles above the diseased stem become chlorotic and die. The dead plant residue also becomes overgrown with gray
mycelial growth during warm, wet weather. Eventually, hard, black sclerotia that appear as relatively large, black objects form on the diseased stems.
Management
2. Plants that are too close together and excessive nitrogen may encourage lodging and more severe disease.
Pasmo
Cause.
Mycosphaerella linicola (syn. M. linorum), anamorph Septoria linicola. Fungi overwinter as conidia produced within pycnidia on infested residue, and as mycelia in
infested residue and seed. Most primary inoculum is

Page 238
conidia from pycnidia, but cotyledons may become infected from seedborne inoculum. During warm, wet weather, conidia are exuded from pycnidia and
disseminated by wind and rain. Secondary inoculum comes from conidia produced in pycnidia on lesions of diseased plants. Lodged plants are more susceptible to
infection than standing flax plants. Low temperatures, which are conducive to flowering, are not favorable for disease development.
Distribution.
Symptoms.
Symptoms are not prevalent on cultivars with long flowering periods. Initially, circular, greenyellow to dark brown lesions develop on diseased cotyledons and then,
later, on lower leaves. Pycnidia develop in the older lesions on diseased cotyledons and leaves. Diseased leaves die and defoliate or cling tightly to stems.
As flax ripens later in the growing season, stem symptoms develop as small, brown, and elongated lesions. Stem lesions enlarge and coalesce, forming brown bands
that encircle diseased stems and alternate with bands of healthy, green tissue to give the stem a mottled appearance, a typical pasmo symptom. Eventually, entire stems
become brown and diseased plants defoliate. Pycnidia develop on stem lesions and appear as numerous, small, black "specks" scattered throughout the lesion.
Flowers and young bolls may also be blighted. Lesions form on older bolls, and seed inside the diseased boll may not develop properly or may be shriveled. The
slender stems, or pedicels, supporting bolls may become weakened and cause ripe bolls to break off during wind or rain.
Management
1. Grow resistant or tolerant cultivars. Earlymaturing cultivars tend to be more susceptible than latermaturing cultivars.
3. Plow under infested residue to bury inoculum.
Phytophthora Root Rot (Phytophthora aphanidermatum)
Cause.
Phytophthora aphanidermatum. Disease is favored by watersaturated soil.
Distribution.
The United States (Arizona and Missouri).
Symptoms.
Initial symptoms of a general chlorosis of plant foliage, stems, and petioles are followed by a necrosis of the leaves as the disease progresses. Taproots have a cortical
rot, but the bright pink discoloration symptomatic of disease caused by P. nicotianae var. parasitica is lacking.
Management.
Not reported.

Page 239
Phytophthora Root Rot (Phytophthora nicotianae var. parasitica)
Cause.
Phytophthora nicotianae var. parasitica. Disease is favored by watersaturated soil.
Distribution.
Symptoms.
Initial symptoms of a general chlorosis of plant foliage, stems, and petioles are followed by a necrosis of the leaves as the disease progresses. Taproots have a cortical
rot, and lateral roots have a bright pink discoloration.
Management.
Not reported.
Powdery Mildew
Cause.
Oidium lini, teleomorph Erysiphe polygoni, generally overwinters as cleistothecia on infested residue. However, frequently only the conidial stage occurs and
cleistothecia are not present. In such cases, it is not known for certain how E. polygoni overwinters but it is presumed overwintering occurs on volunteer flax or other
hosts. Primary infection either may be by conidia from mycelium or ascospores from cleistothecia. Secondary infection is from conidia disseminated by wind from
diseased plants to other hosts.
Distribution.
Wherever flax is grown; however, powdery mildew is not considered an important disease.
Symptoms.
A white, powdery growth consisting of mycelium, conidiophores, and conidia develops on diseased stems, both surfaces of leaves, and sepals. Cleistothecia appear as
small, round, black structures intermingled within the white mycelial growth.
Management.
No management is necessary in the field. In the greenhouse, apply a sulfur fungicide as a foliar spray.
Rhizoctonia Seedling Blight and Root Rot
Cause.
Rhizoctonia solani survives as sclerotia and mycelium in soil or as saprophytic mycelium in residue. Disease is most severe in warm, moist soils that have been
summerfallowed.
Distribution.
Symptoms.
Single plants and groups of seedlings in a row or within a circular area may become diseased. Diseased seedlings become chlorotic, wilt, and die. Root rot symptoms
occur at flowering time when plants appear to ripen prematurely. Roots are stunted or rotted and have brown to redbrown, superficial lesions. Eventually, roots turn
dark brown or black, shrivel, and dry up. Few or no seeds are formed.

Page 240
Management
1. Sow healthy seed that is free of cracks in the seed coat.
2. Sow as early as feasible so plants are well developed when conditions conducive to root rot occur.
3. Do not sow into summerfallowed soil.
Rust
Rust is also called flax rust.
Cause.
Melampsora lini is an autoecious longcycled rust fungus that produces uredinia, telia, pycnia, and aecia on the flax plant. Melampsora lini overwinters as
teliospores within telia on infested residue and seed. In the spring, teliospores germinate to produce basidiospores that infect young flax tissues. Pycnia then develop
and each pycnium produces pycniospores and special mycelia called receptive hyphae. Pycniospores are exuded out of the pycnium in a thick, sticky, sweet liquid that
is attractive to insects. Pycniospores are splashed by water or carried by insects from one pycnium to another, where they become attached to receptive hyphae. The
pycniospore germinates and the nucleus from the spore enters into the receptive hypha. Aecia are usually initiated on the opposite side of the leaf or stem, and the
resultant aeciospores are disseminated by wind to host tissue. Uredinia are initiated in aeciospore infections, and urediniospores are disseminated by wind to other flax
plants. Secondary infections from urediniospores account for most of the spread of rust throughout the summer. Telia, which form around uredinia as flax matures,
provide the overwintering stage.
Several physiologic races exist.
Distribution.
Symptoms.
Telia are brown to black structures covered by epidermis that occur mostly on stems but also on leaves and capsules. Pycnia and aecia occur on leaves and stems
early in the growing season as light orangeyellow sori. Uredinia are redyellow and occur on leaves, stems, and bolls.
Management
1. Grow resistant varieties. There are at least 30 genes for resistance to rust.
2. Sow cleaned seed treated with a seedprotectant fungicide.
3. Sow as early as possible in the growing season to allow susceptible plants to escape early infection.

Page 241
Scorch
Scorch is also called flax fire.
Cause.
Pythium megalacanthum survives in infested soil as oospores. The life cycle is presumed to be typical of most Pythium spp. Slow growth of earlysown crops due
to cool and wet soil conditions favors disease.
Distribution.
Northern Europe.
Symptoms.
Scorch symptoms occur within circular areas of a field. Symptoms start at the bottom of diseased plants and progress upward. Leaves become brown and shriveled
approximately half way up the stem. Leaves just above this point are yellow with brown margins, and higher on the diseased plant, leaves are only partially yellow and
flaccid. Leaves at the very top of a diseased plant may appear green and healthy. If soils dry and warm up, diseased plants may recover unless they are too severely
diseased.
Management.
Sow later in the growing season after soils have warmed up.
Seed Rot, Seedling Blight, and Root Rot
Cause.
Several fungi, including Aureobasidium lini; Fusarium spp.; Olpidium brassicae; Pythium aphanidermatum, P. debaryanum, P. intermedium, P. irregulare, P.
mamillatum, P. megalacanthum, P. splendens, P. vexans; Rhizoctonia spp.; and Thielaviopsis basicola. The most important fungi are the Pythium spp.
Infection of susceptible plants usually occurs under wet soil conditions and when mechanically injured seed is sown. However, some fungi may cause more injury
under cool soil temperatures, while other fungi grow better at higher soil temperatures.
Distribution.
Generally distributed wherever flax is grown.
Symptoms.
Seeds do not germinate and become soft, mushy, and overgrown with white mycelium that causes soil to adhere to the seeds. Seeds that do not germinate are difficult
to find in soil because of the adhering soil. Seeds may germinate but seedlings may be killed before they emerge and will be brown and watersoaked. Again, such
plants would be difficult to find in the soil. Postemergence infection is characterized by stunted plants whose lower leaves become brown and necrotic. Diseased roots
are light brown and rotted. The entire root system is destroyed if soils remain wet.
Management
2. Rotate flax with other crops. However, this is a questionable practice as many causal fungi can also infect a large number of host plants.

Page 242
Stem Mold and Rot
Stem mold and rot is also called Sclerotinia disease.
Cause.
Sclerotinia sclerotiorum survives for several years in soil as sclerotia. Sclerotia produced on other hosts, such as canola, common bean, soybean, and sunflower,
also may provide a source of primary inoculum. Sclerotia on or close to the soil surface germinate during wet conditions to form apothecia on which ascospores are
produced in a layer of asci. Ascospores are then disseminated by wind to host plants. Initially, plant stems are infected at or just above the soil line. Sclerotia,
eventually formed in mycelia growing on and in diseased stems, are returned to soil during harvest. Sclerotinia sclerotiorum has a wide host range.
Distribution.
Canada (Alberta), England, the warmer flaxgrowing areas of the United States, and Russia. However, Sclerotinia disease is not considered serious.
Symptoms.
Diseased plants are quickly killed, lodge, become pale brown in color, and dry up. White, fluffy mycelial growth occurs on diseased stems, which are easily shredded.
Eventually, sclerotia of variable sizes and shapes are frequently formed in mycelium growing in the stem pith cavity and less frequently on stems. Sclerotia are easily
seen as large, sphericalshaped bodies that initially are white but shortly become the characteristic black color.
Management
1. Rotate flax with resistant crops, such as small grains and maize.
2. Control weeds in and around a flax field.
3. Cultural practices that promote rank, thick growth should be avoided.
Thielaviopsis Root Rot
Cause.
Thielaviopsis basicola survives in infested residue and soil as chlamydospores. Most primary inoculum, in addition to the inoculum that causes infections throughout
the growing season, is presumed to be chlamydospores that germinate to produce infective hyphae. The infective hyphae penetrate only roots. Conidia are produced
on diseased roots but their function in the etiology and epidemiology of Thielaviopsis root rot is not well understood. Chlamydospores are produced within diseased
roots and released into the soil upon their decomposition. Thielaviopsis basicola is disseminated by any means that transports soil.
Distribution.
Symptoms.
Diseased aboveground plant parts are stunted and chlorotic. Diseased roots, in which dark brown chlamydospores are borne in short chains, are black and necrotic.

Page 243
Management
1. Crop rotation. Do not grow flax in the same soil for several years.
2. Control weeds in a field since they may be a host for T. basicola.
Wilt
Wilt is also called Fusarium wilt, soil sickness, and dead stalks.
Cause.
Fusarium oxysporum f. sp. lini (syn. F. lini) survives as chlamydospores in soil and as chlamydospores and saprophytic mycelia in infested residue. Microconidia
and macroconidia are seedborne on the outside of weathered seed. Fusarium oxysporum f. sp. lini is disseminated by seed, wind, and any means that moves soil.
Infection hyphae enter host plants through the root hairs of young seedlings; the resulting mycelia grow into the xylem tissue, inhibiting water uptake and causing
diseased plants to wilt.
Soil temperatures of 25°C and higher and low soil moisture favor wilt development. During moist weather, both microconidia and macroconidia are produced on
diseased plant parts, particularly near the soil line. Chlamydospores, formed from macroconidia, microconidia, and mycelia, survive for several years in soil and intact
infested residue.
Several physiologic races of F. oxysporum f. sp. lini exist.
Distribution.
Widespread. Wilt is thought to occur wherever flax is grown.
Symptoms.
Wilt symptoms are classified into four types: Early, or seedling, wilt; late wilt; partial wilt; and onesided, or unilateral, wilt. Symptoms appear at any stage of plant
growth and vary with plant age, plant cultivar, environmental conditions, and the physiologic race that caused the disease.
Early wilt is the most common type. Seedlings wilt and die from the cotyledonary stage until they are approximately 15 cm tall. Diseased plants wilt at their tops and
become dry and brown. Stems become constricted at the soil level, and seedlings fall over. If the soil is moist, abundant mycelial growth and sporulation of
macroconidia and microconidia occur on the outside of the dead seedling.
Late wilt occurs from flowering through boll set. Diseased internal and external stem tissues become discolored, necrotic, and brittle. Stem discoloration is a uniform
light brown but is darker than the color symptomatic of premature ripening caused by root rot or other causes.
Partial wilt occurs when a seedling wilts and dies except for the roots and buds at the base of the stem. During cool weather, these buds at the stem base develop
into new shoots after the death of the original shoot. With a return to high temperatures, lateral shoots wilt and the whole plant dies.
Unilateral wilt occurs when only one side of the stem is diseased. All branches on the diseased side become brown and necrotic.
Management.

Page 244
Aster Yellows
Cause.
The aster yellows phytoplasma survives in several dicotyledonous plants and leafhoppers. The phytoplasma is transmitted primarily by the aster leafhopper,
Macrosteles fascifrons, and less commonly by the leafhoppers M. laevis and Endria inimica.
Distribution.
Central and western North America.
Symptoms.
Symptoms are most conspicuous during and after flowering and appear only on the lateral branches of plants infected late in the growing season. Diseased plants are
stunted and chlorotic. Flower parts are distorted and petals remain green and leaflike. Sometimes diseased and normal flowers are both present on the same diseased
plant. No seed is ordinarily set.
Management.
Not reported.
Crinkle
Cause.
Oat blue dwarf virus (OBDV) is in the marafivirus group. OBDV overwinters in several species of plants and is transmitted by the adult aster leafhopper,
Macrosteles fascifrons. Immature leafhoppers may occasionally transmit OBDV.
Distribution.
Canada and the north central United States.
Symptoms.
The only leaves that are affected and display symptoms are those formed after exposure of plants to viruliferous leafhoppers. A ''crinkle" of diseased leaves occurs due
to a swelling of lateral veins on the margins of leaves, small indentations along the upper surfaces of veins, and enations or pimples on the lower leaf surfaces. Diseased
plants are also stunted and have reduced boll development and seed set.
Management.
Not reported.
Curly Top
Cause.
The curly top virus (CTV) overwinters in a large number of perennial plants. CTV is transmitted by the beet leafhopper, Circulifer tenellus.
Distribution.
Western North America.
Symptoms.
Diseased seedlings turn bronze, then yellow, with the leaves curled along the stem. Severely diseased plants die prematurely, while sur

Page 245
viving plants are stunted and have a reduced number of tillers. Terminal leaves and flower parts are discolored, crinkled, and distorted, and there is little or no seed
set.
Management
2. Sow at times during the growing season that avoid high populations of the beet leafhoppers.
Diseases Caused by Physiologic or Weatheroriented Problems
Boll Blight
Cause.
Warm, dry weather following cool, moist weather.
Distribution.
Not known.
Symptoms.
Buds, flowers, and young bolls fail to develop.
Management.
Not reported.
Heat Canker
Cause.
High temperature at the soil line.
Distribution.
Generally distributed in semihumid plains and at high altitudes throughout the world.
Symptoms.
Cortical tissues collapse, resulting in seedling death or sunken brown lesions on affected stems. Plants that survive have an enlarged stem just above the canker.
Cankers provide an entrance wound for secondary microorganisms that decay stems.
Management
1. Sow early to avoid high soil temperature.
2. Rows should be sown in a north and south direction to provide maximum shading.
Top Dieback
Cause.
Physiologic. High temperatures at seed ripening.
Distribution.
Not known. Affected plants may occur in a limited area or throughout an entire field.
Symptoms.
The top portion of affected plants turns brown, which results in thin and lightweight seed.
Management.
Not reported.

Page 246
Selected References
Christensen, J. J. 1954. The present status of flax diseases other than rust. Adv. Agron. 6:161168.
Ferguson, M. W., Lay, C. L., and Evenson, P. D. 1987. Effect of pasmo disease on flower production and yield components of flax. Phytopathology 77:805808.
Frederiksen, R. A., and Goth, R. W. 1959. Crinkle, a new virus disease of flax. (Abstr.) Phytopathology 49:538.
Hoes, J. A. 1975. Diseases of flax in western Canada. In Oilseed and Pulse Crops in Western Canada. Modern Press, Saskatoon, Sask.
Mederick, F. M., and Piening, L. J. 1982. Sclerotinia sclerotiorum on oil and fibre flax in Alberta. Can. Plant Dis. Surv. 62:11.
Mihail, J. D. 1993. Diseases of alternative crops in Missouri. Can. J. Plant Pathol. 15:119122.
Muskett, A. E. 1947. The diseases of the flax plant. Northern Ireland Flax Development Committee, Belfast.
Turner, J. 1987. Linseed Law: A Handbook for Growers and Advisors. Alderman Printing CI, Ipswich, United Kingdom. 356 pp.
Vanterpool, T. C. 1947. Selenophoma linicola sp. nov. on flax in Saskatchewan. Mycologia 39:341348.

Page 247
9.
Diseases of Maize (Zea mays)
Bacterial Leaf Blight and Stalk Rot
Cause.
Acidovorax avenae subsp. avenae (syn. Pseudomonas avenae and P. alboprecipitans) does not survive well in infested residue or soil. Vaseygrass, Paspalum
urvillei, is considered a primary source of inoculum in Florida. Contaminated farm equipment is a primary means of dissemination within fields and, likely, between
fields.
Infection typically occurs through stomata of leaves that are in whorls and harbor large populations of A. avenae subsp. avenae and other epiphytic bacteria.
Moisture in the whorl is considered necessary for infection to occur. Bacteria also are splashed and blown onto the plant and enter stalks through hail wounds and
other injuries. Warm, rainy weather favors disease development but leaf blight will occur below 18°C.
Distribution.
The central and southern United States. The disease is of relatively minor importance.
Symptoms.
In Illinois, symptoms, which occur on diseased leaves from late April to early June, were severe following heavy rains. Leaves emerging from whorls have water
soaked, brown lesions that become elliptical and gray or white. Lesions may coalesce during wet weather and form large necrotic areas that cause leaves to shred
when diseased plants are buffeted by the wind.
Plant tops become gray to brown and have shortened internodes. The outside of the stalk may be brown to black and appear watersoaked. The inside of the
diseased stalk is brown and slimy and has a foul odor that somewhat resembles that of silage. Diseased plants may be stunted.
Management.
Grow the most resistant hybrid. Fullseason field maize hybrids are more susceptible than shortseason hybrids and sweet maize. Bacterial leaf blight and stalk rot is
not considered a serious disease.

Page 248
Bacterial Leaf Spot
Cause.
Xanthomonas campestris pv. holcicola ( syn. X. campestris pv. zeae).
Distribution.
Bacterial leaf spot occurs in most warm and humid maizegrowing areas of the world.
Symptoms.
Narrow, watersoaked streaks (33 × 20 mm long) occur on diseased leaves. Reddishbrown streaks covered by dried bacterial exudate coalesce and form large,
irregularshaped, necrotic areas that destroy most of the leaf.
Management.
Differences in resistance and susceptibility occur in maize inbreds.
Bacterial Stalk and Top Rot
Bacterial stalk and top rot is also called bacterial stalk rot.
Cause.
Erwinia carotovora subsp. carotovora and E. chrysanthemi pv. zeae (syn. E. carotovora var. zeae and E. chrysanthemi) live as saprophytes on infested residue
in soil and are seedborne. Bacteria disseminated by wind or splashed onto host plants during wet conditions caused by rainfall or overhead irrigation enter the host
plant through hydathodes, stomares, or wounds on leaves and stalks.
Disease development is aided by high temperatures (30° to 35°C) and poor air circulation. The enzyme xylanase is produced by E. chrysanthemi pv. zeae and has
been shown to kill cells and macerate tissue in monocotyledonous plants.
Distribution.
Generally wherever maize is grown.
Symptoms.
Initially, watersoaked lesions in diseased leaf sheaths extend, as streaks, into leaf laminae and cause decay in the pith. Diseased nodes are tan to dark brown, water
soaked, soft, and slimy and have a foul odor that resembles spoiled silage. At midseason, plants fall to the ground as one to several diseased internodes twist and
collapse. The fallen plant may remain green for several days because the vascular strands remain intact and do not decay.
Management.
No disease management is practical, but chlorine in irrigation water has been reported to reduce disease incidence and severity.
Bacterial Stripe
Bacterial stripe is also called bacterial stripe and leaf spot.
Cause.
Pseudomonas andropogonis overwinters in residue. During extended periods of warm and wet weather, bacteria enter into leaves through stomata and possibly leaf
wounds caused by different means.

Page 249
Distribution.
The central and eastern United States.
Symptoms.
Lesions occur first on diseased lower leaves and progress up the plant, but leaves above the ears are rarely infected. Lesions (sometimes described as stripes) initially
are watersoaked, long and narrow with parallel sides, and olive to amber in color. Some investigators have described lesion color as pale yellow or greenish white.
Lesions eventually enlarge, or elongate further, and coalesce with other lesions to involve a large area of the diseased leaf. As lesions enlarge and coalesce, their color
becomes lighter. Severely diseased leaves are easily shred by wind.
Although upper leaves are normally not diseased, they become completely white, a secondary effect of the infection of the lower leaves. In susceptible inbred lines,
most leaves below the ear may be killed.
Other foliar symptoms are slightly sunken, circular to ellipsoidalshaped (14 mm in diameter) spots that are tan to brown with one or more darker brown rings and
irregular margins. Some spots are surrounded by a chlorotic ring 1 mm wide. Sometimes spots coalesce into elongated blotches.
Management.
Grow resistant hybrids and varieties. Bacterial stripe is not normally economically important but has been severe on a few susceptible inbred lines.
Chocolate Spot
Cause.
Pseudomonas syringae pv. coronafaciens (syn. P. coronafaciens pv. zeae). Bacteria are disseminated by wind and enter through wounds or leaf stomates.
Chocolate spot occurs only in fields with potassiumdeficient soils.
Distribution.
The United States (Minnesota and Wisconsin).
Symptoms.
Lesions occur only on leaves. The translucent, dark brown, elongated and elliptical (2 × 5 mm) lesions are surrounded by a broad chlorotic halo. Lesions are most
numerous along diseased leaf edges, where potassiumdeficiency symptoms first appear. Eventually, lesions coalesce and cause large areas of the leaf to die.
Management.
Maintain proper fertility levels.
Goss's Bacterial Wilt and Blight
Goss's bacterial wilt and blight is also called bacterial wilt, blight, freckles, Goss's leaf freckles, leaf freckles and wilt, and Nebraska bacterial wilt.
Cause.
Clavibacter michiganensis subsp. nebraskensis (syn. Corynebacterium michiganense pv. nebraskense) survives in infested residue that consists of leaves, stalks,
cobs, and ears on or near the soil surface; in or on seed; and in irrigation water. Bacteria are disseminated primarily in residue and less frequently by seed.

Page 250
Infested maize residue is the major primary inoculum source for Goss's wilt. Seedborne inoculum is of minor concern as an inoculum source in an area where the
disease is already established. However, infected or contaminated seeds could introduce the pathogen into new areas. Small abrasions and wounds caused by sand
blasting, hail, severe rainstorms, and wind allow bacteria to enter plant tissue and become established in the vascular system. Infection occurs either during wet
weather or under irrigation at temperatures of 27°C and higher.
Plants can be infected at all growth stages, but seedlings are more susceptible than older plants. Disease development is greatest when sweet maize hybrids are
inoculated at the three to fiveleaf stage. Different strains of C. michiganense subsp. nebraskense have been classified into several groups.
Distribution.
The United States (Colorado, Iowa, Kansas, Nebraska, and South Dakota).
Symptoms.
Infection of seedlings causes diseased plants to wilt, wither, and die. Infection of older plants causes stunting, wilting, and various degrees of leaf blight.
Young lesions are yellow to graygreen streaks that are parallel to leaf veins. In certain hybrids, red streaks that are also parallel to veins occur. The streaks enlarge
and appear "greasy," and their margins become wavy. Dark green to black, watersoaked, angularshaped spots resembling freckles occur along the edge of the
enlarged streak. Streaks eventually coalesce and form larger lesions that kill diseased leaves and cause them to dry up. Droplets of driedup bacterial exudate leave a
glistening crystalline residue on dead leaf surfaces.
Systemically diseased plants display either discolored waterconducting tissues from which orange bacterial exudate oozes when a stalk is cut in cross section, or leaf
symptoms that resemble those of drought stress. A dry or watersoaked, slimy, brown rot of roots and lower stalks may occur. Seedlings and older plants may be
killed following systemic infection.
Bacteria are in the chalazal region (the area between the scutellum and the endosperm) and in the vicinity of the embryo in heavily infected kernels.
Management
1. Grow resistant hybrids.
2. Rotate maize with soybean, small grains, and alfalfa.
3. Plow residue deep to reduce inoculum.
Holcus Spot
Cause.
Pseudomonas syringae pv. syringae (syn. P. holci) overwinters in infested residue. During temperatures of 25° to 30°C and wet, windy weather early in the growing
season, bacteria are splashed or blown onto host

Page 251
plants, where they invade the leaf either through stomates or small injuries.
Distribution.
The eastern and midwestern United States.
Symptoms.
Lesions are more numerous toward the tips of diseased lower leaves and initially are dark green with watersoaked margins. Later, lesions dry up and become tan to
brown, round to ellipticalshaped (210 mm in diameter) areas with reddish to brown margins, depending on the maize hybrid. Larger lesions may be surrounded by a
yellowish halo.
Holcus spot initially may appear to be a serious disease on young plants, but warm and dry weather conditions arrest bacterial spread on the plant and little injury
usually occurs. Holcus spot has little or no effect on yield.
Management
1. Grow hybrids that are more resistant than others.
2. Rotate maize with resistant crops.
Pseudomonas fuscovaginae Disease
Cause.
Pseudomonas fuscovaginae is an opportunisitic pathogen favored by low temperatures that occur above 1300 m.
Distribution.
Burundi.
Symptoms.
Symptoms first occur at the silking stage of plant growth. Initially, glossy, brownblack, watersoaked spots occur on the adaxial side of diseased leaf sheaths. Spots
are distinct and approximately 2 mm in diameter but later coalesce to form areas up to 20 cm long. Inside the diseased leaf sheath, light brown patches, which occur
on the abaxial side, have withered centers and sharp, dark purplishbrown borders that fade into healthy tissue. Similar purplebrown lesions occur on husks.
Management.
Not reported.
Purple Leaf Sheath
Cause.
Hemiparasitic bacteria plus fungi. Some of the microorganisms may grow on exogenous substrate, such as pollen, then into the surrounding leaf sheath.
Distribution.
Widespread.
Symptoms.
A dark brown to purplish discoloration of the diseased leaf sheath occurs when excess moisture is present. Symptoms are more pronounced on inner leaf sheath than
on the exterior. Although discoloration frequently is limited to discrete areas, the entire inner leaf sheath may be discolored in some plants. The integrity and strength of
the plant is normally not harmed.

Page 252
Management.
Not necessary. Apparently no injury occurs to the plant; there simply is a discoloration of the leaf sheath tissue.
Seed Rot and Seedling Blight
Cause.
Bacillus subtilis.
Distribution.
Widespread.
Symptoms.
The insides of seeds have a light to dark brown discoloration. Diseased seeds become soft and lose their integrity. If seeds germinate, the resuiting seedlings have a
soft rot with a light brown discoloration.
Management.
Stewart's Wilt
Stewart's wilt is also called bacterial leaf blight, bacterial wilt, maize bacteriosis, Stewart's bacterial wilt, and Stewart's leaf blight.
Cause.
Pantoea stewartii (Erwinia stewartii) overwinters primarily in bodies of the corn flea beetle, Chaetocnema pulicaria. Warm winter weather favors beetle and
bacterial survival, thereby favoring disease development the following growing season. If the sum of the mean monthly temperatures for December, January, and
February in the Northern Hemisphere total 37.8°C or more, Stewart's wilt may be potentially severe. Little or no disease is likely to occur when the sum of the mean
temperatures is below 32.2°C.
Some researchers have reported that P. stewartii is rarely spread through infected dent maize seed but is commonly spread by infected sweet maize seed. Bacteria
may spread through the vascular system and pass into kernels. It has been reported that P. stewartii was isolated from the endosperm of seed produced on diseased
plants and from the interior of seed 5 months after harvest. Khan et al. (1996) reported P. stewartii was detected in seed produced on hybrids that had systemic
Stewart's wilt following leaf inoculation. The bacterium was not detected in seed from hybrids or inbreds with nonsystemic Stewart's wilt. They also reported no
evidence of seedtoseedling transmission of P. stewartii when seeds from diseased plants were sown in field and greenhouse trials. This may have been due, in part,
to low rates of planttoseed transmission in seed produced on plants that were not systemically diseased.
Adult beetles feed on maize seedlings in late spring and early summer and place bacteria in wounds made by their feeding. Disease development is greatest when
plants are infected at the three to fiveleaf stage. Beetles continue to spread bacteria throughout the growing season by feeding on diseased plants, then flying to host
plants. The twelvespotted cucumber beetle, Diabrotica undecimpunctata howartii; toothed flea beetle, Chaetocnema denticulata; larvae of the seed corn
maggot, Hylemya cilicrura; wheat wireworm, Agriotes mancus; and May beetle, Phyllophaga sp., may infrequently spread P. stewartii but are not important in its
overwintering.

Page 253
High levels of ammonium and phosphorus increase plant susceptibility, whereas high calcium and potassium tend to decrease susceptibility of maize plants to P.
stewartii infection.
Distribution.
Central America, China, eastern and southern Europe, eastern United States, and Russia.
Symptoms.
Except for a few susceptible inbreds, dent maize is not as susceptible as sweet maize. In sweet maize, bacteria may be found in every part of the plant, including the
roots.
Conspicuous streaks occur on leaves after tasseling. Initially, streaks tend to follow leaf veins and are long, have irregular or wavy margins, and are light green to
yellow but later turn tan as the diseased tissue dies. Streaks may coalesce and kill the whole leaf. When the leaf is held up to light, streaks will show beetlefeeding
scars that appear as tiny scratches at right angles to the streak.
Tassels may die, and brown cavities form in stalk pith at the soil line of severely diseased plants. Bacteria may spread through the vascular system and pass into
kernels. Bacteria may ooze as yellow, moist beads from cut ends of stalks or stream from cut edges of leaf tissue.
Management
1. Grow resistant cultivars or hybrids.
2. Apply insecticides early to control corn flea beetles.
3. Experimental results with insecticide seed treatments have been effective in managing disease in young maize plants.
Yellow Leaf Blotch
Cause.
Pseudomonas sp. Plants are infected in the seedling stage.
Distribution.
West Africa.
Symptoms.
Scattered cream, yellow, or light tan, rectangular lesions (1015 × 1445 mm) occur on diseased leaves. There is a tendency for streaks, or runners, to follow veins.
Entire leaves of some plants become watersoaked, wither, and die. Seedlings may outgrow the disease and produce healthy kernels.
Management.
Not necessary.
Alternaria Leaf Blight
Cause.
Alternaria alternata (syn. A. tenuis) is a common saprophyte of infested residue. Infection occurs during heavy dew periods 16 to 20 hours after injury has
occurred.

Page 254
Distribution.
The midwestern United States.
Symptoms.
Chlorotic streaks that form on diseased leaves of all ages later become necrotic. Leaves may be killed in 1 week if heavy and prolonged dews occur.
Management.
Not practiced.
Anthracnose Leaf Blight
Cause.
Colletotrichum graminicola. No teleomorphic stage is known. Colletotrichum graminicola survives as mycelia and conidia in infested residue on top of the soil
and as stroma or hyphae in endosperm. When exposed directly to soil, mycelia and conidia will lyse in approximately 16 and 14 days, respectively. Therefore, surface
residue or any infested residue that is not buried is an important source of inoculum.
During warm, wet weather early in the growing season, conidia are produced in acervuli on residue and disseminated by splashing rain or wind to leaves. Disease
development is optimum at 30°C and long periods of cloudy weather since low light intensity enhances lesion development.
Seedlings may be infected, but lower leaves of older plants are the most conducive for disease development. Leaf blight is most severe in continuous maize, and the
spread of inoculum is more rapid within a row, in relation to inoculum sources, than across rows. Infection by the lesion nematode, Pratylenchus hexincisus, also
increases disease severity.
Isolates of C. graminicola from sorghum, shatter cane, johnsongrass, and barnyard grass cause chlorotic flecks on juvenile maize leaves and susceptibletype lesions
on senescing maize leaves. Isolates that infect small grains do not infect maize.
Distribution.
France, Germany, India, the Philippines, Thailand, and the eastern United States.
Symptoms.
Plants are susceptible as seedlings and, again, as mature plants, resulting in disease development early and late in the growing season. Chlorotic flecks occur on
diseased leaves, enlarge, and become graygreen lesions that mature into brown, spindleshaped lesions (515 mm long) with yellow to reddishbrown borders.
Lesions sometimes have concentric rings or zones, and their centers become gray with numerous acervuli that, under magnification, appear as black spines. When
lesions coalesce, leaves may rapidly dry up (top dieback), which can cause stalk lodging during warm, wet conditions later in the season. Symptoms may appear as a
variety of more restricted lesion types in cultivars with different levels of resistance.
Management
1. Grow resistant hybrids. However, hybrids susceptible to leaf blight may be resistant to the stalk rot phase, and vice versa.

Page 255
2. Rotate maize with nongrass crops.
5. Severity of stalk rot has been reported to decrease in artificially and naturally infected plants with increased nitrogen rates applied in either spring or autumn as
anhydrous ammonia.
Anthracnose Stalk Rot
Cause.
Colletotrichum graminicola survives as mycelia and conidia in infested residue on the soil surface and as stroma or hyphae in endosperm. When infested residue is
buried, mycelia and conidia lyse in 16 and 14 days, respectively, because they are exposed directly to soil. During warm, wet weather early in the growing season,
conidia are produced in acervuli on residue and disseminated by splashing rain or wind to host plants. Conidia may wash behind leaf sheaths and invade stalks or
roots. The lower internodes may become infected as normal plant senescence progresses.
When inoculated with conidia prior to the rapid stalk elongation (late whorl) stage of plant growth, susceptible hybrids were resistant to stalk rot. Transition of the
maize plant to susceptibility occurs during rapid stalk elongation just prior to tasseling and extends through anthesis. Therefore, plants are most susceptible to
anthracnose stalk rot at tasseling or after tasseling. Subsequently, maximum stalk rot development occurs by the kernel dent stage. Susceptibility of young tissue to
stalk rot is not consistent in all maize hybrids; moderately susceptible hybrids have delayed and reduced stalk rot development.
Disease is more severe in continuous maize and is associated, in New York, with early or midseason infestations by the European corn borer, Ostrinia nubilalis.
Distribution.
France, Germany, India, the Philippines, Thailand, and the eastern United States. Anthracnose stalk rot may also occur where no leaf blight is present.
Symptoms.
Symptoms may occur at different stages of plant growth, depending on susceptibility of the plant. Very susceptible plants may be killed before pollination. Initially,
narrow, oval, watersoaked lesions that occur on the surfaces of diseased lower internodes after tasseling become tan to reddish and finally dark brown to black linear
streaks. Frequently, large oval areas develop and cause internodes to be dark brown or shiny black. When such stalks are split, the pith, starting at the nodes, is a
dark brown. Some genotypes may have a soft and watery pith. Sometimes internal discoloration may be present when there is little or no blackening of the surface.
Severely diseased stalks are likely to lodge.
Although stalks above the ear sometimes become grayish green and die several weeks after pollination, the lower stalk remains green. Upper leaves

Page 256
may turn yellow or a reddish color and drop off, sometimes just before lower leaves begin to normally senesce.
Management
1. Grow resistant hybrids; however, resistance is not correlated with resistance to other stalk rot fungi.
2. Rotate maize with other crops.
4. Ensure that soils have a balanced fertility.
Ascochyta Leaf and Sheath Spots
Cause.
Ascochyta ischaemi (syn. A. zeae), A. maydis, and A. zeina survive as pycnidia in infested residue. During wet weather, conidia are produced in pycnidia and
disseminated by splashing rain or wind to host plants.
Distribution.
The United States.
Symptoms.
Lesions, which initially are ellipsoidal and reddish purple to brown, become elongated and irregularshaped and have brown margins. Tiny black dots in the lesion are
pycnidia, whose flasklike structures develop in rows below the leaf surface.
Management.
Ascochyta leaf and sheath spots has not been considered important enough to warrant management.
Aspergillus Ear Rot
Cause.
Several species of Aspergillus, including A. flavus, A. glaucus, A. niger, and A. parasiticus. Aspergillus flavus is generally considered to have a greater potential
to naturally infect maize kernels than most other Aspergillus spp.
All Aspergillus spp. presumably survive as sclerotia on infested residue. However, A. flavus overwinters as sclerotia more successfully in the southern than in the
northern United States maizegrowing areas. This may partially explain the lower incidence of infection of maize by A. flavus in the northern maizegrowing areas.
Sclerotia of A. flavus var. flavus and A. flavus vat. parasiticus survived burial in soil for 36 months in Georgia and Illinois. Apparently, sclerotia did not germinate
sporogenically when placed on sand in moist chambers after 36 months burial in soil. However, sclerotia may have germinated sporogenically earlier in their soil burial
and produced large numbers of fungal propagules in the soil. Aspergillus flavus and A. parasiticus also were isolated from soils in Iowa. Deposits of waste maize
infested with A. flavus are frequently found in the vicinity of maize storage cribs and bins and may be potential sources of inoculum.
Growth and sporulation of A. flavus is favored by temperatures of 32° to 38°C and high humidity. Because airborne spores of A. flavus and other Aspergillus spp.
are an important source of inoculum, openpollinated maize is more susceptible to infection than hybrid maize. Spores enter kernels

Page 257
through injuries from growth cracks, insect damage from corn earworms, senescing silks, and cracks caused by drought stress. Aspergillus niger is observed most
frequently in dry years; therefore, it is suspected that this fungus enters the plant through droughtstress cracks.
Aspergillus flavus readily infects wounded kernels at 32% or less moisture content or when physiological maturity occurs. The fungus does not normally infect
uninjured kernels with higher moisture contents. However, A. flavus colonizes senescing silks at optimal temperatures of 32° to 38°C in the absence of injuries and
grows on the senescent silk into the ear. Aspergillus flavus grows onto the adjacent pericarp at the silk attachment site on the kernel, then over the kernel surface and
eventually penetrates the tipcap region. Spread to other kernels is by mycelial growth on pericarps or glumes.
Aflatoxin accumulation in silkinoculated ears follows a similar pattern to that produced in injured kernels except toxin levels are lower and decline as kernel moisture
decreases to 14%.
Optimum moisture for toxin production may be higher than that for infection. Most aflatoxin is produced in wounded kernels that are not representative of the moisture
content of intact kernels from the same ear. In mature maize kernels, A. flavus is reported to produce aflatoxin at kernel moisture contents of 18.0% to 18.5% but not
at lower moisture contents. Other reports state maximum aflatoxin production occurred in maize at 41% to 58% moisture. Maize sown and harvested late in the
growing season and produced under nitrogen stress is a better substrate for preharvest aflatoxin production than maize grown under good management practices and
supplied with adequate nitrogen. When kernel moisture content is 16% to 21%, aflatoxin appears in woundinoculated ears within 1 week and increases linearly until 7
to 9 weeks after inoculation. All Aspergillus spp. will grow on kernels stored at 15% and higher moisture content.
Common fungal colonists of maize kernels, such as Fusarium moniliforme and Acremonium strictum, interfere with the ability of A. flavus to infect maize before
harvest. However, this interference is associated primarily with uninjured kernels.
Distribution.
Symptoms.
Aspergillus niger is a black mold that is sometimes scattered over the whole ear. Aspergillus flavus appears as a greenyellow mold. Aspergillus glaucus is a
greenish mold. Most other Aspergillus spp. are similar greenyellowbrowncolored molds. Frequently, A. flavus can be seen growing in the tracks of corn
earworms or other insect damage and on injured kernels at the ear tip. However, kernels at any position on the ear may be diseased.
Management
1. Harvest maize as early as possible to limit aflatoxin contamination.
2. Dry maize to 15% or less moisture content soon after harvest.

Page 258
3. Use tillage practices, such as irrigation, that reduce water stress.
4. Differences in aflatoxin levels exist between genotypes. However, any comparison of maize lines for resistance to aflatoxin accumulation should be done during the
linear phase of aflatoxin accumulation.
5. Sources of resistance exist in F1 maize hybrids to ear rot caused by A. flavus.
Banded Leaf and Sheath Spot
Banded leaf and sheath spot is also called banded leaf and sheath blight.
Cause.
Rhizoctonia solani (syn. R. microsclerotia) infects plants under warm, humid conditions.
Distribution.
Semitropics and tropics.
Symptoms.
Twentyfive to 30 days after sowing, symptoms appear on the lowest leaf sheaths as watersoaked areas that later become dirty white bands 3 to 5 cm wide. Lesions
increase in size and become discolored gray, tan, or brown areas that alternate with dark bands. Mycelium radiates and spreads upward to leaf blades, causing a
similar band within 24 hours, then mycelium grows progressively to the diseased upper leaf sheaths, eventually killing the leaf blades. Infection continues until all leaves
and ears have died and dried up. Mycelium on dried leaf sheaths and blades condenses to form sclerotia (1.42.7 mm in diameter) that are initially white but later
become brown. Ears have a brownish rot under warm, humid conditions.
Management
1. Grow resistant genotypes.
Black Bundle Disease
Cause.
Acremonium strictum (syn. Cephalosporium acremonium) is seedborne and soilborne, surviving on infested residue in the soil. Infection of the stalk may be directly
through the epidermis or through wounds. There are reports of transmission from seeds to seedlings and eventually to adult plants.
Distribution.
Symptoms.
Initially, diseased leaves become purple or red at the dough stage of plant development. Vascular bundles in the diseased stalk are blackened or reddened through
several internodes. Diseased plants tiller excessively and are barren or have either small ears or multiple ears at one node.
Management
1. Resistance has been identified in some inbreds.

Page 259
Black Kernel Rot
Cause.
Lasiodiplodia theobromae (syn. Botryodiplodia theobromae).
Distribution.
Unknown.
Symptoms.
Diseased kernels have a brown discoloration that later becomes black and has small eruptions containing pycnidia. A dry rot develops.
Management.
Not reported.
Borde Blanco
Borde blanco is also called white border.
Cause.
Marasmiellus sp. is primarily a pathogen of the leaf blade and sheath and is not associated with roots or the basal regions of the stalk.
Distribution.
Costa Rica, Mexico, and Nicaragua. Borde blanco occurs in humid lowlands and highlands where ''hanging mists" occur during the rainy season.
Symptoms.
Leaf blight is characterized by blanched marginal lesions that always begin at the leaf margin but originate at any point along the diseased leaf from the sheathblade
juncture to the apex. Lesions (13 × 525 cm) on diseased leaves of all ages are characterized by concentric zones of slightly different discoloration. The white border
lesions of severely infected plants glisten in sunlight.
Stalk lesions originate at the sheath margin and Marasmiellus sp. penetrates through several sheath layers into the stalk. Stalk lesions are numerous in fields with a high
percentage of diseased leaves. Severe stalk rot has been observed in humid areas where foliage is dense.
Management.
Not reported.
Brown Spot and Stalk Rot
Brown spot is also called black spot, Physoderma brown spot, and Physoderma disease.
Cause.
Physoderma maydis (syn. P. zeaemaydis) overwinters as thickwalled, brown sporangia in infested residue and soil. Sporangia released from infection pustules,
disintegrating infested residue, and soil are disseminated by wind, water, insects, and machinery.
A sporangium germinates by a lid, or cap, opening on one side of the sporangium to release a vesicle that, in turn, ruptures to release 20 to 50 zoospores. Zoospores
swim for 1 to 2 hours then become amoebalike and germinate to form infection hyphae that penetrate meristematic tissue of the host plant. The resulting mycelium
enters mesophyll or parenchyma cells and forms vegetative structures from which sporangia develop in 16 to 20 days. Secondary spread is by zoospores produced
within the thin

Page 260
wailed sporangia. Infection commonly occurs in a diurnal cycle that resuits in alternating bands of diseased and healthy tissue as the diseased leaf emerges from the
whorl. Germination is optimum when moisture is present in whorls or behind leaf sheaths and temperatures are 22° to 32°C.
Plants become increasingly susceptible to infection until they are 45 to 50 days old. Disease development is favored by warm, wet weather and is more severe on
plants sown into infested residue that has overwintered.
Distribution.
Central America and the southeastern and midwestern United States.
Symptoms.
Initially, lesions occur near the base of the leaf blade as small, round, yellowish spots. Lesions may occur in bands across the leaf blade, with diseased tissues turning
chocolate brown to reddish brown and merging to form large, irregular to angularshaped blotches. Cells of diseased maize tissue disintegrate and expose dusty
pustules or brown blisters containing large numbers of microscopic light to dark brown sporangia.
Infections at the nodes beneath the leaf sheaths and premature death of diseased plants due to leaf blighting cause stalk rot and lodging. Symptoms of stalk infections
are watersoaked lesions that occur initially on the stalk nodes beneath the leaf sheaths and later coalesce to form brown blotches. Small pockets of brown sporangia
may form in the diseased stalk.
Management
2. Do not grow susceptible hybrids in river bottoms or other highhumidity locations.
3. Shred and bury infested maize residue.
Brown Stripe Downy Mildew
Cause.
Sclerophthora rayssiae var. zeae survives as oospores in infested residue in the soil and as mycelia in different grasses. Oospores germinate in a film of free water
and form sporangia in which zoospores are produced. Sometimes sporangia germinate directly and form a germ tube. Mycelia in other plant hosts give direct rise to
sporangia. Zoospores liberated from sporangia germinate in free water on leaves at optimum temperatures of 22° to 25°C; thereafter, temperatures of 28° to 32°C
favor disease development. Secondary spread is by the formation of sporangia, at temperatures of 20° to 22°C, that are disseminated by wind and water.
Distribution.
India, Nepal, and Thailand.
Symptoms.
Narrow (37 mm wide), yellow stripes with definite margins that are limited by veins develop on diseased leaves. Later, the stripes become reddish to purple. Further
development of lesions causes a severe striping and blotching of leaves that may either kill plants or suppress seed devel

Page 261
opment if the symptoms occur prior to plant flowering. Sporangia, sporangiophores, and mycelia develop on both sides of leaf lesions and appear as a downy growth.
Floral and vegetative plant parts are not malformed nor are diseased leaves shredded.
Management
1. Grow resistant cultivars or hybrids.
2. Sow before the rainy season begins.
3. Apply fungicides as a foliar spray after symptoms appear or as a soil drench.
Cephalosporium Kernel Rot
Cephalosporium kernel rot is the kernel rot phase of black bundle disease.
Cause.
Acremonium strictum (syn. Cephalosporium acremonium) is seedborne and survives within infested residue in the soil.
Distribution.
Symptoms.
A white, cottony growth occurs on and between kernels on the diseased ear. A white streaking on the kernels has been associated with the disease, but this has been
disputed by some researchers.
Management
1. Resistance has been identified in some inbreds.
Cause.
Cercospora sp. The fungus presumably survives in infested residue in soil.
Distribution.
The United States (Pennsylvania).
Symptoms.
Greenhouse inoculations caused pale tan lesions on diseased leaves. Lesions are limited in lateral spread by the major leaf veins, and lesion ends are more irregular
shaped than the rectangular lesions caused by C. zeaemaydis.
Management.
Not reported.
Charcoal Rot
Cause.
Macrophomina phaseolina (syn. M. phaseoli, Botryodiplodia phaseoli, and Sclerotium bataticola) survives as sclerotia in infested residue and soil. Strains of M.
phaseolina that infect other host plants produce pycnidia, but strain(s) that infect maize do not. Sclerotia are disseminated by any means that moves residue and soil.
Sclerotia germinate in dry soil at optimum temperatures of 37° to 38°C

Page 262
and produce infection hyphae that infect the roots of seedlings, young plants, and mature plants. Hyphae eventually grow through the cortical tissues and into the stalks.
Small sclerotia are eventually produced on diseased tissues.
Association with high populations of the Banks grass mite, Oligonychus pratensis, and the twospotted spider mite, Tetranychus urticae, is reported to increase
incidence and severity of stalk rot. Low soil temperatures or high soil moisture will hinder the development of charcoal rot.
Distribution.
Europe, North America, and South Africa.
Symptoms.
Plants nearing maturity are most likely to display disease symptoms. Brown, watersoaked lesions, which later become black, appear on roots. As plants mature, M.
phaseolina grows into the lower stalk internodes and causes premature ripening and shredding. Diseased stalks frequently break over at the crown. The surface of
rotted stalk internodes may turn gray due to the growth of numerous tiny, black sclerotia that grow through the epidermis of stalks and roots. The interiors of diseased
stalks disintegrate and are covered with sclerotia, leaving only the vascular bundles intact. The numerous sclerotia give the diseased plant tissue the appearance of
being covered with charcoal, hence the name charcoal rot. Kernels are also diseased and become completely black.
Management
1. Keep soils moist.
2. Rotate with resistant plants for 2 to 3 years.
3. Grow fullseason, adapted hybrids.
Common Corn Rust
Common corn rust is also called common rust and common maize rust.
Cause.
Puccinia sorghi is a heteroecious longcycled rust fungus whose alternate host is wood sorrel, Oxalis spp. Commonly, urediniospores overwinter in warmer climates
and are disseminated by wind into temperate maizegrowing regions, thereby serving as primary inoculum and bypassing the alternate host. Temperatures of 16° to
23°C and high relative humidity favor disease development and spread.
The full cycle is as follows: Teliospores replace urediniospores in pustules as maize nears maturity. In the spring, teliospores germinate and form basidiospores that
infect only Oxalis spp. The spermatial (pycnial) stage occurs on the diseased upper leaf surface at the points of infection by the basidiospores. Pycniospores
(spermatia) and receptive hyphae are formed in pycnia (spermagonia) together with a sticky, sweet liquid that is attractive to insects. The pycniospores are extruded
from the pycnia and

Page 263
disseminated by insects to the receptive hyphae of an opposite mating type. Nuclei of the pycniospores and receptive hyphae merge to initiate development of aecia on
the diseased lower leaf surface. Aeciospores from aecia are disseminated by wind and infect only maize. These infections give rise to urediniospores.
Distribution.
Uredinial and telial stages are generally distributed wherever maize is grown. The aecial stage occurs infrequently in temperate areas of Europe, India, Mexico, Nepal,
Russia, South Africa, and the United States.
Symptoms.
Symptoms appear soon after the silking stage of plant growth, but older tissue is usually resistant. Sweet maize is generally more susceptible than field maize. Oval to
elongate, goldenbrown to reddishbrown pustules, which consist of urediniospores breaking through the epidermis, are sparsely scattered over both surfaces of
diseased leaves but may appear on any aboveground plant part. As maize matures, pustules become brownish black with the formation of teliospores that also break
through the epidermis.
The rupture of the epidermis by urediniospores and teliospores differentiates common rust from southern corn rust. The epidermis over a southern corn rust uredinia
remains intact for a long period of time but eventually does rupture.
During severe disease conditions, chlorosis and death of diseased leaf sheaths and leaves may occur.
Management
1. Grow resistant maize hybrids.
2. Apply foliar fungicides when pustules first appear, particularly in seed production fields.
Common Smut
Common smut is also called boil smut.
Cause.
Ustilago zeae (syn. U. maydis) overwinters as teliospores (chlamydospores) in the soil. Teliospores germinate either directly or indirectly in the presence of moisture
at a wide range of temperatures (10° to 35°C). Direct germination is by an infection hypha produced directly from a germinating teliospore. Indirect germination is by
a promycelium first being formed by a teliospore and on which sporidia (basidiospores) are borne. Sporidia are then disseminated by wind to host leaves, where they
germinate. The resultant mycelium fuses with the mycelium from an opposite mating type to form an infection hypha that infects meristematic tissues. Ears of maize are
infected by infection hyphae growing through silk.
The parasitic mycelium stimulates host cells to increase in size and numbers, which results in the formation of a gall. Eventually, teliospores

Page 264
develop within the mycelium and gall, causing the galls to be converted to a black, powdery mass consisting of teliospores.
Disease development is favored by dry conditions that retard plant growth and temperatures of 26° to 34°C. Abnormally cool, wet weather, which retards growth of
young maize plants, is also conducive to disease development. Smut incidence is higher when plants are grown in soil high in nitrogen, particularly where heavy
applications of manure have been made. Injuries from hail, cultivation, herbicide, and detasseling increase the infection incidence and the resulting disease severity.
Distribution.
Worldwide; however, smut rarely occurs in tropical areas.
Symptoms.
All aboveground plant parts are susceptible, but meristematic tissue is particularly susceptible to infection and disease. Galls are first covered with a glistening white
membrane that eventually ruptures within a few weeks to expose a black, powdery mass of teliospores. Galls on ears and stalks grow to 15 cm in diameter or even
larger in some instances. However, galls on leaves rarely develop beyond the size of peas (0.61.2 cm in diameter), become hard and dry, and contain few spores.
Large galls on the ear and on the stalk above the ear are more destructive than galls on the stalk below the ear.
Early infection may kill seedlings. Galls on the lower part of the stalk may cause plants to be barren or to produce several small ears. Such plants become a reddish
color in the autumn.
Management
2. Maintain a wellbalanced soil fertility.
3. Avoid mechanical injuries to plants.
4. Remove and burn galls from infected plants before they rupture.
Corticium Ear Rot
Cause.
Thanatephorus cucumeris (syn. Corticium sasakii). The fungus presumably overseasons as sclerotia in infested residue. Ear rot occurs under extremely wet
conditions.
Distribution.
India.
Symptoms.
Initially, watersoaked spots that vary in size and shape occur on diseased leaf sheaths. The spots gradually enlarge in moist and warm weather and profuse fungal
growth sometimes appears on their surfaces. Brown mycelium grows upward from the base of the ear and is observed late in the season on husks, floral bracts, and
pericarps of rotted kernels. Sclerotia are formed on diseased ears in the later stages of disease.
Management.
Not reported.

Page 265
Crazy Top Downy Mildew
Crazy top downy mildew is also called crazy top.
Cause.
Sclerophthora macrospora (syn. Sclerospora macrospora and Phytophthora macrospora) survives in infested residue and wild grasses as oospores that
germinate and form sporangia in which zoospores are produced. Zoospores are liberated in watersaturated soil and "swim" to seedlings, where they germinate to
produce mycelia that penetrate the plant and become systemic.
Germination and infection occur over a wide range of temperatures and in soil saturated with water for 24 to 48 hours before plants are in the fourto fiveleaf stage.
Sporangia are rarely produced directly on sporangiophores projecting from stomates on leaves, but numerous oospores are produced within diseased leaves and leaf
sheaths. Over 140 grass species are hosts of S. macrospora.
Distribution.
Africa, Asia, Canada, Europe, Mexico, and the United States. Crazy top downy mildew occurs in localized wet areas within a field.
Symptoms.
The most conspicuous symptom is the partial to complete replacement of the tassel by a large, bushy mass of small leaves. No pollen is produced since flower parts
within the tassel are completely deformed. Ear shoots may be numerous, elongated, leafy, and barren. Diseased plants vary in height. Some plants are severely stunted
and have narrow, yellow to brown streaks on leaves and numerous tillers. Other plants are taller than normal and have an increased number of nodes and leaves
above the ear and in the shank.
Management
1. Provide adequate soil drainage.
3. Do not grow in low, wet spots.
Curvularia Leaf Spot
Cause.
Curvularia clavata, C. eragrostidis (syn. C. maculans), C. inaequalis, C. intermedia, C. lunata, C. pallenscens, C. senegalensis, and C. tuberculata.
Distribution.
Generally wherever maize is grown in warm or mild climates.
Symptoms.
Initially, circular (12 mm in diameter), strawcolored lesions with reddish or dark brown margins develop on diseased leaves and may coalesce and form necrotic
areas up to 1 cm long. The centers of some lesions have circular (1 mm in diameter), grayish spots that may have a chlorotic halo.
Management.
Not reported.

Page 266
Didymella Leaf Spot
Cause.
Didymella exitialis. It is presumed D. exitialis overseasons as perithecia in infested residue.
Distribution.
Not reported.
Symptoms.
Small, lightcolored, elongate to ellipticalshaped spots with brown margins form on diseased leaves. Later, spots enlarge and coalesce to form streaks, or irregular
shaped areas, in which perithecia may be formed.
Management.
Not practiced.
Diplodia Ear Rot
Diplodia ear rot is also called white ear rot. Diplodia ear rot, Diplodia seedling blight, and Diplodia stalk rot caused by Diplodia maydis are considered as parts of a
single disease complex.
Cause.
Diplodia maydis (syn. D. zeae, D. zeaemaydis and Stenocarpella maydis). Diplodia maydis overwinters as conidia within pycnidia and mycelium in infested
residue, and as conidia and mycelium on seed. During warm, moist weather in the late summer, conidia are exuded from pycnidia in long cirri and disseminated by
splashing rain or, after cirri have dried up, by wind. Insects are reported to disseminate spores.
Infection occurs late in the development of the kernel. Some researchers state ears are most susceptible during a plant growth stage beginning at silking and continuing
for 21 to 24 days afterward, when kernels have reached a moisture level of 75.4% to 90.0%. During this time, a decrease of 5% moisture in kernels is reported to be
associated with a decrease of up to 22% in ear rot incidence. Resistance occurs 28 days after midsilk, when moisture is approximately 66%. As ears approach
maturity, rot slows and ceases completely when kernels reach approximately 21% moisture content.
Infection commonly starts at the base of husks or on an exposed ear tip, but mycelium can advance from the stalk through the shank. Diplodia maydis enters the
pedicel and penetrates through the hilar region. The hilar layer (black layer) of the hilum is impermeable to the fungus; therefore, entrance into the kernel occurs before
the closing layer is formed or delayed, or if suberization of testa membrane is incomplete. As ears grow in length, husks become loose and provide less protection at
the ear tip, allowing kernels to be more accessible to spores.
Pycnidia may be found on rotted ears, particularly on the inner husks. During wet weather, conidia are exuded and become disseminated by wind. Dry weather early
in the growing season followed by wet conditions before and after silking favors ear infection.

Page 267
Distribution.
Africa, Australia, the Philippines, Romania, and the United States.
Symptoms.
Disease on the kernels of maturing plants begins at the ear base and progresses toward the tip. In contrast to the green color of healthy ears, the husks of diseased
ears that were infected early in the growing season appear to be bleached. When infection occurs 2 weeks after silking, the entire ear becomes grayish brown,
shrunken, and light in weight by harvest time. Such ears remain upright and have tight husks that adhere to the ear due to the growth of the fungus between the ear and
the husk. Black pycnidia are found at the base of husks and on the faces of kernels. Ears infected later in the growing season have no apparent symptoms until the ear
is broken or kernels are removed. White mycelium of D. maydis will be found growing between the kernels on a diseased ear.
The germination of diseased kernels is reduced.
Management.
Diseased stalks may produce inoculum that will infect ears. Therefore, any management practice that lessens stalk rot will likely lessen the incidence of ear rot.
1. Grow the most resistant hybrid.
2. Balance soil fertility. Excess levels of nitrogen may predispose plants to stalk rot. Stalk rot is lowest when the level of nitrogen is adequate enough to allow a hybrid
to reach its yield potential. The severity of stalk rot in artificially inoculated plants has been reported to decrease with increasing rates of nitrogen applied as anhydrous
ammonia in either spring or autumn.
3. Plant the recommended plant population. Higher than recommended plant populations cause plants to be stressed and have less resistance to infection.
4. Harvest early to prevent grain from being weathered.
5. Dry maize kernels to 15% or less moisture content.
6. In programs for breeding resistance to ear rot, ear inoculations should be made at or shortly after midsilk.
Diplodia Ear Rot and Stalk Rot
Cause.
Diplodia frumenti, teleomorph Botryosphaeria festucae. Diplodia frumenti is seedborne, but it is not known if this is important in the life cycles of the fungi. The
fungus presumably overseasons either as pycnidia or perithecia.
Distribution.
Brazil and the United States (Florida).
Symptoms.
Stalk pith is discolored black. Pycnidia occur in longitudinal cracks on the outer diseased stalk tissues. Diseased ears have a dark brown, feltlike growth at the butt
end. Seeds are black and embedded with pycnidia.

Page 268
Management.
Not reported. The disease is of minor importance.
Diplodia Leaf Spot
Diplodia leaf spot is also called Diplodia leaf streak, southern leaf spot, and Stenocarpella leaf spot.
Cause.
Stenocarpella macrospora (syn. Diplodia macrospora) survives as mycelium within infested residue and seed. Ears, leaves, and leaf sheaths are generally
considered to be most susceptible to infection. However, all plant tissue can be infected at any stage of growth. Disease occurs in the semitropics under warm, humid
conditions with a minimum of 50% relative humidity during the day and 95% relative humidity at night.
Distribution.
Central America and the United States (North Carolina).
Symptoms.
Diseased seeds or seedlings may damp off. Initially, small, yellowish spots occur on leaves. Later, the spots become watersoaked lesions with chlorotic margins. The
lesions enlarge and become long, narrow, chlorotic lesions or streaks (1.5 × 10.0 cm). Pycnidia, which appear as numerous black specks, are scattered throughout
the lesion. Frequently, S. macrospora grows along the borders of leaf veins. Inoculated plants had lesions along veins the entire length of a diseased leaf blade. Toxin
production was indicated.
A leaf spot caused by S. macrospora has been described from North Carolina. However, these symptoms were described as circular to elongate lesions that were up
to 25 cm long.
Management.
Differences in resistance exist between genotypes.
Diplodia Seedling Blight
Diplodia ear rot, Diplodia seedling blight, and Diplodia stalk rot caused by Diplodia maydis are considered as parts of a single disease complex.
Cause.
residue, and as conidia and mycelium on seed. During warm, moist weather in late summer, conidia are exuded from pycnidia in long cirri and disseminated by
splashing rain or, after cirri have dried up, by wind. Insects are also reported to disseminate spores.
Infection occurs late in the development of the kernel. Some researchers state ears are most susceptible to infection beginning at the silking stage of plant growth and
continuing for 21 to 24 days afterward, when kernels have reached a moisture level of 75.4 to 90.0%. A decrease of 5% in the moisture content of kernels is
associated with a reported de

Page 269
crease of up to 22% in the incidence of ear rot. Resistance to infection occurs 28 days after midsilk, when the moisture content of kernels is approximately 66%. As
ears approach maturity, rot slows and ceases completely when kernels reach approximately 21% moisture.
Infection commonly starts at the base of husks or on an exposed ear tip, but mycelium can advance from the stalk through the shank. Diplodia maydis enters the
pedicel and penetrates through the hilar region. The hilar layer (black layer) of the hilum is impermeable to the fungus; therefore, entrance into the kernel occurs before
the closing layer is formed or delayed, or if suberization of testa membrane is incomplete. As ears grow in length, husks become loose and provide less protection at
the ear tip, allowing kernels to be more accessible to spores.
Pycnidia may be found on rotted ears, particularly on the inner husks. During wet weather, conidia are exuded and become windborne. Dry weather early in the
season followed by wet conditions before and after the silking stage of plant growth favors ear infection.
Diplodia maydis causes diplodiosis in sheep and cattle.
Distribution.
Symptoms.
Diseased seeds fail to germinate and become soft or overgrown with white mycelium. Seedling mesocotyls become watersoaked and seedlings die in 2 to 3 days.
Management
2. Harvest early to prevent grain from being weathered.
3. Dry maize to 15% or less moisture content.
4. In programs for breeding resistance to ear rot, ear inoculations should be made at or shortly after midsilk.
Diplodia Stalk Rot
Diplodia ear rot, Diplodia seedling blight, and Diplodia stalk rot caused by Diplodia maydis are considered as parts of a single disease complex.
Cause.
residue, and as conidia and mycelium on seed. During warm, moist weather in late summer, conidia are exuded from pycnidia in long cirri and disseminated by
splashing rain or, after cirri have dried up, by wind. Insects are reported to disseminate spores.
Stalk rot infection occurs most frequently at the origin of leaf sheaths at any of the first three nodes above the soil line and infrequently at a higher

Page 270
node. Some infections also occur at the junction of the brace roots with stalks, on roots at the soil level, and through the mesocotyl from infected seed or infested soil.
Stenocarpella maydis then grows up into the stalk and down into roots, but the entire plant is usually not invaded. Temperatures of 28° to 30°C and wet weather 2
to 3 weeks after silking favor spread and development of disease. Date of inoculation has little effect on rate of disease development in stalks.
Plants are predisposed to infection by a number of factors, such as excess nitrogen and low potassium, higher than recommended plant populations, and loss of leaf
area by hail, insects, and other diseases. Earlymaturing hybrids are more susceptible to stalk rot than longerseason hybrids. All of the factors are combined in the
photosynthetic stresstranslocation balance concept of predisposition hypothesis: Predisposition of maize to stalk rot is associated with a carbohydrate shortage in root
tissue caused by a combination of the reduction in photosynthesis by leaves and intraplant competition for carbohydrates by developing kernels. The carbohydrates,
formerly in root and stalk tissue, conferred a resistance to these tissues. When carbohydrates are transferred into the developing kernels, root tissue then has a
weakened defense system, which allows soil microorganisms to invade and decompose roots and stalks. Parenchyma rot and crown rot have been reported to be
more severe in plants with greater numbers of kernels, which is possibly related to the competition for carbohydrates.
Distribution.
Symptoms.
Stalk rot does not have a direct physiological effect on yield but is an important factor in stalk breakage. Symptoms appear several weeks after silking as grayish
green leaves that later turn brown, seemingly in a day or two, and give the impression of frost damage. Dark brown lesions extend in either direction from a diseased
node. The stalk pith is discolored and disintegrated, with only vascular bundles remaining intact, which causes stalks to become weak. In the autumn, dark brown to
black pycnidia form in clusters just beneath the epidermis of the lower diseased internodes. White fungal growth of D. maydis may be present on the surface of
nodes.
Management
1. Grow the most resistant hybrid. No inbred line or hybrid is completely resistant to stalk rot.
2. Balance soil fertility. Excess levels of nitrogen may predispose plants to stalk rot. Stalk rot is lowest when the level of nitrogen is adequate enough to allow a hybrid
to reach its yield potential. The severity of stalk rot in artificially inoculated plants has been reported to decrease

Page 271
with increasing rates of nitrogen applied as anhydrous ammonia in either spring or autumn.
3. Grow the recommended plant population. Higher than recommended plant populations cause plants to be stressed and have less resistance to infection.
Dry Ear Rot
Dry ear rot is also called cob rot and Nigrospora ear rot.
Cause.
Nigrospora oryzae overwinters as mycelium in infested soil residue. Conidia are formed on mycelium and are disseminated by wind. Nigrospora oryzae is a weak
parasite that infects either dead plants or plants stressed by other factors, such as stalk rot, leaf blight, cold weather, and root injury. Maize grown on soil with poor
fertility is more susceptible to infection than maize grown in fertile soil. Infection normally starts either at the butt end or at the tip of the ear.
Distribution.
Symptoms.
Diseased ears are light in weight but do not have external symptoms until harvest time. The ear cobs are soft and easily broken and have kernels that are either
bleached or have white streaks which start at the kernel tip and extend toward its crown. Kernels may be overgrown with gray mycelium and covered with groups of
spores that resemble small, round, black dots. When viewed under magnification, individual spores appear to be the size of pinpoints.
Management
1. Grow fullseason, adapted hybrids that are resistant to stalk rots and leaf blights.
Ergot
Ergot is also called horse's tooth and diente de caballo.
Cause.
Claviceps gigantea, anamorph Sphacelia sp., survives as sclerotia either on the soil surface or mixed with seed. In the spring, sclerotia germinate to produce stroma
on the ends of stipes. The stromatic head contains perithecia in which ascospores are produced, then are disseminated by wind to flowers. Macroconidia and
microconidia are produced in a sweet, sticky substance called honeydew, which is attractive to insects. Insects inadvertently carry conidia from diseased to healthy
flowers while feeding on honeydew. Disease development is optimum at temperatures of 13° to 15°C and high rainfall.
Distribution.
At higher elevations in central Mexico.

Page 272
Symptoms.
Sclerotia replace kernels. Sclerotia initially are creamcolored but later become dark gray, enlarge to 5 × 8 cm in size, and become commashaped, superficially
resembling a horse's tooth. Insects are present on honeydew, which becomes darkcolored due to dust and other material adhering to it.
Management.
No disease management is practiced, but some lines are more susceptible than others.
Eyespot
Eyespot is also called brown spot.
Cause.
Aureobasidium zeae (syn. Kabatiella zeae) overwinters as mycelium in infested residue on the soil surface and is seedborne. Conidia produced on residue are
disseminated by wind to nearby plants. Secondary infection is by conidia produced on new lesions and disseminated by wind and splashed by rain to other host plants.
Disease development is favored by cool, humid weather. Older leaves are more susceptible to infection than younger ones. Maize is the only plant that is known to be
a host for A. zeae.
Distribution.
Argentina, Austria, Brazil, Canada (Ontario), France, Germany, Japan, New Zealand, the United States (north central states and Pennsylvania), and Yugoslavia.
Symptoms.
The first symptoms on leaves are small, translucent or watersoaked, ovoid to circular spots (25 mm in diameter). These symptoms may be confused with genetic
spotting or Curvularia leaf spots. Later, the centers of the spots die, become tancolored, and are surrounded by a narrow, brown to purple ring with a chlorotic halo.
Spots develop in zones or patches on diseased leaves rather than occurring randomly scattered over leaf blades. Eventually, the spots coalesce and form large necrotic
areas that are still distinguishable as spots after leaf death. Spots also develop on leaf sheaths, husks, and kernels.
Management
3. Rotate maize with resistant crops.
False Smut
Cause.
Ustilaginoidea virens. Disease development is favored by hot, wet weather. Rice and other grasses in the Graminae are hosts.
Distribution.
Generally wherever maize is grown, but false smut is rare.
Symptoms.
Sclerotia, sometimes referred to as galls or smut balls, usually replace a few to several flowers on diseased tassels. Sclerotia are irregular and

Page 273
subsphericalshaped (415 mm in diameter), olivegreen to black, and have a velvety texture. A sclerotium is composed of three layers: (1) an outer greenish layer of
mature spores, (2) a middle layer of a light yellowishgreen mass composed of mycelium, and (3) an inner yellowish layer consisting of host tissue, growing mycelium,
and spores. As sclerotia mature, the membrane ruptures and exposes and liberates spores. The surface of the gall gradually becomes roughened.
Management.
Not necessary.
Fusarium avenaceum Stalk Rot and Seedling Root Rot
Fusarium avenaceum stalk rot may be the same or similar to Gibberella stalk rot.
Cause.
Fusarium avenaceum. The fungus is reported to form toxins harmful to animals.
Distribution.
Widely distributed.
Symptoms.
Diseased stalks are brown to graygreen and have a pinkish, disintegrated pith in which just the vascular bundles remain. Dark lesions may sometimes appear at nodes
and extend into internodes. Roots of seedlings have a brown discoloration typical of symptoms of other root rots.
Management
1. Grow the least susceptible hybrid.
3. Grow the recommended plant population.
Fusarium globosum Kernel Infection
Cause.
Fusarium globosum.
Distribution.
South Africa.
Symptoms.
Fusarium globosum was isolated from harvested maize kernels that were asymptomatic.
Management.
Not reported.
Fusarium Kernel Rot
Fusarium kernel rot is also called Fusarium ear rot.
Cause.
Fusarium moniliforme, teleomorph Gibberella fujikuroi. According to Nelson et al. (1983), F. subglutinans and F. proliferatum share many morphological
characteristics with F. moniliforme and may be involved in the same disease syndrome.
Fusarium subglutinans is separated taxonomically from F. moniliforme on

Page 274
the following basis: Fusarium subglutinans bears microconidia on polyphialides only in false heads and not on microconidial chains, whereas F. moniliforme bears
microconidia both in false heads and in long chains. Fusarium proliferatum is separated from F. moniliforme in that F. proliferatum also bears microconidia in
chains of various lengths and in false heads but it forms microconidia in chains on polyphialides, whereas F. moniliforme forms microconidia in chains on
monophialides. It is likely these fungi have been misidentified or confused with each other. Some researchers still consider the three fungi to be synonymous,
presumably on the basis of their morphology.
Fusarium moniliforme survives in crop residue as thickened hyphae or chlamydosporelike structures and in kernels, but the fungus does not survive for long periods
in soil. Macroconidia and abundant microconidia are thought to be produced on crop residue and disseminated by wind to host plants. The pathway of infection into
kernels can occur by one of four ways:
1. Airborne conidia infect exposed kernels. This entry may be facilitated by injuries from cracks made by weather or other means and by insects, including corn
earworms; corn borers, particularly the European corn borer, Ostrinia nubilalis; and rootworm beetles, such as the western corn rootworm beetle, Diabrotica
virgifera. The insects also may be important in spreading fungi to ears and kernels. It has also been suggested that a relatively thin pericarp layer, which is found in
susceptible hybrids, allows access of the fungus into the kernels, especially through insect wounds.
2. Spores germinate and mycelia grow down silks through the tip ends of ears, over the surface of kernels into bracts and pedicels, into the vascular cylinder of the
cob, and, finally, into kernels. The location of F. moniliforme in asymptomatic kernels is the pedicel, or tip cap end, of kernels, suggesting the point of entry is the
same. Sporulation of the fungus on the tassels may contribute to silk infection.
3. A systemic invasion of the shank, where fungal growth proceeds through the stalk from some entryway, or by entering the ruptured scar on the pericarp produced
by the emerging coleorhiza after kernel germination. The fungus then proceeds to grow through the stalk into the cob, rachilla, and pedicel.
4. Symptomless infection can exist throughout an infected plant, and seedtransmitted strains of the fungus can develop systemically to infect kernels in an endophytic
relationship.
Munkvold et al. (1997) concluded that systemic development of F. moniliforme from maize seed and stalk infections can contribute to kernel infection, but silk
infection is a more important pathway for this fungus to reach the kernels.

Page 275
Extensive colonization of kernel surfaces occurs early in the season, but little internal infection occurs until kernel moisture is lower than 34%. Disease development is
generally favored by dry, warm weather. The presence of F. moniliforme increases as harvest is delayed beyond physiological maturity. Fusarium moniliforme
does not grow in grain with a moisture content below 18 to 20%.
Generally fumonisin (a class of mycotoxins that have cancerous activity) concentrations are not thought to increase during storage as long as proper conditions of grain
moisture and temperature are maintained. Fusarium moniliforme undergoes extensive growth and sporulation in the embryo and endosperm of kernels associated
with toxicity to animals.
Gibberella fujikuroi consists of at least seven distinct mating populations, designated A through G. Populations of A, D, and E are the most common on maize and
correspond to the particular anamorph species. Both A and F mating populations are considered to be F. moniliforme; population A contains many prolific
fumonisinproducing strains, while members of the F population produce little or no fumonisin. Most strains of F. moniliforme found on maize are population A, and
most found on sorghum are F. Population D is considered to be F. proliferatum and contains many strains that produce copious amounts of fumonisins. Fusarium
proliferatum was demonstrated to produce beauvericin, fumonisin B1, and moniliformin in maize grown in Italy. Populations B and E are considered to be F.
subglutinans and produce little or no fumonisin. In maize grown in temperate regions, F. moniliforme and F. proliferatum represent the greatest threat of fumonisin
production.
Distribution.
Symptoms.
Fusarium kernel rot does not involve the entire ear; it occurs on kernels at the tips of ears, scattered over the ear, or where there has been insect damage. The color of
diseased kernels varies from faint pink to reddish brown. As disease progresses, kernels have an external powdery or cottony pink mold growth on them.
Symptomless infections can exist throughout some plants in an endophytic relationship. Such kernels are a source of inoculum for seedling blight and stalk rot.
Asymptomatic kernels are as toxic as cracked kernels and plant parts obviously colonized by fungi. Hyphae are restricted to intercellular spaces during symptomless
infection, while the hyphae of diseasecausing strains are found in both intercellular and intracellular sites.
Seedlings grown from inoculated kernels had suppressed shoot diameter, plant height, leaf length, and plant weight 7 days after sowing. However, at 28 days, seedling
growth from inoculated kernels was similar to or greater than that from noninoculated kernels. Histological modifications in seedlings grown from inoculated kernels
included accelerated lignin deposition in shoots and modified chloroplast orientation in leaves.

Page 276
Fumonisins are most common in maize screenings, which are the broken kernels and other fine material removed from grain passed over a wire screen. In Nebraska,
fumonisins are responsible for the moldy corn disease of horses, cattle, mules, hogs, and chickens. The most dramatic manifestation of moldy corn disease is equine
leucoencephalomalacia (ELEM), a fatal brain disease of horses, donkeys, mules, and rabbits. In horses, this disease results in death within a few hours to 1 week after
fumonisin B1 is ingested at concentrations of 5 to 10 ppm. ELEM in horses is known by the popular term ''blind staggers."
Other mycotoxins include fusarin C and moniliformin. Infested maize is carcinogenic, immunosuppressive, hepatotoxic, and nephrotoxic to animals. Fumonisin
contaminated maize has also been associated with porcine pulmonary edema in swine and is reported to be a mild carcinogen or tumor promoter in animals.
Management.
There are no proven, practical methods for significantly reducing fumonisin concentrations in maize. The following are aids in disease management:
1. Avoid growing hybrids that are most susceptible. Hybrids with poor husk covers or weak seed coats, in which kernels pop or silkcut, are susceptible to infection.
Differences in resistance are conditioned by genotype of the pericarp. In mature stages, sweet maize and some highlysine hybrids are very susceptible to Fusarium ear
rot. Commercial hybrids differ in their tendency to accumulate fumonisins. Hybrids grown outside their adapted range tend to accumulate higher concentrations of
fumonisins.
2. Harvest grain early to prevent deterioration from weather.
4. Resistance has been identified in a sweet maize inbred.
Fusarium Leaf Spot
Cause.
Fusarium moniliforme is a fungus that also causes kernel rot and stalk rot. Disease is favored by dry, warm weather.
Distribution.
The Caribbean region.
Symptoms.
Watersoaked spots that initially appear on whorl leaves eventually become white with brown borders and have a papery texture. The whorl does not open, and leaf
tips turn down. Occasionally, necrotic spots develop high on a stalk.
Management.
Not reported.
Fusarium scirpi in Grain
Cause.
Fusarium scirpi (syn. F. equiseti).

Page 277
Distribution.
Australia, China, South Africa (Transkei).
Symptoms.
Fusarium scirpi was isolated from grain and is toxic to animals when grown both in vivo and in vitro. Fungal metabolites induced chromosomal aberrations in animal
cells.
Management.
Not reported.
Fusarium Stalk Rot
Cause.
Fusarium moniliforme, F. proliferatum, and F. subglutinans, teleomorph Gibberella fujikuroi. According to Nelson et al. (1983) F. subglutinans and F.
proliferatum share many morphological characteristics with F. moniliforme and may be involved in the same disease syndrome.
Fusarium subglutinans is separated taxonomically from F. moniliforme on the following basis: Fusarium subglutinans bears microconidia on polyphialides only in
false heads and not on microconidial chains, whereas F. moniliforme bears microconidia both in false heads and in long chains. Fusarium proliferatum is separated
from F. moniliforme in that F. proliferatum also bears microconidia in chains of various lengths and in false heads but it forms microconidia in chains on
polyphialides, whereas F. moniliforme forms microconidia in chains on monophialides. It is likely these fungi have been misidentified or confused with each other.
Some researchers still consider the three fungi to be synonymous, presumably on the basis of their morphology.
Fusarium moniliforme is seedborne and survives as thickened hyphae or chlamydosporelike structures and mycelium in infested corn residue that was either
precolonized parasitically or colonized when placed in soil. Residue of other plants may also be colonized in the soil by F. moniliforme. The teleomorph, G.
fujikuroi, survives more than 1 year in residue that is buried in the soil. Fusarium moniliforme does not survive in soil outside of residue. Infected kernels lacking
symptoms are a source of inoculum for seedling blight and stalk rot.
Before pollination, stalks are infected by conidia produced on residue and disseminated by wind to the bases of leaf sheaths and into corn borer wounds, where
infective hyphae enter the plant. Roots are infected, either through direct penetration or insect wounds, by mycelia that grow through soil from a previously colonized
substrate. Fusarium moniliforme also attracts the root lesion nematodes, Hoplolaimus indicus, Meloidogyne incognita, M. javanica, Pratylenchus brachyurus,
P. zeae, and Tylenchorhynchus vulgaris, and aids their penetration into seedling roots.
Disease development is aided by warm, dry conditions, excess soil nitrogen, and higher than recommended plant populations, which stress plants, predisposing them
to infection. Stalk rot is reported to be less in notillage systems than in either conventional tillage systems or plowing harvested fields in the autumn. Senescing tissues
caused by water stress, high

Page 278
populations of the Banks grass mite, Oligonychus pratensis, and the twospotted spider mite, Tetranychus urticae, are reported to increase incidence and severity
of stalk rot. Parenchyma rot and crown rot are reported to be more severe in diseased plants with a greater numbers of kernels.
Gibberella fujikuroi consists of at least seven distinct mating populations, designated A through G. Populations of A, D, and E are the most common on maize and
correspond to the particular anamorph species. Both A and F mating populations are considered to be F. moniliforme; population A contains many prolific
fumonisinproducing strains, while members of the F population produce little or no fumonisin, a class of mycotoxins that have cancerous activity. Most strains of F.
moniliforme found on maize are population A, and most found on sorghum are F. Population D is considered to be F. proliferatum and contains many strains that
produce copious amounts of fumonisins. Fusarium proliferatum was demonstrated to produce beauvericin, fumonisin B1, and moniliformin in maize grown in Italy.
Populations B and E are considered to be F. subglutinans and produce little or no fumonisin. In maize grown in temperate regions, F. moniliforme and F.
proliferatum represent the greatest threat of fumonisin production.
Distribution.
Symptoms.
Symptoms are generally similar to Gibberella stalk rot. Rotting affects diseased roots and lower internodes. Nodes have dark lesions without definite margins, and
leaves become brown, resembling frost injury. Pith disintegration begins after pollination, although plants are infected earlier in the season. Pith tissue is shredded; only
the vascular bundles remain intact. White to pale pinkcolored mycelium grows on the surface of diseased nodes in wet weather.
Symptomless infections can exist throughout some infected plants in an endophytic relationship. Hyphae are restricted to intercellular spaces during symptomless
infection, whereas hyphae of diseasecausing strains are found in both intercellular and intracellular sites.
Management
1. Grow the most resistant hybrids.
Fusarium thapsinum Infection
Cause.
Fusarium thapsinum, teleomorph Gibberella thapsina. Fusarium thapsinum and F. moniliforme are similar morphologically and may be confused in the
literature.
Distinguishing F. thapsinum from F. moniliforme is accomplished by crosses with standard femalefertile tester strains. Fusarium thapsinum produces a yellow
pigment in culture; F. moniliforme does not. Fusarium thapsinum does not produce fumonisins; F. moniliforme does. Fusarium

Page 279
thapsinum produces moniliformin; F. moniliforme does only rarely. Fusarium thapsinum is sensitive to hygromycin; F. moniliforme is not. Therefore, it is
suggested that the numerous reports in the literature assigning the predominant Fusarium species associated with head blight of sorghum to F. moniliforme and
consider this organism to be the same one responsible for stalk and ear rot in maize may be erroneous.
It is implied that the nonproduction of fumonisins or the production of large amounts of moniliformin by isolates of F. moniliforme from sorghum probably refer to
strains of F. thapsinum rather than to strains of F. moniliforme. This difference also implies that sorghum is more likely to be naturally contaminated with moniliformin
than with fumonisins, and maize is more likely to be naturally contaminated with fumonisins instead of moniliformin.
Distribution.
Egypt, the Philippines, South Africa, Thailand, and the United States (Alabama, Arkansas, Georgia, Illinois, Kansas, Mississippi, Missouri, Ohio, and Texas).
Symptom.
Fusarium thapsinum has been isolated from diseased stalks and seeds. The fungus has also been isolated from asymptomatic seed, stems, roots, and crowns of
sorghum, suggesting F. thapsinum may be endophytic in this plant. Pathogenicity of the fungus has not been tested under field conditions on maize, but under
greenhouse conditions some strains can cause lesions in sorghum stalks following toothpick inoculations.
Management.
Not reported.
Gibberella Ear Rot
Gibberella ear rot is also called red ear rot.
Cause.
Gibberella zeae, anamorph Fusarium graminearum, overwinters as chlamydospores in soil, perithecia and mycelia in residue, and mycelia and conidia on seed. The
fungus F. crookwellense has been isolated from ears that bear symptoms similar to those caused by F. graminearum. To date, no teleomorphic stage is known for
F. crookwellense.
Perithecia are produced on residue in the autumn or spring. Rainfall may be needed for perithecial and ascospore formation and maturity on crop residue but not to
trigger the actual release of ascospores. Perithecial drying during the day followed by sharp increases in relative humidity may provide the stimulus for release of
ascospores. In eastern Canada, ascospores were released during the first 3 weeks of July in a diurnal pattern that began around 1600 to 1800 hours and reached a
peak before midnight, then declined to low levels by 0900 the following morning. The beginning of ascospore release was correlated with a rise in relative humidity
during the early evening hours.
During warm, moist weather early in the season, conidia of F. gramin

Page 280
earum are produced from mycelia in 1yearold infested residue. Shortly after pollination, during similar weather conditions, ascospores are exuded from perithecia.
Both conidia and ascospores are disseminated by wind to host plants. Sap beetles, Glischrochilus quadrisignatus, also disseminate conidia and ascospores to ears,
primarily as secondary inoculum. In some areas, Group 2 isolates, which are mostly windborne and cause disease of aboveground plant parts, dominate. These
eventually form perithecia. On wheat, F. graminearum Group 2 readily produces perithecia in culture, but F. graminearum Group 1, which is associated with crown
and root rot of wheat, does not.
Entry of F. graminearum into the ear often occurs via the silk and/or the silk channel and through bird or insect wounds. The pathogen spreads down the ear from the
ear tip, with the silks possibly providing a pathway to the kernels and rachis. Silk is most susceptible to infection when it has some brown tips after elongation and
pollination.
Cool, wet weather at silking favors development of disease. Ears with loose, open husks are more susceptible than those with good husk coverage. Inbreds and
hybrids differ in susceptibility.
Distribution.
Symptoms.
A reddish mold starts at the ear tip. Ears infected early in the growing season may rot completely. Husks adhere tightly to the ear because of mycelial growth between
husks and ears. Blueblack perithecia, which can be easily scraped off, are sometimes found on husks and ear shanks.
Fusarium graminearum produces the mycotoxins zearalenone, deoxynivalenol (vomitoxin), 3acetyldeoxynivalenol, and 15acetyldeoxynivalenol. Fusarium
crookwellense is known to produce the toxins nivalenol and fusarenone. The toxins deoxynivalenol and zearalenone are toxic to swine and may be produced in corn
affected by G. zeae. Zearalenone concentration may vary according to corn line and fungus isolate; however, it is interesting to note that lessvirulent isolates have
been reported to produce large quantities of zearalenone in culture and in diseased ears. Swine may refuse to eat maize containing vomitoxin, which causes vomiting,
dizziness, and, in severe cases, death. Infected maize is also toxic to humans, dogs, and other animals with similar digestive systems. Zearalenone produces estrogenic
disturbances that cause young gilts to come in heat and mammary glands of boar pigs to enlarge.
The highest concentration of deoxynivalenol is in the cob, followed by symptomatic kernels, with the lowest concentrations in symptomless kernels.
Management
1. Harvest early.

Page 281
3. Several inbreds display resistance. High concentrations of kernel (E)ferulic acid confer resistance.
4. Complete burial prevents inoculum production on infested residues.
5. Avoid successive crops of wheat or maize.
Gibberella Stalk Rot
Cause.
Gibberella zeae, anamorph Fusarium graminearum, overwinters as chlamydospores in soil, perithecia and mycelia in infested residue, and mycelia and conidia on
seed. Perithecia are produced on infested residue in the autumn or spring.
During warm, moist weather early in the season, conidia of F. graminearum are produced from mycelia in 1yearold residue. Shortly after pollination, ascospores
are exuded from perithecia. Rainfall may be needed for perithecial and ascospore formation and maturity on crop residue but not to trigger the actual release of
ascospores. Perithecial drying during the day followed by sharp increases in relative humidity may provide the stimulus for release of ascospores. In eastern Canada,
ascospores were released during the first 3 weeks of July in a diurnal pattern that began around 1600 to 1800 hours and reached a peak before midnight, then
declined to low levels by 0900 the following morning. The beginning of ascospore release was correlated with a rise in relative humidity during the early evening hours.
Both spore types are disseminated by wind and infect nodes just above the soil line. Fusarium graminearum grows into pith tissue late in the growing season as
tissues senesce. In some areas, Group 2 isolates, which are mostly windborne and cause disease of aboveground plant parts by infecting at the leaf sheaths, dominate.
These eventually form perithecia. On wheat, F. graminearum Group 2 readily produces perithecia in culture, but F. graminearum Group 1, which is associated with
crown and root rot of wheat, does not.
Another mode of infection common in some areas is the infection of roots by chlamydospores or mycelia. Eventually, the fungus grows into the crown and stalk.
Seedborne infection is not thought to result in stalk rot.
Gibberella stalk rot is prevalent in plants subjected to stresses that resuited in early senescence and a reduction of sugar to roots and stalks. Such plants are readily
invaded by fungi. Stresses are caused by a variety of factors, such as excessively high levels of nitrogen, low levels of potassium, and high plant populations.
The incidence and severity of stalk rot is lowest when the nitrogen level is adequate enough to allow a hybrid to reach its yield potential. Severity of stalk rot is
reported to decrease with increasing rates of nitrogen applied as anhydrous ammonia in spring or autumn. Stalk rot is less in notillage systems than in either
conventional tillage or fall plowing. There is evi

Page 282
dence that Gibberella stalk rot is prevalent in plants growing under favorable conditions early in the season but subjected to unfavorable conditions after silking.
Parenchyma rot and crown rot are reported to be more severe in plants with greater numbers of kernels.
Distribution.
Wherever maize is grown. In the United States, Gibberella stalk rot is most common in the eastern and northern maizegrowing areas.
Symptoms.
Symptoms appear several weeks after pollination. Leaves become grayish green, then quickly turn brown, which resembles damage caused by low temperatures.
Stalks are brown to graygreen and have a pinkish, disintegrated pith in which just the vascular bundles remain intact. Dark lesions appear at nodes and extend into
internodes. Infrequently, concentric rings appear in lesions on the outside of the stalk. Small, round, black perithecia, which are easy to scrape off, may occur on
diseased tissue.
Management
1. Grow the leastsusceptible hybrid.
Gray Ear Rot
Cause.
Botryosphaeria zeae (syn. Physalospora zeae), anamorph Macrophoma zeae, overwinters as sclerotia in infested ear and kernel residue and as pycnidia and
perithecia in infested leaf residue. In the spring, ascospores from perithecia and conidia from pycnidia are disseminated by wind or splashing rain to infection sites on
leaves and ears. Occasionally, infection occurs on the tassel neck or under the sheath of the uppermost leaf. Perithecia and pycnidia are eventually formed only in leaf
lesions, and sclerotia only in ears and kernels. Disease development is favored by long periods of warm to hot, wet weather for several weeks after silking.
Distribution.
The eastern United States.
Symptoms.
Gray ear rot resembles Diplodia ear rot in its early stages. A gray mycelial growth develops on and between kernels near the base of the ear. Early infection results in
bleached husks that adhere tightly to ears. At harvest, ears are slate gray, light in weight, and remain upright. Cobs will have sclerotia, evident as black specks,
scattered within them. Kernels may have black streaks beneath the seed coat.
Management.
Grow hybrids resistant to Diplodia ear rot since these genotypes may also be resistant to gray ear rot.
Gray Leaf Spot
Gray leaf spot is also called Cercospora leaf spot.

Page 283
Cause.
Cercospora zeaemaydis and C. sorghi (syn. C. sorghi var. maydis). A Mycosphaerella sp. is thought to be the teleomorph of C. zeaemaydis.
Cercospora zeaemaydis overwinters as mycelium in infested residue on the soil surface. Conidia are then produced from mycelia during wet weather and
disseminated by wind to host plants. In the north central United States, sporulation does not occur on overwintered tissue buried in soil.
Infested residue has a significant effect on disease severity. Any tillage method leaving residue on the soil surface favors gray leaf spot development. Disease incidence
and severity increases proportionately to the amount of infested residue on the soil surface. Tillage systems leaving greater than 35% residue cover may result in high
disease levels, especially under environmental conditions favorable for disease development.
Plants are infected at all stages of growth. Although early infection favors disease development, symptoms develop best later in the growing season, possibly due to a
thick plant canopy creating a favorable microclimate. Research in Maryland found low populations of maize sown early in the growing season had more severe disease
than latersown maize. No differences were observed between low and high plant populations with latesown maize.
Disease development is favored by temperatures of 22° to 30°C and long daily periods of high relative humidity and leaf wetness. Maize dwarf mosaic virus is
reported to predispose plants to gray leaf spot.
Genetic differences exist between isolates of C. zeaemaydis. Barnyard grass, johnsongrass, and Sorghum spp. are susceptible to C. zeaemaydis. Zeae
diploperennis, Z. mays subsp. luxurians, and Z. mays subsp. mexicana develop typical eyespot lesions when inoculated.
Distribution.
Africa, Central America, China, Europe, India, Mexico, the Philippines, northern South America, Southeast Asia, and the eastern and midwestern United States.
Symptoms.
General symptoms appear on the lower leaves of mature plants that are at or near anthesis and on the higher leaves of diseased plants later in the season. Initially,
reddish, watersoaked spots occur that later become narrow, rectangularshaped (5 cm long), tan or pale brown lesions restricted by leaf veins. Lesions may have a
grayish cast when C. zeaemaydis sporulates. Lesions may eventually coalesce and kill the leaf. During severe disease conditions, all leaves may be killed. Severe
stalk rot and breakage may occur.
Lesion type influences disease progress. Many susceptible inbreds display necrotic lesions, moderately resistant hybrids display chlorotictype lesions, and resistant
inbreds display flecktype lesions.
Management

Page 284
Green Ear Downy Mildew
Green ear downy mildew is also called Graminicola downy mildew.
Cause.
Sclerospora graminicola overwinters as oospores in soil and on seed. Primary infection likely occurs by oospores germinating to form germ tubes that penetrate corn
leaves. Infection is favored by temperatures of 24° to 32°C for 2 days after planting. Secondary spread is by formation on diseased leaves of sporangia, which are
disseminated by wind to host leaves. Sporangia commonly germinate indirectly by releasing three or more zoospores. Each zoospore then germinates to form a germ
tube. Infrequently, sporangia germinate directly to form only a single germ tube. Oospores are eventually formed in diseased tissue later in the growing season. Disease
development is favored by high humidity, light rains or heavy dews, and a temperature of 17°C (optimum).
Distribution.
Israel and the United States. Green ear downy mildew occurs on various grasses throughout the world, but it is not an economically important disease on corn.
Symptoms.
Symptoms appear about 10 days after the plumule emerges. Diseased plants are stunted, and chlorotic streaking, together with gray blotching and mottling, occurs on
leaves. A white, downy growth consisting of mycelium and sporangia occurs on discolored areas. Leaves may be thick, corrugated, and fragile. Sometimes diseased
plants will outgrow the disease.
Management.
Not necessary.
Head Smut
Head smut is also called ear and tassel smut.
Cause.
Sporisorium holcisorghi (syn. Sphacelotheca reiliana, Sorosporium reilianum, and Ustilago reiliana) overwinters as teliospores in soil and on seed. Survival is
better in dry than in moist soil. Teliospores germinate to infect seedlings either directly by producing a germ tube or indirectly by producing a basidium on which
sporidia (basidiospores) are formed. Sporidia of opposite mating types fuse to form a germ tube or hyphae. Soil temperatures of 23° to 30°C and moderate to low
soil moistures (1.5 bar is the maximum) are optimum for seedling infection. Mycelia develop systemically and invade undifferentiated floral tissues that partly or wholly
develop into smut sori in which teliospores are produced. Disease is accentuated by nitrogen deficiency.
Other hosts include pitscale grass, sorghum, and sudangrass. Pathogenic specialization occurs. It has been determined that a single race infects maize; another race
infects grain sorghum, foragesorghum hybrids,

Page 285
and some sudangrass varieties. A "hybrid" of S. reiliana has been identified that infects both maize and sorghum.
Distribution.
Drier soils of Australia, southeastern Europe, India, western Mexico, New Zealand, Russia, South Africa, the United States, and Yugoslavia.
Symptoms.
The most obvious symptom is the development of sori (galls) on tassels and infrequently on "normalappearing" vegetative leaves. Occasionally, sori develop as long,
thin stripes in leaves. Galls are covered by a membrane that breaks open to expose a powdery spore mass and the host vascular bundles. The appearance of vascular
bundles and leafy proliferations on tassels or ears when they are only partially converted to galls distinguishes head smut from common smut. Plants with smutted
tassels do not produce pollen, and they may be dwarfed and have numerous tillers. When the tassel is not diseased, most ears except for a few "nubbins" will be
smutted, rounded, and lack silks. Sometimes multiple ears appear at nodes. Less obvious chlorotic spots begin to develop on the fourth or fifth emerged leaf of
seedlings and, thereafter, on successive leaves.
Management
3. Fungicides applied to soil at or before sowing may be useful in reducing inoculum.
4. Apply a fungicide seed protectant.
Hormodendrum Ear Rot
Hormodendrum ear rot is also called Cladosporium rot.
Cause.
Cladosporium herbarum and C. cladosporioides (syn. Hormodendrum cladosporioides) infect kernels through growth cracks or cracks caused by early frost.
Distribution.
Symptoms.
Symptoms are not obvious until harvest, when greenishblack streaks occur on kernels. The discoloration starts where kernels are attached to the cob and grows
upward but seldom reaches the crown. After harvest, deterioration may occur if maize is stored when its moisture content is too high.
Management.
Not necessary.
Hyalothyridium Leaf Spot
Cause.
Hyalothyridium maydis causes disease under humid conditions.

Page 286
Distribution.
Colombia, Costa Rica, and Mexico.
Symptoms.
Two types of symptoms occur on diseased leaves. One symptom is small, tan, elliptical spots with brown borders. The other is large (1.5 cm in diameter), tan, circular
blotches that cover much of the leaf surface. Pycnidia are found in both types of lesions. In some areas only the smaller leaf spots are found.
Management.
Not reported.
Java Downy Mildew
Cause.
Peronosclerospora maydis (syn. Sclerospora maydis) overseasons in diseased maize plants. The fungus is seedborne as internal mycelium, but this is not thought to
be an important source of inoculum. Peronosclerospora maydis is not known to form oospores. Conidia are produced at 18° to 23°C in the presence of dew for S
to 6 hours.
All Java downy mildew outbreaks on maize and sweet maize in northern Australia since 1970 have been in areas where plume sorghum, Sorghum plumosum, occurs,
suggesting it is an alternate host. It is not known for certain if resting spores are produced in plume sorghum.
Conidia are disseminated by wind to young plants and germinate under conditions of darkness, free moisture, and temperatures below 24°C. However, some
researchers state the temperature range for optimum germination is 10° to 30°C and for optimum germ tube growth, 18° to 30°C. Germ tubes enter plants through
stomata. High levels of systemic infection occur at temperatures of 8° to 36°C. Conidia are produced on wet leaves in the dark. Maize sown late in the growing
season is most vulnerable to infection early in the rainy season, particularly if maize follows maize or sugarcane and is overfertilized with nitrogen.
Distribution.
Australia and Indonesia.
Symptoms.
Diseased leaves of plants younger than 4 weeks initially have white to chlorotic streaking that later becomes necrotic. A white, downy growth consisting of mycelium,
conidiophores, and conidia commonly occurs in chlorotic streaks. Systemic infection results in chlorosis of the upper leaves. Diseased plants may be stunted and
sterile, and lodge.
Management
1. Grow resistant hybrids and varieties.
2. Treat seed with a systemic fungicide.
Late Wilt
Cause.
Cephalosporium maydis is soil and seedborne. Seedlings are more susceptible to infection than older plants. Infection occurs through the roots and mesocotyls of
host plants, then develops slowly in the xylem tissue

Page 287
until rapid plant growth occurs at tassel emergence. Disease development is favored by light, sandy and heavy, clay soils.
Distribution.
Egypt and India.
Symptoms.
Diseased leaves wilt at the tasseling stage of plant growth, turn dull green, then dry up. Vascular bundles are discolored, and the lower portions of stalks dry up and
become hollow and shrunken. Secondary organisms may cause a wet rot.
Management
Cause.
Leptosphaeria maydis.
Distribution.
Humid areas at high altitudes in the Himalayas.
Symptoms.
Leptosphaeria leaf spot is most obvious on lower diseased leaves at silking and tasseling stages of plant development. Small, light tan lesions form that enlarge to
become either concentricshaped or streaked. These latter symptoms suggest two separate diseases.
Management.
Not reported.
Nigrospora Stalk Rot
Nigrospora stalk rot is associated with dry ear rot.
Cause.
Nigrospora oryzae overwinters as mycelium in infested soil residue. Conidia are formed on mycelia and are disseminated by wind to host plants. Plants nearing
maturity and weakened by poor fertility, diseases, or injury are infected through stomates in the stalks.
Distribution.
Generally wherever maize is grown, but Nigrospora stalk rot is not a serious disease.
Symptoms.
Superficial, dark gray to black lesions with a slight bluish cast form on diseased lower internodes. Discoloration may appear as several tiny lesions or larger, irregular
shaped blotches.
Management.
Maintain wellfertilized soil.
Northern Leaf Blight
Northern leaf blight is also called crown stalk rot, northern blight, northern corn leaf blight, stripe, Turcicum leaf blight, and white blast.

Page 288
Cause.
Exserohilum turcicum (syn. Bipolaris turcica, Dreschlera turcica, and Helminthosporium turcicum), teleomorph Setosphaeria turcica. Exserohilum turcicum
is a heterothallic ascomycete that overwinters as chlamydospores (converted from conidia), conidia, and mycelia in leaf midribs and sheaths. Successive nights of
temperatures at approximately 10°C induce formation of chlamydospores. In Israel, E. turcicum also overwinters on sorghum plants.
In spring, conidia are formed from mycelia in residue and are disseminated for long distances by wind or splashed by rain to lower leaves. Infection occurs when leaf
surfaces are wet during temperatures of 18° to 27°C. Successive spores are produced following warm nights with 10 to 12 hours of 90% or more relative humidity
and are spread to higher leaves. The proximal portions of leaf blades are less susceptible than distal portions. Disease is more severe under notillage conditions and
when no tillage has occurred before or after sowing than with mulchtillage and with autumn and spring cultivation without the use of a moldboard plow.
Five physiologic races were known to exist and several new races have now been reported from maize grown in China, Mexico, Uganda, and Zambia. Race 0 is
widely distributed in many parts of the world. Race 1 was first detected in 1974 in Hawaii but is now widespread in the maize belt of the United States. Race 23 and
race 23N are restricted to the continental United States. Race 2N was reported in Hawaii. Other races have been reported from matings of isolates in the laboratory.
Sweet maize is more susceptible than field maize. Sorghum, sudangrass, johnsongrass, garnagrass, and teosinte also become diseased.
Distribution.
Wherever maize is grown in a humid area. Northern corn leaf blight is common in the eastern United States.
Symptoms.
Lesions first appear on diseased lower leaves. As the season progresses, lesions develop on upper leaves. Susceptible plants that become severely diseased may be
killed and their leaves covered with lesions that give the appearance of low temperature or frost injury. Because lesions compete for resources within a leaf, heavy
disease pressure often results in smaller, numerous lesions, rather than fewer, larger ones. Typically, lesions on susceptible plants are graygreen to tan and elliptical
shaped. Lesions usually are 1.3 × 5.010.0 cm but occasionally grow as large as 3.8 × 15.0 cm. During damp weather, dark olive to black conidia produced on leaf
surfaces often form concentric zones that give lesions a targetlike appearance. Husks can be infected, but ears and kernels are not.
Symptoms on plants with monogenic resistance conferred by genes Ht1, Ht2, and Ht3 are characterized by chlorotic lesions with little or no sporulation. When the
Ht2 gene is present, lesions on some hybrids will be long, narrow, chlorotic streaks extending the length of leaves and may be confused with symptoms of Stewart's
wilt. The HtN gene delays lesion de

Page 289
velopment until shortly after pollination. Plants with polygenic resistance have fewer and smaller lesions.
A chlorotic halotype symptom is governed by a single recessive gene. The symptom is characterized by a distinct dark orangebrown pigment that later becomes
surrounded by a circular chlorotic halo about 1 cm in diameter. Most infection points in this genetic stock retain the chlorotic halo phenotype until plant senescence,
but some develop into typical elongated, necrotic northern leaf blight lesions.
Management
1. Grow resistant hybrids. Resistance is of two types: monogenic and polygenic. Monogenic resistance genes are Ht1, Ht2, Ht3, and HtN. Polygenic resistance is
partial resistance effective against all biotypes.
3. Plow under infested residue to reduce inoculum.
Northern Leaf Spot
Northern leaf spot is also called Carbonum corn leaf spot, Helminthosporium leaf spot, and northern corn leaf spot.
Cause.
Bipolaris zeicola (syn. Drechslera carbonum, D. zeicola, Helminthosporium carbonum, and H. zeicola) teleomorph Cochliobolus carbonum. Bipolaris zeicola
overwinters as mycelia and conidia in infested residue. Conidia are produced from mycelia in the spring during moderate temperatures and wet weather and are
disseminated by wind or splashed to the lower leaves of maize. Wet weather also favors infection and subsequent disease development. Five physiologic races of B.
zeicola are known. These are designated 0 through 4. Northern corn leaf spot does not occur on commercial single or doublecross hybrids.
Distribution.
In the temperate maizegrowing areas of the world.
Symptoms.
Race 0 is avirulent on maize genotypes susceptible to races 1, 2, and 3.
Race 1 produces the hostspecific HC toxin, is highly virulent, and infects only a few inbred lines. Symptoms on diseased leaves are tan, oval to circular lesions that
vary from small spots to larger lesions (1 × 3 cm). A pattern of concentric zones often occurs in the lesions. During optimum disease conditions, lesions become
numerous. A black mold grows over kernels to give the diseased ear a charred appearance.
Race 2 isolates do not produce HC toxin, are not considered pathogenic, and show no distinct host specialization. However, Race 2 will infrequently penetrate leaves
and elicit small necrotic lesions. These Race 2 lesions are small, round to oblong or ovalshaped, chocolatecolored or necrotic spots that range in size from barely
visible to 0.5 × 2.5 cm. The ear rot caused by Race 2 is indistinguishable from that caused by Race 1.

Page 290
Race 3 causes symptoms on most maize inbred lines and hybrids and is frequently referred to as northern leaf spot or Helminthosporium leaf blight. Lesions are on
diseased leaf blades, sheaths, husks, and ears. Lesions on leaves are narrow and linear (0.52.0 × 15.020.0 mm), grayish tan, and surrounded by a light to dark
border. Ears are infected from the tip, butt, or through sides of the husk. A black mold develops over kernels.
Race 4 causes early and sudden leaf death. Leaves become reddish brown, which is suggestive of a toxin being produced by the fungus. Lesions within dead tissue are
oval to circularshaped (510 mm in diameter) and often contain concentric circles. Most susceptibility was expressed in inbreds with B73 background. Lesions on
some hybrid genotypes are smaller, nearly creamcolored, and without concentric circles. There is no seed infection.
A similar pathotype from Wisconsin caused foliage damage, which reduced yields of inbreds having a B73 background. Seed size, but not germination, was also
affected. A dry, brown to black internal and external discoloration of crowns occurred, but roots were unaffected.
Bipolaris zeicola also causes stalk rot characterized by rapid and severe necrosis of the nodes and internode pith.
Management
3. Differences in resistance exist among inbreds to Race 3. Some are highly resistant, others are susceptible, and many are intermediate in reaction. Inbreds are usually
more susceptible than hybrids.
Penicillium Rot
Penicillium rot is also called blueeye.
Cause.
Penicillium chrysogenum, P. expansum, and P. oxalicum occur on ears that have been injured by corn earworms or other causes. Penicillium spp. are soil
inhabiting fungi that enter kernels through uninjured pericarps (even at moisture contents as low as 14%), grow in the germ, and sporulate beneath the pericarp.
Penicillium spp. may invade seed embryos and cause seedling blight at low temperatures of 15§ to 20§C. Penicillium oxalicum loses its viability in seeds after
storage at room temperatures of 20§ to 25§C for 12 months.
Distribution.
Wherever maize is grown.
Symptoms.
Rot is most likely to occur on tips but may be found on other parts of ears. Kernels infected with P. oxalicum will have a grayish bluegreen mold, while other
Penicillium spp. cause a brighter bluishgreen mold.
Management.
Grain should be dried to 14% or less moisture content during storage.

Page 291
Phaeocytostroma Stalk Infection
Cause.
Phaeocytostroma ambiquum (syn. Phaeocytosporella zeae) overwinters as pycnidia in infested residue.
Distribution.
France and the United States (Illinois).
Symptoms.
Light tan, oblong blotches appear near the soil line on maturing stalks. Elongated pycnidia appear within lesions and have a short to long slit as an opening.
Management.
Not necessary.
Phaeosphaeria Leaf Spot
Cause.
Phaeosphaeria maydis (syn. Leptosphaeria zeamaydis, Metasphaeria maydis, and Sphaerulina maydis), anamorph Phoma sp. Phaeosphaeria maydis
survives in infested residue, presumably as pseudothecia and less commonly as pycnidia. Disease is favored by high rainfall and low night temperatures.
Distribution.
Brazil, Colombia, Costa Rica, India, and the United States (Florida).
Symptoms.
Initially, round to oblong, light green or chlorotic lesions (0.32.0 cm in diameter) occur randomly over diseased leaves. Later, lesions become white to light tan and
have distinct dark brown margins. Lesions may coalesce and form larger irregularshaped diseased areas in which perithecia and, infrequently, pycnidia are formed.
Management.
Most germplasm in the United States is not susceptible.
Philippine Downy Mildew
Cause.
Peronosclerospora philippinensis (syn. Sclerospora philippinensis). Some researchers consider P. philippinensis to be conspecific with P. sacchari.
Conidia are disseminated by wind and splashed by water to young plants. Peronosclerospora philippinensis is also seedborne. Leaves are penetrated by germ tubes
growing into stomata and then into the stem, where P. philippinensis becomes established in the shoot apex.
Conidia are produced at temperatures of 18§ to 23§C in the presence of moisture for 5 to 6 hours. Germination occurs at temperatures of 10§ to 30§C, and germ
tube growth occurs at 18§ to 30§C.
Other hosts include johnsongrass, sorghum, sugarcane, and teosinte.
Distribution.
Africa, India, Indonesia, Nepal, and the Philippines.
Symptoms.
The first diseased leaf may have systemic symptoms of either a general chlorosis or chlorotic streaks. The chlorotic streaks will commonly develop a downy growth
consisting of mycelium, conidia, and conidio

Page 292
phores. Ears may abort, which results in partial or complete sterility, and tassels may be malformed, resulting in less pollen. Infection of plants early in the growing
season results in stunted and dead plants.
Infection by maize streak virus often masks symptoms of Philippine downy mildew.
Management
2. Rogue and destroy diseased plants.
3. Apply systemic fungicide seed treatment and foliar spray.
Phomopsis Seed Rot
Cause.
Phomopsis sp.
Distribution.
The United States.
Symptoms.
Dark, ostiolate, globose, and erumpent pycnidia are present on diseased seed. Thin, smooth, creamywhite cirri emerge from pycnidia. A loss in germination occurs.
Management.
Not reported.
Physalospora Ear Rot
Physalospora ear rot is also called Botryosphaeria ear rot.
Cause.
Botryosphaeria festucae (syn. Physalospora zeicola), anamorph Diplodia frumenti, overseasons as perithecia and pycnidia in infested residue. Disease is favored
by warm, humid weather.
Distribution.
In tropical maizegrowing areas.
Symptoms.
Partially diseased ears have a few blackened kernels near the base. Severely diseased ears are covered by a dark brown to black, ''feltlike" mold.
Management.
Not reported.
Pyrenochaeta Stalk Rot and Root Rot
Pyrenochaeta stalk rot and root rot is also called red root rot.
Cause.
Phoma terrestris (syn. Pyrenochaeta terrestris) survives as pycnidia in infested soil residue. Plants are usually infected before pollination.
Distribution.
The United States (Delaware and Maryland), but Pyrenochaeta stalk rot and root rot is likely more widely spread.
Symptoms.
Only stalks below the soil surface are infected. Dark brown, shallow blotches occur on stalks. Later, a pink discoloration that is evident in the outer rind blends into
the dark brown areas.

Page 293
Management.
Maize hybrids vary in susceptibility. Pyrenochaeta stalk infection is not a serious disease.
Pythium Root Rot
Cause.
Pythium arrhenomanes and P. graminicola. Pythium torulosum and P. dissotocum are also reported to be associated to a lesser degree with Pythium root rot.
Pythium graminicola is reported to be the dominant causal fungus.
Pythium spp. survive in infested residue and soil as oospores and sporangia; however, some isolates do not form oospores. Infection is either by direct germination of
oospores and sporangia to form a germ tube or indirectly by zoospores formed in either structure and released into watersaturated soil. Zoospores "swim" to root
surfaces, where they encyst and germinate to form a germ tube.
Disease severity is greatest in poorly drained, wet soils. Pythium root rot is prevalent in the early spring and late summer.
Distribution.
Symptoms.
Secondary roots of diseased young plants have scattered yellowishbrown lesions that eventually coalesce and become dark brown to black, resulting in dark streaks
and girdling of roots. Diseased primary roots become black and necrotic. Similar lesions will be formed on new roots under wet soil conditions later in the growing
season. Sometimes new roots form above a lesion.
Stunting and chlorosis of lower leaves occurs on young plants. Diseased older plants may be generally stunted and also display chlorosis, rolling, and wilting of leaves.
Management.
Sow seeds into welldrained soil.
Pythium Seed and Seedling Blight
Cause.
Several Pythium species, including P. debaryanum, P. irregulare, P. paroecandrum, P. rostratum, P. splendens, P. ultimum, and P. vexans. The fungi survive
either as oospores, sporangia, or mycelia in infested residue.
Disease is severest in wet soils at temperatures of 10§ to 13§C. Under these conditions, seed germination and growth is slow, causing plants to become more
susceptible to infection. Sporangia either germinate directly to form a germ tube or germinate indirectly to form a vesicle in which zoospores are formed. Similarly,
oospores either germinate directly to form a germ tube or germinate indirectly to form a zoosporangium in which zoospores are formed. Zoospores "swim" by means
of flagella through soil water to host seeds and roots. Upon contact with a plant, a zoospore will encyst and germinate to produce a germ tube that directly penetrates
the seed or root. As mycelium grows through a plant, sporangia and oospores

Page 294
are produced both on and in the diseased plant.
Generally sweet maize is more susceptible than dent maize. Popcorn is the most resistant.
Distribution.
Symptoms.
Seeds may be rotted before germination and seedlings may be infected before or after emergence. Seeds are brown, soft, and overgrown with mycelia. It is difficult to
find diseased seeds in soil because of their rapid decomposition after infection and because of adhering soil that is bound to the seed by mycelium, making a diseased
seed indistinguishable from the surrounding soil. Roots are brown and watersoaked and have a "sloughed" appearance.
Aboveground symptoms are chlorosis, wilting, and death of leaves. Lesions on mesocotyls are initially brown and sunken. Eventually, mesocotyls become soft and
watersoaked.
Management
2. Do not sow seed stored for 2 or more years at temperatures between 15.5§ and 35.0§C.
3. Do not sow seed with cracked or split seed coats because cracks are an entrance for fungi.
4. Delay sowing until the soil temperature is 13§C and above.
Pythium Stalk Rot
Cause.
Pythium aphanidermatum (syn. P. butleri) survives as oospores, sporangia, or mycelia in infested soil residue. During humid weather at temperatures of 32§C and
higher or where air and soil drainage is poor, sporangia germinate either directly to form a germ tube or indirectly by releasing zoospores into the soil. Oospores
likewise may germinate either directly to form a germ tube or indirectly to form a zoosporangium in which zoospores are formed. Zoospores "swim" through soil water
to a host plant, where it germinates to form a germ tube that penetrates the plant.
Distribution.
Wherever maize is grown under hot, humid conditions.
Symptoms.
Pythium stalk rot can occur any time during the growing season but is most frequent at the tasseling stage of plant growth. The disease is recognized when plants twist
and fall over due to a loss of strength at a brown, watersoaked, and softened internode(s) on the diseased stalk immediately above the soil line. Vascular bundles
within the fallen stalk remain intact, which causes the fallen plants to remain green and turgid for several weeks.
Management.
Grow resistant hybrids.

Page 295
Red Kernel Disease
Cause.
Epicoccum nigrum is a weak parasite that infects injured or weakened kernels.
Distribution.
The United States.
Symptoms.
A red discoloration occurs in the endosperm of sweet maize.
Management.
Not reported.
Rhizoctonia Ear Rot
Rhizoctonia ear rot is also called sclerotial rot.
Cause.
Rhizoctonia zeae, teleomorph Waitea circinata, overseasons as mycelia and sclerotia on or in infested residue, in kernels, and in soil. Sclerotia are the main means of
dissemination. Disease is favored by warm, humid weather.
Distribution.
Asia, Europe, North America, and South America.
Symptoms.
Initially, pink mycelial growth occurs on diseased ears. Later, the mycelium becomes dull gray. Numerous white, salmoncolored, dark brown or black sclerotia
develop on the outer husks.
Management.
Not reported.
Rhizoctonia Root Rot and Stalk Rot
Cause.
Several anastomosis groups of Rhizoctonia solani and R. zeae.
Distribution.
Symptoms.
AG2 causes the most severe symptoms. Rhizoctonia solani causes postemergence damping off, stunting, leaf chlorosis, and necrosis of diseased seedlings. Isolates
from other plant species cause brown to black lesions on the seminal, crown, and brace roots. Roots frequently decay and disintegrate 2 to 5 cm from the crown.
Rhizoctonia zeae, which causes buff to tan lesions with dark brown borders on diseased corn roots, is less virulent than R. solani.
Management.
Not practiced.
Rostratum Leaf Spot
Rostratum leaf spot is also called Helminthosporium leaf disease, and Helminthosporium leaf disease, ear, and stalk rot.
Cause.
Setosphaeria rostrata, anamorph Exserohilum rostratum (syn. Bipolaris rostrata, Drechslera rostrata, D. halodes, E. halodes, and Helminthosporium ro

Page 296
stratum), survives as mycelia and conidia in infested residue. Conidia are produced from mycelia and disseminated by wind or splashing rain to maize. Mature plants
or older leaves are more susceptible to infection than younger leaves. A temperature of 30§C and a watersaturated atmosphere are conditions for optimum infection.
Sudangrass, pearl millet, and several other grasses are also hosts.
Distribution.
Where maize is grown under hot, humid conditions. Rostratum leaf spot is more severe in India and parts of Asia.
Symptoms.
Initially, small, pale yellow, elongated spots (12 × 25 mm) on diseased leaves gradually elongate into longitudinal stripes between the leaf veins. In cases of severe
disease, the lesions will coalesce and extend across the veins. Older lesions become light tan to cream with a light brown margin and enlarge to 23 × 240 mm.
A stalk rot with typical symptoms in the nodal and internodal tissue has been reported from Florida.
Management.
Sclerotium Ear Rot
Sclerotium ear rot is also called southern blight.
Cause.
Sclerotium rolfsii. Disease occurs under extremely wet conditions.
Distribution.
India.
Symptoms.
Initially, watersoaked spots on diseased leaf sheaths vary in size and shape, but they gradually enlarge during moist and warm weather. Profuse fungal growth
sometimes appears on the surface of diseased spots. White mycelium grows upward from the base of a diseased ear and is observed late in the growing season on
husks, floral bracts, and pericarps of rotted kernels. In the later stages of disease, sclerotia form on ears.
Management.
Not reported.
Seed and Seedling Blight Other Than Pythium
Cause.
Stenocarpella maydis, Gibberella zeae, Fusarium moniliforme, Rhizoctonia solani, and possibly other fungi. Aspergillus flavus vat. columnaris is reported from
South Africa to be a seed storage fungus that can colonize seedlings grown from sporecontaminated seed. Most of these fungi are discussed under the stalk rot or ear
and kernel blight caused by each. Seedling blight generally occurs under wet, cool, soil conditions that do not vary appreciably from those favoring Pythium blight.
Distribution.

Page 297
Symptoms.
Symptoms are nondescript and may be entirely absent. Failure of seeds to germinate, the failure of seedlings to emerge, the killing of seedlings after emergence, or
short, stunted plants are general symptoms. Diseased seed, which may be rotted and overgrown with mycelium, eventually disintegrates. The mesocotyl may be rotted
and discolored, cutting off water and nutrients from the seed and primary root. If the adventitious roots from the first node above the mesocotyl are not well
developed, leaves wilt and plants die. Roots have brown to black, watersoaked, flaccid lesions.
Management.
Treat seed with a fungicide seed protectant.
Selenophoma Leaf Spot
Cause.
Selenophoma sp. Disease occurs at low temperatures (10§ to 18§C).
Distribution.
Colombia, at an altitude of 2700 m.
Symptoms.
Lesions on diseased leaves are typical "eyespots" with concentric zonations bordered by a yellow halo. When relative humidity is 70% or greater, lesions grow to 2
cm long and eventually coalesce and cause severe leaf necrosis.
Management.
Not reported.
Septoria Leaf Blotch
Cause.
Septoria sp. causes disease under cool, humid conditions.
Distribution.
Septoria leaf blotch is presumed to be common in cool, humid climates.
Symptoms.
Small, light green, chlorotic or brown lesions form on diseased leaves. Lesions coalesce and form large necrotic areas in which numerous pycnidia may be produced.
Management.
Not necessary.
Sheath Blight
Cause.
Rhizoctonia solani. The causal fungus is probably multinucleate and has been tentatively identified as a sasakii form. Disease occurs in irrigated fields with over 100
units of N fertilizer applied and a history of rice production in the last 1 to 6 years.
Distribution.
The United States (east central Arkansas).
Symptoms.
Reddish eyespot lesions with dark red to purple margins occur on diseased stalks near the soil line and develop upward to approximately 2 m above the soil line. The
fungus penetrates leaf sheaths to the rind and ap

Page 298
pears as a yellowgreen discoloration with a thin black border. Prolific sclerotial development occurs in the older lesions on diseased leaf sheaths, ear husks, and silks.
Management.
Not reported.
Sheath Rot
Sheath rot is also called Gaeumannomyces graminis root rot.
Cause.
Gaeumannomyces graminis. Inoculum likely originates as mycelia and perithecia in the infested residue of cereals, especially wheat. Maize was reported to be
severely infected during the early seedling stages but not later in the growing season. Maize may act as a "carrier" crop from season to season for the fungus to infect
small grains.
Distribution.
Europe. However, disease is likely widespread wherever maize and small grains are grown in rotation.
Symptoms.
Primarily the cortical tissue of roots becomes diseased. Diseased roots have a dark brown to black discoloration. Apparently the disease on corn is not severe and
little damage occurs.
Management.
Not necessary.
Shuck Rot
Cause.
Myrothecium gramineum. The Myrothecium spp., in general, are soil inhabitants and widespread facultative parasites. Disease development is normally favored by
wounds and hot, humid weather. Infection of the shucks is presumably by inoculum within soil that is disseminated by wind to host plants.
Distribution.
Not known.
Symptoms.
Small, dark, watersoaked lesions occur that expand into larger necrotic areas on diseased shucks. Sporodochia may develop in lesions. It is not known if the fungus
grows into the kernels from diseased shucks.
Management.
Not necessary.
Silage Mold
Cause.
Monascus purpureus and M. tuber.
Distribution.
Widespread.
Symptoms.
Silage is stained a reddishpurple to dark purple color.
Management.
Not reported.

Page 299
Sordaria fimicola Stalk Infection
Cause.
Sordaria fimicola is an opportunistic inhabitant of maize stalks.
Distribution.
South Africa.
Symptoms.
Sordaria fimicola was isolated only from the nodes of diseased stalks. Plants grown in infested soil showed a significant reduction in dry matter. Root length was
reduced by 33.3% and plant height by 34.0%. A reduction in seedling vigor is possibly due to phytotoxic byproducts released by the fungus into the soil.
Management.
Not reported.
Sorghum Downy Mildew
Sorghum downy mildew is also called downy mildew.
Cause.
Peronosclerospora sorghi (syn. Sclerospora sorghi) survives for several years as oospores in infested residue and in soil after the infested residue has decomposed.
Isolates from Java or Thailand do not form oospores. Peronosclerospora sorghi is not seedborne but does survive for a short time in immature seeds that are sown
shortly after harvest. Oospores germinate and infect young plants that are emerging in warm soil. Conidia are also reported to provide primary inoculum. Mycelium
grows systemically in infected plants and, eventually, conidia are produced on leaf surfaces. Conidia are disseminated by wind but infect only the leaves of host plants
that are younger than 3 weeks old.
Reports of temperatures for optimum disease development differ. Some researchers report optimum germination occurs at high humidity and temperatures of 12§ to
20§C for some isolates and 12§ to 32§C for other isolates. Others report temperature ranges are 10§ to 30§C for optimum germination and 18§ to 30§C for
optimum germ tube growth. Conidia are produced at temperatures of 18§ to 23§C in the presence of dew for 5 to 6 hours. High levels of systemic infection occur at
temperatures of 8§ to 36§C. Eventually, oospores are formed in diseased tissues. Johnsongrass, sorghum, and teosinte are also hosts.
Distribution.
Africa, Asia, Central America, Israel, Italy, South America, and the United States (primarily in the south central and midwestern states).
Symptoms.
Systemic infection occurs only in young plants. Initially, chlorotic to white streaks develop parallel to the leaf midrib. Sometimes half of an entire leaf will be chlorotic.
A downy growth consisting of conidia and conidiophores appears in chlorotic tissue on both surfaces of the diseased leaf. Severely diseased plants are stunted and
chlorotic and have narrow, erect leaves. Tassels are phyllodied, with floral parts converted to small leaves, which results in an abnormal seed set. Symptoms of sec

Page 300
ondary infections are small lesions that contain downy growth scattered over the leaves of older plants.
A remission of symptoms, which is possibly a resistance mechanism, has been reported from Nigeria. Cobs from such plants formed normally but weighed significantly
less than those from uninfected plants. When seeds that were produced on maize plants with symptom remission were sown, seedlings did not develop downy mildew
symptoms. Infection by maize streak virus will mask symptoms of downy mildew.
Management
2. Rogue out and destroy diseased plants as they appear in the field.
3. Do not rotate maize with sorghum, and vice versa.
5. Sow in cool soil at the onset of the rainy season.
Southern Corn Leaf Blight
Southern corn leaf blight is also called Maydis leaf blight, southern blight, and southern leaf blight.
Cause.
Cochliobolus heterostrophus, anamorph Bipolaris maydis (syn. Drechslera maydis and Helminthosporium maydis), overwinters as conidia and mycelia in
infested residue. Race T also survives on kernels in storage. In the spring, conidia are disseminated by wind or splashed by rain to host plants, where infection occurs
in the presence of free moisture and temperatures of 15.5§ to 26.5§C. Lesions form and expand more rapidly at 30§C than at lower temperatures. Secondary
sporulation occurs in lesions in 60 to 72 hours. Race T produces five times more spores than Race O at 22.5§C and twice as many at 30§C.
Races O and T are the most common physiologic races, but other races are present. Race O infects only leaves, while Race T infects leaves, stalks, leaf sheaths, ear
husks, and kernels. Race C has been designated from China, where isolates of Bipolaris maydis induced significantly larger lesions on leaves of inbred lines of maize
with cmsC than on leaves of the same lines with cmsT, cmsS, or normal (N) cytoplasm. Maize infected with maize dwarf mosaic virus is more susceptible to
infection by B. maydis than are healthy maize plants. Disease is most severe when susceptible cultivars are grown in continuous maize culture utilizing a minimumtillage
system and overhead irrigation.
Distribution.
Generally wherever maize is grown, but Race O is most likely to be present in the southeastern and midwestern United States.
Symptoms.
Lesions on leaves caused by Race O are tan with buff to brown borders and parallel sides (26 × 322 mm). Race T lesions are larger (0.61.2 × 0.62.7 cm),
elliptical or spindleshaped, and surrounded by yel

Page 301
lowgreen or chlorotic halos. Lesions often may have dark reddishbrown borders. Lesions may coalesce and kill leaves.
Race T produces similar lesions on other plant parts. Such lesions are usually very large (several centimeters in length) and tan with dark purplebrown borders.
Mycelium grows through husks to the kernels, where a grayblack color from the production of conidia gives ears and kernels a moldy or charcoal appearance.
Seedlings from infected kernels wilt and die a few days after sowing.
During temperatures of 20§ to 30§C and a relative humidity of 100%, race T produces large numbers of spores, which give lesions a black "velvety" appearance.
Severely diseased plants are predisposed to stalk rot.
Management
2. Apply foliar fungicides before disease becomes too severe and when weather conditions are conducive to disease development.
Southern Corn Rust
Southern corn rust is also called Polysora rust and southern rust.
Cause.
Puccinia polysora is a rust fungus that produces the urediniospore stage and rarely the teliospore stage. No alternate host is known.
Urediniospores constitute both primary and secondary inoculum. Optimum infection occurs at a temperature of 26§C and a minimum of 16 hours of dew. Subsequent
disease development occurs at temperatures of 21§ to 27§C and high relative humidity, with temperature being the limiting factor to disease development in the
northern United States. Disease becomes progressively more severe as plants develop and is greatest on maize sown later in the growing season.
Epiphytotics coincide with an increase in double cropping of maize in the lower Mississippi River Valley and the Coastal Plain of the southeastern United States. This
cropping practice may provide conditions for development of large quantities of inoculum to infect maize in the northern corn belt at an early growth stage.
Nine physiologic races of P. polysora have been described.
Distribution.
Africa, Central and South America, Southeast Asia, the United States (primarily the southeastern states but occasionally the Midwest), and the West Indies.
Symptoms.
Pustules occur on both leaf surfaces and resemble common rust pustules except they are smaller (0.22.0 mm). Pustules are a light cinnamon brown, circular to oval
shaped, and densely scattered over the diseased upper leaf surface. Pustule development on lower leaf surfaces is slower and less abundant than on the upper leaf
surfaces. The epidermis

Page 302
remains intact over the pustules for a longer time than common rust but eventually ruptures. Telia, which are chocolate brown to black and circular to elongateshaped
(0.2 to 0.5 mm in diameter), often form a ring around the initial uredinium. The epidermis over the telia will eventually rupture, but it also remains intact longer than
common rust. Severely diseased leaves may become chlorotic and eventually dry up. During severe disease conditions, pustules may occur on leaf sheaths and stalks.
Management
Spontaneum Downy Mildew
Cause.
Peronosclerospora spontanea (syn. Sclerospora spontanea).
Distribution.
The Philippines and Thailand.
Symptoms.
The first leaf may have systemic symptoms of either general chlorosis or chlorotic streaks. The most common symptom is long, chlorotic streaks with downy growth
consisting of mycelium, conidia, and conidiophores that occurs on diseased leaves. Diseased plants are generally stunted and chlorotic. During humid conditions at
night, diseased leaves are covered with a white ''fuzz" consisting of mycelium, conidia, and conidiophores.
Ears may abort, resulting in partial or complete sterility, and tassels may be malformed, thus producing less pollen. Early infection results in stunted and dead plants.
Management
2. Rogue and destroy diseased plants.
3. Apply systemic fungicide seed treatment and foliar spray.
Sugarcane Downy Mildew
Cause.
Peronosclerospora sacchari (syn. Sclerospora sacchari) survives as mycelium in sugarcane. Sporangia produced from mycelia at nightly temperatures of 20§ to
25§C and in the presence of free water are disseminated by wind to maize. Sporangia germinate in the presence of free water and form mycelia that penetrate through
the stomata of plants that are less than 1 month old. Mycelia then develop systemically in the infected plant. Sporangia are eventually produced in diseased tissue and
serve as secondary inoculum. Oospores are also produced, but their function is not known. Older plants are resistant.
Other hosts are broomcorn, gamagrass, grain sorghum, sugarcane, and teosinte.

Page 303
Distribution.
Southeast Asia.
Symptoms.
Initially, small, round, chlorotic spots appear on diseased leaves. Eventually, systemic infection occurs as yellow to white streaks, or stripes, starting at the base of the
third to sixth oldest leaf and extending the length of the leaf. Streaks may be discontinuous in some hybrids or varieties and may disappear on plants that are infected
later in the growing season or are less severely diseased. Downy masses of sporangia appear at night on both leaf surfaces, leaf sheaths, and husks during periods of
high humidity and an optimum temperature of 25§C. Plants, especially tassels, are distorted and have poorly filled ears and elongated ear shanks.
Management
1. Do not grow maize near sugarcane.
Tar Spot
Cause.
Phyllachora maydis; however, at least two other organisms, Monographella maydis and Coniothyrium phyllachorae, can be found in tar spot lesions. The fungus
M. maydis is commonly found on the surface of leaves, generally without any apparent reaction by the plant to the presence of the fungus. It is only in association with
P. maydis that M. maydis becomes pathogenic and highly virulent. The effect of C. phyllachorae is not completely known but it seems to be a hyperparasite of both
P. maydis and M. maydis.
Phyllachora maydis is an obligate parasite and M. maydis requires its presence to become pathogenic. Ascospores of P. maydis are disseminated by wind to host
plants. The presence of a toxin produced by P. maydis has been associated with the rapid killing of plant tissue.
Disease development is favored by cool, humid weather.
Distribution.
Central America and South America in moderately cool and humid, tropical or subtropical, mountainous areas.
Symptoms.
Different disease symptoms have been reported. Disease development generally starts on the lower leaves at flowering time and moves rapidly up the diseased plant.
Disease becomes most severe after pollination and may cause premature desiccation of the spike.
Phyllachora maydis initially induces small (0.52.0 mm in diameter), oval to circularshaped, light brown lesions that may be surrounded by a dark brown border.
This border is caused by M. maydis and has been described as a brown, elliptic, necrotic halo that surrounds each P. maydis lesion. The development of P. maydis
lesions is frequently followed by the development of M. maydis lesions.
Lesions coalesce and form longer lesions (up to 10 mm in length).

Page 304
Glossy, black, sunken spots frequently occur in the middle of a lesion but are also abundant outside a lesion, particularly when plants are severely diseased.
Management.
Grow the most resistant genotype.
Trichoderma Ear Rot and Root Rot
Cause.
Trichoderma viride (syn. T. lignorum) is a common soilborne fungus that is considered to be a secondary invader of ears and roots.
Distribution.
Widespread.
Symptoms.
A greenish, cottony fungal growth occurs on and between seeds. Roots are generally discolored, and diseased plants are reported to be stunted.
Management.
Treat seed with a fungicide seed treatment.
Tropical Corn Rust
Tropical corn rust is also called tropical rust.
Cause.
Physopella pallescens and P. zeae (syn. Angiospora zeae) are rust fungi that produce the urediniospore and teliospore stages on maize. No alternate host is known.
Urediniospores constitute both the primary and secondary inoculum. Disease development is favored by warm to hot, and humid weather.
At least two races of P. zeae are known. Teosinte is also a host.
Distribution.
Central America, South America, and the Caribbean.
Symptoms.
Uredinial pustules occur in small groups (0.31.0 mm long) on diseased upper leaf surfaces. Pustules are yellow or creamcolored and covered by an epidermis
except for a small pore or split. Later, pustules develop into purple blotches that are circular to oblongshaped (0.5 cm in diameter) with creamcolored centers. Dark
brown to black telia develop in groups around uredinia.
Management.
Yellow Leaf Blight
Yellow leaf blight is also called Phyllosticta leaf spot.
Cause.
Ascochyta ischaemi and Phyllosticta maydis, teleomorph Mycosphaerella zeaemaydis. Phyllosticta maydis overwinters as pycnidia or pseudothecia in infested
maize or grass residue. Under cool, wet conditions, primarily in the spring, conidia ooze from pycnidia and are disseminated to host plants by diseased leaves rubbing
against healthy leaves, by wind for a short distance, and by splashing rain. Ascospores are produced that are also wind

Page 305
borne. Young plants growing through residue on the soil surface are especially vulnerable to infection; however, plants may be infected at any stage of their growth.
Conidia from pycnidia on older lesions provide secondary inoculum. Sudangrass and foxtail are also susceptible.
Distribution.
Africa, Argentina, Asia, Brazil, Canada, Romania, Taiwan, and the United States (primarily in the northern corngrowing areas but also in the midwestern and southern
states).
Symptoms.
Phyllosticta maydis does not spread rapidly over a large area; it is usually restricted to isolated fields. Plants growing in fields containing infested residue from last
year's crop may be most vulnerable to disease since residue harbors the pathogen.
Lesions develop first on lower leaves. The gray, tan, or brown lesions surrounded by a narrow red or purple margin with a wide yellowishgreen halo are oval to
ellipticalshaped (0.3 × 1.3 cm). The yellow discoloration surrounding lesions gives the disease its name. Lesions on older leaves contain pycnidia that look like tiny,
brownishblack specks but, under magnification, resemble small "flaskshaped" structures.
Severe disease results in yellowed leaves that resemble symptoms of nitrogen deficiency. Diseased leaves eventually die, and plants are stunted and more susceptible
to stalk rot. Leaf sheaths and outer husks are also diseased.
Management
1. Grow the most resistant hybrids. Hybrids containing T cytoplasm are more susceptible than hybrids containing other cytoplasms.
2. Apply a foliar fungicide if economic and disease conditions warrant it.
Zonate Leaf Spot
Cause.
Gloeocercospora sorghi survives as sclerotia and mycelia in infested residue. Conidia are produced in sporodochia, exuded in a slimy matrix, and disseminated by
splashing rain. Sclerotia develop in diseased tissue later in the growing season. Bentgrass, johnsongrass, sudangrass, and sugarcane are also hosts.
Distribution.
Africa, Central America, South America, and in the southern maizegrowing areas of the United States.
Symptoms.
Lesions on leaves initially are watersoaked, then become reddish brown and enlarge to 5 cm in diameter, forming a targetlike or zonate pattern. Small (0.10.2 mm
diameter), black sclerotia develop in dead tissue.
Management.
Not reported. Zonate leaf spot is not known to cause severe damage.

Page 306
Diseases Caused By Nematodes
Several kinds of nematodes attack maize, but in most cases the distribution is not well known. Disease management tends to be general for all nematodecaused
diseases. Following are practices that tend to reduce effects of nematode injury. Specific management practices are mentioned, where applicable, to control a disease
caused by nematodes.
1. Fertilize soils according to soil tests. Plants suffering from nutrient deficiency are more susceptible to injury.
2. Maintain good weed control. Weeds act as reservoirs of nematodes to infect next year's crop.
4. Apply nematicides to severely affected areas.
Awl
Cause.
Dolichodorus heterocephalus and likely other Dolichodorus spp. Awl nematodes are ectoparasites that are limited to wet soils. Some dissemination of the
nematode occurs by water. Feeding is generally restricted to the root tips.
Distribution.
Symptoms.
The aboveground symptom is plant stunting. The belowground symptom is stubby, thick roots that have some lesions present.
Bulb and Stem
Cause.
Ditylenchus dipsaci occurs in association with heavy soils, high rainfall, and cool temperatures.
Distribution.
Widespread, but usually occurring in small areas within a field. This is not a serious disease.
Symptoms.
Ditylenchus dipsaci feeds on leaves and stems, where it may cause cell hypertrophy and hyperplasia. Stalks may be slightly stunted and distorted. Infrequently, a
growing point may be destroyed.
Burrowing
Cause.
Radopholus similis is an endoparasite that reproduces within roots and is capable of surviving for only a few months outside of host tissue. Feeding occurs in the
cortex. Some dissemination occurs by water.
Distribution.
Tropical and subtropical areas around the world.
Symptoms.
The aboveground symptom is a slight stunting of diseased plants. Belowground symptoms are root lesions and decay.

Page 307
Columbia Lance
Cause.
Hoplolaimus columbus is an ectoparasitic, semiendoparasitic, and endoparasitic nematode.
Distribution.
Widespread.
Symptoms.
Lesions occur on diseased roots. Foliage is chlorotic and a severely diseased plant may be stunted.
Corn Cyst
Cause.
Heterodera avenae, Hzeae, and Punctodera chalcoensis.
Distribution.
Egypt, India, Pakistan, and the United States (Maryland and Virginia).
Symptoms.
The aboveground symptom is a general stunting. The belowground symptom is white to tan cysts on the roots of diseased plants.
Dagger
Cause.
Xiphinema americanum and X. mediterraneum are ectoparasites.
Distribution.
Not known.
Symptoms.
The aboveground symptom is a slight to moderate stunting of diseased plants. The belowground symptom is a reduction in feeder roots accompanied by necrosis of a
portion of the root system.
False Root Knot
Cause.
Naccobus dorsalis. Maize grown in a rotation with susceptible crops becomes infrequently infected.
Distribution.
The United States.
Symptoms.
Epidermal and cortical cells of the diseased root hypertrophy and give the impression of a swelling along portions of the root. The "swellings" bear a superficial
resemblance to root knots caused by Meloidogyne spp.
Lance
Cause.
Hoplolaimus galeatus and H. indicus are primarily endoparasites but sometimes feed as semiendoparasites and ectoparasites. Hoplolaimus indicus does more
damage to maize when it is in association with Fusarium moniliforme than it does alone. Other lance nematodes may also be parasitic to maize.
Distribution.
Not known.

Page 308
Symptoms.
Aboveground symptoms are stunting and chlorosis of diseased plants. The belowground symptom is lesions that reduce root growth.
Lesion
Cause.
Pratylenchus brachyurus, P. crenatus, P. hexincisus, P. neglectus, P. penetrans, P. scribneri, P. thornei, and P. zeae are endoparasites that feed and
reproduce in the root cortex. Some species thrive in warm, sandy soils, while others grow and reproduce better in heavy textured soils. Maize is tolerant to
populations up to 500 nematodes per gram of dry root tissue if plant growth conditions are favorable. Pratylenchus brachyurus and P. zeae cause more injury to
maize when they are in association with Fusarium moniliforme than they do alone. Disease is most severe during the seedling stage.
Distribution.
Temperate climates of the world.
Symptoms.
Aboveground symptoms include plant stunting. Leaves are chlorotic and a purple to reddish discoloration may occur. Diseased roots have reduced growth with few
fibrous roots. Brown lesions may be present and a general brown to blackish root decay may occur.
Management.
A seaweed concentrate from Ecklonia maxima suppressed reproduction of P. zeae on excised maize roots in vitro; however, in greenhouse experiments,
reproduction of P. zeae was not affected.
Needle
Cause.
Longidorus breviannulatus.
Distribution.
Sandy soils in temperate regions. Longidorus breviannulatus can potentially cause severe disease in the United States (Illinois, Indiana, and Iowa).
Symptoms.
The aboveground symptom is thin stands of severely stunted and chlorotic plants. Occasionally plants are killed in irregular patches during the first 6 to 8 weeks after
sowing. Later, damaged plants may grow as tall as healthy plants, but stalks remain slender. If ears are present, they are reduced in size.
Belowground symptoms include yellow discoloration, slightly swollen root tips, stubby roots, pruning of lateral roots, and fewer small feeder roots than healthy plants.
When soil moisture is high, seminal roots are destroyed and bushlike crown roots proliferate near the soil surface. The prop root system is unaffected.
Ring
Cause.
Criconemoides ornata and C. citui are ectoparasites.
Distribution.
Southeastern United States.

Page 309
Symptoms.
The aboveground symptom is a mild stunting. Belowground symptoms are lesions on roots and some decay.
Root Knot
Cause.
Meloidogyne arenaria, M. chitwoodi, M. incognita, and M. javanica are endoparasitic nematodes. Populations of M. incognita are highest under minimumtillage
systems and irrigation. Meloidogyne incognita and M. javanica are more restrictive of maize growth when they are in association with Fusarium moniliforme than
they are alone. Meloidogyne arenaria, M. incognita, and M. javanica do not survive if the temperature averages below 3§C during the coldest month.
Distribution.
Warmer regions of the world.
Symptoms.
Aboveground symptoms are stunting and chlorosis. Belowground symptoms are galls on roots and stunted and abnormally branched roots.
Management.
No commercial hybrids have been identified as resistant to M. incognita, but some are resistant to M. arenaria.
Spiral
Cause.
Helicotylenchus spp. are either ectoparasites, semiendoparasites, or endoparasites.
Distribution.
Symptoms.
The aboveground symptom is plant stunting. Belowground symptoms are a reduction in number of feeder roots and some root rot.
Sting
Cause.
Belonolaimus longicaudatus is an ectoparasite, found only in sandy soils, that produces a phytotoxic enzyme.
Distribution.
Symptoms.
Aboveground symptoms are stunting and chlorosis. The belowground symptom is deep necrotic lesions on roots. The frequent destruction of root tips results in thick,
stubby roots.
Stubby Root
Cause.
Paratrichodorus christiei, P. minor, Quinisulcius acutus, and Trichodorus christiei are ectoparasites found primarily in sandy soils. Most nematode feeding is
around root tips.
Distribution.
Not known.

Page 310
Symptoms.
Aboveground symptoms include severe stunting and chlorosis. The belowground symptom is a "devitalizing" of the root tips that causes stubby lateral roots. Roots
sometimes appear thicker than normal.
Stunt
Cause.
Tylenchorhynchus dubius and T. vulgaris are ectoparasites that are more restrictive of maize growth when they are in association with Fusarium moniliforme than
when they are alone.
Distribution.
Symptoms.
Aboveground symptoms are moderate plant stunting and chlorosis. The belowground symptom is a reduction in root growth.
Diseases Caused By Phytoplasmas
Corn Stunt
Corn stunt is also called achaparramiento, maize stunt, Rio Grandetype maize stunt, and Rio Grande corn stunt.
Cause.
Spiroplasma kunkelii, or corn stunt spiroplasma (CSS), is a helical, motile phytoplasma. CSS is not seedborne or mechanically transmitted and it is not known how it
survives in the absence of maize. In areas where maize is grown continuously, CSS is transmitted from maturing to newly sown fields by the leafhoppers Dalbulus
maidis, D. elimatus, Graminella nigrifrons, and Baldulus tripsaci. The mollicute is introduced into the sieve tubes of host plants by phloemfeeding leafhoppers.
Spiroplasmas move into tassels as they develop.
The age and/or size of the plant at the time of infection affects pathogen movement. Spiroplasmas are detected earlier in roots of plants inoculated at the oneleaf
seedling stage than in roots of plants inoculated at the fourleaf stage.
CSS tolerates wide temperature regimes (18§ to 31§C).
Distribution.
Argentina, Central America, Mexico, and the United States (Texas and possibly throughout the southern and southwestern United States and California). Infected
plants have been found at 940 m above sea level in Mexico, but corn stunt is more prevalent in tropical lowlands than at higher elevations.
Symptoms.
The following symptoms are observed in the United States. A chlorosis that initially occurs on the margin of the whorl leaf is followed by a reddening of the tops of
older leaves. Small, circular to elongated, chlorotic spots develop at the bases of leaves on young plants and often coalesce to become elongated stripes that may or
may not have a distinct

Page 311
margin. Plants are stunted and bear numerous small ear shoots and suckers. When disease is severe, there is a proliferation of roots.
Three types of symptoms are described from Mexico. First, leaves of stunted plants observed 60 to 940 m above sea level have welldefined, broad, chlorotic
streaking. Second, diseased plants are not always stunted, but leaf margins have red to purple streaks. Third, diseased plants usually are not stunted, but their leaves
have either a diffuse yellow or a chlorotic stripe with or without red margins. Both the second and third symptom types are observed at all elevations in Mexico and
appear 7 days before or after anthesis.
Symptoms of diseased plants from Argentina include chlorotic streaks that originate at the bases of young leaf blades. Older leaf margins are reddened, and there is a
progressive shortening of upper stalk internodes and a proliferation of ears.
Management.
Resistant germplasm is being sought.
Maize Bushy Stunt
Maize bushy stunt is also known as Mesa Central corn (maize) stunt.
Cause.
Maize bushy stunt phytoplasma (MBSP) is a nonhelical or pleomorphic phytoplasma found only in the phloem of diseased plants that is, to date, not culturable. It is
not known how MBSM survives in the absence of maize. MBSM is transmitted by several leafhoppers but only Dalbulus maidis and D. elimatus are efficient
vectors. Maize and annual teosinte are the only known hosts for MBSM.
Distribution.
Central America, Mexico, South America, and the southern United States.
Symptoms.
An initial chlorosis of the whorl leaf margin occurs and is followed by a reddening of older leaf tips. Reddening may not occur in certain hybrids. Subsequent leaves
develop a chlorosis of the margins, turn yellow or red, tear, twist, and are shortened. Plants are stunted, have numerous small ears, and have a bushy appearance due
to numerous tillers that develop at the leaf axils and base.
Management.
Not reported.
Unnamed Disease
Cause.
Spiroplasma. Disease occurs in lateplanted corn.
Distribution.
Symptoms.
The leaf blades of diseased plants are bright red at harvest time.
Management.
Not reported.

Page 312
Diseases Caused By Viruses
American wheat striate mosaic is also called wheat striate mosaic.
Cause.
American wheat striate mosaic virus (AWSMV) is in the rhabdovirus group. AWSMV is transmitted mainly by the painted leafhopper, Endrla inimica, and less
frequently by the leafhopper Elymana virenscens.
Distribution.
Symptoms.
Diseased plants are stunted and have slight to moderate leaf striation that consists of thin yellow to white parallel streaks.
Management.
Not reported.
Australian Maize Stripe
Cause.
The Australian maize stripe agent is thought to be a virus. The agent is vectored by the planthopper Peregrinus maidis. The major reservoir host is Sorghum
verticilliflorum. Acquisition and inoculation threshold periods were approximately 1 hour each.
Distribution.
Australia (Queensland). Incidence may be high in sweet maize grown in coastal districts where the vector and plant reservoir is common; however, the disease is rare
in the major inland agricultural areas.
Symptom.
Broad yellow stripes occur on leaves of diseased plants.
Management.
Not reported.
Cause.
Barley stripe mosaic virus (BSMV) is in the hordeivirus group. BSMV is transmitted by seed. Maize is more susceptible to systemic infection at 25§C than at higher
temperatures.
Distribution.
Symptoms.
Chlorotic stripes occur on leaves of diseased plants.
Management.
Not practiced.
Barley Yellow Dwarf
Cause.
Barley yellow dwarf virus (BYDV) is in the luteovirus group. BYDV is transmitted by several aphids. Irrigated maize is a reservoir of BYDV and its aphid vectors
between summer harvest and autumn sowing of winter grains in eastern Washington. Several grasses are hosts. See Barley Yellow Dwarf in Chapter 2, ''Diseases of
Barley."

Page 313
Distribution.
Africa, Asia, Australia, Europe, New Zealand, and North America.
Symptoms.
Leaves of diseased plants become chlorotic at the tips and margins. Later, beginning with the oldest leaves, all leaves become reddish to purple in color. Little or no
stunting occurs.
Management.
Disease is normally not severe enough to warrant management; however, avoid growing maize adjacent to or following diseased grass hosts.
Brome Mosaic
Cause.
Brome mosaic virus (BMV) is in the bromovirus group. BMV is transmitted by the corn rootworms Diabrotica undecimpunctata and D. virgifera and the
nematodes Longidorus macrosoma, Xiphinema coxi, and X. diversicaudatum. Several grasses and some dicotyledons are hosts.
Distribution.
Worldwide in other hosts.
Symptoms.
Chlorotic stripes of varying widths occur on young diseased leaves. Occasionally, young plants may wilt and die.
Management.
Avoid growing maize adjacent to or following diseased grasses in a rotation.
Cause.
Cereal chlorotic mottle virus (CeCMV) is in the rhabdovirus group. CeCMV is transmitted by the leafhopper Nesoclutha pallida. Several other grasses are hosts.
Distribution.
Australia (Queensland).
Symptoms.
The initial chlorotic stripes on diseased leaves are followed by a slight chlorotic mottling.
Management.
Not reported.
Cereal Tillering Disease
Cause.
The causal virus is unknown. It is disseminated by the planthoppers Laodelphax striatellus and Dicranotropis hamata. Barley, oat, and several grasses are also
hosts.
Distribution.
Sweden.
Symptoms.
Diseased plants are stunted and have numerous shoots. Leaves have vein enations.
Management.
Not reported.

Page 314
Corn Chlorotic Vein Banding
Corn chlorotic vein banding is also called Brazilian maize mosaic.
Cause.
Corn chlorotic vein banding virus (CCVBV) is transmitted by the corn planthopper, Peregrinus maidis. CCVBV may be related to maize mosaic virus.
Distribution.
Brazil.
Symptoms.
The disease occurs sporadically in a field. Chlorotic vein banding occurs along the leaf veins. Diseased plants are generally stunted. The disease is generally not
considered serious, and significant losses have not occurred.
Management.
Not necessary.
Corn Lethal Necrosis
Cause.
Corn lethal necrosis is caused by the synergistic action of maize chlorotic mottle virus (MCMV) in combination with either maize dwarf mosaic virus (MDMV) strain B
or wheat streak mosaic virus (WSMV). (See "maize chlorotic mottle virus" (MCMV), "maize dwarf mosaic virus" (MDMV), and "wheat streak mosaic
virus" (MSMV) in this chapter for specific information.)
It is presumed that maize plants are susceptible at all stages of development.
Distribution.
Mexico in winter seed maize nurseries, the United States (Hawaii in winter seed maize nurseries, Kansas, and Nebraska).
Symptoms.
An initial bright yellow mottling in diseased leaves is followed by a necrosis inward from the leaf margins and, eventually, premature death of plants. In diseased
maturing plants, necrosis normally begins at the tassel and progresses downward, causing plants to die from the top down. Ears may be small and distorted and have
little or no kernel development. Developed kernels are often wrinkled and shriveled. Losses of 75% to 80% may occur in susceptible hybrids.
Management
1. Grow a nonhost crop, such as alfalfa, a small grain, sorghum, or soybean, in fields where corn lethal necrosis has occurred.
2. Grow a tolerant hybrid.
Cucumber Mosaic
Cause.
Cucumber mosaic virus (CMV) is in the cucumovirus group. CMV is disseminated by several aphid species. Other hosts include numerous dicotyledons and
monocotyledons.

Page 315
Distribution.
Worldwide in several other hosts.
Symptoms.
A mild symptom is chlorotic, elliptical spots that eventually form stripes on diseased leaves. Severe symptoms are the death of seedlings or the stunting of diseased
plants that have necrotic leaf spots.
Management.
Not reported.
Cynodon Chlorotic Streak
Cause.
Cynodon chlorotic streak virus (CCSV) is in the rhabdovirus group. CCSV is transmitted by the planthopper Toya propinqua, but it is not mechanically transmitted.
CCSV is endemic in Bermuda grass, Cynodon dactylon.
Distribution.
Morocco.
Symptoms.
Diseased plants are stunted and have narrow, longitudinal, chlorotic streaks on leaves.
Management.
Not reported.
Elephant Grass Mosaic
Cause.
Elephant grass mosaic virus (EGMV). EGMV has been tentatively identified as a potyvirus that causes a mosaic of elephant grass but has a very limited host range. In
greenhouse tests, EGMV was transmitted mechanically, but not by aphids.
Distribution.
Brazil.
Symptoms.
Chlorotic spots and streaks developed on diseased leaves 1 to 2 weeks after inoculation.
Management.
Not reported.
High Plains Virus
Cause.
High plains virus (HPV) is transmitted by the wheat leaf curl mite, Aceria tosichella, which also transmits wheat streak mosaic virus, resulting in mixed infections by
these two viruses. HPV is also transmitted at a low rate in the infected seed of sweet maize. The virus is associated with a 32kDa protein that resembles tenuiviruses;
however, it is also suggested there is some resemblance to tospoviruses.
HPV is also transmitted to barley and wheat.
Distribution.
The midwestern United States (Colorado, Idaho, Kansas, Nebraska, Texas, and Utah). Dent maize, sweet maize, and blue maize are susceptible.

Page 316
Symptoms.
Disease is often worse on the side of the maize field that is near wheat. It is speculated that, generally, higher temperatures or fluctuating day/night temperatures may
exacerbate symptom expression. Symptoms are often most severe on diseased lower leaves and develop more slowly on upper leaves. Many other viruses are
typically more noticeable on the upper leaves.
The first symptoms appear when the plants are small, approximately at the 30 to 45cm stage. The incidence and severity increase for several weeks. In some
reports, the incidence appears to decline because the smaller, more severely diseased plants die, while the healthy and less severely diseased plants survive and
improve the appearance of the field.
The first symptoms on diseased plants infected early in their growth are plant stunting and a pronounced chlorosis in the form of an interveinal general mosaic and
flecking, or streaking, in the youngest leaves. The chlorosis is discrete, small, white spots in linear clusters or rows that roughly follow the veins. There is no sharp
delimitation between symptomatic and nonsymptomatic areas of a diseased leaf.
As diseased plants develop, new growth continues to be chlorotic, while older tissue reddens at the leaf margin, beginning at the leaf tip. The reddening progresses
down the leaf and is followed by necrosis that begins at the tip and moves down the leaf. In the most severe cases, the plants die. In mild cases, some plants eventually
recover from the shock phase and grow to sexual maturity. However, in sweet maize, these plants produce unacceptable ears; in field maize, the ear matures but is
often stunted or deformed and ear and kernel size are reduced. At maturity, the infected dent maize plants are stunted (2 m tall versus a normal 2.7 m tall) and display
a striking chlorosis with red stripes, sectors, and flecks. Mature plants approaching harvest have clearly defined red sectors and stripes on the leaves.
Symptoms of the disease are very severe in susceptible genotypes, killing maize plants in as little as 2 weeks following infection. Dent maize yields are reduced by 25%
to 75%. Severely infected sweet maize is a total loss.
Management.
Genetic variability for resistance to HPV exists among maize inbred lines.
Johnsongrass Mosaic
Cause.
Johnsongrass mosaic virus (JGMV) is in the potyvirus group. JGMV now consists of former strain JG of sugarcane mosaic virus from Australia and strain O of maize
dwarf mosaic virus from the United States. JGMV is transmitted mechanically and nonpersistently by the corn leaf aphid, Rhopalosiphum maidis.
Distribution.
Likely wherever maize is grown near johnsongrass.

Page 317
Symptoms.
Initially, diseased plants have a stippled mottle or mosaic of light and dark green that develops into narrow streaks on the youngest leaves. Symptoms may occur on all
diseased leaves, leaf sheaths, and husks that develop after the plant is infected by JGMV. As diseased plants mature, the mosaic disappears and leaves become
yellowish green and frequently show blotches or streaks of red.
Management
2. Destroy johnsongrass or other overwintering hosts.
Maize Chlorotic Dwarf
Cause.
Maize chlorotic dwarf (MCDV) is composed of at least two strains: MCDVT, the type isolate; and MCDVM1. Although the two strains are similar in host plant
range, vector range, and retention of inoculativity by the vector, they can be distinguished from one another by symptomatology as well as by transmission rate by
some vector species. MCDVM1 can also be differentiated from MCDVT on the basis of serology and the electrophoretic patterns of the coat proteins.
MCDV overwinters primarily in johnsongrass, but other plants, such as beard grass, Andropogon virginicus; muhly, Muhlenbergia sobolifera; indian grass,
Sorghastrum nutans; and blue stem, Schizachyrium scoparium, are also susceptible. MCDV is semipersistently transmitted by several leafhoppers, including
Amblysellus grex, Dalbulus maidis, Graminella nigrifrons, G. sonora, Planicephalus flavicostatus, and Stirellus bicolor. Graminella nigrifrons is the most
efficient vector. Amblysellus grex, P. flavicostatus, and S. bicolor transmit MCDVT at higher rates than they transmit MCDVM1. A helper component produced
in MCDVinfected plants is necessary for the transmission of MCDV by leafhopper vectors, but MCDV is not transmitted mechanically.
In single infections, each isolate causes no stunting or only mild stunting and vein banding, but in infections together, a synergistic interaction between MCDVT and
MCDVM1 causes severe stunting.
Distribution.
Symptoms.
There is a more severe chlorosis and stunting of plants when MCDVT infects maize in combination with MCDVM1 than in infections by either virus alone. Singly,
each isolate causes only mild symptoms, with isolate M1 causing the mildest symptoms.
Initially, chlorosis occurs on young leaves in the whorl. As diseased leaves unfurl, a fine chlorotic striping associated with the smallest visible leaf veins (tertiary leaf
veins) runs for some length parallel to the veins. This diagnostic symptom is more pronounced when induced by MCDVT than by MCDVM1. The early striping may
become obscured as diseased

Page 318
plants mature and their leaves become yellowish and reddish. Additional symptoms are plant stunting and a reddening, yellowing, and eventual necrosis of leaf margins
that are horizontally split. Diseased leaves are duller than bright, shiny healthy leaves.
Athough leaf discoloration and plant stunting are correlated with MCDV infection, these symptoms are not diagnostic since not all plants infected with MCDV are
stunted and discolored.
Management
1. Grow tolerant hybrids.
2. Sow early in the growing season to avoid large leafhopper populations.
3. Control johnsongrass to eliminate overwintering hosts.
Maize Chlorotic Mottle
Cause.
Maize chlorotic mottle virus (MCMV) is in the sobemovirus group. MCMV survives in corn residue and is transmitted by six species of beetles: the cereal leaf beetle,
Oulema melanopa; the corn flea beetle, Chaetocnema pulicaria; the flea beetle, Systena frontalis; the southern corn rootworm, Diabrotica undecimpunctata; the
northern corn rootworm, D. longicornis; and the western corn rootworm, D. virgifera. MCMV is also transmitted by seed, by thrips (Frankliniella williamsi),
mechanically, and possibly by soil. In the absence of fresh maize roots, newly hatched larvae of vectors forage on infested crop residues and acquire MCMV, which is
transmitted later by larvae feeding on developing maize roots.
MCMV survival in maize tissues, and perhaps viability of beetle eggs in soil, may occur only in soils with high waterholding capacities. Such soils can maintain infected
crop residues in a "proper" state of hydration and preserve virus particles. Continuous maize production greatly increases the incidence of MCMV. Other hosts of
MCMV include barley, johnsongrass, rye, sorghum, and wheat.
MCMV, together with either maize dwarf mosaic virus strain B or wheat streak mosaic virus, is one of the viruses that causes corn lethal necrosis. At least two strains
of MCMV exist: the Peru strain, MCMVP; and the Kansas strain, MCMVK.
Distribution.
Brazil, Peru, and the United States (Hawaii, Kansas, Nebraska, and Texas).
Symptoms.
Initially, fine, chlorotic stripes are parallel to the veins of the youngest diseased leaves. Stripes coalesce and produce elongated, chlorotic blotches that eventually
become necrotic. Eventually, leaves curl downward and plant death follows. Diseased plants are stunted, have distorted tassels, and form fewer ears. Significant yield
losses may occur from infection by MCMV alone.

Page 319
Management
1. Grow tolerant hybrids.
2. Rotate maize with soybean.
Maize Dwarf Mosaic
Cause.
Maize dwarf mosaic virus (MDMV) now consists of former MDMV strains A, D, E, and F; former sugarcane mosaic virus strain J infective to johnsongrass in the
United States; and maize mosaic virus, European type, from Yugoslavia.
MDMV is transmitted mechanically from the mouthparts of several aphids, and is seedborne in sweet maize. Disease appearance and spread are likely related to
aphid numbers. Plants infected when young are more severely diseased than plants infected when they are older; however, late sowings of sweet maize are more
severely diseased than early sowings. Soil moisture and nitrogen availability are associated with virus infection.
Several wild and cultivated grasses are susceptible to MDMV. In Mississippi, 70% of all grass species are susceptible in various degrees to MDMV.
Distribution.
Symptoms.
Symptoms are variable and most severe on plants infected when young; those infected at the pollination stage of plant growth or later may appear normal. Initially,
plants have a stippled mottle or mosaic of light and dark green that develops into narrow streaks on the youngest diseased leaves. Sometimes the mosaic appears as
dark green "islands" on a chlorotic background. Symptoms may occur on all leaves, leaf sheaths, and husks that develop after infection. As diseased plants mature, the
mosaic disappears and leaves become yellowish green and frequently show blotches or streaks of red that are generally observed after periods of cool night
temperatures of 15.5§C and below.
Pollen germ tube lengths are shortened and virus may be present in silks of some sweet maize cultivars. Severely diseased plants are barren. Plants are predisposed to
root rot, and stalk strength is reduced because diseased stalks become smaller in diameter than those of healthy plants. Upper internodes may be shortened, giving a
"feather duster" appearance to diseased plants.
Infection of sweet maize by MDMV and drought stress are additive in effect on ear and plant characteristics. Weight of ears is reduced by 16%, butt blanking of ears
is increased, leaf area is reduced, and plant height is reduced.
Management
3. Plant sweet maize early.

Page 320
Maize Leaf Fleck
Cause.
Maize leaf fleck virus is disseminated in a persistent manner by the aphids Myzus persicae, Rhopalosiphum padi, and R. maidis. Another host is harding grass,
Phalaris stenoptera.
Distribution.
The United States in the San Francisco Bay area of California.
Symptoms.
Older diseased leaves and the tips of other leaves have small, round, yellowish to orange spots and tip and marginal burning. Eventually, diseased leaves become
necrotic.
Management.
Not reported.
Maize Line
Cause.
Maize line virus (MLV) is disseminated by the corn planthopper, Peregrinus maidis.
Distribution.
East Africa.
Symptoms.
Wide, chlorotic bands occur on diseased leaves. Veins on leaf undersurfaces become thickened and give a rough texture to the surface. Diseased plants are slightly
stunted.
Management.
Not reported.
Maize Mosaic
Maize mosaic is also called corn leaf stripe, corn stripe, corn mosaic, enanismo rayado, and sweet corn mosaic stripe. In some literature, maize mosaic has been
confused with maize dwarf mosaic.
Cause.
Maize mosaic virus (MMV) is in the rhabdovirus group. MMV is transmitted by the corn planthopper, Peregrinus maidis, and may be seedborne. MMV infects
sorghum and wild grasses, which provide another means for MMV to overseason.
Distribution.
In tropical areas of Africa, Australia, Caribbean, India, northern South America, and the United States (Hawaii and the mainland).
Symptoms.
Symptoms vary. Initially, small, white flecks associated with whitening of leaf veins occur on one side of the midrib near the base of a young leaf. The specks elongate
and form fine, discontinuous stripes parallel to the midrib. Sometimes stripes coalesce and cause yellow bands to form on leaves. Severely diseased tissue becomes
red to purple, with a necrosis of the formerly chlorotic areas of diseased leaves. Stripes also occur on sheaths, husks, and stalks. Sometimes only broad, chlorotic
bands occur on leaves that have both veins and interveinal tissue affected. Bands,

Page 321
which may appear on one or both sides of the midrib, are not continuous but fade into spots or yellow areas at different lengths on the leaf. Moderate to severe
dwarfing of new growth can occur.
Management.
Grow resistant hybrids and inbreds.
Maize Mottle
Maize mottle and chlorotic stunt have been viewed as the same disease complex (Rossel 1984).
Cause.
Mottle strain of maize streak virus (MSVMS) is in the geminivirus group. MSVMS is transmitted mainly by the leafhopper Cicadulina mbila, but other leafhoppers
also are vectors. MSV is not seedborne or mechanically transmitted.
Distribution.
East Africa.
Symptoms.
Symptoms are not described well but generally have been characterized as a chlorotic mottling of leaves and a stunting of diseased plants.
Management.
Some maize genotypes have been described as having levels of resistance.
Maize Necrotic Lesion
Cause.
Maize necrotic lesion virus infects roots of maize. Isometric viruslike particles (17 and 29 nm in diameter) have been found in crude extracts from lesions and
mesophyll cells, suggesting a satellite and/or helper virus may be involved in the disease syndrome.
Distribution.
Not known.
Symptoms.
Symptoms on rubinoculated leaves of seedlings first appear as chlorotic local lesions, then become necrotic after 24 to 36 hours. Masses of amorphous inclusions
and fibrilcontaining vesicles occur in the cytoplasm.
Management.
Not known.
Maize Pellucid Ringspot
Cause.
Maize pellucid ringspot virus is thought to be disseminated by an aphid.
Distribution.
New Guinea and western Africa.
Symptoms.
Diseased leaves have round, watersoaked spots.
Management.
Not reported.

Page 322
Maize Raya Gruesa
Cause.
Maize raya gruesa virus (MRGV) is transmitted in a persistent manner by the corn planthopper, Peregrinus maidis. MRGV is acquired by a feeding acquisition
period of 48 to 72 hours and an incubation period in the insect vector of 4 to 22 days.
Distribution.
Colombia.
Symptoms.
Chlorotic stripes 1 mm wide occur on diseased leaves.
Management.
Not reported.
Maize Rayado Fino
Maize rayado fino is also called fine striping disease and rayado fino. Maize Colombian stripe (del rayado Colombiana del maize) and Brazilian corn streak are
diseases of maize caused by strains of MRFV.
Cause.
Maize rayado fino virus (MRFV) is in the marafivirus group. MRFV virions are isometric (approximately 30 nm in diameter) and contain a singlestranded RNA
genome. The virus is able to replicate in both maize and in the leafhopper Dalbulus maidis. MRFV often occurs in field infections associated with mollicutes (corn
stunt spiroplasma and maize bushy stunt phytoplasma) that are transmitted by the same vector.
MRFV is transmitted by nymphs and adults of the leafhoppers Baldulus tripsaci, D. maidis, D. elimatus, Graminella nigrifrons, and Stirellus bicolor. The
incubation period is 7 to 21 days, with leafhoppers retaining MRFV for prolonged periods, sometimes for life.
Distribution.
Central America, South America, and the United States (Florida and Texas). MRFV is the only maizeinfecting virus existing solely in the center of origin of maize.
Symptoms.
Initially, a few small, chlorotic dots or short stripes develop at the base and along veins of young diseased leaves. Dots become numerous and begin to fuse; however,
long continuous stripes are seldom found and a characteristic chlorotic stipple striping of veins prevails. As diseased plants become older, symptoms become less
conspicuous and may disappear when plants reach maturity. Diseased plants may be partially stunted and chlorotic.
Management.
Genotypes have been identified that display mild, delayed symptoms and low virus concentrations in diseased plants.
Maize Red Stripe
Cause.
Maize red stripe virus (MRSV). It is not known how MRSV is spread.

Page 323
Distribution.
Bulgaria.
Symptoms.
Red streaks occur on leaves. Diseased plants are dwarfed and have small ears.
Management.
Not reported.
Maize Ring Mottle
Cause.
Maize ring mottle virus is transmitted by seed.
Distribution.
Bulgaria.
Symptoms.
Chlorotic spots and rings occur on diseased leaves.
Management.
Not reported.
Maize Rio Cuarto Disease
Cause.
A reolike virus.
Distribution.
Argentina.
Symptoms.
Diseased plants are severely stunted, malformed, and dark green and have stiff or brittle stalks and leaves. Enations on leaf veins may be present.
Management.
Grow resistant inbreds or hybrids.
Maize Rough Dwarf
Maize rough dwarf is also called nanismo ruvido.
Cause.
Maize rough dwarf virus (MRDV) is in the fijivirus group. MRDV is disseminated only by the planthopper Laodelphax striatellus.
Distribution.
Southern and southeastern Europe.
Symptoms.
Early infection results in severely stunted plants that have numerous enations on the undersides of diseased leaves and leaf sheaths. Root systems are reduced in size
and discolored. Ears are not formed or if they are, tend to be small and malformed. Later infection does not result in noticeable stunting but enations are still formed.
Management.
Not reported.
Maize Sterile Stunt
Cause.
Maize sterile stunt virus (MSSV) is in the rhabdovirus group. MSSV is present in several grassy weeds and is transmitted by planthoppers.
Distribution.
Australia, on some inbreds.

Page 324
Symptoms.
Mild chlorosis occurs on emerging leaves; older diseased leaves become red to purple. Tassels will not form and ears become malformed.
Management.
Maize Streak
Maize streak is also called corn streak, maize streak disease, and streak disease. Bajra streak (Chapter 10) and maize mottle are caused by strains of the same virus.
Cause.
Maize streak virus (MSV) is in the geminivirus group. MSV is transmitted mainly by the leafhopper Cicadulina mbila, but other leafhoppers are also vectors. MSV is
not seedborne or mechanically transmitted.
Several specialized strains of MSV from maize, sugarcane, and grasses exist. Fiftyfour grass species are hosts, including African millet, barley, broomcorn, millet, oat,
rice, rye, sugarcane, wheat, and several wild grasses. In South Africa, isolates MSVCT and MSVPe caused different symptoms in maize and also differed
antigenically. In Nigeria, MSV isolated from many grasses was not readily transmissible to susceptible field maize, but the grasses Axonopus compressus, Brachiaria
lata, and Setaria barbata were likely to be involved in perpetuating strains of MSV pathogenic to maize.
Infection by MSV will mask symptoms of Peronosclerospora philippinensis and P. sorghi.
Distribution.
Kenya, Nigeria, and South Africa.
Symptoms.
Initially, circular (0.52.0 mm in diameter), colorless spots occur on the lowest exposed portions of the youngest diseased leaves. With incident light, lesion color
varies from white to yellow. In transmitted light, white lesions appear translucent. Spots are scattered but eventually become more numerous and grouped together.
Eventually, narrow, broken, chlorotic stripes that may consist of only a few flecks or small dots occur along veins. However, symptoms may become more severe and
stripes may coalesce and form wider stripes that are evenly distributed on leaves formed after infection. Eventually, the broad chlorotic stripes diffuse together,
producing both yellow and white lesions that cause an entire leaf to become chlorotic.
Insect toxin is responsible for stunting, leaf curling, and vein enations often associated with symptoms caused by MSV. Plants infected early are more severely
diseased than plants infected when older; consequently, yield losses are directly proportional to the age of the plant at infection. Virus strains from maize cause severe
stunting if plants are infected before the 4 to 5leaf stage.

Page 325
Management
1. Grow resistant hybrids. Some lines of Zea mays are resistant but mildly susceptible at the 1 to 2leaf stage. Perennial species of maize, Z. perennis and Z.
diploperennis, are resistant to MSV.
2. Apply insecticides.
3. Do not grow maize adjacent to other hosts.
Maize Stripe
Maize stripe is also called maize chlorotic stripe, maize hoja blanca (white leaf of corn), and maize white leaf and may be the same as Tsai's disease.
Cause.
The maize stripe virus (MStpV) is a member of the tenuivirus group. MStpV persists and multiplies with a minimum latent period of more than 1 week in the
planthoppers Toya catilina and Peregrinus maidis. MStpV is generally transovarially transmitted, but an isolate from Venezuela was mechanically transmitted to the
sweet maize cultivar 'Iochief' but not to field maize. Other hosts include barley, sorghum, and teosinte.
Distribution.
In all tropical areas where P. maidis occurs.
Symptoms.
Initially, numerous chlorotic spots and streaks appear at the bases and extend outward on the youngest diseased leaves. As leaves expand, spots and stripes coalesce
and form broad chlorotic bands that later cause leaves to be completely yellow. Diseased plants may have acute bending at the apical tip, causing them to become
necrotic and die. Severe infection results in reduced yields.
Management.
Not reported.
Maize Tassel Abortion
Cause.
Maize tassel abortion virus is disseminated by the insect Malaxodes farinosus.
Distribution.
East Africa.
Symptoms.
The tassels are aborted. Small leaves grow at right angles to the stalk.
Management.
Not reported.
Maize Vein Enation
Cause.
Maize vein enation virus (MVEV) is disseminated by the leafhopper Cicadulina mbila. Other hosts of MVEV include numerous grasses, oat, rice, rye, sorghum,
sugarcane, and wheat.
Distribution.
India.

Page 326
Symptoms.
Galls form on the lower surfaces of diseased leaves. Leaves become dark green. Diseased plants are stunted.
Management.
Not reported.
Maize Wallaby Ear
Cause.
Maize wallaby ear virus (MWEV) is transmitted by the leafhoppers Cicadulina bipunctella bimaculata, C. bimaculata, and Nesoclutha pallida. Other hosts for
MWEV are rice, rye, sorghum, sugarcane, wheat, and several other grasses.
Distribution.
Australia.
Symptoms.
There are two types of symptoms. Mild symptoms consist of galls and enations from which diseased plants recover. Severe symptoms consist of numerous galls on
most veins and upright dark green leaves with edges that roll upward and inward and stand stiffly at right angles to the stalk. Diseased plants may be severely stunted
and have reduced yields.
Management.
Not reported.
Maize White Line Mosaic
Maize white line mosaic is also called white line mosaic and stunt.
Cause.
Maize white line mosaic virus (MWLMV) is not mechanically transmitted but has been transferred from diseased roots placed in sterile soil with zoospores of an
Olpidiumlike fungus considered to be the likely vector. Infection is associated with time of season rather than plant age. Maize white line mosaic often occurs locally
in poorly drained areas of a field and along edge rows. A satellite virus (SVMWLMV),which is serologically related to a satellitelike particle associated with maize
dwarf ringspot virus, is associated with MWLMV.
Distribution.
The United States (Michigan, New York, Ohio, Vermont, and Wisconsin).
Symptoms.
An interveinal mosaic pattern that varies in intensity from a mild mottle to severe necrosis develops on leaves. Mild mottling consisting of small, discrete, chlorotic lines
that are seen in the early growth stages of diseased plants develops into chlorotic, white lines (12 × 14 cm) near the veins. In the latter stages of growth, diseased
plants may be severely stunted, develop a severe mosaic and mottled appearance, and may develop a crozierlike hooking of the terminal portions. Plants may be
barren or produce small ears with reduced kernel numbers. Diseased plants may be symptomless.

Page 327
Management.
Grow the most resistant genotype. There is no difference in susceptibility to MWLMV among 11 tested sweet maize cultivars.
Maize Yellow Stripe
Cause.
leafhopper Cicadulina chinai. Acquisition and inoculation threshold times are 30 minutes each, with a latent period of 4.5 to 8.0 days, depending on temperature
(14§C minimum and 25§C maximum). The maximum retention period is 27 days.
Wheat, barley, and graminaceous weeds are winter hosts. Different strains of MYSV exist.
Distribution.
Egypt.
Symptoms.
Three symptom types exist: fine stripe, coarse stripe, and chlorotic stunt. Each type may represent different MYSV strains. Experimentally, fine stripes appear on the
first leaves of diseased plants, followed by coarse stripes on younger leaves; however, some leaves have both symptom types.
Management.
Not reported.
Mal De Rio Cuarto
Cause.
Mal de rio cuarto virus (MRCV) is in the fijivirus group. MRCV is transmitted in a persistent, propagative way by the planthopper Delphacodes kuscheli. The insects
develop mainly on oat and wheat, then migrate to maize during their first stages of growth. Disease is most severe when infection takes place during the early stages of
plant development and during periods of high rainfall. MRCV has been detected in 12 species of weeds in the families Poaceae and Cyperaceae.
Distribution.
Argentina. Mal de Rio Cuarto is the most important disease of maize in Argentina.
Symptoms.
Diseased plants have shortened internodes, thickened and flattened stalks, degenerated leaves or leaves reduced to sheaths, malformed cobs, and proliferating
grainless ears. Enations protrude from the veins in the backs of leaves.
Management.
Not reported.
Millet Red Leaf
Cause.
Millet red leaf virus (MRLV) is disseminated by the aphids Macrosiphum granarium, Rhopalosiphum maidis, and the greenbug, Schizaphis graminum. Other
hosts of MRLV include species of Panicum and Setaria.

Page 328
Distribution.
China.
Symptoms.
Chlorosis to a reddening discoloration occurs on diseased leaf blades.
Management.
Not reported.
Cause.
Northern cereal mosaic virus (NCMV) is in the rhabdovirus group. NCMV is disseminated by the planthoppers Delphacodes albifascia, Laodelphax striatellus,
Meuterianella fairmairei, and Unkanodes sapporonus. Other hosts include barley, grasses, oat, rye, and wheat.
Distribution.
Japan and Korea.
Symptoms.
Chlorotic striping occurs along one side of diseased leaf blades.
Management.
Not reported.
Oat Pseudorosette
Oat pseudorosette is also known as zakuklivanie.
Cause.
Oat pseudorosette virus (OPRV) is disseminated by the planthopper Laodelphax striatellus. Other hosts of OPRV include barley, oat, rice, wheat, and several
species of grassy weeds.
Distribution.
Russia (western Siberia).
Symptoms.
Diseased plants have numerous tillers and malformed tassels. Leaves have a reddish discoloration.
Management.
Not reported.
Oat Sterile Dwarf
Cause.
Oat sterile dwarf virus (OSDV) is in the fijivirus group. OSDV is disseminated by the planthoppers Dicranotropis hamata, Javesella discolor, J. obscurella, and J.
pellucida.
Distribution.
Sweden.
Symptoms.
Diseased plants have narrow leaves with enations that last a short time.
Management.
Not reported.
Cause.
Rice blackstreaked dwarf virus (RBSDV) is in the fijivirus group. RBSDV is disseminated by the planthoppers Laodelphax striatellus, Ribautodel

Page 329
phax albifascia, and Unkanodes Sapporonus. Other hosts include barley, several grasses, rice, and wheat.
Distribution.
Japan.
Symptoms.
Diseased plants are stunted and have chlorotic streaks on leaves.
Management.
Not reported.
Rice Stripe
Cause.
Rice stripe virus (RSV) is in the tenuivirus group. RSV is disseminated by the planthoppers Laodelphax striatellus, Ribautodelphax albifascia, and Unkanodes
sapporonus. Other hosts of RSV include barley, millet, rice, and wheat.
Distribution.
Japan.
Symptoms.
Diseased plants are stunted and have chlorotic streaks on the leaves.
Management.
Not reported.
Sorghum Stunt Mosaic
Cause.
Sorghum stunt mosaic virus (SSMV) is in the rhabdovirus group. SSMV is disseminated by the leafhopper Graminella sonora.
Distribution.
The United States (Arizona and California).
Symptoms.
Diseased plants are stunted and leaves are chlorotic and have a mosaic pattern. Seed may not set.
Management.
Do not grow maize in the vicinity of sorghum.
Sugarcane Fiji Disease
Cause.
Sugarcane Fiji disease virus (FDV) is in the fijivirus group. FDV is disseminated by the leafhoppers Perkinsiella saccharicida and P. vastatrix. Other hosts include
sorghum and sugarcane.
Distribution.
Australia (New South Wales), Java, New Guinea, and the Philippines.
Symptoms.
Galls occur on veins of diseased leaves.
Management.
Not reported.
Sugarcane Mosaic
Cause.
Sugarcane mosaic virus (SCMV) is in the potyvirus group. SCMV is now grouped as follows and consists of the former SCMV strains A, B, D, E,

Page 330
and MB; the former SCMV strains SC, BC, and Sabi from Australia; and the former maize dwarf mosaic virus (MDMV) strain B in the United States.
A new strain of SCMV in Yugoslavia occurs on maize mixed with MDMV.
SCMV is transmitted by several aphid species in a nonpersistent manner and by sap inoculation. SCMV is seedborne at a low rate in sweet maize seed but not in
seed of other types of maize. SCMV does not normally cause severe disease in maize except for sweet maize.
Distribution.
Tropical and subtropical areas.
Symptoms.
Initially, a mild mottle occurs in interveinal areas of diseased leaves. Chlorotic patterns soon occur and elongate to produce streaks or stripes with irregular margins.
Plants may become severely stunted, are lighter in appearance than healthy plants, and produce ears with few or no kernels.
Management
1. Do not grow maize near sugarcane.
3. Grow resistant hybrids, especially for sweet maize.
Vein Enation
Vein enation is also called leaf gall.
Cause.
Unknown virus that is spread by the leafhopper Cicadulina bipunctella.
Distribution.
The Philippines.
Symptoms.
Diseased plants are stunted, and leaves are reduced in length and width. Vein enation, or galling, makes leaves appear corrugated or creased. The young leaves
enveloping the tassel often will fail to unfurl.
Management
1. Rogue diseased plants.
2. Application of insecticides has been effective.
Wheat Spot Mosaic
Cause.
Wheat spot mosaic virus (WSMV) is disseminated by the wheat curl mite, Aceria tulipae (syn. Eriophyes tulipae). Other hosts of WSMV include barley, numerous
grasses, rye, and wheat.
Distribution.
Canada and the United States (Ohio).
Symptoms.
Chlorotic spots, streaks, and mottling occur on diseased leaves.
Management.
Not reported.

Page 331
Wheat Streak Mosaic
Cause.
Wheat streak mosaic virus (WSMV) is in the potyvirus group. WSMV overwinters in winter wheat, other winter small grains, and a number of wild grasses. WSMV
is transmitted in the field by the wheat curl mite, Aceria tulipae (syn. Eriophyes tulipae), and mechanically, but WSMV is not seedborne, even though the virus can
be isolated from kernels before maturity.
Young plants are most susceptible to infection. Some maize lines are more susceptible to infection at 35°C than at lower temperatures; however, many lines are
susceptible regardless of temperature. Other hosts include cereals and numerous grasses.
Distribution.
Europe, northern Africa, and North America.
Symptoms.
Small, oval to ellipticalshaped spots occur at the tips of younger diseased leaves and later elongate parallel to leaf veins. Older diseased leaves may become chlorotic
at the tips. Ears may be poorly developed, and there may be a general yellowing and stunting of diseased plants.
Management.
Not necessary, but differences in resistance exist among inbreds.
Wheat Striate Mosaic
Cause.
American wheat striate mosaic virus is in the rhabdovirus group. See ''American Wheat Striate Mosaic" in Chapter 23, Diseases of Wheat.
Distribution.
South central Canada and north central United States.
Symptoms.
Upper diseased leaves have distinct, long, thin, white to chlorotic streaks.
Management.
Not reported.
Unknown Virus
Cause.
Unknown virus that is possibly in the tenuivirus group.
Distribution.
The United States (Kansas).
Symptoms.
Diseased plants are severely stunted and have a pronounced chlorosis of the youngest leaves. The chlorosis is a general mosaic with flecking or streaking. As plants
mature, new growth becomes chlorotic, while older tissue reddens along the leaf margins, beginning at the tip. Reddening progresses down the leaf and is followed by
a necrosis that also begins at the tip. Severely diseased plants die. Ear and kernel sizes are reduced. Blue maize and popcorn are also affected.
Management.
Not reported.

Page 332
North Queensland Stripe
Cause.
Unknown. Virus particles have not been found.
Distribution.
Northern Australia.
Symptoms.
Symptoms closely resemble leaf stripe symptoms of Java downy mildew caused by Peronosclerospora maydis.
Management.
Not known.
Selected References
Adipala, E., Lipps, P. E., and Madden, L. V. 1993. Occurrence of Exserohilum turcicum on maize in Uganda. Plant Dis. 77:202205.
Ammar, E. D., Elnagar, S., AbulAta, A. E., and Sewify, G. H. 1989. Vector and hostplant relationships of the leafhopperborne maize yellow stripe virus. J.
Amy, D. C., et al. 1971. Eyespot of maize, a disease new to North America. Phytopathology 61:5457.
Assabgui, R. A., Reid, L. M., Hamilton, R. I., and Arnason, J. T. 1993. Correlation of kernel (E)ferulic acid content of maize with resistance to Fusarium
graminearum. Phytopathology 83:949953.
Attwater, W. A., and Busch, L. V. 1982. The role of sap beetles (Glischrochilus quadrisignatus (Say)) in the epidemiology of Gibberella corn ear rot. (Abstr.)
Bacon, C. W., Bennett, R. M., Hinton, D. M., and Voss, K. A. 1992. Scanning electron microscopy of Fusarium moniliforme within asymptomatic corn kernels
and kernels associated with equine leukoencephalomalacia. Plant Dis. 76:144148.
Bains, S. S., Jhooty, J. S., Sokhi, S. S., and Rewal, H. S. 1978. Role of Digitaria sanquinalis in outbreaks of brown stripe downy mildew of maize. Plant Dis. Rptr.
62:143.
Bajet, N. B., and Renfro, B. L. 1989. Occurrence of corn stunt spiroplasma at different elevations in Mexico. Plant Dis. 73:926930.
Biddle, J. A., McGee, D.C., and Braun, E. J. 1990. Seed transmission of Clavibacter michiganense subsp. nebraskense in corn. Plant Dis. 74:908911.
Bonde, M. R., Peterson, G. L., and Duck, N. B. 1985. Effects of temperature on sporulation, conidial germination, and infection of maize by Peronosclerospora
sorghi from different geographical areas. Phytopathology 75:122126.
Bonde, M. R., Peterson, G. L., Kenneth, R. G., Vermeulen, H. D., Sumartini, and Bustaman, M. 1992. Effect of temperature on conidial germination and systemic
infection of maize by Peronosclerospora species. Phytopathology 82:104109.
Boosalis, M. G., Sumner, D. R., and Rao, A. S. 1967. Overwintering of conidia of Helminthosporium turcicum on corn residue and in soil in Nebraska.
Boothroyd, C. W. 1981. Virus diseases of sweet corn, pp. 103109. In D. T. Gordon, J. A.

Page 333
Knoke, and G. E. Scott (eds.). Virus and viruslike diseases of maize in the United States. Southern Cooperative Series Bull. 247. 218 pp.
Boothroyd, C. W., and Israel, H. W. 1980. A new mosaic disease of corn. Plant Dis. 64:218219.
Bowden, R. L., and Stromberg, E. L. 1982. Chocolate spot of corn in Minnesota. Plant Dis. 66:744.
Bradfute, O. E., and Louie, R. 1988. Maize necrotic lesion virus (MNLV) and satellitelike particles. (Abstr.) Phytopathology 78:1585.
Bradfute, O. E., Teyssandier, E., Marino, E., and Dodd, J. L. 1981. Reolike virus associated with maize rio cuarto disease in Argentina. (Abstr.) Phytopathology
71:205.
Burns E. E., and Shurtleff, M. C. 1973. Observations of Physoderma maydis in Illinois: Effects of tillage practices in field corn. Plant Dis. Rptr. 57:630633.
Bustamante, P. I., Hammond, R., and Ramirez, P. 1998. Evaluation of maize germplasm for resistance to maize rayado fino virus. Plant Dis. 82:5056.
Campbell, K. W., and Carroll, R. B. 1991. Red root rot, a new disease of maize in the Delmarva Peninsula. Plant Dis. 75:1186.
Campbell, K. W., White, D. G., and Toman, J. 1993. Sources of resistance in F 1 corn hybrids to ear rot caused by Aspergillus flavus. Plant Dis. 77:1169.
Carrera, L. M., and Grybauskas, A. 1992. Effect of planting dates and plant density on the development of gray leaf spot of corn. (Abstr.). Phytopathology 82:718.
Carson, M. L. 1995. A new gene in maize conferring the "chlorotic halo" reaction to infection by Exserohilum turcicum. Plant Dis. 79:717720.
Carson, M. L., and Goodman, M. M. 1991. Phaeosphaeria leaf spot of maize in Florida. Plant Dis. 75:968.
Castillo, J., and Herbert, T. T. 1974. Nueva enfermedat virosa afectano al maiz en al Peru (A new virus disease of maize in Peru). Fitopatologia 9:7984.
Ceballos, H., and Deutsch, J. A. 1992. Inheritance of resistance to tar spot complex in maize. Phytopathology 82:505512.
Chambers, K. R. 1987. Isolation of Sordaria fimicola from maize stalks. J. Phytopathology 120:369.
Chambers, K. R. 1988. Effect of time of inoculation on Diplodia stalk and ear rot of maize in South Africa. Plant Dis. 72:529531.
Christensen, J. J., and Wilcoxson, R. D. 1966. Stalk Rot of Corn. Monograph No. 3. The American Phytopathological Society, St. Paul, MN.
Cohen, Y., and Sherman, Y. 1977. The role of airborne conidia in epiphytotics of Sclerospora sorghi on sweet corn. Phytopathology 67:515521.
Cook, G. E., Boosalis, M. G., Dunkle, L. D., and Odvody, G. N. 1973. Survival of Macrophomina phaseoli in corn and sorghum stalk residue. Plant Dis. Rptr.
57:873875.
Cullen, D., Caldwell, R. W., and Smalley, E. B. 1983. Susceptibility of maize to Gibberella zeae ear rot: Relationship to host genotype, pathogen virulence, and
zearalenone contamination. Plant Dis. 67:8991.
Damsteegt, V. D., Bonde, M. R., and Hewings, A. D. 1993. Interactions between maize streak virus and downy mildew fungi in susceptible maize cultivars. Plant Dis.
77:390392.
Davis, R. M., Farrar. J. J., Peters, T. L., Kegel, F. R., and Mauk, P. A. 1991. Relationship between ear husk morphology and Fusarium ear rot of corn. (Abstr.)

Page 334
De Agudelo, F. V., and MartinezLopez, G. 1983. Maize raya gruesa: A rhabdovirus transmitted by Peregrinus maidis. (Abstr.) Phytopathology 73:125.
de Nazareno, N. R. X., Lipps, P. E., and Madden, L. V. 1991. Gray leaf spot of corn as influenced by the amount of surface corn residue. (Abstr.) Phytopathology
81:1143.
de Nazareno, N. R. X., Lipps, P. E., and Madden, L. V. 1992. Survival of Cercospora zeaemaydis in corn residue in Ohio. Plant Dis. 76:560563.
de Nazareno, N. R. X., Lipps, P. E., and Madden, L. V. 1993. Effect of levels of corn residue on the epidemiology of gray leaf spot of corn in Ohio. Plant
Dis.77:6770.
De Waele, D., McDonald, A. H., and De Waele, E. 1988. Influence of seaweed concentrate on the reproduction of Pratylenchus zeae (Nematoda) on maize.
Nematologica 34:7177
Dodd, J. L. 1980. Grain sink size and predisposition of Zea mays to stalk rot. Phytopathology 70:534535.
Dodd, J. L., and Hooker, A. L. 1990. Previously undescribed pathotype of Bipolaris zeicola on corn. Plant Dis. 74:530.
Doupnik Jr., B., and Jensen, S. G. 1991. Suppression of maize chlorotic mottle virus by soybean rotation in firstyear corn and fumigation in thirdyear corn. (Abstr.)
Duveiller, E., Snacken, F., Maraite, H., and Autrique, A. 1989. First detection of Pseudomonas fuscovaginae on maize and sorghum in Burundi. Plant Dis. 73:514
517.
Farr, D. F., Bills, G. R., Chamuris, G. P., and Rossman, A. Y. 1989. Fungi on Plants and Plant Products in the United States. The American Phytopathological
Society, St. Paul, MN. 1252 pp.
Forster, R. L., Strausbaugh, C. A., Jensen, S. G. Ball, E. M., Harvey, T., and Seifers, D. L. 1997. Seed transmission of the High Plains virus in sweet corn. (Abstr.).
Phytopathology 87:S31.
Gamez, R. 1969. A new leafhopperborne virus of corn in Central America. Plant Dis. Rptr. 53:929932.
Garcia, A. S., Reloba, R. G., and Castro, F. B. 1985. Field symptoms, spread and signs of the banded leaf and sheath blight disease of corn hybrids in Mindanao.
(Abstr.) Philipp. Phytopathol. 21:4.
Gendloff, E. H., Rossman E. C., Casale, W. L., Isleib, T. G., and Hart, L. P. 1986. Components of resistance to Fusarium ear rot in field corn. Phytopathology
76:684688.
Gilbertson, R. L., Brown, W. M., Jr., and Ruppel, E.G. 1985. Effect of tillage and herbicides on Fusarium stalk rot of corn. (Abstr.) Phytopathology 75:1296.
Gilbertson, R. L., Brown, W. M., Jr., Ruppel, E. G., and Capinera, J. L. 1986. Association of corn stalk rot Fusarium spp. and western corn rootworm beetles in
Colorado. Phytopathology 76:13091314.
Gingery, R. E., and Nault, L. R. 1990. Severe maize chlorotic dwarf disease caused by double infection of mild virus strains. Phytopathology 80:687691.
Gingery, R. E., Nault, L. R., Tsai, J. H., and Lastra, R. J. 1979. Occurrence of maize stripe virus in the United States and Venezuela. Plant Dis. Rptr. 63:341343.
Gordon, D. T., Bradfute, O. E., Gingery, R. E., Knoke, J. K., Louie, R., Nault, L. R., and Scott, G. E. 1981. Introduction: History, geographical distribution,
pathogen characteristics, and economic importance, pp. 112. In D. D. Gordon, J. K. Knoke, and G. E. Scott (eds.), Virus and viruslike diseases of maize in the
United States. Southern Cooperative Series Bull. 247. 218 pp.
Greber, R. S. 1982. Maize sterile stunt: A delphacidtransmitted rhabdovirus affecting some maize genotypes in Australia. Aust. J. Agric. Res. 33:1323.

Page 335
Guthrie, E. J. 1978. Measurement of yield losses caused by maize streak disease. Plant Dis. Rptr. 62:839841.
HalfonMeiri, A, and Solel, Z. 1990. Factors affecting seedling blight of sweet corn caused by seedborne Penicillium oxalicum. Plant Dis. 74:3639.
Headrick, J. M., and Pataky, J. K. 1989. Resistance to kernel infection by Fusarium moniliforme in inbred lines of sweet corn and the effect of infection on
emergence. Plant Dis. 73:887892.
Herold, F. 1972. Maize mosaic virus. CMI/A.A.B. Descriptions of plant viruses. Set 5. No. 94.
Hirrel, M. C., Lee, F. N., Dale, J. L., and Plunkett, D. E. 1988. First report of sheath blight (Rhizoctonia solani) on field corn in Arkansas. Plant Dis. 72:644.
Hoenisch, R. W., and Davis, R. M. 1994. Relationship between kernel pericarp thickness and susceptibility to Fusarium ear rot in field corn. Plant Dis. 78:517519.
Hollier, C.A., and King, S. B. 1985. Effect of dew period and temperature on infection of seedling maize plants by Puccinia polysora. Plant Dis. 69:219220.
Hsia, C. C., Kommedahl, T., Tziang, B. L., and Wu, J. L. 1988. Toxigenic Fusarium scirpi in maize grain from midnorthern China. Phytopathology 78:978980.
Huff, C. A., Ayers, J. E., and Hill, R. R., Jr. 1988. Inheritance of resistance in corn (Zea mays) to gray leaf spot. Phytopathology 78:790794.
Hunt, R. E., Nault, L. R., and Gingery, R. E. 1988. Evidence for infectivity of maize chlorotic dwarf virus and for a helper component in its leafhopper transmission.
Jamil, F. F., and Nicholson, R. L. 1987. Susceptibility of corn to isolates of Colletotrichum graminicola pathogenic to other grasses. Plant Dis. 71:809810.
Jardine, D. J., Bowden, R. L., Jensen, S. G., and Seifers, D. L. 1994. A new virus of corn and wheat in western Kansas. (Abstr.). Phytopathology 84:1117.
Jensen, S. G., Lane, L. C., and Seifers, D. L. 1996. A new disease of maize and wheat in the High Plains. Plant Dis. 80:13871390.
Jiang, X. Q., Meinke, L. J., Wright, R. J., Wilkinson, D. R., Campbell, J. E., and Berry, J. A. 1991. Corn thrips (Frankliniella williamsi Hood) a major vector
associated with a 1990 maize chlorotic mottle virus epiphytotic in Hawaii. (Abstr.) Phytopathology 81:1243.
Jones R. K., and Duncan, H. E. 1981. Effect of nitrogen fertilizer, planting date, and harvest date on aflatoxin production in corn inoculated with Aspergillus flavus.
Plant Dis. 65:741744.
Jones, R. K., Duncan H. E., Payne, G A., and Leonard, K. J. 1980. Factors influencing infection by Aspergillus flavus in silkinoculated corn. Plant Dis. 64:859
863.
Jons, V. L., Timian, R. G., Gardner, W. S., Stromberg, E. L., and Berger, P. 1981. Wheat striate mosaic virus in the Dakotas and Minnesota. Plant Dis. 65:447448.
Jordann, E. M., Loots, G. C., Jooste, W. J., and De Waele, D. 1987. Effects of rootlesion nematodes (Pratylenchus brachyurus Godfrey and P. zeae Graham)
and Fusarium moniliforme Sheldon alone or in combination, on maize. Nematologica 33:213219.
Keller, N. P., and Bergstrom, G. C. 1988. Developmental predisposition of maize to anthracnose stalk rot. Plant Dis. 72:977980.
Keller N. P., Bergstrom, G. C., and Carruthers, R .I. 1986. Potential yield reductions in maize associated with an anthracnose/European corn borer pest complex in
New York. Phytopathology 76:586589.
Khan, A., Ries, S. M., and Pataky, J. K. 1996. Transmission of Erwinia stewartii through seed of resistant and susceptible field and sweet corn. Plant Dis. 80:398
403.

Page 336
Khonga, E. B., and Sutton, J. C. 1988. Inoculum production and survival of Gibberella zeae in maize and wheat residues. Can. J. Plant Pathol. 10:232239.
Kingsland, G. C. 1980. Effect of maize dwarf mosaic virus infection on yield and stalk strength of corn in the field in South Carolina. Plant Dis. 64:271273.
Kitajima, E. W., and Costa, A. S. 1982. The ultrastructure of the corn chlorotic vein banding (Brazilian maize mosaic) virusinfected corn leaf tissues and viruliferous
vector. Fitopatologia Brasileria 7:247259.
Klittich, C. J. R., Leslie, J. F., Nelson, P. E., and Marasas, W. F. O. 1997. Fusarium thapsinum (Gibberella thapsina): A new species in section Liseola from
sorghum. Mycologia 89:643652.
Kloepper, J. W., Garrott, D. G., and Kirkpatrick, B. C. 1982. Association of spiroplasmas with a new disease of corn. (Abstr.) Phytopathology 72:1004.
Kommedahl, T., Sabet, K. K., Burnes, P.M., and Windels, C. E. 1987. Occurrence and pathogenicity of Fusarium proliferatum on corn in Minnesota. Plant Dis.
71:281.
Kucharek, T. A. 1973. Stalk rot of corn caused by Helminthosporium rostratum. Phytopathology 63:13361338.
Kumar, V., Vasanthi, H.J., and Shetty, H. S. 1987. Detection, location and transmission of Nigrospora oryzae in maize. Int. J. Tropical Plant Diseases 5:153163.
Lastra, R., and Carballo, O. 1985. Mechanical transmission, purification and properties of an isolate of maize stripe virus from Venezuela. Phytopathol. Z. 114:168
179.
Latterell, F. M., and Rossi, A. E. 1983. Stenocarpella macrospora (Diplodia macrospora) and S. maydis (D. maydis) compared as pathogens of corn. Plant Dis.
67:725729.
Latterell, F. M., and Rossi, A. E. 1984. A Marasmiellus disease of maize in Latin America. Plant Dis. 68:728731.
Latterell, F. M., and Rossi, A. E. 1984. An unidentified species of Cercospora pathogenic to corn. (Abstr.) Phytopathology 74:852.
Latterell, F. M., Rossi, A. E., and Trujillo, E. E. 1986. A previously undescribed Selenophoma leaf spot of maize in Colombia. Plant Dis. 70:472474.
Leach, C. M., Fullerton, R. A., and Young, K. 1977. Northern leaf blight of maize in New Zealand: Relationship of Drechslera turcica airspora to factors influencing
sporulation, conidium development, and chlamydospore formation. Phytopathology 67:629636.
Leonard, K. J., and Thompson, D. L. 1976. Effects of temperature and host maturity on lesion development of Colletotrichum graminicola on corn.
Leonard, K. J., Levy, Y., and Smith, D. R. 1989. Proposed nomenclature for pathogenic races of Exserohilum turcicum on corn. Plant Dis. 73:776777.
Levy, Y. 1984. The overwintering of Exserohilum turcicum in Israel. Phytoparasitica 12:177182.
Levy, Y., and Leonard, K. J. 1987. Development of northern corn leaf blight lesions as affected by position and density of lesions on leaves. (Abstr.) Phytopathology
77:409.
Lipps, P. E. 1988. Spread of corn anthracnose from surface residues in continuous corn and cornsoybean rotation plots. Phytopathology 78:756761.
Lland, A., and Schieber, E. 1980. Diplodia macrospora of corn in Nicaragua. Plant Dis. 64:797.
Lockhart, B. E. L., Khaless, N., E1 Maataoui, M., and Lastra, R. 1985. Cynodon chlorotic streak virus, a previously undescribed plant rhabdovirus infecting
Bermuda grass and maize in the Mediterranean area. Phytopathology 75:10941098.

Page 337
Logrieco, A., Moretti, A., Ritieni, A., Bottalico, A., and Corda, P. 1995. Occurrence and toxigenicity of Fusarium proliferatum from preharvest maize ear rot, and
associated mycotoxins, in Italy. Plant Dis. 79:727731.
Lopes, J. R. S., Nault, L. R., and Gingery, R. E. 1994. Leafhopper transmission and host plant range of maize chlorotic dwarf waikavirus strains. Phytopathology
84:876882.
Louie, R., Gordon, D. T., and Lipps, P. E. 1981. Transmission of maize white line mosaic virus. (Abstr.) Phytopathology 71:1116.
Louie, R., Gordon D. T., Madden, L. V., and Knoke, J. K. 1983. Symptomless infection and incidence of maize white line mosaic. Plant Dis. 67:371373.
Maiti, S. 1978. Two new ear rots of maize from India. Plant Dis. Rptr. 62:10741076.
Malek, R. B., Norton, D. C., Jacobsen, B. J., and Acosta, N. 1980. A new corn disease caused by Longidorus breviannulatus in the Midwest. Plant Dis.
64:11101113.
March, G. J., Balzarini, M., Ornaghi, J. A., Beviacqua, J. E., and Marinelli, A. 1995. Predictive model for "Mal de Rio Cuarto" disease intensity. Plant Dis. 79:1051
1053.
Marcon, A., Kaeppler, S. M, and Jensen, S. G. 1997. Genetic variability among maize inbred lines for resistance to the High Plains viruswheat streak mosaic virus
complex. Plant Dis. 81:195198.
Martins, C. R. F., and Kitajima, E. W. 1993. A unique virus isolated from elephant grass. Plant Dis. 77: 726729.
Martinson, C. A., Foley, D. C., and Marton, C. 1988. The effect of plant density and kernel sink level on stalk rot and strength of maize. (Abstr.) Phytopathology
78:1525.
Matyac, C. A., and Kommedahl, T. 1985. Factors affecting the development of head smut caused by Sphacelotheca on corn. Phytopathology 75:577581.
Matyac, C. A., and Kommedahl, T. 1985. Occurrence of chlorotic spots on corn seedlings infected with Sphacelotheca reiliana and their use in evaluation of head
smut resistance. Plant Dis. 69:251254.
McDaniel, L. L., and Gordon, D. T. 1985. Identification of a new strain of maize dwarf mosaic virus. Plant Dis. 69:602607.
McKee, D. C. 1988. Maize Diseases: A Reference Source for Seed Technologists. The American Phytopathological Society. St. Paul, MN. 150 pp.
McLennan, S. R., and Rijkenberg, F. H. J. 1987. Stenocarpella (Diplodia) macrospora on maize (Zea mays). (Abstr.) Phytophylactica 19:122.
Mesfin, T., BosquePerez, N. A., Budenhage, I. W., Thottappilly, G., and Olojede, S. O. 1992. Studies on maize streak virus isolates from grass and cereal hosts in
Nigeria. Plant Dis. 76:789795.
Misra, A. P. 1959. Diseases of millets and maize. Indian Agriculturist 3:7589.
Muller, G. J. et al. 1973. A Compendium of Corn Diseases. The American Phytopathological Society. St. Paul, MN.
Munkvold, G. P., and Desjardins. A. E. 1997. Fumonisins in maize. Can we reduce their occurrence? Plant Dis. 81:556565.
Munkvold, G. P., McGee, D. C., and Carlton, W. M. 1997. Importance of different pathways for maize kernel infection by Fusarium moniliforme. Phytopathology
87:209217.
Mycock, D. J., Lloyd, H. L., and Berjak, P. 1987. Infection of Zea mays seedlings by Aspergillus flavus var. columnaris. (Abstr.) Phytophylactica 19:121.
Nankam, C., and Pataky, J. K. 1996. Resistance to kernel infection by Fusarium moniliforme in the sweet corn inbred IL125b. Plant Dis. 80:593598.

Page 338
Nault, L. R., and Gordon, D. T. 1988. Multiplication of maize stripe virus in Peregrinus maidis. Phytopathology 78:991995.
Nelson, P. A., Toussoun, T. A., and Marasas, W. F. O. 1983. Fusarium Species: An Illustrated Manual for Identification. The Pennsylvania State University Press,
University Park. 193 pp.
Niblett, C. L., and Claflin, L. E. 1978. Corn lethal necrosis, a new virus disease of corn in Kansas. Plant Dis. Rptr. 62:1519.
Nicholson, R. L., Bergeson, G. B., Degennaro, F. P., and Viveiros, D. M. 1985. Single and combined effects of the lesion nematode and Colletotrichum
graminicola on growth and anthracnose leaf blight of corn. Phytopathology 75:654661.
Norton, D. C., and De Agudelo, F. V. 1984. Plantparasitic nematodes associated with maize in Cauca and Valle del Cauca, Colombia. Plant Dis. 68:950952.
Nwigwe, C. 1974. Occurrence of Phomopsis on maize (Zea mays). Plant Dis. Rptr. 58:416417.
Ochor, T. E., Trevathan, L. E., and King, S. B. 1987. Relationship of harvest date and host genotype to infection of maize kernels by Fusarium moniliforme. Plant
Dis. 71:311313.
Olanya, O. M., and Fajemisin, J. M. 1992. Remission of symptoms on maize plants infected with downy mildew in northern Nigeria. Plant Dis. 76:753.
Olanya, O. M., Hoyos, G. H., Tiffany, L. H., and McGee, D. C. 1997. Waste corn as a point source of inoculum for Aspergillus flavus in the corn agroecosystem.
Plant Dis. 81:576581.
Paulitz, T. C. 1996. Diurnal release of ascospores by Gibberella zeae in inoculated wheat plots. Plant Dis. 80:674678.
Payne, G. A., and Leonard, K. J. 1985. Stenocarpella macrospora on corn in North Carolina. Plant Dis. 69:613.
Payne, G. A., and Waldron, J. K. 1983. Overwintering and spore release of Cercospora zeaemaydis in corn debris in North Carolina. Plant Dis. 67:8789.
Payne, G. A., Cassel, D. K., and Adkins, C. R. 1985. Reduction of aflatoxin levels in maize due to irrigation and tillage. (Abstr.) Phytopathology 75:1283.
Payne, G. A., Cassel, D. K., and Adkins, C. R. 1986. Reduction of aflatoxin contamination in corn by irrigation and tillage. Phytopathology 76:679684.
Payne, G. A., Duncan, H. E., and Adkins, C. R. 1987. Influence of tillage on development of gray leaf spot and number of airborne conidia of Cercospora zeae
maydis. Plant Dis. 71:329332.
Payne, G. A., Hagler, W. M., Jr., and Adkins, C. R. 1988. Aflatoxin accumulation in inoculated ears of fieldgrown maize. Plant Dis. 72:422424.
Payne, G. A., Thompson, D. L., Lillehoj, E. B., Zuber, M. S., and Adkins, C. R. 1988. Effect of temperature on the preharvest infection of maize kernels by
Aspergillus flavus. Phytopathology 78:13781380.
Payne, G. A., Kamprath, E. J., and Adkins, C. R. 1989. Increased aflatoxin contamination in nitrogenstressed corn. Plant Dis. 73:556559.
Pedersen, W. L., and Brandenburf, L. J. 1986. Mating types, virulence, and cultural characteristics of Exserohilum turcicum race 2. Plant Dis. 70:290292.
Pedersen, W. L., and Oldham, M. G. 1992. Effect of three tillage practices on development of northern corn leaf blight (Exserohilum turcicum) under continuous
corn. Plant Dis. 76:11611164.

Page 339
Pinner, M. S., Markham, P. G., Markham, R. H., and Dekker, E. L. 1988. Characterization of maize streak virus: Description of strains, symptoms. Plant Pathol.
37:7487.
Pordesimo, A. N., and Aday, B. A. 1984. Vein enation or leaf gall of corn. (Abstr.) Philipp. Phytopathol. 20:15.
Raid, R. N., Pennypacker, S. P., and Stevenson, R. E. 1988. Characterization of Puccinia polysora epidemics in Pennsylvania and Maryland. Phytopathology
78:579585.
Ramsey, M. D., and Jones, D. R. 1988. Peronosclerospora maydis found on maize, sweet corn and plume sorghum in Far North Queensland. Plant Pathol. 37:581
587.
Rao, B., Schmitthenner, A. F., Caldwell, R., and Ellett, C. W. 1978. Prevalence and virulence of Pythium species associated with root rot of corn in poorly drained
soil. Phytopathology 68:15571563.
Reid, L. M., Bolton, A. T., Hamilton, R. I., Woldemariam, T., and Mather, D. E. 1992. Effect of silk age on resistance of maize to Fusarium graminearum. Can. J.
Reid, L. M., Mather, D. E., and Hamilton, R. I. 1996. Distribution of deoxynivalenol in Fusarium graminearuminfected maize ears. Phytopathology 86:110114.
Reifschneider, F. J. B., and Arny, D. C. 1980. Host range of Kabatiella zeae, causal agent of eyespot of maize. Phytopathology 70:485487.
Reifschneider, F. J. B., and Lopes, C. A. 1982. Bacterial top and stalk rot of maize in Brazil. Plant Dis. 66:519520.
Rheeder, J. P., Marasas, W. F. O., and Nelson, P. E. 1996. Fusarium globosum, a new species from corn in southern Africa. Mycologia 88:509513.
Rich, J. R., and Schenck, N. C. 1981. Seasonal variations in populations of plantparasitic nematodes and vesiculararbuscular mycorrhizae in Florida field corn.
Plant Dis. 65:804807.
Roane, M. K., and Roane, C. W. 1983. New grass hosts of Polymyxa graminis in Virginia. (Abstr.) Phytopathology 73:968.
Robinson, R. K., and Lucas, R. L. 1967. Observations on the infection of Zea mays by Ophiobolus graminus. Plant Pathol. 16:7577.
Rossel, H. W. 1984. On geographical distribution and control of maize mottle/chlorotic stunt in Africa. Maize Virus Dis. Newsl. 1, 1719.
Rupe, J. C., Siegel, M. R., and Hartman, J. R. 1982. Influence of environment and plant maturity on gray leaf spot of corn caused by Cercospora zeaemaydis.
Sardanelli, S., Krusberg, L. R., and Golden, A. M. 1981. Corn cyst nematode, Heterodera zeae, in the United States. Plant Dis. 65:622.
Schneider, R. W., and Pendery, W. E. 1983. Stalk rot of corn: Mechanism of predisposition by an early season water stress. Phytopathology 73:863871.
Schurtleff, M. C. (ed.). 1980. Compendium of Corn Diseases. The American Phytopathological Society, St. Paul, MN. 105 pp.
Seifers, D. L., Harvey, T. L., Martin, T. J., and Jensen, S. G. 1997. Identification of the wheat curl mite as the vector of the High Plains virus of corn and wheat. Plant
Dis. 81:11611166.
Sharma, H. S. S., and Verma, R. N. 1979. False smut of maize in India. Plant Dis. Rptr. 63:996997.
Sinha, R. C., and Benki, R. M. 1972. American wheat striate mosaic virus. CMI/A.A.B. Descriptions of Plant Viruses. Set 6, No. 99.

Page 340
Smidt, M. L., and Vidaver, A. K. 1986. Population dynamics of Clavibacter michiganense subsp. nebraskense in fieldgrown dent corn and popcorn. Plant Dis.
70:10311036.
Smidt, M. L., and Vidaver, A. K. 1987. Variation among strains of Clavibacter michiganense subsp. nebraskense isolated from a single popcorn field.
Stevens, C., and Gudauskas, R. T. 1982. Relation of maize dwarf mosaic virus infection to Helminthosporium maydis race O. Phytopathology 72:15001502.
Sumner, D. R., and Bell, D. K. 1980. Root diseases of corn caused by Rhizoctonia solani and Rhizoctonia zeae. (Abstr.) Phytopathology 70:572.
Sumner, D. R., and Bell, D. K. 1982. Root diseases induced in corn by Rhizoctonia solani and Rhizoctonia zeae. Phytopathology 72:8691.
Sumner, D. R., and Schaad, N.M. 1977. Epidemiology and control of bacterial leaf blight of corn. Phytopathology 67:11131118.
Suparyono, and Pataky, J. K. 1989. Influence of host resistance and growth stage at the time of inoculation on Stewart's wilt and Goss's wilt development and sweet
corn hybrid yield. Plant Dis. 73:339345.
Tosic, M., Ford, R. E., Shukla, D. D., and Jilka, J. 1990. Differentiation of sugarcane, maize dwarf, johnsongrass, and sorghum mosaic viruses based on reactions of
oat and some sorghum cultivars. Plant Dis. 74:549552.
Traut, E. J., and Warren, H. L. 1991. Reactions of corn inbreds to Bipolaris zeicola races 1, 2 and 3, and the new pathotype. (Abstr.) Phytopathology 81:1189.
Trujillo, G. E., Acosta, J. M., and Pinero, A. 1974. A new corn virus disease found in Venezuela. Plant Dis. Rptr. 58:122126.
Tsai, J. H. 1979. Occurrence of a corn disease in Florida transmitted by Peregrinus maidis. Plant Dis. Rptr. 59:830833.
Ullstrup, A. J. 1970. A comparison of monogenic and polygenic resistance to Helminthosporium turcicum in corn. Phytopathology 60:15971599.
Ullstrup, A. J. 1978. Corn Diseases in the United States and Their Control. USDA Agric. Res. Serv. Agric. Hdbk. No. 199 (Rev.).
Uyemoto, J. K. 1983. Biology and control of maize chlorotic mottle virus. Plant Dis. 67:710.
Uyemoto, J. K., Phillips, N. J., and Wilson, D. L. 1981. Control of maize chlorotic mottle virus by crop rotation. (Abstr.) Phytopathology 71:910.
Vakili, N. G., and Booth, G. D. 1981. Helminthosporium carbonum, a cause of stalk rot of corn in Iowa. (Abstr.) Phytopathology 71:910.
VanGessel, M. J., and Coble, H. D. 1993. Effect of nitrogen and moisture stress on severity of maize dwarf mosaic virus infection in corn seedlings. Plant Dis.
77:489491.
Vidaver, A. K., and Carlson, R. R. 1978. Leaf spot of field corn caused by Pseudomonas andropogonis. Plant Dis. Rptr. 62:213216.
Vidaver, A. K., Gross, D. C., Wysong, D. S., and Doupnik, B. L., Jr. 1981. Diversity of Corynebacterium nebraskense strains causing Goss's bacterial wilt and
blight of corn. Plant Dis. 65:480483.
Visconti, A., Chelkowski, J., Solfrizzo, M., and Bottalico, A. 1990. Mycotoxins in corn ears naturally infected with Fusarium graminearum and F. crookwellense.
Wallin J. R. 1986. Production of aflatoxin in wounded and whole maize kernels by Aspergillus flavus. Plant Dis. 70:429430.

Page 341
Warren, H. L. 1975. Temperature effects on lesion development and sporulation after infection by races O and T of Bipolaris maydis. Phytopathology 65:623626.
Warren, H. L. 1977. Survival of Colletotrichum graminicola in corn kernels. Phytopathology 67:160162.
Warren, H. L., Huber, D. M., and Tsai, C. Y. 1987. Nutrient interactions with stalk rot of maize. (Abstr.) Phytopathology 77:1745.
Waudo, S. W., and Norton, D. C. 1986. Pathogenic effects of Pratylenchus scribneri in maize inbreds and related cultivars. Plant Dis. 70:636638.
Weston, W. J., Jr. 1921. Another conidial Sclerospora of Philippine maize. J. Agric. Res. 20:669685.
White, D. G., Hoeft, R. G., and Touchton, J. T. 1978. Effects of nitrogen and nitrapyrin on stalk rot, stalk diameter and yield of corn. Phytopathology 68:811814.
Wicklow, D. T., Horn, B. W., Shotwell, O. L., Hesseltine, C. W., and Caldwell, R. S. 1988. Fungal interference with Aspergillus flavus infection and aflatoxin
contamination of maize grown in a controlled environment. Phytopathology 78:6874.
Wicklow, D. T., Wilson, D. M., and Nelsen, T. C. 1993. Survival of Aspergillus flavus sclerotia and conidia buried in soil in Illinois or Georgia. Phytopathology
83:11411147.
Widham, G. L., and Williams, W. P. 1988. Resistance of maize inbreds to Meloidogyne incognita and M. arenaria. Plant Dis. 72:6769.
Windels, C. E., and Kommedahl, T. 1984. Lateseason colonization and survival of Fusarium graminearum Group II in cornstalk in Minnesota. Plant Dis. 68:791
793.
Wei, J.K; Lui, K.M; Chen, J.P, Luo, P.C., and LeeStadelmann, O. Y. 1988. Pathological and physiological identification of race C of Bipolaris maydis in
China. Phytopathology 78:550554.
Welz, H. G., and Leonard, K. J. 1993. Phenotypic variation and parasitic fitness of races of Cochliobolus carbonum on corn in North Carolina. Phytopathology
83:593601.
Williams, R. J., Frederiksen, R. A., and Mughogho, L. K. (eds.). 1978. Proceedings of the International Workshop on Sorghum Diseases. ICRISAT, Patancheru,
India. 469 pp.
Worf, G. L., and Delahaut, K. A. 1991. Effects and control of northern corn leaf spot disease in Wisconsin. (Abstr.) Phytopathology 81: 1201.
Wright, W. R., and Billeter, B. A. 1974. ''Red kernel" disease of sweet corn on the retail market. Plant Dis. Rptr. 58:10651066.
Yates, I. E., Bacon, C. W., and Hinton, D. M. 1997. Effects of endophytic infection by Fusarium moniliforme on corn growth and cellular morphology. Plant Dis.
81:723728.
Young, G. V., Lefebvre, C. L., and Johnson, A. G. 1947. Helminthosporium rostratum on corn, sorghum and pearl millet. Phytopathology 47:180183.
Zeyen, R. J., and Morrison, R. H. 1975. Rhabdoviruslike particles associated with stunting of maize in Alabama. Plant Dis. Rptr. 59:169171.
Zhang, L., Zitter, T. A., and Lulkin, E. J. 1991. Artificial inoculation of maize white line mosaic virus into corn and wheat. Phytopathology 81:397400.
Zuber, M. S., Darrah, L. L., Lillehoj, E. B., Josephson, L. M., Manwilier, A., Scott, G. E., Gudauskas, R. T., Horner, E. S., Widstrom, N. W., Thompson, D. L.,
Bockholt, A. J., and Brewbaker, J. L. 1983. Comparison of openpollinated maize varieties and hybrids for preharvest aflatoxin contamination in the southern United
Zummo, N. 1976. Yellow leaf blotch: A new bacterial disease of sorghum, maize, and millet in West Africa. Plant Dis. Rptr. 60:798799.

Page 343
10.
Diseases of Millet
The species included are foxtail millet, or Italian millet, Setaria italica (syn. Chaeotchloa italica); proso, or browntop, millet, Panicum miliaceum; Japanese millet,
or sawan millet, Echinochloa crusqalli var. frumentacea; jungle rice millet, E. colonum; pearl millet, or bajra, Pennisetum glaucum; and finger millet, or ragi or
African millet, Eleusine coracana. Certain diseases are reported to affect some millets. Any known differences between millets in susceptibility to pathogens are
noted in the text.
Diseases Caused By Bacteria
Bacterial Blight
Cause.
Xanthomonas campestris pv. coracanae.
Distribution.
India on ragi, or African millet.
Symptoms.
Initially, watersoaked, translucent, pale yellow, linear to elongate spots (510 mm long) develop parallel to the midribs of diseased leaves. Eventually, spots become
brown and coalesce to cover the entire leaf, causing it to wither.
Management.
Not reported.
Bacterial Leaf Streak
Cause.
Xanthomonas campestris pv. pennamericanum. A Xanthomonas spp. causing a leaf streak has been described in Colorado; however, this may be different than
bacterial leaf streak caused by X. campestris.
Distribution.
Northern Nigeria and the United States (northeastern Colorado).
Symptoms.
Symptoms are not fully reported, but they are presumed to be

Page 344
streaks on the diseased foliage. The bacterial streak from Colorado is described as a brownred, watersoaked streak on diseased leaves.
Management.
Not reported.
Bacterial Leaf Stripe
Cause.
Acidovorax avenae subsp. avenae (syn. Pseudomonas avenae) is not known to be seedborne; however, the high incidence of disease on pearl millet in Nigeria
could be due to infected seed. Hydathodes are the possible portals of entry into host plants by the bacteria.
Distribution.
Nigeria, but it is thought to be present in most areas of Africa where pearl millet is grown.
Symptoms.
Watersoaking normally occurs at the tips of diseased leaves, to where the ends of interveinal lesions (several centimeters to more than 25 cm long) have elongated.
Older lesions are a uniform light brown. Lesions are similar to those of yellow leaf blotch, but lesions of yellow leaf blotch are reported to not be limited by veins.
Management.
Not reported.
Bacterial Spot
Cause.
Pseudomonas syringae. The gramnegative bacterium produces fluorescing, opaque, colorless, smoothmargined, domed colonies. Disease appears after hard rains.
Distribution.
The United States.
Symptoms.
Watersoaked spots on diseased leaves expand to form oval to elongated, tan, necrotic lesions with a thin dark brown margin.
Management.
Not reported.
Bacterial Stripe
Cause.
Pseudomonas syringae pv. panici.
Distribution.
The United States on proso millet.
Symptoms.
Stripes on diseased leaves initially are watersoaked and later become brown. Dried scales of bacterial exudate may be present on the lesion surface.
Management.
Not reported.
Pantoea agglomerans Leaf Spot
Cause.
Pantoea agglomerans (syn. Erwinia herbicola).
Distribution.
India and Zimbabwe.

Page 345
Symptoms.
Initially, watersoaking occurs at the leaf tips and margins. About a day later, necrotic lesions that are surrounded by chlorotic halos occur at the leaf tips and margins.
Strawcolored lesions with a chlorotic edge often extend the length of the diseased leaf.
Management.
Not reported.
Yellow Leaf Blotch
Cause.
Pseudomonas sp. is seedtransmitted.
Distribution.
West Africa.
Symptoms.
Symptoms occur at the fiveleaf stage of plant growth as large (30 × 150 mm), cream yellow or light tan lesions that elongate to the tips of diseased leaves. Young
plants that become infected in the two to threeleaf stage are sometimes severely stunted or killed, but plants that become infected later in the growing season are not
severely stunted. Maturing diseased plants have large lesions on young leaves but outgrow the disease.
Management.
Not reported.
Bipolaris Leaf Spot
Cause.
Bipolaris setariae. Drechslera setariae is considered a synonym by Farr et al. (1989), but since the two fungi are reported to cause separate disease syndromes by
some researchers, D. setariae is considered as a separate pathogen.
Disease becomes severe during humid conditions with intermittent rains and temperatures of 20° to 25°C. Disease symptoms in the form of lesions are fewer and
smaller during dry, hot weather.
Distribution.
India.
Symptoms.
Bipolaris setariae causes elliptical, brown spots with dark brown centers that are often surrounded by a pale yellow halo.
Management.
Blast
It has been suggested "Pyricularia leaf spot" is a more appropriate name, since millet is not "blasted" in the same way that foliage is severely diseased on rice.
Cause.
Pyricularia setariae. Some researchers consider P. grisea to be the proper name for this organism.
Distribution.
India on finger millet, or ragi.

Page 346
Symptoms.
Small, brown, circular to elongated spots, which occur on diseased leaves and leaf sheaths, eventually develop into large elongated or spindleshaped areas that
coalesce to cover most of the leaf blade. The centers of spots are grayish and have irregular redbrown margins. During humid conditions, olive gray fungal growth
occurs in the middle of spots on the upper diseased leaf surfaces.
Elongated, irregularshaped patches occur just below the ear head, resuiting in a condition known as rotten neck. The main stalk below the lowest spike becomes
discolored brown to black and sunken for 25 to 51 mm. An olive gray fungal growth may be seen in the center of these spots. Kernels may not develop or may be
light in weight and "chaffy." A seedling blight phase also occurs and causes heavy losses.
Management.
Apply foliar fungicides before disease becomes severe.
Brown Leaf Spot
Cause.
Bipolaris urochloae (syn. Drechslera urochloae and Helminthosporium urochloae).
Distribution.
Zimbabwe.
Symptoms.
Leaf spots are extremely variable in shape and size. Initially, spots develop in various ways: as small dots, brown flecks, fine streaks, or small oval to large rectangular
or spindleshaped lesions (215 × 225 mm). Under humid conditions, spots develop brown margins and coalesce to cover large areas of the leaf and leaf sheath. The
centers of the spots are covered with a dense, grayish growth of mycelium, conidia, and conidiophores of the fungus. At the latter stages of disease, the affected
tissues die and severely diseased plants fail to produce heads.
Management.
Some genotypes may have degrees of resistance.
Cause.
Cercospora penniseti. This fungus may be synonymous with C. apii.
Distribution.
Symptoms.
Symptoms develop late in the growing season, usually in September or October. Spots on diseased leaves are usually oval (0.82.5 × 1.08.0 mm), but occasionally
may be oblong to rectangularshaped, and have pale tan to gray or chalky white centers that are dotted with rows of black conidiophore tufts and surrounded by a
dark brown margin. In moist weather, spots are covered with silvery layers of conidia.
Spots similar to those on leaves sometimes occur on stems (0.52.0 × 1.05.0 mm). Sometimes dark brown runners extend longitudinally for 3 mm from the ends of
these spots.

Page 347
Management.
Some cultivars appear to have more resistance than others. Management is usually not necessary since the disease occurs too late in the season to cause much damage
to foliage. Disease management may be desirable if millet is grown for seed.
Curvularia leaf spot is also called leaf mold.
Cause.
Curvularia penniseti. Other Curvularia species reported to cause leaf spots are C. affinis, C. geniculata, C. lunata, and C. maculans. It is not certain if fungi are
primary pathogens or secondary organisms. While no pathogenicity tests have been made, the organisms are often the only fungi associated with various spots and
blotches.
Distribution.
Symptoms.
Oval to oblong, brown spots with yellow margins occur on diseased leaves. Heads are also diseased.
Management.
Not necessary.
Dactuliophora Leaf Spot
Dactuliophora leaf spot is also called circular leaf spot.
Cause.
Dactuliophora elongata presumably overseasons as sclerotia in infested residue.
Distribution.
Higher rainfall areas of western Africa.
Symptoms.
Diseased leaves have circular lesions, sometimes with zonate circles. The inside of the spot is frequently speckled with black sclerotia.
Management.
Not reported.
Downy Mildew (Plasmopara penniseti)
Cause.
Plasmopara penniseti survives as oospores in soil and as mycelia and zoosporangia in seed. During wet soil conditions in the spring, oospores germinate to produce
zoosporangia in which zoospores are formed. Eventually, zoospores are released from the zoosporangia and "swim" to roots, where they encyst and germinate to form
a germ tube that infects the plant host.
Distribution.
Presumed to be worldwide but most common in the temperate milletgrowing regions.
Symptoms.
During wet weather, downy, whitish, fungal growths consisting of zoosporangia and mycelium occur on the undersides of diseased leaves,

Page 348
opposite yellow areas on the topsides of these leaves. As diseased plants continue to grow, leaves become wrinkled and distorted and the entire plant is stunted.
Management.
Not reported.
Downy Mildew (Sclerospora graminicola)
This disease is also called green ear disease. Symptoms are similar to those caused by Sclerospora macrospora and confusion regarding these two diseases appears
in the literature. Singh (1995) describes S. graminicola as causing two types of symptoms, downy mildew and green ear, and implies the downy mildews caused by
S. macrospora and S. graminicola are the same disease. However, Farr et al. (1989) do not list S. graminicola. Both symptoms, as described by Singh, will be
discussed here.
Cause.
Sclerospora graminicola produces asexual spores in the form of sporangia, in which zoospores are formed, and sexual spores called oospores. Oospores are thick
walled resting spores produced in diseased leaves. Sclerospora graminicola has been reported to survive for several years in soil as oospores and as oospores on
seed. However, Singh and King (1988) reported isolates from different hosts are highly hostspecific and considerable variability occurs in S. graminicola. Therefore,
when a host is withdrawn, the population of the pathogen dies out.
Sclerospora graminicola is disseminated by seedborne oospores and by any means that moves oosporeinfested residue or soil. Oospores germinate to produce one
to many germ tubes that directly penetrate meristematic tissue of young plants.
Sporangia (conidia) are produced from 0100 to 0400 hours during the night on the ends of conidiophores that have emerged through stomatal openings at
temperatures of 20° to 25°C and a relative humidity of 95% to 100%. Sporangia are disseminated by wind to other hosts and germinate either directly by germ tubes
or, more commonly, by releasing one to 12 zoospores that first encyst, then germinate to produce a germ tube that infects meristematic tissue. Zoospores retain their
infectivity for about 4 hours at 30°C and for a longer time at lower temperatures.
Downy mildew is most severe under moist conditions.
Distribution.
Wherever millet is grown. Although downy mildew s a serious disease in Africa and India, it is found only on the weed Setaria viridis in the United States. Downy
mildew is considered the most important disease of pearl millet in India and in the Sahelian and subSahelian zones of Africa.
Symptoms.
Downy mildew symptoms may appear on the first leaf but normally occur on the second and third leaves in the form of chlorosis of the leaf lamina, beginning at the
base of the diseased leaf. Chlorosis progresses to successively higher leaves on the plant and covers the entire lamina on the third or fourth leaf. A downy, grayish
growth consisting of sporangia

Page 349
and conidiophores develops on diseased tissue during wet or humid weather, generally on the abaxial leaf surface. As diseased plants approach maturity, leaves
become brown, necrotic, and either split or shred.
Another characteristic symptom is the halfleaf symptom, which is a distinct margin between the diseased area toward the basal portion of the leaf and the nondiseased
area toward the leaf tip. Because of the systemic nature of the disease, after leaf symptoms develop, all the subsequent leaves and the panicle have symptoms except
in the case called recover resistance, where plants outgrow the disease.
Green ear symptoms appear on panicles due to the transformation of floral parts into leaf structures, which have no kernel development. Sometimes symptoms may
appear as local lesions on the leaves.
Symptomless shoots have been reported to develop from plants that showed typical systemic symptoms of downy mildew. Injection of the growing points of the
symptomless shoots with a sporangial suspension or clipping the stems and shoots of recovered plants growing under high disease pressure generally does not result in
subsequent disease development. Lines produced from recovered plants maintained their resistance at three locations in India. This phenomenon was also observed in
Mall and Niger.
Severely diseased plants remain stunted and do not produce particles. Plants are dwarfed, have excessive tillering from the crown, and develop axillary buds along the
culm.
Management
2. Control weeds that may serve as alternate hosts.
3. Grow the most resistant cultivar. Recovery resistance may be an effective defense mechanism that could be exploited in breeding pearl millet for resistance to
downy mildew.
4. Practice good fertilizer management. Phosphorous as superphosphate (16% P) decreased severity of downy mildew in field trials.
Downy Mildew (Sclerospora macrospora)
Downy mildew is sometimes called green ear.
Cause.
Sclerospora macrospora (syn. Sclerophthora macrospora) survives as oospores in soil and infested residue. Oospores germinate to produce mycelia, which may
directly infect the host plant. More commonly, sporangia are produced in which zoospores are formed. Zoospores are liberated from sporangia and "swim" to
meristematic tissue, where they encyst and germinate to form a germ tube that penetrates the host plant. Secondary infection occurs by production of sporangia borne
on the ends of sporangiophores that have emerged through stomates. Sporangia are disseminated by wind to host plants, where zoospores are again released and
germinate to form germ tubes that penetrate meristematic tissue.

Page 350
Oospores are eventually formed in diseased tissue. The disease is most severe under wet conditions.
Distribution.
Africa and India.
Symptoms.
Diseased plants are stunted, have shortened internodes, and are chlorotic or pale green. There is a proliferation of the first glumes of the lower spikelets. Ultimately,
the whole inflorescence becomes involved, giving the diseased plant a bushlike appearance.
Management.
Drechslera Leaf Spot
Cause.
Drechslera dematioidea (syn. Helminthosporium dematioidea). Overwintering is likely as mycelia in infested residue. Conidia are disseminated by wind from
residue to plant hosts.
Distribution.
Africa, temperate Europe, and southern North America.
Symptoms.
Symptoms on diseased leaves are primarily lesions that are elliptical, yellowish to grayish or tan, and several centimeters long. The centers of lesions are usually grayish
to tan with a tan margin. In warm, humid weather, sporulation gives lesions a dark gray appearance. During humid conditions, lesions enlarge and kill large parts of
diseased leaves.
Management.
Not reported.
Ergot
Cause.
Claviceps fusiformis overseasons as sclerotia in the soil and in stored grain. Sclerotia germinate, coinciding with flowering, and produce one to 16 stipes, which
terminate in a globular capitulum in which perithecia are produced. Ascospores are produced in perithecia and infect inflorescences through young, fresh stigmas.
Infection is prevented or reduced after the stigmas wither either subsequent to pollination or during aging. Honeydew containing macroconidia is produced in 4 to 6
days. The macroconidia germinate and produce microconidia in 2 to 3 days.
Several insects function in the secondary spread of the fungus by being attracted to the honeydew and becoming contaminated with conidia. Included are Aphis
indica, Dysdercus ungulatus, Monomorium salomonis, Musca domestica, Syrphus confractor, Tabanus rubidus, Vespa orientalis, and V. tropica. Aphis
indica and M. domestica are the most efficient disseminators.
Infection is favored by 16 to 24 hours of panicle wetness and moderate temperatures. Minimum temperature is more critical for infection than maximum temperature.
In susceptible genotypes, temperatures in the range of 14° to 35°C with 8 hours/day at less than 20°C and 4.6 hours/day at greater than 30°C are favorable for
infection.
Cytoplasmic male sterility is associated with increased susceptibility.

Page 351
Distribution.
India on pearl millet. Ergot also occurs throughout Africa, but it is not considered a serious disease.
Symptoms.
Symptoms are typical of ergot found on other plants. Hard, black sclerotia, or ergot bodies, replace grain kernels. Sclerotia vary in shape from elongated to round
(1.31.8 × 3.66.1 mm), are light to dark brown, and are hard to brittle. Sweet, sticky honeydew containing conidia is produced on diseased inflorescences and
becomes black from adhering dust and attracts insects.
Management.
Exserohilum Leaf Blight
Exserohilum leaf blight is also called zonate eyespot.
Cause.
Exserohilum rostratum (syn. Helminthosporium rostratum) survives as mycelium in infested residue and is seedborne. Conidia production from mycelium is
optimum during wet conditions at a temperature of 30°C; conidia are disseminated by wind to plant hosts. Conidia produced in leaf spots during warm, wet conditions
provide secondary inoculum.
Distribution.
The United States (Georgia) on pearl millet. Exserohilum leaf blight is considered to be of minor importance.
Symptoms.
Lesions on diseased leaves are small (12 × 25 mm) and limited laterally by veins. Lesions may later coalesce and form large, necrotic areas that extend across veins.
Lesions are dark brown at first but later become light brown, particularly on older leaves. The necrotic center of all lesions may bleach to a straw color with a slight
browning at the edges and some yellowing at the lesion ends. Exserohilum rostratum has also been found associated with head mold.
Management.
Not necessary, as Exserohilum leaf blight occurs infrequently.
False Mildew
Cause.
Beniowskia sphaeroidea. Disease is favored by humid weather.
Distribution.
Malawi and Uganda.
Symptoms.
Typical white growth consisting of conidia, conidiophores, and mycelium occurs on diseased leaves.
Management.
Not reported.
Fusarium nygamai Disease
Cause.
Fusarium nygamai. Fusarium nygamai is considered very similar to F. moniliforme. Polyphialides and chlamydospores are produced in cultures that are 21 days
or older.

Page 352
Distribution.
Southern Africa. However, F. nygamai likely occurs in other areas where millet is grown.
Symptoms.
The mycotoxin moniliformin is produced. Fusarium moniliforme produces moniliformin in small amounts or not at all.
Management.
Not reported.
Head Mold
Cause.
Several fungi, including Alternaria spp., Aspergillus flavus, Bipolaris setariae, B. stenospila (syn. Helminthosporium stenospilum), Curvularia lunata,
Drechslera dematioidea, Epicoccum spp., Exserohilum rostratum (sometimes incorrectly spelled rostrata), Fusarium moniliforme, Gloeocercospora sorghi,
Olpitrichum tenellum, and Phyllosticta penicillariae. Other Fusarium species reported to cause head mold are F. chlamydosporum, F. equiseti, F. napiforme,
F. nygamai, and F. pallidoroseum (syn. F. semitectum). Infection is favored by high rainfall and low maximum temperatures.
Fusarium moniliforme infects mature millet; the disease severity is increased by dew or other moisture. Other pathogens infect in a similar manner, with disease
incidence increasing more on latesown millet than on earlysown millet. Head mold is most severe following insect injury and under humid, wet weather conditions.
Distribution.
Africa, India, and the United States.
Symptoms.
Oidium tenellum causes a mealy, white coating on diseased heads. Under magnification, the coating appears as white hairs with white beads at their tips.
Helminthosporium spp. and C. lunata cause a black woolly mat to grow over heads. Fusarium moniliforme initially causes a whitish mycelial growth on spikelets
of immature heads that later turns pink or causes individual grains to be covered with an orange crust. Moldy spikelets are easily shaken off. Seed quality and
germination are greatly reduced.
Aspergillus flavus causes a typical browngreen discoloration of seed. The aflatoxins deoxynivalenol, nivalenol, zearalenone, and 15acetylscirpentriol have been
detected in pearl millet.
Incidence of F. chlamydosporum has been positively correlated with concentrations of trichothecenes and zearalenone.
Management.
No acceptable management is known except timely harvest of millet grown for grain. It may be possible to avoid disease in wet milletgrowing areas by timing sowing
so heads mature after heavy rains have stopped.
Head Smuts
Cause.
Sporisorium destruens (syn. Sphacelotheca destruens) is a pathogen of proso millet. Ustilago trichophora (syn. U. crusgalli) is a pathogen of Japan

Page 353
ese barnyard millet. Both S. destruens and U. trichophora are smut fungi that survive in soil as chlamydospores.
Distribution.
Wherever millet is grown.
Symptoms.
Sporisorium destruens completely destroys the inflorescence except for the vascular strands. The sorus is covered with a gray mycelium that does not persist long
before exposing redbrown chlamydospores that become windborne.
Ustilago trichophora forms sori in galllike swellings on nodes and flowers that remain covered by host tissue. When exposed, chlamydospores are yellow to olive
brown.
Management
2. Rotate millet with other crops.
Helminthosporiosis
Helminthosporiosis is also called blight.
Cause.
Bipolaris nodulsa (syn. Helminthosporium nodulosum) survives in infested soil residue and is seedborne. The fungus is present in the pericarp and endosperm but
not in the embryo. Helminthosporiosis is most severe at temperatures of 30° to 32°C and high moisture.
Distribution.
Africa and India on finger millet, or ragi.
Symptoms.
Roots, culms, leaves, heads, and inflorescences are diseased. Numerous small, oval, brown spots commonly occur on upper leaf surfaces and gradually elongate to an
approximate size of 1 ° 10 mm. Other descriptions note the spots are pale yellow to black.
Spots on leaf sheaths are larger than the spots on diseased leaves, are dark brown to nearly black, and usually occur at the junction of the leaf blade and sheath.
Lesions on culms and internodes are similar to those on leaf sheaths. Diseased heads dry up, especially at the rachis.
Diseased seed is discolored gray or black. Preemergence damping off may occur with seeds and seedlings. Most infected seed does not germinate, and the fungus
sporulates heavily on ungerminated seeds and dead seedlings. In less severe disease instances, rot develops as a browning of the coleoptile and slowly progresses
upward. The main roots of such seedlings are discolored and there is a tinge of brown discoloration on root hairs. Emerged seedlings have discolored, dull brown
coleoptiles with some etiolation at the tip. With time, browning and etiolation of the coleoptile increases and seedlings collapse within 9 to 12 days. Yield losses as high
as 50% have been reported.
Management

Page 354
Helminthosporium leaf spot is also called Bipolaris leaf spot.
Cause.
Bipolaris stenospila (syn. Helminthosporium stenospilum), B. sacchari (syn. H. saachari), and B. setariae (syn. H. setariae). Optimum disease development
caused by B. setariae is at temperatures of 15° to 21°C.
Distribution.
The United States (Georgia) on pearl millet.
Symptoms.
Disease symptoms usually develop extensively during August through October after plants head. Lesions on diseased leaves will vary in size and shape from brown
flecks, fine linear streaks, and small oval spots to large, irregularshaped, oval, oblong, or almost rectangular spots (0.53.0 × 1.010.0 mm). Sometimes large,
elongated lesions are produced. Spots may expand and coalesce and form long streaks (2.55.0 × 20.090.0 mm). Lesions may be dark brown initially but later
become tan or graybrown with a less distinct dark brown border. During moist weather, a dense graybrown growth consisting of mycelium, conidiophores, and
conidia grows in lesions. A black conidial and mycelial growth may also occur over individual grains in the head.
Management.
Some cultivars are more resistance than others; however, management is usually not necessary since disease occurs too late in the season to cause much damage to
foliage production. Management may be desirable if millet is grown for seed.
Kernel Smuts
Cause.
Ustilago crameri and Sporisorium neglectum (syn. U. neglecta). Both U. crameri and S. neglectum survive in dry soil as chlamydospores. Chlamydospores
germinate and produce a basidium on which either lateral branches or sporidia, both of which infect seedlings, are formed.
Distribution.
Africa, Asia, and the United States. Ustilago crameri is a pathogen of foxtail millet.
Symptoms.
Sori resemble enlarged kernels and are enclosed in floral bracts. The floral bracts rupture during the growing season or at harvest time and release yellowbrown to
olive green chlamydospores of U. crameri or purplebrown chlamydospores of S. neglectum.
Management
Leaf Spot (Drechslera setariae)
Cause.
Drechslera setariae infects only areas of leaves infected by Sclerospora graminicola.

Page 355
Distribution.
India.
Symptoms.
Lesions vary in size and have ashcolored centers with dark margins. Sometimes under severe disease conditions, diseased leaves are completely blighted.
Management.
Not reported.
Leaf Spot (Helminthosporium frumentacei)
Cause.
Helminthosporium frumentacei.
Distribution.
India on Japanese millet.
Symptoms.
Initially, numerous, yellowish spots (12 mm in diameter) occur on both sides of diseased leaves and on leaf sheaths. Spots gradually increase in size and have a light
brown center with a yellow margin that becomes dark brown as the spots mature. Spots elongate or coalesce and form long stripes.
Management.
Not reported.
Long Smut
Long smut is also called pearl millet smut and pearl millet kernel smut. Much confusion surrounds the etiology of this disease and the proper name(s) of the causal
organism.
Cause.
Moesziomyces penicillariae (syn. Tolyposporium penicillariae). Ustilago penniseti has also been reported to be a synonym. Moesziomyces penicillariae survives
as chlamydospores in soil. Chlamydospores are the only source of inoculum and germinate during humid conditions and produce a basidium on which sporidia bud,
germinate, and infect host plants through the flowers. Flowers are most susceptible at an early stage of development, before the stigma or anthers are visible. After
pollination, flowers are virtually immune from infection. Later in the growing season, chlamydospores are formed on grain instead. The chlamydospores are released
and fall to the soil when their enclosing membrane ruptures.
Distribution.
Africa and Asia on pearl millet.
Symptoms.
The membrane enclosing the chlamydospores and the chlamydospores themselves is collectively called a sorus. The sorus is brown to black, is somewhat pear
shaped, and protrudes from the floral bracts of the diseased plant. Upon rupturing of the sori membranes, the exposed chlamydospores are greenbrown.
Management.
In experimental plots, applying foliar fungicides shows promise of partial control.

Page 356
Cause.
Myrothecium roridum.
Distribution.
Worldwide, but most common in warmer areas.
Symptoms.
Necrotic spots occur on diseased leaves. Sometimes the centers of the spots fall out and give leaves a shothole appearance.
Management.
Not reported.
Phyllosticta Leaf Blight
Cause.
Phyllosticta penicillariae survives as pycnidia in infested residue and is seedborne. Dissemination is by any method that moves residue and by airborne conidia.
Distribution.
Africa and the United States (Georgia).
Symptoms.
Diseased plants are stunted and chlorotic and have numerous leaf lesions that are approximately 2.55.0 mm in size. Lesions are parallelsided and have light brown
necrotic tissue in the center and dark brown margins. Coalesced lesions usually result in tattered leaf tissue. Leaf margins are frequently necrotic. Pycnidia, which
average 75.8 µm in diameter, frequently can be observed in the necrotic tissue. Husks also become diseased.
Management.
Not reported.
Pyricularia Leaf Spot
Pyricularia leaf spot is also called blast and may be the same disease as blast. Some researchers consider Pyricularia grisea and P. setariae to be synonymous.
Cause.
Pyricularia grisea is seedborne in finger millet. The fungus is present in the pericarp and endosperm but not in the embryo. Disease is favored by wet conditions or
extended periods of high relative humidity.
Distribution.
Australia, India, Kenya, Russia, Uganda, and the United States (Georgia).
Symptoms.
Numerous small, brown flecks enlarge and become brown, spindleshaped spots on diseased leaves. Later, ash gray, watersoaked spots with brown margins
develop. Spots increase in size (0.51.5 × 3.08.0 mm), become necrotic and eventually coalesce and give leaves a blasted appearance. Severe disease is usually
accompanied by extensive chlorosis.
Culm nodes blacken, become fragile, and may lodge at these weakened areas. Brown to black spots appear at the particle base, enlarge, and often girdle the neck
below the panicle.
The diseased neck becomes shriveled and covered with mycelium, coni

Page 357
diophores, and conidia. Abundant conidia and conidiophores are also formed on nodes and necks in wet weather. When neck blast is severe, panicles fail to emerge
and spikelets become diseased and blackened. When neck infection occurs early in the growth of the host plant, the grains do not fill and panicles remain erect. Later
infection in the life of the plant resuits in lodging of partially filled panicles.
Diseased seed is discolored gray or black. Most diseased seed does not germinate and the fungus sporulates heavily on ungerminated seeds and dead seedlings. Less
severe disease results in a rot that develops as a browning of the coleoptile and slowly progresses upward. The main roots of such seedlings are discolored and there
is a light brown discoloration of the root hairs.
Emerged seedlings have discolored, dull brown coleoptiles with some etiolation at the tip. With time, browning and etiolation of the coleoptile increases and seedlings
collapse within 9 to 12 days. Yield losses as high as 50% have been reported.
Management
1. Apply foliar fungicide before disease becomes severe.
2. Treat seed with fungicide seed treatments.
Rhizoctonia Blight
Cause.
Rhizoctonia solani and R. zeae survive in soil and infested residue as sclerotia. Sclerotia are disseminated by wind, splashing water, or any means that transports soil
or residue. When sclerotia are deposited on a host plant, they germinate and form infective hyphae that penetrate the plant. Disease is more severe on millet types with
a low, dense growth habit, which creates high humidity conditions that are more conducive to disease development.
Distribution.
Symptoms.
Lesions are irregularshaped blotches (47 cm long) that occur mostly on diseased leaf sheaths and the bases of leaf blades. Lesions are watersoaked at first but
eventually become light tan and have an indistinct brown border. Diffuse white to tan mycelia grow over the surfaces of lesions and adjacent green tissue. Older lesions
may be covered with tiny, brown sclerotia that are usually associated with R. solani. Rhizoctonia zeae is distinguished by tiny, globular, red sclerotia that may occur
on the same lesions and be mixed together with R. solani.
Apparently little damage is caused except that an occasional tiller may be killed. Rarely, an entire plant may be so severely blighted that it has the appearance of being
scalded.
Management.
Not necessary.

Page 358
Rust (Puccinia substriata var. indica)
Cause.
Puccinia substriata var. indica (syn. P. penniseti) is a macrocyclic heteroecious rust that overwinters as teliospores in the United States and has eggplant, Solanum
melongena, as an alternate host. Other aecial hosts include S. anguivi, S. ferox, S. gilo, S. incanum, S. linaeanum, S. nodiflorum, and S. rostratum. Solanum
americanum and S. aviculare are resistant. Uredinia and telia are produced on millet; pycnia are produced on the upper leaf surfaces of eggplant and aecia on the
lower leaf surfaces of eggplant.
Optimal temperatures for urediniospore germination on artificial media is 19° to 22°C for incubation periods of 6 to 7 hours. Continuous light for 2 hours incubation
delayed germination, but exposure to light during the first hour of incubation followed by 1 hour of dark is stimulatory.
At least 11 races of P. substriata var. indica have been identified.
Distribution.
India and the United States on pearl millet. Rust is a lateseason disease in the southeastern United States.
Symptoms.
Uredinia occur as orangebrown pustules that rupture the leaf epidermis. Uredinia occur on both leaf surfaces but are more abundant on the upper surfaces of
diseased leaves.
Management
2. Remove eggplants from vicinity of millet.
Rust (Puccinia substriata var. pennicillariae)
Cause.
Puccinia substriata var. pennicillariae (syn. P. penniseti). The aecial stage is not known.
Distribution.
Africa.
Symptoms.
Typical brownish uredinia occur on both leaf surfaces but are most abundant on the upper surfaces of diseased leaves.
Management.
Not reported.
Smut
Cause.
Melanopsichium eleusinis (syn. Ustilago eleusinis). Chlamydospores are disseminated by wind to flowers, where infection occurs. Melanopsichium eleusinis is not
seedborne.
Distribution.
India.
Symptoms.
After flowering, symptoms are evident on scattered diseased kernels throughout the ear. Diseased grains are transformed into galls that are

Page 359
five to six times the size of a normal grain. Initially, diseased grains, which are slightly greenish and 2 to 3 mm in diameter, project slightly beyond the glumes.
Eventually, galls reach a diameter up to 16 mm and turn pinkish green and have cracks in the outer wall of the sorus, which is the membrane plus the enclosed
chlamydospores. The sorus eventually ruptures and the chlamydospores are disseminated by wind to developing flowers or fall to the soil surface.
Management
1. Some cultivars are apparently more resistant than others.
Other Smuts Reported on Millet
Sorosporium paspali var. verrucosum
Tilletia barclayana (syn. Neovossia barclayana)
Tilletia ajrekari
Tolyposporium senegalense
Ustilago paradoxa
Southern Blight
Southern blight is also called foot rot, and southern blight and wilt.
Cause.
Sclerotium rolfsii overwinters as sclerotia in soil and as mycelia in infested residue and seeds. Mycelia from germinated sclerotia, residue, or seed serve as the
primary inoculum. High soil temperatures and a low soil pH of 3 to 6 favor disease development. High relative humidity stimulates aerial growth of mycelia on stems,
branches, and leaves. Cool temperatures in winter kill sclerotia and mycelia. The disease is reported to be most severe under wet soil conditions, although on other
crops southern blight is more severe under relatively dry soil conditions.
Distribution.
Africa and India on finger millet, or ragi.
Symptoms.
Symptoms develop when diseased plants are 6 to 8 weeks old. Single tillers and occasionally an entire plant may be killed. Diseased plants are stunted and chlorotic
and have a poorly developed root system. A brown to black discoloration is present on crowns, and the root cortex is rotted. Later, the basal portion of stems
becomes discolored brown and the cortical tissue disintegrates and rots, causing plant death. White mycelia, in which black sclerotia eventually develop, grow on
crowns and lower stems.
Aboveground symptoms are white mycelial mats that grow upward inside leaf sheaths for as much as 30 cm above the soil line. Tissue beneath mats becomes
discolored and is eventually killed and shredded. Sclerotia form inside the leaf sheaths and around the base of the diseased plant.

Page 360
Management.
Grow the most resistant cultivar.
Top Rot
Top rot is also called pokkah boeng.
Cause.
Fusarium subglutinans (syn. F. moniliforme var. subglutinans). Fusarium subglutinans overwinters as mycelia and perithecia in infested residue and is seedborne
as mycelia and conidia. Conidia are produced from mycelia growing on residue during wet weather and disseminated by wind or splashed by rain to plant hosts,
where they lodge in the leaf sheaths or whorls and germinate. During wet weather, F. subglutinans also grows upward on the outside of stalks. Metabolites produced
by F. subglutinans cause distortions in plants.
Distribution.
Tropical or semitropical milletgrowing areas. Top rot is not a common disease of millet.
Symptoms.
Mild symptoms on diseased leaves may appear as a mosaic that somewhat resembles a virus symptom. Leaves near the top of diseased plants are deformed and
discolored and have wrinkled bases and numerous transverse cuts in the leaf margin. Leaves may be so wrinkled that they do not unfold properly. In severe cases, F.
subglutinans may grow from whorls and sheaths into stalks, causing the tops of plants to die.
Management.
No management measures are necessary.
Zonate Leaf Spot
Cause.
Gloeocercospora sorghi overwinters as sclerotia in infested soil residue. Most primary inoculum presumably comes from residue, However, G. sorghi is also
seedborne as mycelia and possibly sclerotia that contaminate seed, thus affording another potential source of primary inoculum. In the spring, sclerotia germinate and
produce conidia, which are disseminated by splashing rain or wind to millet. During warm, wet weather, sporulation occurs within lesions in the form of pink
sporodochia that form above the leaf stomates. Conidia produced in sporodochia are borne in a pinkish, gelatinous mass and serve as secondary inoculum by being
splashed by rain to nearby plant hosts. Sclerotia are eventually formed in lesions.
Distribution.
The United States (Georgia). Zonate leaf spot is of minor importance.
Symptoms.
Lesions on diseased leaves initially appear as watersoaked spots (2.03.5 × 3.55.0 mm) that eventually develop tan centers with dark brown borders. Spots enlarge
to form roughly semicircular blotches that

Page 361
may cover half or more of the leaf width. Blotches are different shades of dark brown mottled with light tan spots that tend to arrange in circles. This gives the
appearance of incomplete tan rings alternating with dark brown rings. This ''zonation" pattern is often absent on narrowleafed strains of millet. During moist weather,
tiny, salmoncolored globules consisting of masses of spores are visible under magnification on both surfaces of spots. As leaves die, lenticular black sclerotia appear
in the dead tissue.
Management.
Not necessary.
Burrowing
Cause.
Radopholus similis is an endoparasite that survives for a few months outside of host tissue. Some dissemination occurs by water. Feeding occurs in the cortex and
reproduction occurs in the roots.
Distribution.
Tropical and subtropical areas around the world.
Symptoms.
The aboveground symptom is a slight stunting of diseased plants. Belowground symptoms are root lesions and decay.
Management.
Not reported.
Cyst
Cause.
Heterodera gambiensis.
Distribution.
Gambia and Niger.
Symptoms.
Small, whitish to light yellow sacs of immature females can be observed without magnification on the outside of diseased roots. Plant growth is stunted and unthrifty.
Management.
Not practiced.
Dagger
Cause.
Distribution.
Not known.
Symptoms.
The aboveground symptom is a slight to moderate stunting of the entire diseased plant. Belowground symptoms are a reduction in feeder roots accompanied by
necrosis of portions of the root system.
Management.
Not reported.

Page 362
Lance
Cause.
Hoplolaimus indicus is an endoparasite that sometimes feeds as a semiendoparasite and an ectoparasite.
Distribution.
Not known.
Symptoms.
Aboveground symptoms are stunting and chlorosis of the entire diseased plant. The belowground symptom is lesions that occur on roots and reduce root growth.
Management.
Not reported.
Ring
Cause.
Criconemella ornata is an ectoparasite.
Distribution.
Symptoms.
The aboveground symptom is a mild stunting of the whole diseased plant. Belowground symptoms are lesions on roots and some root decay.
Management.
Not reported.
Root Knot
Cause.
Meloidogyne incognita, M. incognita, and M. javonica do not survive if the temperature averages below 3°C during the coldest month.
Distribution.
Symptoms.
Diseased plants are stunted and chlorotic and have reduced yields. Roots have galls, elongated swellings, and discrete knots or swellings. Root proliferation is
common.
Management.
Not reported.
Root Lesion
Cause.
Pratylenchus brachyurus, P. mulchandi, and P. zeae are endoparasites.
Distribution.
Worldwide.
Symptoms.
Plants are stunted and chlorotic. Roots are poorly developed and have necrotic lesions.
Management.
Not reported.
Sting
Cause.
Belonolaimus longicaudatus is an ectoparasite found only in sandy soils. It produces a phytotoxic enzyme.

Page 363
Distribution.
Symptoms.
Aboveground symptoms are stunting and chlorosis of the entire diseased plant. Belowground symptoms include deep necrotic lesions on the roots. Root tips are
frequently destroyed, resulting in thick, stubby roots.
Management.
Not reported.
Stubby Root
Cause.
Paratrichodorus minor is an ectoparasite found primarily in sandy soils. Most nematode feeding is around the root tips.
Distribution.
Not known.
Symptoms.
Aboveground symptoms include severe stunting and chlorosis of the entire diseased plant. Roots are stubby and sometimes appear thicker than healthy roots.
Management.
Not reported.
Stunt
Cause.
Tylenchorhynchus phaseoli, T. vulgaris, and T. zeae are ectoparasites.
Distribution.
Not reported.
Symptoms.
Diseased plants may be stunted and chlorotic. The root system is poorly developed and has fewer feeder roots than healthy plants. Numerous root tips may be short
and thickened.
Management.
Not reported.
Bajra (Pearl Millet) Streak
Cause.
Bajra streak virus (BSV) is transmitted by the leafhopper Cicadulina mbila. BSV is not mechanically transmitted. BSV is considered to be a strain of maize streak
virus. Plants may become infected at all stages of growth. Maize, sorghum, finger millet, barley, oat, and wheat are also infected.
Distribution.
India.
Symptoms.
Long, parallel, chlorotic streaks develop the entire length of diseased leaves. Plants infected early in their growth are stunted and produce empty heads.
Management.
Not reported.

Page 364
Guinea Grass Mosaic
Cause.
Guinea grass mosaic virus is transmitted by several species of aphids. Millet was inoculated.
Distribution.
Ivory Coast.
Symptoms.
Leaves had a slight green mosaic, and diseased plants were slightly stunted.
Management.
Not reported.
Maize Dwarf Mosaic
Cause.
Maize dwarf mosaic virus (MDMV) now consists of former MDMV strains A, D, E, and F; former sugarcane mosaic virus strain J infective to johnsongrass in the
United States; and maize mosaic virus, European type (Et), from Yugoslavia.
MDMV persists in several annual and perennial grasses. In the spring, aphids, particularly the corn leaf aphid, Rhopalosiphus maidis, and the greenbug Schizaphis
graminum, feed on overwintering hosts and acquire the virus.
Distribution.
Potentially, wherever millet is grown.
Symptoms.
Symptoms of MDMV infection can vary according to virus strain and temperature. Symptoms are most evident on the upper two or three leaves as an irregular
mottling of dark and light green areas interspersed with longitudinal white or light yellow streaks.
Management.
Control grassy weeds, particularly johnsongrass, in a field.
Maize Streak
Cause.
not seedborne or mechanically transmitted in maize.
Distribution.
Symptoms.
Chlorotic streaks and stripes occur on diseased leaves.
Management.
Not reported.
Panicum Mosaic
Cause.
Panicum mosaic virus (PMV) is in the sobemovirus group. PMV is mechanically transmitted. The grasses Panicum spp.; crabgrass, Digitaria sanguinalis; foxtail
millet, Setaria italica; and barnyard grass, Echinochloa crusgalli are also susceptible. Different strains of PMV are present.
Distribution.
The United States.

Page 365
Symptoms.
Diseased plants may be stunted and chlorotic. Other symptoms include a yellowgreen mosaic and mottling of leaves and stunted, deformed, or blasted heads. In
severe disease cases, plants may die. Some cultivars of millet may be symptomless carriers.
Management.
Grow resistant cultivars. Generally, vigorousgrowing types are more susceptible and slowgrowing plants with smaller leaves are more resistant.
Wheat Streak Mosaic
Cause.
Wheat streak mosaic virus (WSMV). WSMV is vectored by the wheat curl mite, Aceria tosichella (syn. A. tulipae).
Distribution.
Symptoms.
Symptoms on diseased leaves range from a mosaic with interveinal reddening to a mosaic with interveinal reddening and necrosis within the red areas.
Management.
Not reported.
Diseases Caused By Unknown Factors
Brown Leaf Mottle
Cause.
Unknown.
Distribution.
Unknown.
Symptoms.
Initially, a faint brown, irregular mottle of the leaf and sheath appears at about the time of rapid stem elongation of the affected plant. Symptoms become more
pronounced as plants mature. Affected tissue eventually becomes necrotic before normal senescence occurs, and leaves on affected plants senesce sooner than
healthy plants.
Management.
Not reported.
Red Leaf Spot
Cause.
Unknown.
Distribution.
Unknown.
Symptoms.
Symptoms first appear about the time of flower initiation. Irregular or zonate, watersoaked blotches appearing on leaves soon become a mahogany color. As affected
plants mature, the discolored areas coalesce and become necrotic.
Management.
Not Reported.

Page 366
Selected References
Burton, G. W., and Wells, H. D. 1981. Use of nearisogenic host populations to estimate the effect of three foliage diseases on pearl millet forage yield.
Claflin, L. E., Ramundo, B. A., Leach, J. E., and Erinle, I.D. 1989. Pseudomonas avenae, causal agent of bacterial leaf stripe of pearl millet. Plant Dis. 73:1010
1014.
Desaum S. G., Thirumalachar, M. J., and Patel, M. K. 1965. Bacterial blight disease of Eleusine coracana Gaertn. Indian Phytopathol. 18:384386.
Deshmukh, S. S., Mayee, C. D., and Kulkarni, B. S. 1978. Reduction of downy mildew of pearl millet with fertilizer management. Phytopathology 68:13501353.
Frederickson, D. E., Monyo, E. S., King, S. B., and Odvody, G. N. 1997. A disease of pearl millet in Zimbabwe caused by Pantoea agglomerans. Plant Dis.
81:959.
Govindu, H. C., Shivanandappa, N., and Renfro, B. L. 1970. Observations on diseases of Eleusine coracana with special reference to resistance to the
Helminthosporium disease, pp. 415424. In Plant Disease Problems. International Symposium on Plant Pathology. Indian Phytopathology Society, New Delhi.
Jensen, S. G., Lambrecht, P., Odvody, G. N., and Vidaver, A. K. 1991. A leaf spot of pearl millet caused by Pseudomonas syringae. (Abstr.) Phytopathology
81:1193.
Keshi, K. C., and Mohanty, N. N. 1970. Efficacy of different fungicides and antibiotics on control of blast of ragi, pp. 425429. In Plant Disease Problems.
International Symposium on Plant Pathology. Indian Phytopathology Society, New Delhi.
Lee, T. A., Jr., and Toler, R. W. 1977. Resistance and susceptibility to Panicum mosaic virusSt. Augustine decline strain in millets. Plant Dis. Rptr. 61:6062.
Luttrell, E. S. 1954. Diseases of pearl millet in Georgia. Plant Dis. Reptr. 38:507514
Marasas, W. F. O., Rabie, C. J., Lubben, A., Nelson, P. E., Toussoun, T. A., and Van Wyk, P. S. 1987. Fusarium napiforme, a new species from millet and
sorghum in southern Africa. Mycologia 79:910914.
Marasas, W. F. O., Rabie, C. J., Lubben, A., Nelson, P. E., Toussoun, T. A., and Van Wyk, P. S. 1988. Fusarium nygamai from millet in southern Africa.
Mycologia 80:263266.
Mehta, P. R., Singh, B., and Mathur, S. C. 1952. A new leaf spot of bajra (Pennisetum typhoides Stapf. & Hubbard) caused by a species of Piricularia. Indian
Misra, A. P. 1959. Diseases of millets and maize. Indian Agriculturist 3:7589.
Mohan, L., Sivaprakasam, K., and Jeyarajan, R. 1988. A new leaf blight disease of pearl millet caused by Exserohilum rostratum Leonard and Suggs. Madras
Agric. J. 75:414415.
Ohobela, M., and Claflin, L. E. 1987. Identification of the causal agent of bacterial leaf streak of pearl millet (Pennisetum americanum (L.) Leeke). (Abstr.)
Onesirosan, P. T. 1975. Head mold of pearl millet in southern Nigeria. Plant Dis. Rptr. 59:336337.
Onyike, N. B., and Nelson, P. E. 1987. Distribution of Fusarium species on millet from Nigeria, Lesotho and Zimbabwe. (Abstr.) Phytopathology 77:1617.
Pande, S., Mukuru, S. Z., Odhiambo, R. O., and Karunakar, R. I. 1994. Seedborne infection

Page 367
of Eleusine coracana by Bipolaris nodulosa and Pyricularia grisea in Uganda and Kenya. Plant Dis. 78:6063.
Pathak, V. N., and Gaur, S. C. 1975. Chemical control of pearl millet smut. Plant Dis. Rptr. 59:537538.
Ramakrishnan, R. S., and Soumini, C. K. 1948. Studies in cereal rust. I. Puccinia penniseti Zimm and its alternate host. Indian Phytopathol. 1:97103.
Rangawami, G., Prasad, N. N., and Eswaran, K. S. S. 1961. Bacterial leaf spot diseases of Eleusine coracana and Setaria italica in Madras State. Indian
Phytopathol. 14:105107.
Safeeulla, K. M. 1970. Studies on the downy mildews of bajra, sorghum and ragi, pp. 405414. In Plant Disease Problems. International Symposium on Plant
Pathology. Indian Phytopathology Society, New Delhi.
Seifers, D. L., Harvey, T. L., Kofoid, K. D., and Stegmeier, W. D. 1996. Natural infection of pearl millet and sorghum by wheat streak mosaic virus in Kansas. Plant
Dis. 80:179185.
Seth, M. L., Raychaudhuri, S. P., and Singh, D. V. 1972. Bajra (pearl millet) streak: A leafhopperborne cereal virus in India. Plant Dis. Rptr. 56:424428.
Sharma, S. B., Waliyar, F., and Ndunguru, B. J. 1990. First report of Heterodera gambiensis on pearl millet in Niger. Plant Dis. 74:938.
Singh, S. D. 1990. Sources of resistance to downy mildew and rust in pearl millet. Plant Dis. 74:871874.
Singh, S. D. 1995. Downy mildew of pearl millet. Plant Dis. 79:545550
Singh, S. D., and King, S. B. 1988. Recovery resistance to downy mildew in pearl millet. Plant Dis. 72:425428.
Singh, S. D, and Williams, R. J. 1980. The role of sporangia in the epidemiology of pearl millet downy mildew. Phytopathology 70:11871190.
Singh, S. D., de Milliano, W. A. J., Mtisi, E., and Chingombe, P. 1990. Brown leaf spot of pearl millet caused by Bipolaris urochloae in Zimbabwe. Plant Dis.
74:931932.
Sundaram, N. V., Palmer, L. T., Nagarajan, K., and Prescott, J. M. 1972. Disease survey of sorghum and millets in India. Plant Dis. Rptr. 56:740743.
Swift, C. E., Ishimaru, C. A., and Brown, W. M., Jr. 1991. Bacterial streak of millet caused by Xanthomonas spp. in Colorado. (Abstr.) Phytopathology 81:1159.
Tapsoba, H., and Wilson, J. P. 1997. Effects of temperature and light on germination of urediniospores of the pearl millet rust pathogen, Puccinia substriata var.
indica. Plant Dis. 81:10491052.
Thakur, R. P., and Williams, R. J. 1980. Pollination effects on pearl millet ergot. Phytopathology 70:8084.
Thakur, R. P., Ras, V. P., and Williams, R. J. 1984. The morphology and disease cycle of ergot caused by Claviceps fusiformis in pearl millet. Phytopathology
70:201205.
Thakur, R. P., Rao, V. P., and King, S. B. 1989. Ergot susceptibility in relation to cytoplasmic male sterility in pearl millet. Plant Dis. 73:676678.
Thakur, R. P., Rao, V. P., and King, S. B. 1991. Influence of temperature and wetness duration on infection of pearl millet by Claviceps fusiformis. Phytopathology
81:835838.
Thirumalachar, M. J., and Mundkur, B. B. 1947. Morphology and the mode of transmission of ragi smut. Phytopathology 37:481486.
Verma, O. P., and Pathak, V. N. 1984. Role of insects in secondary spread of pearl millet ergot. Phytophylactica 16:257258.

Page 368
Weber, G. F. 1973. Bacterial and Fungal Diseases of Plants in the Tropics. University of Florida Press, Gainesville, FL.
Wells, H. D. 1967. Effects of temperature on Helminthosporium setariae on seedlings of pearl millet, Pennisetum typhoides. Phytopathology 57:1002.
Wells, H. D. 1978. Eggplant may provide primary inoculum for rust of pearl millet caused by Puccinia substriata var. indica. Plant Dis. Rptr. 62:469470.
Wells, H. D., Burton, G. W., and Hennen, J. F. 1973. Puccinia substriata var. indica on pearl millet in the Southeast. Plant Dis. Rptr. 57:262.
Wilson, J. P. 1994. Field and greenhouse evaluations of pearl millet for partial resistance to Puccinia substriata var. indica. Plant Dis 78:12021205.
Wilson, J. P., and Burton, G. W. 1990. Phyllosticta penicillariae on pearl millet in the United States. Plant Dis. 74:331.
Wilson, J. P., and Hanna, W. W. 1991. Fungal flora of pearl millet grain as affected by date of planting. (Abstr.) Phytopathology 81:1200.
Wilson, J. P., Hanna, W. W., Wilson, D. M., Beaver, R. W., and Casper, H. H. 1993. Fungal and mycotoxin contamination of pearl millet grain in response to
environmental conditions in Georgia. Plant Dis 77:121124.
Wilson, J. P., Phatak, S. C., and Lovell, G. 1996. Aecial host range of Puccinia substriata var. indica. Plant Dis. 80:806808.
Young, G. V., Lefebvre, C. L., and Johnson, A. G. 1947. Helminthosporium rostratum on corn, sorghum, and pearl millet. Phytopathology 47:180183.
Zummo, N. 1976. Yellow leaf blotch: A new bacterial disease of sorghum, maize, and millet in West Africa. Plant Dis. Rptr. 60:798799.

Page 369
11.
Diseases of Oat (Avena sativa)
Bacterial Blight (Acidovorax avenae subsp. avenae)
Cause.
Acidovorax avenae subsp. avenae (syn. Pseudomonas avenae). Infection and disease development is most severe at high temperatures.
Distribution.
Symptoms.
Lesion shape varies from circular to linear. Lesions are watersoaked, then dry up and become brown to black.
Management.
Sow later in the autumn when temperatures are cool.
Bacterial Blight (Pseudomonas syringae pv. coronafaciens)
Bacterial blight is also called halo blight and blade blight.
Cause.
Pseudomonas syringae pv. coronafaciens (syn. P. coronafaciens) can survive for 2 or more years on seed and infested soil residue. During wet weather in the
spring, bacteria are splashed by rain onto the first leaves, where they enter the plant through wounds or natural openings, such as stomates. The bacteria are spread in
cool, wet weather by plants rubbing against each other during a stormy or windy period. Bacteria are also spread by insects, particularly aphids that feed on diseased
tissue and inadvertently carry bacteria to a plant host. Warm, dry weather stops spread of the bacteria and subsequent disease development.
Distribution.
Australia, Europe, North America, and South America.
Symptoms.
Symptoms of halo blight occur earlier in the season than any diseases caused by leafspotting fungi. Symptoms are first noticeable on leaves as small, light green, oval
to oblong, watersoaked spots with slightly sunken centers. The spots eventually change color from light green to yel

Page 370
low to light brown and the tissue around the spots forms a watersoaked and light yellow halo. Due to an increased number of spots that eventually coalesce, severely
diseased leaves turn brown and die back from the tip. Portions of leaves of highly susceptible cultivars may die when lesions are not present.
Management
3. Plow under residue to reduce inoculum.
Bacterial Stripe Blight
Bacterial stripe blight is also called stripe blight.
Cause.
Pseudomonas syringae pv. striafaciens (syn. P. striafaciens) survives on seed and in infested residue for at least 2 years. During cool, wet weather, bacteria are
disseminated by splashing rain and by wind to leaves. Warm, dry weather stops the spread of bacteria and subsequent disease development.
Distribution.
Australia, Europe, North America, and South America.
Symptoms.
Bacterial stripe blight is seldom a serious disease. Symptoms first appear on leaves as sunken, watersoaked dots. If dots are abundant, the leaf may die. Dots enlarge
into watersoaked stripes or blotches, often with narrow yellowish margins, that may extend the length of the diseased leaf blade. As stripes age, they become a
translucent rusty brown. In moist weather, bacteria are exuded in droplets from the stripes; the droplets of bacteria later dry and form white scales on diseased leaves.
Management
1. Grow resistant cultivars if they are available.
Black Chaff
Cause.
Xanthomonas campestris pv. translucens (syn. X. campestris and X. translucens pv. undulosa). The taxonomy of the causal organism(s) continues to be in flux.
Black chaff is considered to be caused by five of the former X. campestris pathovars (pv. cerealis, pv. hordei, pv. secalis, pv. translucens, and pv. undulosa) that
are often grouped together under the name "translucens group" or are considered to be a single species, X. translucens, or a pathovar named X. campestris pv.
translucens. Bragard et al. (1997) agreed that X. translucens pv. translucens and X. translucens pv. hordei are true synonyms. They also reported that when using
restriction fragment length polymorphism and fatty acid methyl esters analysis, the pathovars X. translucens pv. cerealis, X. translucens pv. translucens, and X.
translucens

Page 371
pv. undulosa cluster in different groups and correspond to true biological entities.
The bacteria overwinter in soil residue, on seed, and directly in soil. Primary infection occurs by bacteria being disseminated from soil, host plants, and infested residue
by splashing water and insects, particularly aphids. Primary infection may also occur by seedborne bacteria, but seed stored 6 or more months is not considered an
important source of inoculum. Bacteria enter into plants through natural openings such as stomata and wounds. Since free water is necessary for bacteria to enter
plants, small spaces and grooves that contain water may act as a reservoir for bacteria. Secondary spread of bacteria occurs by planttoplant contact, splashing rain,
and sucking and chewing insects.
On other small grains, black chaff is called bacterial blight, bacterial streak, bacterial leaf streak, or black chaff.
Distribution.
Wherever oat is grown.
Symptoms.
Symptoms of black chaff, which occur after several days of damp or rainy weather, are more obvious on leaves than on heads. The inner portions of the glumes have
brown or black spots. In moist weather, tiny, yellow beads of bacteria ooze to the surface of these discolored areas.
Small watersoaked spots occur on tender green leaves, on leaf sheaths of older plants, and sometimes on seedlings. The spots enlarge and coalesce, becoming
glossy, olive green, translucent stripes, or streaks, of various lengths that later turn yellowbrown. Stripes may extend the length of a diseased leaf and are usually
narrow, being limited by leaf veins. Occasionally, a spot becomes large and blotchlike, causing the leaf to shrivel, turn light brown, and die. Severely diseased leaves
die back from the tips. Under humid conditions early in the morning, droplets of bacterial exudate may be seen on the surface of spots. Droplets dry into hard,
yellowish granules that may be easily removed as dry flakes from leaf surfaces. Grain is not destroyed, but it may be brown and shrunken and may carry bacteria to
infect next year's crop.
Management
1. Do not sow seed from diseased plants. Seed should be cleaned to remove lightweight, infected kernels.
3. Rotate oat with other crops, preferably noncereals.
Anthracnose
Cause.
Colletotrichum graminicola, teleomorph Glomerella graminicola, overwinters as mycelium and spores on infested residue, but the fungus is not seedborne.
Optimum production of conidia from mycelia occurs during

Page 372
wet weather at a temperature of 25°C; conidia are disseminated by wind to plant hosts.
Distribution.
Wherever oat is grown, but anthracnose is most severe when oat is grown on sandy soils that are low in fertility.
Symptoms.
Redbrown, elongated, lensshaped spots are produced on diseased leaves, especially where they are attached to the leaf sheath. After the death of leaf tissue,
acervuli appear as dark brown objects scattered throughout the spots. During severe disease, most of the diseased leaf tissue is covered with acervuli. Diseased basal
and crown tissue becomes bleached, then turns brown and is covered with acervuli. Under magnification, acervuli appear ''hairy" or have a pincushion appearance.
Roots and stems are also infected. Infection of panicles results in lightweight, shriveled grain. Later in the season, severely diseased plants are small and have few
tillers.
Management
1. Ensure soils have adequate fertility.
2. Rotate oat with legumes.
Cause.
Hymenula cerealis (syn. Cephalosporium gramineum) survives for up to 5 years as conidia and mycelia within infested residue in the top 8 cm of soil. Conidia
serve as primary inoculum and infect roots through mechanical injuries caused by soil heaving and insects during the winter and early spring. Infection is most severe in
wet, acid soils (pH 5.0) due to a combination of increased fungal sporulation and root growth. Subcrown internodes can also be infected as seed germinates. After
infection, conidia enter xylem vessels and are carried upward, where they lodge and multiply at nodes and leaves. No further damage is done to roots. Hymenula
cerealis prevents water movement up plants and also produces metabolites that are harmful to plants. At harvest time, H. cerealis is returned to the soil in infested
residue, where it is a successful saprophytic competitor with other soilborne microorganisms.
Distribution.
Great Britain, Japan, and most oatgrowing areas of North America.
Symptoms.
Oat is ordinarily not severely diseased. Diseased plants are scattered throughout a field but are most numerous in the lower and wetter areas of the field.
Diseased plants are dwarfed. At jointing and heading time, one to four—but normally one or two—distinct yellow stripes develop the length of the plant on leaf
blades, sheaths, and stems. Thin brown lines consisting of infected veins occur in the middle of the stripes. The stripes eventu

Page 373
ally become brown and are highly visible on green leaves. The stripes continue to remain noticeable, even on yellow straw. Toward harvest, culms at or below nodes
become darkly discolored due, in part, to fungal sporulation and discoloration of diseased tissue. Heads of diseased plants are white and contain shriveled seed or no
seed at all.
Management
1. Rotate oat with a noncereal for at least 2 years.
2. Plow residue deeper than 8 cm.
Covered Smut
Cause.
Ustilago segetum (syn. U. kolleri) is seedborne and seed is the only source of inoculum. After infected seed is sown, mycelium from the seed grows into the
developing oat shoots. Plants cease to be susceptible to infection when the first seedling leaves have emerged more than 1 cm beyond the leaf sheaths. Once inside the
seedlings, mycelium grows systemically, keeping pace with the growing tip of the plant and finally entering the young, developing kernels. By heading time, the kernels
and hulls are completely replaced with chlamydospores.
Chlamydospores are scattered by wind and harvesting operations. Some chlamydospores lodge either outside or inside the hulls of healthyappearing seed, where
they remain dormant until the seed is sown. Other chlamydospores germinate immediately after being disseminated by wind to healthy kernels. The infective mycelia
then grow into hulls or seed coats, where they remain inactive until the infected seed is sown.
Soil temperature and moisture at the time of seed germination have an influence on infection. Infection occurs at 5% to 60% soil moisture (35%40% is optimum) and
at soil temperatures of 5° to 30°C (15°25°C is optimum).
Distribution.
Symptoms.
All spikelets and panicles on a diseased plant are usually smutted. Smutted panicles do not spread as much as healthy panicles. As a smutted oat panicle emerges from
its enclosing sheath, a dark brown to black, powdery mass of chlamydospores enclosed within a whitegray membrane has replaced the grains and, often, the awns
and glumes. The whitegray membrane is more persistent than that of loose smut and remains intact until the chaff dries or until grain is harvested. The persistence and
the extent of damage to panicles vary with the oat cultivar. Smutted plants are generally shorter than healthy plants.
Management
2. Treat seed with a systemic fungicide seed protectant.

Page 374
Crown Rust
Crown rust is also called oat leaf rust.
Cause.
Puccinia coronata is a heteroecious longcycled rust fungus that has the buckthorn species Rhamnus carthartica, R. dahurica, and R. lanceolata as alternate hosts
to oat and other grasses.
Puccinia coronata causes crown rust of oat by following either one of two distinct life cycles. Depending on weather conditions, urediniospores are produced in
uredinia on oat every 8 to 10 days and are disseminated by wind to other oat plants. The urediniospores germinate in the presence of moisture and infect leaves and
less frequently leaf sheaths, stems, and panicles. This cycle will continue indefinitely as long as susceptible oat plants are available.
Urediniospores produced in northern oatproducing areas are blown south during the summer and autumn and infect oat and grasses in Mexico and the southern
United States. Urediniospores continue to recycle on oat in these southern oatproducing areas until they are disseminated north and infect oat during late winter and
spring.
A second, but complete, life cycle that utilizes both plant hosts occurs where species of buckthorn are present in climates with low temperatures. As oat ripens and
during periods of drought, excessive moisture, or high temperatures, telia containing teliospores form in or around uredinia. Teliospores, which function as the means of
survival through the winter, germinate in the spring and form basidiospores that are disseminated by wind to buckthorn, where the leaves are infected. At the point of
basidiospore infection, a pycnium forms on the upper leaf surface.
By exchanging genetic material between different fungal strains, pycnia are the means by which new races of crown rust arise. Each pycnium produces pycniospores
and special mycelia called receptive hyphae. Pycniospores are exuded from pycnia in a thick, sticky, sweet liquid that is attractive to insects. Pycniospores are then
splashed by water or carried by insects from one pycnium to another, where they become attached to receptive hyphae. The nucleus from the pycniospore enters the
receptive hypha, which results in the formation of an aecium on the lower leaf surface.
Aeciospores differ genetically from both pycniospores and receptive hyphae. The aeciospores are disseminated by wind to oat, where infection occurs. Each infection
gives rise to a uredinium in which urediniospores are again formed. The urediniospores serve as the repeating stage, reinfecting only oat.
The production of urediniospores is optimum at a temperature of 21°C in the presence of dew, fog, or some other form of moisture. The higher relative survival ability
of some races on Avena sterilis is due to a shorter time between inoculation and uredinia appearance, higher infection density, higher yield of urediniospores per
uredinium, and extended longevity of

Page 375
urediniospores. Telia are again produced as oats mature, thus completing the life cycle. Numerous physiologic races exist.
Experimentally, oat becomes resistant when incubated at 35°C for 8 hours at the vegetative stage of fungal development. The effect of this temperature stress
disappears by cutting the stem prior to the heat treatment, which suggests the effect of heat treatment on disease is through its effect on the host.
Distribution.
Symptoms.
Uredinia appear primarily on leaves as bright orangeyellow, round to oblong pustules. There is no loose epidermis around pustules, which distinguishes crown rust
from stem rust. Similar pustules may occur on sheaths, stems, and panicles. Pustules burst open and release urediniospores that look like orange powder. Under
conditions favorable for infection, uredinia become numerous and may coalesce. Stems may be so weakened that severe lodging results.
As plants begin to ripen, telia form either in a ring around old uredinia or develop independently of uredinia. Telia remain covered indefinitely by epidermis, giving them
a grayblack, oblong, and slightly raised appearance.
Pycnia on buckthorn leaves are bright orange to yellow spots that sometimes have a small drop of liquid consisting of pycniospores in the middle. Opposite pycnial
spots on the underleaf surface are aecia that resemble raised, orange cluster cups.
Management
2. Plant oat early in spring to escape rust.
3. Eradicate buckthorn shrubs within 1.5 km of oat fields.
Downy Mildew
Cause.
Sclerophthora macrospora (syn. Sclerospora macrospora) survives as oospores in infested leaf and stem residue in soil. When residue decays, oospores are
liberated into soil, where they may persist for long periods of time. Oospores are disseminated by seed and within soil and residue by wind or water. Oospores
germinate in saturated soil and form sporangia in which zoospores are formed. Zoospores are released from sporangia and "swim" for a short distance to a host,
where they encyst, then germinate and form a germ tube that penetrates the host plant. Disease is most severe during wet, cool environmental conditions.
Distribution.
Wherever oat is grown in wet areas.
Symptoms.
Symptoms are most noticeable within a field at heading time in areas that are low or liable to flood. Diseased plants are stiff, upright,

Page 376
and remain green for several days after healthy plants have ripened. Severely diseased plants are dwarfed to less than a third the height of healthy plants and tiller
excessively. Leaves are leathery, and the upper leaves are curled around panicles which, in turn, are also curled and twisted into a cluster of frayed and tangled
spikelets.
Less severely diseased plants may be slightly dwarfed and stiff and may produce distorted heads that stand above those of healthy plants. The flag leaf is curled and
twisted about a poorly developed head. Heads are deformed and spikelets are not recognizable since viable seed is not produced.
Management.
Drain areas in fields that are likely to be flooded.
Ergot
Cause.
Claviceps purpurea survives as sclerotia buried in soil or on the soil surface. Sclerotia germinate before flowering time and produce stromatic heads in which
perithecia are produced at the end of a stipe or stalk. Ascospores form in perithecia and are disseminated by wind to young flowers, where they germinate and form
infective hyphae that penetrate ovaries. Mycelium in an ovary produces conidia in a sweet, sticky, liquid called honeydew on the outside of infected flowers. Insects
are attracted to honeydew and inadvertently disseminate conidia from diseased to healthy flowers. Eventually, sclerotia replace oat kernels.
Distribution.
Wherever oat is grown, but ergot is relatively uncommon on oat.
Symptoms.
Ergot is easily recognized by the purpleblack, hornshaped sclerotia produced in place of one or several kernels on a head. Sticky honeydew covered with dust and
foreign matter gives diseased flowers a grayish to black appearance.
Management
1. Place sclerotia at a soil depth where ascospores cannot be released into the air. Sclerotia are decomposed in a year or so by soil microorganisms.
2. Control grassy weeds around fields.
3. Rotate with crops, such as legumes, that are not susceptible to C. purpurea.
4. Clean seed to remove ergot bodies.
Eyespot
Eyespot is also called Cercosporella foot rot, stem break, foot rot, strawbreaker, and culm rot.
Cause.
Pseudocercosporella herpotrichoides survives as mycelium in infested soil

Page 377
residue for several years in the absence of grain crops. Conidia produced during cool, damp weather in autumn or spring infect crown and basal culm tissue. Roots are
not infected.
Distribution.
Ireland. Reports from Europe and the United States indicate that oat is resistant.
Symptoms.
Characteristic eyespot lesions are found on oat but are not as common as they are on barley, rye, and wheat. Eyespot is most conspicuous near the end of the growing
season when diseased plants lodge. Lodging caused by eyespot causes straw to fall in all directions. In contrast, lodging caused by wind or rain causes straw to fall in
one direction. White heads, similar to symptoms produced in takeall, are also present at maturity.
Eyeshaped or ovate lesions with white to tan centers and brown margins develop first on the basal leaf sheaths. Similar spots form on stems adjacent to sheaths and
eventually cause stems to lodge. Roots are not infected, but necrosis occurs around roots in the upper crown nodes. Under moist conditions, lesions enlarge and the
black stromalike mycelium that develops over the surface of diseased crowns and the base of culms gives them a "charred" appearance. Stems then shrivel and
collapse. Plants that do not collapse are yellowish or pale green and heads are reduced in size and number.
Oat often has an indentation on one or both sides of culms where infection has occurred that extends up from the plant base for 2.5 to 5.0 cm and sometimes causes a
split in the culm. Pseudocercosporella herpotrichoides is often visible when infected stems are cut longitudinally. Oat is usually not stunted but plants that are pulled
up break off above the soil line.
Management.
Rotate with noncereals.
Fusarium Foot Rot
Cause.
Fusarium culmorum survives in soil as chlamydospores or as mycelia in infested residue.
Distribution.
Symptoms.
Seedlings are infected below or at the soil surface. Light brown to redbrown lesions may be noticed at the base of the seedling leaf or just below the soil surface on
the stem. Some seedlings may also have these spots on the mesocotyl near the seed. Seedlings may damp off either before or after emergence.
Management

Page 378
Fusarium head blight is also known as scab, Fusarium blight, and head blight.
Cause.
Gibberella zeae, anamorph Fusarium graminearum. Although not well documented, the Fusarium spp. that cause Fusarium head blight of oat are probably the
same as those that cause Fusarium head blight of wheat.
Gibberella zeae is seedborne and overwinters as mycelia in infested residue and as perithecia on oat, barley, maize, wheat, and other grass residue that was diseased
the previous season. Ascospores produced in perithecia during warm, moist weather are disseminated by wind to plant hosts. Conidia of Fusarium spp. are
produced from mycelia and also are disseminated by wind to hosts. Spores, primarily conidia, are also produced on diseased heads and serve as a source of
secondary inoculum to cause new infections. Wet autumn weather favors disease development on lodged grain and on grain in swaths.
Distribution.
Symptoms.
Fusarium head blight on oat is not as readily detected as it is on wheat or barley because a hull covers the oat kernel. Hulls of infected spikelets are ashen gray and
may be partially covered by a pink growth consisting of mycelium and conidia. In severe cases, hulls are shriveled and rough but do not turn brown. Small, black
perithecia may be produced on hulls as grain nears maturity.
If seed is heavily diseased, seedlings may be killed before emergence. Seedlings frequently are only stunted, but many become chlorotic and die after emergence.
Roots of infected seedlings are redbrown and rotted. Later in the season, roots may be covered by pink mycelium. If a joint on the stem becomes infected, the plant
portion above it becomes white and perithecia are produced on the affected joint.
Management
2. Plow under maize residue when oat follows maize. Fusarium head blight is more severe when maize stalks are left on the soil surface than when they are plowed into
the soil.
3. Rotate oat with legumes rather than cereals. Oat is the least susceptible of the cereals.
Head Blight
Head blight is also called Helminthosporium foot rot and Helminthosporium culm rot.
Cause.
Bipolaris sorokiniana (syn. Drechslera sorokiniana, Helminthosporium sativum, and H. sorokinianum) overwinters as mycelia and conidia in infested residue
and seed.

Page 379
Distribution.
Symptoms.
Roots and basal portion of young diseased seedlings are rotted. Leaves droop and wilt or whole leaves turn chlorotic and die. Disease of older plants appears as a
blackening and weakening of the lower stems. Frequently, diseased stems bend over and lodge on the soil surface but the upper portion of the stems stays alive for
some time after falling over. Often the live tips of fallen stems turn and grow upward.
Management
2. Rotate oat with legumes.
Helminthosporium Seedling Blight, Crown, and Lower Stem Rot
Cause.
Drechslera avenacea (syn. Helminthosporium avenaceum) and D. avenae (syn. H. avenae), teleomorph Pyrenophora avenae. Drechslera spp. overwinter as
mycelium under the seed coat, spores on seed, and mycelia or perithecia in infested residue. Seedborne infection results in spots on seedling leaves in which conidia
are produced during wet weather and disseminated by wind to other leaves. Infections of older leaves may originate either from conidia produced on residue or
primary spots, or from ascospores produced in perithecia on residue during wet weather later in the growing season. Disease development is favored by cool, wet
weather.
Distribution.
Symptoms.
Oat seedlings are stunted. Diseased leaves initially turn yellow, then reddish, and eventually brown as severely diseased plants die. Dark brown to black lesions
develop on lower stems and leaf sheaths. Disease initiated as seedling infections can continue as plants develop, or infections of roots, crowns, and lower stems of
older plants may occur that are characterized by dark brown areas of decay near the oat crown. Severely diseased plants are unproductive, are more subject to
lodging than healthy plants, and may die.
Management
1. Sow highquality seed that was properly harvested. Delayed harvest can result in increased D. avenacea damage to kernels.
3. Rotate oat with other crops.
Leaf Blotch and Crown Rot
Leaf blotch and crown rot is also called blotch, Helminthosporium leaf blotch, Helminthosporium leaf spot, leaf blotch, leaf streak, oat leaf blotch, oat leaf spot, and
Pyrenophora leaf blotch.

Page 380
Cause.
Drechslera avenacea (syn. Helminthosporium avenaceum) and D. avenae (syn. H. avenae), teleomorph Pyrenophora avenae. Drechslera spp. overwinter as
mycelia under the seed coat, as spores on seed, and as mycelia or perithecia in residue. Seedborne infection results in spots on seedling leaves in which conidia are
produced during wet weather and disseminated by wind to other leaves. Infections of older leaves may originate either from conidia produced on residue or primary
spots, or from ascospores produced in perithecia on residue during wet weather later in the growing season. Disease development is favored by cool, wet weather.
Distribution.
Africa, Asia, Australia, Europe, and North America.
Symptoms.
In the seedborne phase of the disease, oblong to elongate, light redbrown spots appear on seedling leaves soon after emergence. Seedling leaves may also be twisted
or contorted.
On older leaves, lesions start as small, brown flecks that develop into longitudinal strips of dead tissue. The brown to yellow or reddish outer edges of spots merge
and frequently spread over the greater part of a diseased leaf blade. Sometimes, welldefined spots are not produced but leaves will have a withered appearance as if
they had been injured by adverse weather. As leaves die, they change from green to yellow or gray and the brown spots fade. When kernels are diseased, they will
turn brown at the basal end.
Management
3. Plow under residue to reduce inoculum originating from the field.
4. Grow the least susceptible cultivars. Several lines of spring oat are identified as having a degree of resistance.
Loose Smut
Loose smut is also called black loose smut, black head, false loose smut, and naked smut.
Cause.
Ustilago avenae is seedborne and seed is the only source of inoculum. After seed is sown, mycelia grow into and infect young oat shoots. Infection occurs when
seeds sprout at soil moistures of 5% to 60% (35% to 40% is optimum) and soil temperatures of 5° to 30°C (15° to 25°C is optimum).
Plants cease to be susceptible to infection when the first leaves have emerged more than 1 cm beyond the sheath. Once inside a seedling, mycelium grows
systemically, keeping pace with the growing tip of the infected plant and finally entering the young, developing kernels. By heading time, kernels and hulls are
completely replaced by chlamydospores, which are released into the air and disseminated by wind to healthy heads before harvest. Some spores lodge outside or
inside hulls of healthy seed,

Page 381
where they remain dormant until the seed is sown. Other spores germinate immediately and grow into the hulls or seed coats of kernels but remain inactive until the
seed is sown.
Distribution.
Symptoms.
Smutted panicles do not spread as much as healthy ones. As a smutted oat panicle emerges from its enclosing sheath, a dark brown to black powdery mass of smut
spores (chlamydospores) contained within a delicate, whitegray membrane has replaced the grains and, often, the awns and glumes. All spikelets and panicles on a
diseased plant are usually smutted. The thin membrane breaks and disintegrates soon after oat panicles emerge. Smutted plants are shorter than healthy ones and often
are overlooked at harvest because the naked mass of chlamydospores quickly scatter by wind and rain and leave a bare panicle, which is difficult to see.
Management
Microdochium Root Rot
Cause.
Microdochium bolleyi (syn. Aureobasidium bolleyi and Gloeosporium bolleyi). Microdochium bolleyi is primarily a saprophyte.
Distribution.
Symptoms.
Disease symptoms are mild and consist of discoloration and necrosis on the subcrown internode.
Management.
Not necessary.
Pink Snow Mold
Pink snow mold is also called snow mold.
Cause.
Microdochium nivale (syn. Fusarium nivale), teleomorph Monographella nivalis (syn. Calonectria nivalis). The causal fungus oversummers as perithecia or
mycelia in infested residue. Plants are infected in the autumn by ascospores disseminated by wind to host plants or by mycelia growing from previously infested residue
to nearby plants. Primary infections occur on leaf sheaths and blades near the soil level. Disease is spread by mycelial growth during cool, wet weather, or by mycelial
growth underneath a snow cover. Secondary infection in the spring occurs in two ways: by ascospores produced in perithecia that developed during cool, humid
weather and by conidia produced on mycelia and sporodochia that grew on oat plants under the winter snow cover. Both types of spores are then disseminated by
wind to other host plants.

Page 382
Distribution.
Canada, central and northern Europe, and the United States.
Symptoms.
Diseased plants have chlorotic and dry necrotic leaves. A good diagnostic characteristic is the pink color of mycelia and sporodochia on leaf and crown tissues as
snow melts in the spring.
Management.
Powdery Mildew
Cause.
Blumeria graminis f. sp. avenae (syn. Erysiphe graminis f. sp. avenae) overwinters as cleistothecia on wild grasses and oat residue. Ascospores form within
cleistothecia in spring and are disseminated by wind to oat plants. Conidia are produced as soon as mycelia become established on leaf surfaces, especially during
cool, humid weather but not in the presence of free water. Conidia account for most of the secondary inoculum and are disseminated by wind from plant to plant.
Cleistothecia are formed on leaf surfaces as diseased plants approach maturity.
Distribution.
Symptoms.
Powdery mildew first appears as patches of white, fluffy mycelium, conidia, and conidiophores on diseased lower leaves and leaf sheaths. As disease progresses, the
patches become powdery and turn gray, then brown. The ''powder" is a combination of mycelium, conidia, and conidiophores that has continued to grow on the leaf
surface. Eventually, when large areas of the leaves are diseased, the leaves become yellow and shrivel up. As plants near maturity, cleistothecia are seen as small,
brown to black, round objects interspersed within the mycelium and spores. Yield may be reduced.
Management.
Management usually is not necessary; however, the following are aids for managing the disease.
1. Apply a sulfur fungicide to foliage.
2. Grow cultivars that have adult resistance.
Pythium Seed and Seedling Rot
Cause.
Pythium debaryanum, P. irregulare, and P. ultimum survive as oospores in residue or soil. In moist soil, oospores germinate and form sporangia in which
zoospores are produced. Zoospores then "swim" in moist soil to root tips or seeds, where they germinate and form germ tubes that infect plants.
Distribution.
Symptoms.
Seed and seedlings may be killed before or after emergence. Plants that are not killed are chlorotic and stunted but may recover and become as green as healthy
plants. However, diseased plants usually remain less

Page 383
vigorous than healthy plants. Watersoaked, translucent areas that occur on roots later turn redbrown.
Management.
Treat seed with a seedprotectant fungicide.
Scoliocotrichum Leaf Blotch
Cause.
Cercosporidium graminis (syn. Scoliocotrichum graminis vat. avenae) presumably survives as mycelium in infested residue. During wet weather in the spring,
conidia are produced and disseminated by wind to plant hosts. Sporulation ceases during dry weather.
Distribution.
Generally distributed in most oatgrowing areas, but Scoliocotrichum leaf blotch is uncommon.
Symptoms.
Oblong to linear, redbrown to purplebrown blotches with definite margins develop on leaves. The necrotic area is dry and sunken. A good diagnostic characteristic
that can be seen with the aid of magnification is the rows or tufts of conidiophores that emerge through stomata.
Management.
Management is not practiced ordinarily, but sanitation will reduce inoculum.
Sharp Eyespot
Sharp eyespot is also called Rhizoctonia root rot.
Cause.
Rhizoctonia cerealis. Survival is as sclerotia in soil and infested residue or as mycelia in infested residue of several susceptible plant species. Plants may be infected
any time during the growing season. Roots and culms are infected by mycelia that grow either from germinating sclerotia or from a precolonized substrate, particularly
in dry, cool soils at less than 20% moistureholding capacity.
Distribution.
Symptoms.
Oat is one of the most susceptible cereals to R. cerealis. Diseased seedlings may be killed. Diamondshaped lesions with tan centers and dark brown margins occur
on lower leaf sheaths. These lesions somewhat resemble the symptoms of eyespot disease. Dark sclerotia and mycelium may develop in lesions; sclerotia also may
develop between culms and leaf sheaths.
When roots are diseased, plants may produce new roots to compensate for those that have rotted off, but plants may still lodge and produce white heads. Diseased
plants generally appear stiff, have a grayish cast, and are delayed in maturity.
Management.
No management measure is effective. Vigorous plants growing in wellfertilized soil are not as likely to become as severely diseased as unthrifty plants.

Page 384
Speckled Blotch
Speckled blotch is also called dark stem of oat, leaf spot of oat, Septoria black stem, Septoria blight, Septoria disease, Septoria leaf blotch, and speckled leaf blotch.
There is a great deal of confusion in the literature concerning the disease name. Farr et al. (1989) list a speckled blotch as being caused by both Stagnospora avenae
and Septoria tritici f. avenae, whereas the list of diseases by the American Phytopathological Society lists only S. avenae as the causal fungi.
Cause.
Stagnospora avenae (syn. Septoria avenae) and Septoria tritici f. avenae. Some researchers consider Leptosphaeria avenaria to be the teleomorph. The causal
fungi overwinter as mycelia and pycnidia (micropycnidia) in infested residue; S. tritici f. avenae is also seedborne, but only in very susceptible cultivars. Conidia
(microspores) are disseminated by wind to plant hosts during cool, wet weather in the spring. Perithecia are not thought to be an important means of overwintering nor
are ascospores important as a means of primary inoculum or in the secondary spread of disease.
Pycnidia form in mature lesions if weather continues to be cool and wet after the initial infections. Conidia, which are disseminated mostly by rain and water, are
primarily responsible for stem infections. Perithecia and ascospores form primarily in spring, but some perithecia form in the summer and overwinter on infested
residue.
Distribution.
Africa, Australia, Europe, and North America.
Symptoms.
Blotches first appear on lower leaves and then spread up a diseased plant. Round to elongate or diamondshaped, yellow to light or dark brown blotches are
surrounded by a band of dull brown that changes to yellow as it blends into the green of healthy plant tissue. As blotches enlarge, the diseased leaf tissue dies. Pycnidia
appear as black dots scattered throughout the centers of older blotches, giving them a speckled appearance. After heading, infection at a leaf base spreads into an
adjoining leaf sheath, which becomes discolored chocolate or redbrown.
Above the upper two joints, graybrown to shiny black lesions develop on the stems or on culms under diseased leaf sheaths. Dark gray mycelium fills the hollow
areas of diseased culms. During cool, wet weather, black or dark brown lesions may extend to lemma and palea and eventually to the groat of the kernel. Diseased
plants frequently lodge as they near maturity.
Management
1. Grow cultivars that mature late; early cultivars are more susceptible.
4. Rotate oat every 3 or 4 years.

Page 385
Speckled Snow Mold
Speckled snow mold is also called gray snow mold and Typhula blight.
Cause.
Typhula idahoensis, T. incarnata (syn. T. itoana), and T. ishikariensis overseason as sclerotia in infested residue and soil or as parasitic growth on live plants.
Saprophytic growth on dead plant tissue provides an inoculum source for increased disease in the spring; however, the fungi are poor saprophytes and depend
primarily on parasitism for existence. Sclerotia germinate during wet weather in autumn and form either a basidiocarp or mycelium. Optimum infection occurs at
temperatures of 1° to 5°C, when basidiospores form on basidiocarps and are disseminated by wind to host plants or when mycelia directly infect plants by growing
over the surface of the soil. Further infection occurs by mycelial growth under snow cover. Sclerotia are formed within necrotic tissue and in mycelia.
Distribution.
Canada, central and northern Europe, Japan, and the northwestern United States.
Symptoms.
At snowmelt, graywhite mycelia are present on leaves and crowns of diseased plants and on the soil. The numerous sclerotia in diseased tissues or scattered in
mycelia growing over diseased plant surfaces give the plants a speckled appearance. Dead leaves are common, but unless the crown is diseased, plants recover during
warm, dry weather although they will not be as vigorous as healthy plants. Dead leaves crumple easily and are covered with gray to white mycelium.
Management
1. Rotate oat with a legume to reduce the inoculum in soil since the fungi are not good saprophytes.
2. In wheat experiments disease incidence was decreased by fungicide seed treatments.
Stem Rust
Cause.
Puccinia graminis (syn. P. graminis f. sp. avenae) is a heteroecious longcycle rust that has the common barberry, Berberis vulgaris, as the alternate host to oat.
Rust is caused by P. graminis in one of two ways. Urediniospores, called summer or repeating spores, are produced in uredinia on oat several weeks before it ripens.
The urediniospores are disseminated by wind to other oat plants, where infection and production of secondary urediniospores in new uredinia occur under moist
conditions and moderate temperatures. This cycle will continue indefinitely as long as green oat plants are available. Urediniospores produced in northern oat
producing areas are blown south during the summer and autumn and infect oat in Mexico and the southern United States. Urediniospores continue to recycle on oat
during

Page 386
the winter in southern oatproducing areas until they are disseminated by wind northward during late winter and spring to infect oat in the north.
In the second method of infection, P. graminis goes through a complete life cycle. Telia containing teliospores form on maturing oat. The teliospores are the means of
survival through the winter. In spring, teliospores germinate and form basidiospores (sometimes called sporidia) that are disseminated by wind to barberry bushes,
where infection of the foliage occurs. At the point of infection by the basidiospore, a pycnium (sometimes called a spermogonium) forms on the upper leaf surface.
Pycnia exchange genetic material between different isolates of P. graminis, thereby creating new races that are genetically different from the parent isolates. Each
pycnium produces pycniospores and special mycelia called receptive hyphae. Pycniospores are exuded from pycnia in a thick, sticky, sweet liquid that is attractive to
insects. Pycniospores are splashed by water or carried by insects from one pycnium to another, where they become attached to receptive hyphae and germinate, with
the nucleus from the spore from one pycnium entering into the receptive hypha of another pycnium. This results in formation of an aecium on the lower leaf surface.
Aeciospores, which differ genetically from both pycniospores and receptive hyphae, are produced in aecia and are disseminated by wind to oat, where infection
occurs. Each infection gives rise to a uredinium in which urediniospores are formed. Urediniospores then serve as the repeating stage, becoming windborne to oat,
where new generations of urediniospores are formed. Telia are once again produced as oat matures, thus completing the life cycle.
Distribution.
Symptoms.
Uredinia and telia occur on diseased stems, leaf sheaths, leaf blades, and panicles. Uredinial pustules are large, oblong, and dark redbrown. The epidermis of leaves
and culms is ruptured and pushed back around the pustule, giving it a jagged appearance and exposing the urediniospores. The dark color and jagged appearance of
the pustule distinguish stem rust from the relatively smooth margin and light orangeyellow color of crown rust. As plants approach maturity, black, oblong telia form in
and around uredinia, particularly on stems and sheaths. Teliospores are exposed when the epidermis ruptures.
Pycnia on barberry leaves appear as bright orange to yellow spots with a small drop of moisture in the middle. Opposite pycnial spots on the under side of leaves are
aecia that resemble raised, orange clusters.
Management
2. Eradicate common barberry shrubs from the vicinity of oat fields.

Page 387
TakeAll
Takeall is also called white head.
Cause.
Gaeumannomyces graminis var. avenae survives as mycelia in plants or as mycelia and perithecia in infested soil residue. However, ascospores produced in
perithecia are not considered important in the dissemination of G. graminis var. avenae, which is a poor saprophyte and does not survive long in soil in the absence
of a host.
In the autumn or spring, seedlings are infected by roots growing into the vicinity of previously colonized residue and coming in contact with mycelia growing from the
residue. Planttoplant spread of G. graminis var. avenae occurs by hyphae growing through soil from a diseased plant to a healthy plant or by a healthy root coming
in contact with a diseased root. Ascospores are produced in perithecia during wet weather but are not disseminated a great distance by splashing water or by wind.
Takeall is usually more severe on oat grown in alkaline soils.
Distribution.
Symptoms.
The first symptoms are light to dark brown necrotic lesions on roots. By the time a diseased plant reaches the jointing stage, most of its roots are brown and dead. At
this point, many plants die, but if plants are still alive, they are stunted and their leaves are chlorotic.
Disease becomes most obvious as plants approach heading. The plant stand is uneven in height and plants appear to be in several stages of maturity. At heading, roots
are sparse, blackened, and brittle, and diseased plants have few tillers, ripen prematurely, and have bleached and sterile heads. When pulled from the soil, diseased
plants easily break free from their crowns. A dark discoloration occurs on stems just above the soil line. Mats of dark brown mycelia grow under the lower sheaths
between the stems and inner leaf sheaths.
Management.
Rotate oat with a nongrass host crop.
Victoria Blight
Victoria blight is also called Helminthosporium blight.
Cause.
Bipolaris victoriae (syn. Helminthosporium victoriae) overwinters as conidia on seeds and as mycelia and spores on infested residue. Bipolaris victoriae
produces a toxin that spreads throughout a plant.
Distribution.
Wherever oat cultivars with the Victoria type of crown rust resistance are grown. Victoria blight is now rare.
Symptoms.
Diseased seed may rot in soil before germination. Usually, plants are infected in the seedling stage as they emerge from the soil. Diseased

Page 388
seedling leaves are a dull bluegray and have redbrown stripes that may cover half a leaf blade and extend the length of a leaf. Later, seedling leaves develop a
reddish color and the entire plant may die. Still later, as the lower joints and leaf sheaths become covered with conidia and conidiophores, the basal parts of stems turn
a brownish color and have a dark, velvety appearance. Severe disease causes root rot and the death of stems, which resuits in lodging and premature ripening of
plants.
Management
1. Grow oat cultivars that do not have the Victoria type of crown rust resistance.
Bulb and Stem
Cause.
Ditylenchus dipsaci. Nematodes are associated with heavy soils, high rainfall, cool growing seasons, and winter grains. Free moisture permits the nematode to
migrate to and feed on aerial plant parts. The nematode penetrates leaves and stems.
Distribution.
Worldwide. Damage is confined to small areas within fields.
Symptoms.
Cell hypertrophy and hyperplasia occur. Stunting distortions and swollen stems are common symptoms. In severely infested soils, the growing points of diseased plants
are destroyed and the plants may die. Other diseased plants have reduced spike growth and reduced grain yields.
Management
1. Rotate with noncereal crops.
2. Grow winter cereals to reduce damage.
Cyst
Cause.
Heterodera hordecalis, H. latipons, and Punctodera chalcoensis.
Distribution.
Heterodera latipons has been reported in Israel.
Symptoms.
Diseased plants are stunted and chlorotic. Cysts are not described on roots.
Management.
Rotate oat with a nongrass crop.
Dagger
Cause.
Xiphinema americanum nematodes are external parasites that prefer to feed on young, succulent roots.

Page 389
Distribution.
Widespread. Damage on oat is likely not very severe.
Symptoms.
Moderate swelling occurs on young roots. Severely diseased plants have clusters of short, stubby branches and a shriveling of small roots at the points of attachment.
The most obvious symptom is one or several light brown to dark brown or black necrotic flecks on roots.
Management.
Not necessary.
Lesion
Lesion is also referred to as the pin nematode.
Cause.
Pratylenchus thornei but other Pratylenchus spp. are also thought to infect oat. Nematodes live free in soil as migratory endoparasites and overwinter as eggs,
larvae, or adults in host tissue or soil. Both larvae and adult nematodes penetrate roots, where they move through cortical cells and the females deposit eggs as they
migrate. Older roots are abandoned and new roots are sought as sites for penetration and feeding.
Distribution.
Symptoms.
Plants in limited areas within a field are chlorotic and under moisture stress. Roots and crowns are rotted when Rhizoctonia solani infects plants through nematode
wounds. New roots become dark and stunted, and the yield of diseased plants is reduced.
Management
1. Sow in autumn when soil temperatures are below 13°C.
2. Use soil fumigants where the high costs warrant them.
3. Application of nitrogen and phosphorous reduced populations of P. thornei on roots of wheat grown in a rotation.
Needle Nematode
Cause.
Longidorus cohni builds to high populations during the winter, but populations decrease during higher soil temperatures in the spring.
Distribution.
Israel.
Symptoms.
Terminal swellings occur on roots. Diseased plants are stunted and chlorotic and can cause large bare patches in a field.
Management.
Rotate oat with a nongrass crop.
Oat Cyst Nematode
Oat cyst nematode is also called the cereal cyst nematode.
Cause.
Heterodera avenae. The life cycle from egg to larva to adult is completed in 9 to 14 weeks. Females enter roots and begin feeding. Shortly after en

Page 390
tering roots, females swell up and break through the root epidermis but remain attached to the plant roots by a thin neck. Females are inseminated by males and
several hundred eggs develop within a female body. Eventually, the female body forms a hard body or cyst that is resistant to physical adversities. The cysts detach or
break off from the roots and can survive in soil for several years. The following spring, secondstage larvae hatch from an average of 75% of the eggs.
Heterodera avenae is also a pathogen of barley, rye, and wheat but is most prevalent on oat.
Distribution.
Africa, Australia, southeastern Canada, Europe, Japan, Russia, and the United States (Oregon).
Symptoms.
The lemonshaped cysts, which are barely visible to the naked eye, are initially white, then become dark brown as they harden. Eggs and larvae are white and can only
be observed with magnification.
The first symptom on oat is poor growth in one or more localized areas within a field. Leaf tips of young, severely diseased plants are red or purple. The discolored
leaves die and the diseased plant becomes chlorotic. Roots are thickened and branched more than healthy roots. Large infestations of nematodes in soils cause
diseased plants to wilt, particularly during times of water stress, followed by stunted growth, poor root development, and early plant death.
Management
1. Grow resistant oat cultivars. However, resistant cultivars will vary from area to area because the oat cyst nematode is known to have up to 20 races. Normally, not
all races are present in one locality.
2. Rotate oat with a legume crop. The number of nematodes will decline the longer oat is not grown in infested soil.
3. Apply a nematicide before planting.
Ring
Cause.
Criconemella spp. and Nothocriconemella mutabilis. The nematodes are ectoparasites.
Distribution.
Not reported.
Symptoms.
Symptoms on oat are not well known. Feeding on roots of other plant species does not result in necrosis.
Management.
Not reported.
Root Gall
Cause.
Subanguina radicicola survives in host roots. Larvae penetrate roots and develop in the cortical tissue, forming a root gall in 2 weeks. Mature females begin egg
production within a gall. Eventually, galls weaken and re

Page 391
lease larvae that establish secondary infections. Each generation is completed in about 60 days.
Distribution.
Canada and northern Europe.
Symptoms.
Diseased seedlings have reduced and chlorotic top growth. Galls on roots are inconspicuous and vary in diameter from 0.5 to 6.0 mm. Roots may be bent at the gall
site. At the center of larger galls is a cavity filled with nematode larvae.
Management.
Rotate oat with a noncereal crop.
Root Knot
Cause.
Meloidogyne chitwoodi and M. naasi are endoparasitic nematodes that overwinter as eggs in the soil. In spring, larvae hatch from eggs but enter roots at any time
during the growing season. By the middle of summer, females inside root knot tissue release eggs into soil.
Distribution.
Symptoms.
Root knots are found on diseased roots in the spring and summer. These root swellings or thickenings are comprised of swollen root cortical cells and the bodies of
nematodes containing egg masses. When root knots are cut open, the inner egg masses turn dark.
Management
1. Sow oat in the autumn.
2. Rotate oat with root crops.
Sheath
Cause.
Hemicycliophora spp. feed near plant root tips as ectoparasites.
Distribution.
Widespread, but probably most common under warmer climate conditions.
Symptoms.
Symptoms on oat are not well known, but galls have been reported to form near the root tips of other grass hosts. Other plant species did not display any obvious
symptoms.
Management.
Not known.
Spiral
Cause.
Distribution.
Not reported.
Symptoms.
Symptoms on oat are not well known. Small necrotic flecks on roots and a general overall decline in plant vigor have been suggested.
Management.
Not reported.

Page 392
Sting
Cause.
Belonolaimus longicaudatus.
Distribution.
Presumably in warmer climates.
Symptoms.
Root tips are injured, which results in stubby roots or a reduced root system. Lesions may occur along diseased roots.
Management.
Not known.
Stubby Root
Cause.
Paratrichodorus minor survives in soil or on roots as eggs, larvae or adults. Paratrichodorus minor feeds only on the outside of oat roots and moves relatively
rapidly through soil at a speed of 5 cm/hour, especially in fine, sandy soils.
Distribution.
Widely distributed in most agricultural soils.
Symptoms.
Diseased roots are thickened, short, and stubby; the root tips may have brown lesions. The tops of diseased plants decline in growth, and the entire plant is easily
pulled from soil due to a lack of a fibrous root system.
Management.
Not reported.
Stunt
Cause.
Quinisulcius capitatus, Tylenchorhynchus spp., and Merlinius spp. Merlinius spp. survive as different morphological stages in soil and in association with host
tissue. They are ectoparasitic nematodes that feed on the outside of wheat roots, often in association with the fungus Olpidium brassicae.
Distribution.
Indigenous to most soils but rarely found in high populations.
Symptoms.
The most severe damage occurs on winter cereals growing in wet soils. The lower leaves die and a few short tillers with small seed form on diseased plants. The
diseased roots of seedlings are shortened, dark in color, and shriveled.
Management.
Not known.
Aster Yellows
Cause.
The aster yellows phytoplasma survives in several dicotyledonous plants and leafhoppers. Aster yellows phytoplasma is transmitted primarily by the aster leafhopper,
Macrosteles fascifrons, and less commonly by the

Page 393
painted leafhopper, Endria inimica, and the leafhopper M. laevis. Leafhoppers acquire the phytoplasma by feeding on diseased plants, then transmit the phytoplasma
by flying to healthy plants and feeding on them. Different strains vary in their ability to infect oat. Canadian workers have designated a western strain of the aster
yellows phytoplasma as CAYA and three eastern strains as DAYA, MAYA, and NAYA.
Distribution.
Eastern Europe, Japan, and North America.
Symptoms.
Aster yellows is rarely severe on oat. Symptoms become most obvious at temperatures of 25° to 30°C. Seedlings either die 2 to 3 weeks after infection or, if
seedlings live, they become stunted and have chlorotic blotches on leaves or have completely chlorotic leaves and distorted and sterile heads. Normalappearing floral
parts may still be nonfunctional.
Infection of older plants causes leaves to be stiff and discolored in shades of yellow, red, or purple, which begins from the leaf tip or margin and moves inward to
include the entire leaf blade. Diseased root systems may not be well developed.
Management.
No management is practical.
Cause.
African cereal streak virus (ACSV) is limited to the phloem, where it induces a necrosis. ACSV is transmitted by the planthopper Toya catilina but is not seed or
mechanically transmitted. The natural virus reservoir is native grasses. Disease development is aided by high temperatures.
Distribution.
East Africa.
Symptoms.
Initially, faint, broken, chlorotic streaks begin near leaf bases and extend upward. The broken nature of young streaks is clearly defined. Later, definite alternate yellow
and green streaks develop along entire leaf blades. Eventually, leaves become almost completely chlorotic. New leaves tend to develop a shoestring habit and die.
Plants infected while young become chlorotic and severely stunted, and die. Seed yield is almost completely suppressed. Plants become soft, flaccid, and velvety to
the touch.
Management.
Not reported.
Cause.
American wheat striate mosaic virus (AWSMV) is in the rhabdovirus group. AWSMV is transmitted mainly by the leafhopper Endria inimica and occasionally by
Elymana virescens.

Page 394
Distribution.
Canada and the central United States.
Symptoms.
Leaves have obvious striations consisting of yellow to white parallel streaks. Older leaves are stunted and chlorotic, then become necrotic.
Management.
Not reported.
Barley Yellow Dwarf
The disease caused by the barley yellow dwarf virus is sometimes called oat red leaf, red leaf, and yellow dwarf.
Cause.
Barley yellow dwarf virus (BYDV) is a phloemrestricted virus in the luteovirus group. Several luteoviruses are grouped under the name BYDV and share the
characteristic of infecting gramineous plants but differ in various other properties, such as virulence, host range, serological behavior, and transmissibility by aphid
vectors.
BYDV survives or is reservoired in grains sown in the autumn and in several perennial grasses. Perennial grasses are a large reservoir of BYDV but may not serve as
the most important source of inoculum. Inoculum carried by aphids from elsewhere in Canada was considered to be the main source of infection, not nearby grasses,
winter wheat, or maize. In areas where oversummering is a factor, maize is a reservoir for both aphids and some isolates of BYDV. A major source of BYDV in
Indiana is exogenous aphid populations moving from distant plants in wind currents, especially in the spring. Transmission from local grasses was sporadic and less
common
BYDV is transmitted by several species of aphids, including the corn leaf aphid, Rhopalosiphum maidis; oat birdcherry aphid, R. padi; rice root aphid, R.
rufiabdominelis; Russian wheat aphid, Diuraphis noxia; early instars of greenbug, Schizaphis graminum; and the English grain aphid, Sitobion avenae. Once
BYDV is acquired, aphids are capable of transmitting it for the rest of their lives. One very active aphid feeding for short periods on different plants is a more
important vector than several stationary aphids. In the autumn, aphids migrate to autumnplanted small grains and perennial grasses.
Based on transmission by different insects, five types of BYDV are recognized. MAV is transmitted specifically by S. avenae; RMV by R. maidis; RPV by R. padi;
SGV by S. graminum; and PAV nonspecifically by R. padi and M. avenae and infrequently by D. noxia. However, some BYDV isolates obtained from cereal
plants in Victoria, Australia, were serologically similar to MAV but distinct in being readily transmissible by the aphid R. padi. Some RMV isolates from Montana
were transmitted efficiently by R. maidis and S. graminum, and two RMV isolates were occasionally transmitted by R. padi. An aphid may transmit BYDV for the
rest of its life.
BYDV is not transmitted through eggs, newborn aphids, seed, soil, or mechanical means. Disease development occurs during temperatures of

Page 395
10° to 18°C and moist conditions that favor grass and cereal growth and aphid reproduction and migration. Storm fronts aid aphid flights, which may cover hundreds
of kilometers from southern areas, where most overwintering occurs, to the upper Midwest in the United States.
Distribution.
Africa, Asia, Australia, Europe, New Zealand, North America, and South America.
Symptoms.
BYDV on oat is first seen in plants along the edges of fields. Areas of diseased plants varying in size from a few to several kilometers in diameter give fields a patchy
and uneven appearance.
The plant discoloration symptoms that lend the oftenused name ''red leaf" to the disease vary considerably. Initially, faint yellowishgreen blotches occur near the leaf
tip, on the margin, or on the leaf blade. The blotches enlarge, coalesce at the leaf base, and turn various shades of yellowred, orange, red, or redbrown; however,
tissue next to the midrib remains green longer than the rest of the diseased leaf. The discoloration eventually involves the entire leaf blade progressively from the leaf
tips to the bases. The entire flag leaf ultimately becomes a yellow to reddishorange discoloration. Margins of symptomatic leaves may show inward curling. The still
green areas of infected plants may be a darker green than that of healthy plants. It has been reported that the bright yellow discoloration occurs on older but not the
youngest leaves except in late infections when only flag leaves show symptoms.
Plants infected early are severely dwarfed and may die prematurely. Eventually, most diseased plants are dwarfed to some extent and leaf color becomes bright yellow
or occasionally red or purple. Root elongation is restricted on spring oat.
Infection of young plants has the most significant influence on yield. Depending on the cultivar, heads of diseased plants have many blasted spikelets. Test weight of
grain is lowered. The biggest losses have been reported on spring oat.
Management
1. Grow resistant cultivars. Resistance has been identified in breeding lines.
2. Properly fertilize soil. Vigorously growing plants are more tolerant of BYDV than weaker ones.
Cause.
Cereal chlorotic mottle virus (CeCMV) is in the rhabdovirus group. CeCMV is transmitted by cicadellids.
Distribution.
Australia and northern Africa.
Symptoms.
Severe necrotic and chlorotic streaks occur on leaves.
Management.
Not reported.

Page 396
Flame Chlorosis
Cause.
Doublestranded RNAs ranging in size from 900 to 2800 base pairs present in vesicles rather than virions is likely the disease agent or its replicative intermediate. The
causal agent is soiltransmitted and has been transmitted by sowing seed or by placing seedlings in soil where diseased plants had previously grown.
The grassy weeds green foxtail, Setaria viridis, and barnyard grass, Echinochloa crusgalli, are also hosts.
Distribution.
Canada (Manitoba).
Symptoms.
A striking flamelike pattern of leaf chlorosis and severe stunting occur in spring barley. Chloroplasts and mitochondria of affected cells are hypertrophied and contain
an extensive proliferation of fibrilcontaining vesicles that form within the organellar envelope. Diseased plants continue to produce leaves with symptoms after being
transferred to sterile potting medium.
Management.
Not reported.
Maize Dwarf Mosaic
Cause.
Maize dwarf mosaic virus strain O (MDMVO) is in the potyvirus group. MDMVO is transmitted from maize to oat by several aphid species. Infections occur on
plants grown near MDMVinfected maize.
Distribution.
The United States, but infection of oat is rare.
Symptoms.
Leaves have a mild mottling.
Management.
Not necessary.
Oat Blue Dwarf
Cause.
Oat blue dwarf virus (OBDV) is in the marafivirus group. OBDV is transmitted by adult aster leafhoppers, Macrosteles fascifrons, and occasionally by immature
leafhoppers. OBDV overwinters in wild grasses in southern oatgrowing areas and is transmitted into northern oatgrowing areas by leafhoppers. OBDV is limited to
the phloem. At least 18 plant species are infected by OBDV.
Distribution.
Symptoms.
Diseased plants are dwarfed, uniformly dark bluegreen, and mature later than healthy plants. The dwarfed condition causes diseased plants to be overlooked.
Leaves, especially flag leaves, and stems are stiffer, shorter, and stand out at a greater angle from the stem than those of healthy plants. Tillers appear in larger numbers
and form above the crown. Severely blasted heads produce little or no seed.
Management.
Not reported.

Page 397
Oat Golden Stripe
Cause.
Oat golden stripe virus (OGSV) is in the furovirus group. OGSV is transmitted by the soilborne fungus Polymyxa betae. Polymyxa betae survives in field soil as
cystosori. Cysts give rise to zoospores, which swim through free soil water until they contact a host root and encyst. Encysted zoospores produce a structure called a
stachel through which zoosporic cytoplasm enters the host cell and becomes a plasmodium. Only primary root tissue of young roots is infected; the optimum
temperature for infection is about 25°C. The host cell then becomes infected with OGSV if P. betae is viruliferous. After a period of time the plasmodium develops
into a zoosporangium, which releases additional zoospores that repeat the infection cycle. However, some plasmodia develop into cysts, and frequently nearly every
cell in the small feeder roots will contain a cyst. As root cells senesce, cysts are eventually released into the soil, where they can remain viable for years without loss of
virulence.
Distribution.
France, United Kingdom, and the United States (North Carolina).
Symptoms.
When plants are systemically infected, a yellow striping occurs on the tips of leaves and on the two youngest leaves. Many plants have infected roots but show no
systemic symptoms.
Management.
Not reported.
Oat Mosaic
Some researchers have reported oat mosaic virus and soilborne mosaic virus to be the same organism causing the same disease. However, because the symptoms are
described somewhat differently in the literature, they are reported as two different diseases here.
Cause.
Oat mosaic virus (OMV) is in the bymovirus group. OMV is transmitted by the soilborne fungus Polymyxa graminis and by mechanical means.
Distribution.
The United Kingdom and the United States.
Symptoms.
Diseased leaves have a general mottling, especially the first leaves formed on the plant.
Management.
Not reported.
Oat Necrotic Mottle
Cause.
Oat necrotic mottle virus (ONMV) is in the rymovirus group. ONMV is a flexuous filament that is transmitted mechanically but not by aphids. Symptoms in the growth
chamber developed optimally at 20°C.
Distribution.
Canada (Manitoba).

Page 398
Symptoms.
Initially, fine chlorotic lines develop on leaves. As leaves mature, the chlorotic lines enlarge and merge to form a general chlorotic mottle. Later, pale orangebrown
spots, some with pale brown borders and green centers, develop at random on leaf blades and sheaths and are accompanied by a reddish pigmentation that varies
with oat variety. Eventually, a necrosis develops at random on leaves and sheaths.
Management.
Not reported.
Oat Soilborne Mosaic
Cause.
Oat soilborne mosaic virus (OSBMV) is soilborne and survives in soil for up to 5 years, possibly in the soil fungus Polymyxa graminis. Circumstantial evidence
suggests that OSBMV is transmitted to roots by soil fungi that previously invaded roots for at least 2 weeks before the virus was transmitted. OSBMV is composed
of at least two different strains.
Distribution.
Symptoms.
The leaves of less severely diseased plants have light green to yellow dashes and streaks and sometimes a necrotic mottling that parallels the axis of leaves. Other
strains of OSBMV cause eyespot lesions that are spindleshaped with light green to ash gray borders and green centers. One strain of OSBMV causes severely
diseased plants to grow in small rosettes.
Management.
Oat Sterile Dwarf
Cause.
Oat sterile dwarf virus (OSDV) is in the fijivirus group. OSDV is transmitted mainly by the planthopper Javesella pellucida but also by J. dubia, J. discolor, J.
obscura, and Dicranotropis hamata.
Distribution.
Czechoslovakia, Finland, Germany, Norway, Poland, Sweden, and the United Kingdom.
Symptoms.
Plants have a general bushy, dwarfed, dark green, grasslike appearance. Leaves are malformed and have yellow or white enations that are centered on veins or vein
swellings on the back of leaves.
Management.
Not reported.
Oat Striate Mosaic
Cause.
Oat striate mosaic virus (OSMV) is in the rhabdovirus group. OSMV is transmitted by the leafhopper Graminella nigrifrons. The highest incidence of disease was
reported in the autumn on voluntary spring oats.
Distribution.
The United States (Illinois). All laboratory isolates are thought to be lost.

Page 399
Symptoms.
Diseased leaves have a striation pattern parallel to the veins, similar to wheat striate. A necrosis of leaves and stems eventually occurs.
Management.
Not reported.
Orchardgrass Mosaic
Cause.
Orchardgrass mosaic virus (OGMV) is mechanically transmitted. Orchardgrass is a source of inoculum.
Distribution.
Canada (Quebec).
Symptoms.
Typical mosaic symptoms on leaves, considerable stunting, and reduced or delayed heading.
Management.
Not reported.
Wheat Streak Mosaic
Cause.
Wheat streak mosaic virus (WSMV) is in the potyvirus group. WSMV survives in infected plants and is transmitted from plant to plant only by the feeding for one or
more minutes of young wheat curl mites, Aceria tosichella (syn. A. tulipae and Eriophyes tulipae). Once a mite has picked up WSMV from a diseased plant, it
carries the virus internally for several weeks. It was thought that neither mites nor WSMV could survive longer than 1 to 2 days in the absence of a living plant,
including seed. However, active virus reportedly has been detected in dead plants.
As plants mature during late summer or early autumn, mites migrate or are windborne for at least 2.4 km to nearby volunteer cereals, grasses, or maize and infect them
with WSMV. Consequently, WSMV is disseminated from volunteer plants to cereals sown in autumn. However, some plants are hosts for mites but not WSMV, and
vice versa. Other plants are susceptible to both mites and WSMV, and some are resistant to both.
WSMV has a wide host range that includes barley, maize, oat, rye, wheat, and several annual and perennial grasses.
Distribution.
Eastern Europe, western and central North America, and Russia.
Symptoms.
The greatest disease severity occurs in autumnsown oat. Oat sown in the spring is generally not severely diseased but may serve as a reservoir for WSMV to be
carried to other autumnsown cereals. The first symptoms on leaves consist of light green to light yellow blotches, dashes, or streaks parallel to veins. Plants become
stunted and develop a large number of tillers that vary in height and an overall yellow mottling. As diseased plants mature, the yellowstriped or yellowmottled leaves
turn brown and die. After harvest, stunted plants with sterile heads remain standing at the same height or shorter than stubble.

Page 400
Management
1. Destroy all volunteer cereals and grasses in adjoining fields 2 weeks before sowing and 3 to 4 weeks in the field to be sown.
2. Sow winter oat as late as practical after the Hessian flyfree date.
Disease Caused by Physiological Disorders
Blast
Blast is also called blight, blindness, or white star.
Cause.
Any factor that interferes with the normal development of the oat plant when heads are forming. Late sowing, lack of moisture, high temperatures, nutrient imbalance,
crowding, disease, insect attacks, or a combination of factors can cause blast.
Distribution.
Symptoms.
Spikelets, recognized by light color, delicate texture, and lack of grain as heads emerge from boots, are blighted and fail to develop. Ordinarily a few spikelets on the
lower half of heads are blasted, but occasionally half and rarely entire heads are affected.
Management.
Not reported.
Selected References
Boewe, G. H. 1960. Disease of wheat, oats, barley and rye. Illinois Nat. Hist. Surv. Circ. 48.
Brodney, V., Wahl, L, and Rotem, J. 1983. Factors affecting the survival of physiologic races of Puccinia coronata avenae on Avena sterilis in Israel. (Abstr.)
Clement, D. L., Lister, R. M., and Foster, J. E. 1986. ELISAbased studies on the ecology and epidemiology of barley yellow dwarf virus in Indiana. Phytopathology
76:8692.
Cohn, E., and Ausher, R. 1973. Longidorus cohni and Heterodera latipons, economic nematode pests of oats in Israel. Plant Dis. Rptr. 57:5354.
Elliott, C. 1927. Bacterial stripe of oats. J. Agric. Res. 35:811824.
Frank, J. A., and Christ, B. J. 1988. Ratelimiting resistance to Pyrenophora leaf blotch in spring oats. Phytopathology 78:957960.
Gildow, F. E., and Frank, J. A. 1988. Barley yellow dwarf virus in Pennsylvania: Effect of the PAV isolate on yield components of Noble spring oats. Plant Dis.
72:254256.
Gill, C. C. 1967. Oat necrotic mottle, a new virus disease in Manitoba. Phytopathology 57:302307.

Page 401
Gough, F. J., and McDaniel, M. E. 1974. Occurrence of oat leaf blotch in Texas in 1973. Plant Dis. Rptr. 58:8081.
Gray, S. M., Smith, D. M., and Sorrells, M. E. 1991. Isolatespecific resistance to barley yellow dwarf virus in spring oats. (Abstr.). Phytopathology 81:122.
Haber, S., and Chong, J. 1993. Flame chlorosis induces vesiculations in chloroplasts and mitochondria: What does it mean? (Abstr.) Can J. Plant Pathol. 15:57.
Haber, S., and Hardener, D. E. 1992. Green foxtail (Setaria viridis) and barnyard grass (Echinochloa crusgalli), new hosts of the viruslike agent causing flame
Harder, D. E., and Bakker, W. 1973. African cereal streak, a new disease of cereals in east Africa. Phytopathology 63:14071411.
Huffman, M. D. 1955. Disease cycle of Septoria disease of oats. Phytopathology 45:278280.
Jedlinski, H. 1976. Oat striate mosaic, a new virus disease in Illinois spread by the leafhopper Graminella nigrifrons (Forbes). (Abstr.) Am. Phytopathol. Soc.
3:208.
Jons, V. L. 1986. Downy mildew (Sclerophthora macrospora) of wheat, barley, and oats in North Dakota. Phytopathology 70:892.
Kolb, F. L., Cooper, N. K., Hewings, A. D., Bauskey, E. M., and Teyker, R. H. 1991. Effects of barley yellow dwarf virus on root growth in spring oat. Plant Dis.
75:143145.
Lockhart, B. E. L. 1986. Occurrence of cereal chlorotic mottle virus in Northern Africa. Plant Dis. 70:912915.
McKay, R. 1957. Cereal Disease in Ireland. Arthur Guiness, Son & Co. Ltd., Dublin.
Peterson, J. F. 1989. A cerealinfecting virus from orchardgrass. Can. Plant Dis. Surv. 69:1316.
Poole, D. D., and Murphy, H. C. 1953. Field reaction of oat varieties to Septoria black stem. Agron. J. 45:369370.
Richardson, M. J., and Noble, M. 1970. Septoria species on cereals: A note to aid their identification. Plant Pathol. 19:159163.
Roane, M. K., and Roane, C. W. 1983. New grass hosts of Polymyxa graminis in Virginia. (Abstr.) Phytopathology 73:68.
Scardaci, S. C., and Webster, R. K. 1982. Common root rot of cereals in California. Plant Dis. 66:3134.
Schaad, N. W., Sumner, D. R., and Wate, G. O. 1980. Influence of temperature and light on severity of bacterial blight of corn, oats and wheat. Plant Dis. 64:481
483.
Simmonds, P. M. 1955. Root disease of cereals. Can. Dept. Agric. Pub. 952.
Simons, M. D., and Murphy, H. C. 1952. Kernel blight phase of Septoria black stem of oats. Plant Dis. Rptr. 36:448449.
Simons, M. D., and Murphy, H. C. 1968. Oat Diseases and Their Control. USDA. Agric. Res. Serv. Agric. Hdbk. No. 343.
Sinha, R. C., and Benk, R. M. 1972. American Wheat Striate Mosaic Virus. Commonwealth Mycological Institute. Descriptions of Plant Viruses, Set 6., No. 99.
Kew, England.
Timian, R. G. 1985. Oat blue dwarf virus in its plant host and insect vectors. Plant Dis. 69:706708.
Walker, J. 1975. Takeall disease of Graminae: A review of recent work. Rev. Plant Pathol. 54:113144.
Yamamoto, H., and Tani, T. 1987. Induction of crown rust resistance in oat by high temperature stress. Ann. Phytopathol. Soc. Japan 53:616621.

Page 403
12.
Diseases of Peanut (Arachis hypogaea)
Bacterial Wilt
Bacterial wilt is also called brown rot and slime disease.
Cause.
Pseudomonas solanacearum survives in soil and may be seedborne. Infection occurs through wounds or lenticels on host roots. Disease development is favored by
heavy clay soils that tend to stay moist and soils in which peanut has been grown for several successive years. Pseudomonas solanacearum has a wide host range.
Distribution.
Wherever peanut is grown. Bacterial wilt is of minor importance in the United States.
Symptoms.
Different symptoms of the disease occur in different geographical peanutgrowing areas. A symptom from the East Indies is sudden wilting with leaves remaining
attached to dead plants. Symptoms from India are a general loss of turgidity, drying and drooping of leaves, and the ultimate death of the plant. Internal symptoms
include browning of the vascular system of the roots and stem.
Symptoms of disease in the United States are not as severe. There are a large number of dead roots. Brown or black streaks occur throughout diseased roots, main
stems, and lower branches and can be observed as dark brown spots in the xylem and pith when stems and roots are cut in cross section. Eventually, diseased tissue
is blackened and has extensive plugging and necrosis. If plants are infected when young, pods are invaded and remain small or become wrinkled and develop a
spongy or soft decay. When mature plants are infected, there is no invasion of pods.
Management

Page 404
3. Grow plants on light, welldrained soils.
4. Rotate peanut with resistant crops, such as sweet potatoes, small grains, and certain legumes.
Aerial Blight
Cause.
Rhizoctonia solani. Fungal propagules are splashed onto leaves during rainstorms.
Distribution.
India, Malaya, and the United States.
Symptoms.
Leaves of diseased plants rot or blight.
Management.
Not reported.
Cause.
Alternaria tenuissima.
Distribution.
India.
Symptoms.
Diseased leaves have light to dark brown spots and frequently are totally blighted.
Management.
Not reported.
Cause.
Alternaria arachidis.
Distribution.
India.
Symptoms.
Orangebrown lesions in interveinal areas of diseased leaves often extend into veins and veinlets.
Management.
Not Reported.
Alternaria Spot and Veinal Necrosis
Cause.
Distribution.
Symptoms.
Orangebrown necrotic spots that occur in the interveinal areas of diseased leaves often extend into veins and veinlets.
Management.
Not reported.

Page 405
Anthracnose
Anthracnose is also called Colletotrichum leaf spot.
Cause.
Colletotrichum arachidis, C. dematium, and C. mangenoti survive as mycelia in infested residue. Conidia are produced in acervuli and disseminated by wind and
splashing rain to host plants.
Distribution.
Africa, Argentina, India, Niger, Taiwan, Uganda, and the United States.
Symptoms.
Different symptoms have been described. When plants are infected by C. mangenoti, browngray, elongate to circular lesions occur on both leaflet surfaces but rarely
on petioles or stems. Lesions may be large and involve up to half the leaflet.
Other symptom descriptions are scattered circular to irregularshaped lesions with graywhite centers surrounded by dark brown borders. Some researchers describe
lesions as initially small, watersoaked, yellow spots that enlarge to 13 mm in diameter and become dark brown. These spots grow rapidly, become irregularshaped,
and spread over the entire leaflet. Spots may extend into petioles and branches and cause the death of the entire plant.
Management.
Management measures usually are not warranted.
Aspergillus Crown Rot
Cause.
Aspergillus niger and A. pulverulentus survive in several different ways: As saprophytes in infested residue and as conidia and mycelia in soil, on seed surfaces, and
in or under tissues of the testae. The abundant spores that are produced are disseminated by wind for long distances and by any agent that moves soil.
Most infection occurs within 10 days after seed germination as elongating hypocotyls come in contact with soilborne inoculum. Hyphae penetrate directly into
hypocotyls or cotyledons. Disease is most severe when plant emergence is delayed, plants are predisposed by high soil and air temperatures, and plants grow in soils
low in organic matter. The causal fungi grow best in warm, moist conditions.
Distribution.
Wherever peanut is grown.
Symptoms.
The most common symptom is that, after seed germinates, the elongating hypocotyl is infected, becomes watersoaked and light brown, and is covered by black
conidia and mycelium. Eventually, the diseased hypocotyl tissue becomes dark brown, then lighter in color, and shreds. Necrosis and shredding eventually extend into
the branches.
The aboveground symptom is a rapid wilting of the entire plant during

Page 406
dry weather. Recovery of the turgidity of diseased plants, which may occur during high soil moisture, is related to the growth of adventitious roots above the infection
site. However, most plants succumb and die in less than 30 days after infection.
Seed is infected when placed in a moist environment, where it becomes covered with sooty black masses of spores.
Management
2. Grow bunchtype cultivars.
Blackhull
Cause.
Thielaviopsis basicola overwinters most commonly as chlamydospores in the endocarp of unharvested peanuts, as saprophytic mycelium in infested residue, and as
endoconidia in soil. As pods deteriorate the following season, chlamydospores germinate and produce mycelia that infect new pods. Dissemination is by any means
that transports soil. Optimum growth of T. basicola in vitro is at 22° to 28°C. Blackhull is more severe in wet soils that are neutral or slightly alkaline.
Distribution.
Occurs in most countries where 'Spanish' and 'Valencia' peanuts are grown.
Symptoms.
Infections occur on external schlerenchymatous shell tissue during development of the fruit and are first seen as tiny black spots. Eventually, shells become black due to
an aggregation of chlamydospores in the developing shells. Dark, crusty patches develop where great numbers of lesions have coalesced. Thielaviopsis basicola
grows throughout shell tissue and produces masses of chlamydospores. Internal shell tissue and testae of kernels are discolored brown.
Management
2. Rotate peanut with grain sorghum, maize, or small grains.
3. Leave soil fallow.
4. Sow as late as feasible in the growing season.
Black Root Rot
Cause.
Thielaviopsis basicola overwinters most commonly as chlamydospores in the endocarp of unharvested peanuts, as saprophytic mycelium in infested residue, and as
endoconidia in soil.
Distribution.
The United States.
Symptoms.
Diseased roots become dark, disintegrate, and die. Leaves become stunted and chlorotic and the entire plant wilts, especially during dry soil conditions. Diseased
plants die slowly.

Page 407
Management
2. Rotate peanut with grain sorghum, maize, or small grains.
3. Leave soil fallow.
4. Sow as late as feasible in the growing season.
Botrytis Blight
Botrytis blight is also called gray leaf mold and stem rot.
Cause.
Botrytis cinerea survives as sclerotia in soil and infested residue. Sclerotia germinate and form either mycelia or support conidiophores and conidia on sclerotial
surfaces. Conidia are abundantly produced on infested tissue and disseminated by wind and water. Sclerotia are disseminated by any means that moves soil.
Disease is most severe during damp, cool weather (20°C or below) in late autumn. Botrytis cinerea requires no wounds or necrotic tissue to infect; however,
senescing frostinjured and mechanically injured tissues are most prone to colonization. Leaves, stems, and subterranean organs are infected. Organic debris on the
soil surface aids in the infection process by serving as an energy source for B. cinerea.
Distribution.
Japan, Nyasaland, Rhodesia, Tanganyika, the United States, and Venezuela. However, Botrytis blight is seldom a severe problem since climatic conditions that favor
disease are rarely present.
Symptoms.
Diseased tissues decay rapidly and are sparsely covered with dark gray mycelium, conidiophores, and conidia. Disease progresses rapidly from leaves and stems
down into pegs and fruit. Flattened, black, irregularshaped sclerotia develop on decayed stems and pods.
Management
1. Regulate sowing dates to prevent plants from growing or maturing during cool, wet weather.
Charcoal Rot and Macrophomina Leaf Spot
Charcoal rot and Macrophomina leaf spot is also called root rot disease.
Cause.
Macrophomina phaseolina (syn. Rhizoctonia bataticola) survives primarily as sclerotia or microsclerotia in infested residue and soil. Other types of survival are as
mycelium in seeds and residue and, presumably, as pycnidia in infested residue. Sclerotia remain viable in dry soil for several years but rapidly lose their viability in wet
soil. Dissemination is by any means that moves soil residue and seed. Disease is most severe at a high soil temperature (35°C) and low soil moisture.
Distribution.
Worldwide. Charcoal rot is of minor importance.

Page 408
Symptoms.
Watersoaked necrotic areas that develop on stems at the soil line become dull brown and extend up stems into the branches and down into the roots. Plants wilt if
stems become girdled by lesions or if roots are decayed. Athough infection of leaflets is rare, symptoms consist of large, marginal, zonate spots in which pycnidia that
resemble small, black bumps are found. Partial defoliation may occur. When diseased plants die, a blackening or sooty appearance caused by numerous sclerotia
occurs over plant parts. A few pycnidia that resemble small, black pimples may also develop.
Root infection can occur independently of stem rot. At first, roots are blackened; later, the taproot is completely rotted.
When peanuts are physically damaged before or after harvest, M. phaseoli grows through shells into the kernels. Sclerotia are evident as a black or sooty growth that
occurs on internal and external shell surfaces.
Management
2. Apply soil fungicides to reduce fruit infection.
3. Reduce row spacing. Incidence of root rot is lower at 30 cm than at either 45 or 60cm row spacings.
4. Grow varieties that are the most resistant.
5. In experimental conditions, gypsum applied at the rate of 150 kg/ha resuited in significant reduction of disease incidence regardless of row spacings or varieties
used.
Choanephora Leaf Spot
Cause.
Choanephora spp.
Distribution.
The Philippines, Senegal, Thailand, and Uganda.
Symptoms.
Brown lesions containing faint concentric circles originate at leaflet margins and eventually spread over the entire leaflet. Abundant sporulation occurs on both leaflet
surfaces. Defoliation of diseased plants may occur.
Management.
Not reported.
Collar Rot
Collar rot is also called Diplodia collar rot.
Cause.
Lasiodiplodia theobromae (syn. Diplodia gossypina) survives as mycelium and pycnidia in infested residue. During wet weather, conidia are produced in pycnidia
and disseminated by splashing water or by wind to host plants. Mycelia in residue are also disseminated by running water, cultivation, or any means that moves soil.
When predisposed by heat injuries, plants of all ages are infected. Lasiodiplodia theobromae rapidly colonizes heatinjured tissue and grows intercellularly through
cortical

Page 409
parenchyma into adjacent nonwounded tissue. Hot, dry weather favors infection.
Distribution.
Worldwide, but collar rot is not considered an important disease.
Symptoms.
Initially, there is a rapid wilting of branches or of entire diseased plants. During warm weather, plants die within a few days of infection and symptom expression. Stem
lesions become graybrown to black and extend toward the taproot. Necrotic stems become shredded. Infection of a branch usually results in death of that branch.
Numerous pycnidia, which appear as tiny, black pimplelike dots, develop in necrotic tissue.
Management
1. Heat canker may be more prevalent in 'Runner' than in 'Spanish' cultivars because the greater leaf development in 'Spanish' cultivars provides shade.
2. Do not rotate peanut with cotton and soybean.
4. Sow peanut rows so plants shade each other.
5. A finely clodded soil surface is most favorable for reducing reflective sunlight energy.
Colletotrichum Leaf Spot
Cause.
Colletotrichum gloeosporioides. Overseasoning is likely as mycelium in seeds, seed coats, infested residue, and on weeds.
Distribution.
Not certain, but presumably occurs in humid tropics and subtropics where peanut is grown.
Symptoms.
Foliar symptoms develop after prolonged periods of high humidity and include dark brown to black spots on leaves, necrosis of laminar veins, petiole cankering, and
premature defoliation. Diseased lower branches and leaves on a plant may be killed.
Management.
Not reported.
Cylindrocladium Black Rot
Cause.
Cylindrocladium parasiticurn (syn. C. crotalariae), teleomorph Calonectria ilicicola, survives as small (35425 gm in diameter), irregularshaped microsclerotia in
infested residue, soil, and possibly seed. Microsclerotia survive better buried in soil than on the soil surface. Primary infection originates from germination of
microsclerotia and from mycelia growing from infested residue. Microsclerotia 150 µm and larger induce root rot more efficiently than do smaller microsclerotia. Seeds
are infected at a higher incidence shortly before storage than after 7 months storage in an unheated building. Hyphae grow intracellularly and intercellularly

Page 410
throughout the testae of discolored seed. Hyphae grow in the cotyledonary tissues from seed with discolored testae.
Longdistance dissemination occurs as propagules on seed surfaces and windborne plant fragments that contain microsclerotia. Other means of dissemination are
birds, farm implements, movement of hay, and dispersal in roots.
During moist conditions, ascospores are formed in newly developed perithecia and disseminated by splashing rain or insects. However, the epidemiological importance
of ascospores is thought to be limited to shortrange spread.
A soil temperature of 25°C and a moisture content near field capacity are most conducive for infection and subsequent root rot development. Disease is most severe
in heavy clay soils that stay wet and waterlogged for long periods of time after a rainfall.
Cylindrocladium crotalariae does not survive well at soil temperatures of 5°C and below. However, at these low temperatures survival is better in moist than in dry
soil.
Distribution.
Australia, India, Japan, and the United States.
Symptoms.
Symptoms typically appear midway through the growing season and may increase rapidly as the season progresses. Some researchers state aboveground symptoms
are optimum early in the growing season after moisture stress follows a period of high rainfall that accentuates root rot and causes loss of functional roots. Diseased
plants are stunted and chlorotic, wilt on warm days, eventually collapse, and remain debilitated although they normally do not die. Taproots, immature pegs, and pods
are blackened and taproots are shredded and have few or no lateral roots. Microsclerotia form in roots and appear as small black structures the size and appearance
of ground pepper.
Perithecia look like small redorange spherical objects in dense clusters on stems, pegs, and pods just above or beneath the soil surface. Perithecia are especially
abundant in moist areas under dense foliage. During wet weather, ascospores are exuded from perithecia as a viscous yellow ooze in 2 to 3 weeks.
Management
2. Disk under all diseased plants prior to digging and combining operations. Avoid passing through these areas with equipment during harvest.
3. Dig and remove all diseased plants and either burn them completely or bury them in a sanitary landfill.
4. Practice sanitation on all equipment since microsclerotia can be moved in soil left on equipment. Wash equipment with a strong stream of water immediately before
equipment is moved from infested areas.

Page 411
5. Cropping history has been reported to not affect disease development. However, some reports suggest rotating peanut every 3 to 5 years with maize, small grains,
or perennial grasses but not with soybean since peanut and soybean have many pathogens in common.
6. Remove all diseased plants prior to harvest in small, localized areas.
7. Perform cultural practices that increase soil temperature. Disease development is slowed when soil temperatures exceed 25°C and stops when soil temperatures
exceed 35°C.
Cylindrocladium Leaf Spot
Cause.
Cylindrocladium scoparium.
Distribution.
Symptoms.
Spots on diseased leaves vary from light to dark brown to black.
Management.
Not reported.
Diplodia Infection
Cause.
Diplodia sp. Disease was favored when stems were wounded with a shallow cut and inoculated plants were placed in a mist chamber during artificial inoculation.
Distribution.
Symptoms.
Black lesions greater than 5 cm in length occur on diseased upper stems. Following wounding, internal necrosis was greater in upper stems than in lower stems.
Management.
Not reported.
Cause.
Bipolaris spicifera (syn. Drechslera spicifera).
Distribution.
Asia.
Symptoms.
Reddish to brown elongated specks occur on diseased leaves.
Management.
Not reported.
Early Leaf Spot
Early leaf spot is also called tikka, viruela, peanut cercosporosis, Mycosphaerella leaf spot, brown leaf spot, and early Cercospora leaf spot.
Cause.
Cercospora arachidicola, teleomorph Mycosphaerella arachidis, survives as conidia, asci, and mycelia either in infested residue or soil. Conidia produced from
mycelium and ascospores produced in asci are splashed or blown to host leaves. Penetration by germ tubes is through open stomata

Page 412
or directly through lateral faces of epidermal cells. Secondary infection occurs from conidia produced in leaf spots and disseminated by wind, rain, insects, and
machinery. Infection is favored by temperatures of 26° to 31°C and long periods of high relative humidity. Perithecia are produced in diseased tissue later in the
growing season.
Disease severity is greatest where peanut follows peanut in a rotation. The incidence and severity is usually greater in sprinkleirrigated plants and in plants receiving
sodic water. Prior infection with peanut green mosaic virus increases susceptibility to infection by C. arachidicola. Different races of C. arachidicola are present.
Distribution.
Symptoms.
Symptoms occur earlier in the season than those of late leaf spot. Cercospora arachidicola is more frequent on domestic cultivars of Arachis hypogaea, while
Phaeoisariopsis personata is more common on wild species; therefore, differences in the occurrence of symptoms may be related to host differences rather than the
time of the growing season. The terms ''early" and "late" leaf spot may not be significant in peanutgrowing areas where both pathogens occur.
Initially, small chlorotic spots occur, then enlarge (110 mm or more in diameter) and become brown to black and subcircular. A chlorotic halo around a spot or lesion
on the upper leaflet surfaces is common but is not always present. The spots will coalesce during wet weather. Sporulation on upper lesion surfaces gives lesions a
sooty appearance. Defoliation may occur. Petioles and stems have dark, elongated, superficial lesions with indistinct margins. Both species of Cercospora may be
present in lateseason infections.
Management
1. Rotate peanut with other crops.
2. Plow under or remove infested residue. Destroy volunteer peanut plants.
Fusarium Peg and Root Rot
Cause.
Several species of Fusarium, including F. roseum, F. solani, F. tricinctum, and F. moniliforme. These fungi survive as chlamydospores in soil and as saprophytic
mycelia in infested residue. Primary inoculum is either chlamydospores that germinate and produce hyphae or conidia produced from mycelia. Conidia are
disseminated by wind, water, or any means that moves soil or residue. Several Fusarium spp. are apparently only parasitic on belowground plant parts and do not
become pathogenic. Injury from Fusarium spp. is ordinarily not serious if host plants are in a vigorous growing condition.

Page 413
Distribution.
The disease occurs wherever peanut is grown.
Symptoms.
Seedlings that haven't emerged have gray, watersoaked tissues that are overgrown with mycelia.
Fusarium solani causes a dry root rot. The lower taproot is brown to redbrown, withers, and often curls. Secondary roots become brown and slough off.
Eventually, disease progresses up the hypocotyl, causing plants to wilt. Sometimes adventitious roots that develop above the diseased area allow plants to survive.
Older plants infected by F. solani have small, elongate, slightly sunken, brown lesions on roots just below the crowns. Eventually, lesions girdle the roots and cause
cortical tissue to become shredded and diseased plants to be chlorotic, wilted, and moribund.
Fusariuminfected pods do not have typical symptoms. However, a violetwhite discoloration of pods is reported to be characteristic.
Management
1. Increase organic matter in the soil.
2. Avoid growing peanut in acid soils.
Fusarium Stem Canker
Cause.
Fusarium oxysporum. Wounding of the central stem by mechanical or environmental means is necessary for infection to occur. Prolonged wet weather enhances
Distribution.
The United States (Alabama).
Symptoms.
Reddish to dark brown, sunken, elongated (0.53.0 cm), girdling lesions occur at varying distances above the soil line along the central stems of diseased plants.
Foliage distal to the cankers becomes chlorotic and wilts. Sporodochia of F. oxysporum may be observed on the surface of some lesions.
Management.
Not reported.
Fusarium Wilt (Fusarium martii vat. phaseoli)
Although the disease is called Fusarium wilt in some literature, the fungus is not systemic in the xylem tissue and the disease is more of a stem or root rot that results in
wilt symptoms. Fusarium martii is not listed in Fart et al. (1989) or in Nelson et al. (1983).
Cause.
Fusarium martii var. phaseoil.
Distribution.
The United States.
Symptoms.
Symptoms first occur 8 to 10 weeks after sowing. The youngest leaves become chlorotic, degenerate rapidly through a drooping or wilt

Page 414
stage, and finally die because of stem lesions at or near the soil line. Roots may also be girdled by lesions. The entire diseased stem may eventually be destroyed.
Management.
Not reported.
Fusariurn Wilt (Fusarium oxysporum)
Cause.
Fusarium oxysporum survives as chlamydospores in soil and as mycelia in infested residue. Primary inoculum is either chlamydospores that germinate and produce
hyphae or conidia produced from mycelia. Conidia are disseminated by wind, water, or any means that moves soil or residue.
Distribution.
Fusarium wilt occurs wherever peanut is grown.
Symptoms.
Fusarium wilt occurs sporadically from year to year and within a field. Wilt is characterized by graygreen leaves that quickly permanently wilt. In dry weather, wilted
leaves become dry and brittle and appear to be bleached. In slower wilting, the leaves may first become chlorotic and the plant defoliates before death occurs.
Taproots have vascular discoloration but secondary roots appear healthy.
Management.
Not reported.
Late Leaf Spot
Late leaf spot is also called brown leaf spot, leaf spot, late Cercospora leaf spot, Mycosphaerella leaf spot, peanut cercosporosis, tikka, and viruela.
Cause.
Phaeoisariopsis personata (syn. Cercospora personata and Cercosporidium personatum), teleomorph Mycosphaerella berkeleyi. Phaeoisariopsis personata
survives as conidia, perithecia, and mycelia in infested residue, and as mycelia in soil. Primary inoculum is conidia produced directly from mycelia growing in infested
residue and disseminated by wind to host plants, and ascospores produced in perithecia and splashed by rain to peanut leaves. Penetration of leaves is by germ tubes
that grow through open stomata or directly through the lateral faces of epidermal cells.
Some report temperatures of 16° to 20°C to be very favorable for germination of conidia. Others report infection is favored by temperatures of 26° to 31°C and long
periods of high relative humidity. However, in experiments using detached leaves, maximum infection occurred at 20°C if leaves were exposed to 12 hours/day of
more than 93% relative humidity. Using this method, infection decreased with increasing temperature, regardless of genotype resistance. Daily periods of high relative
humidity for less than 12 hours also reduced the number of infections on all genotypes, regardless of temperature.
After leaves are infected, conidia that have sporulated in lesions are readily disseminated by wind, rain, insects, and machinery throughout

Page 415
the growing season and function as secondary inoculum. A minimum of 4 hours of relative humidity at or greater than 95% per day is required for conidial production.
The highest numbers of conidia are produced when lesions are subjected to daily periods of 16 or more hours of relative humidity at or above 95% and a temperature
of approximately 20°C. Perithecia are produced in diseased tissue later in the growing season.
Disease severity is greater where peanut follows peanut in a rotation and in fields receiving tractor traffic. Prior infection with peanut green mosaic virus increases
susceptibility to infection by P. personata. Different races of P. personata are present.
Distribution.
Late leaf spot occurs wherever peanut is grown. However, the disease predominates in the tropics and subtropics and is reported to be the major peanut leaf spot in
the southernmost United States.
Symptoms.
Symptoms occur later in the season than those of early leaf spot. However, Cercospora arachidicola is more frequent on domestic cultivars of Arachis hypogaea,
while P. personata is more common on wild species; therefore, differences in occurrence of symptoms may be related to host differences rather than the time of the
growing season. The terms "early" and "late" leaf spot may not be significant in peanutgrowing areas where both pathogens occur.
Initially, small chlorotic spots occur, then enlarge (110 mm in diameter), become dark brown to black, are subcircular, and do not have yellow halos. If halos are
present, they are normally on the upper leaf surfaces. The color of spots on the lower leaf surfaces tends to be black and is a good diagnostic characteristic to
separate symptoms from those of early Cercospora leaf spot.
Sporulation first occurs on the lower leaf surfaces and later will occur sparsely on the upper leaf surfaces. Stroma on which spores are produced are often arranged in
concentric circles and are visibly raised above the lesion surface. Defoliation may occur. Diseased petioles and stems have dark, elongated and superficial lesions with
indistinct margins.
Management
2. Plow under or remove infested residue. Destroy volunteer peanut plants.
Macrophoma Leaf Spot
Cause.
Macrophoma sp. persists as saprophytic mycelia and pycnidia in infested residue.
Distribution.
Europe.

Page 416
Symptoms.
Lesions on diseased leaves are dark and composed of firm necrotic tissue. Marginal necrosis occurs along the apical portions of diseased leaflets. Pycnidia appear as
black pimplelike objects scattered throughout necrotic tissue.
Management.
Since Macrophoma leaf spot is not a serious disease, management is not necessary.
Melanosis
Melanosis also is called Stemphylium leaf spot in the United States. Some researchers consider symptoms similar to those described here as a melanosis disease
caused by Macrosporium sp. and Alternaria sp.
Cause.
Stemphylium botryosum.
Distribution.
Argentina. Melanosis is considered a minor disease.
Symptoms.
Symptoms are most prominent on the diseased lower leaf surfaces. Spots are irregular, circular to oval (0.51.0 mm in diameter), or elongated (1.5 mm long). The
numerous dark brown spots give the impression leaflets are covered with fly specks. Initially, spots are slightly submerged but later become elevated and "crustlike."
Defoliation does not occur even in severe disease conditions.
Management.
Some cultivars are more susceptible than others, but management is usually not necessary.
Myrotheciurn Leaf Blight
Myrothecium leaf blight is also called groundnut leaf blight.
Cause.
Myrothecium roridum.
Distribution.
India.
Symptoms.
Lesions on diseased leaves are gray, round to irregularshaped (510 mm in diameter), and surrounded by chlorotic halos. Lesions eventually coalesce and give
diseased leaves a blighted appearance. Black fruiting bodies, which are frequently arranged in concentric rings, form on diseased lower and upper leaf surfaces.
Management.
Not reported.
Neocosmospora Root Rot
Cause.
Neocosmospora vasinfecta.
Distribution.
South Africa.
Symptoms.
Diseased taproots and lateral roots are discolored and split. External discoloration of stems occurs about 1 cm above the soil surface and in

Page 417
ternal discoloration of vascular bundles and pith occurs about 3 cm above the soil surface. Small, dark lesions and larger dark cracks occur in the surface tissues of
diseased pods and the underlying parenchymatous tissue is brown. Perithecia are produced on diseased tissue.
Management.
Not reported.
Net Blotch
The common name of this disease may be confused with web blotch (sometimes called net blotch) caused by Phoma arachidicola. Net blotch may be the same
disease syndrome as pod wart.
Cause.
The reported cause is Streptomyces sp. in Israel and S. scabies in South Africa. However, disease may be caused by the same fungus at both locations. Disease may
be accentuated when peanut follows potatoes in a rotation.
Distribution.
Israel and South Africa.
Symptoms.
Disease symptoms are accentuated by the herbicide ethalfluralin. The dark brown to black blotches that initially occur on diseased pods become netlike lesions that
eventually may cover the entire pod. Dark brown, necrotic, wartlike lesions were reported on the cultivar 'Sellie' in South Africa.
Management
1. Methyl bromide reduces disease incidence and severity.
2. Do not grow peanut following potatoes.
Olpidium Root Rot
Cause.
Olpidium brassicae.
Distribution.
India and the United States (Texas). Olpidium root rot is a minor disease of peanut.
Symptoms.
Diseased root cortex is brown to black.
Management.
Not necessary.
Pepper Spot and Scorch
Cause.
Leptosphaerulina crassiasca overwinters as pseudothecia and saprophytic mycelia in infested residue. Ascospores are produced in pseudothecia and are forcibly
ejected from the pseudothecia and disseminated a considerable distance by wind. Ascospores become closely attached to leaflet surfaces and germinate when free
water is available. Optimum conditions for germination are a temperature of 28°C and 100% relative humidity. Eventually, numerous pseudothecia are produced in
detached dead leaves.

Page 418
Distribution.
Argentina, India, Madagascar, Malawi, Mauritius, Senegal, South Africa, Taiwan, the United States, and Zambia.
Symptoms.
Symptoms are of two types and occur only on diseased leaves. Pepper spots are less than 1 mm in diameter, dark brown to black, irregularshaped to circular, and
occasionally depressed. Lesions do not rapidly enlarge with age. Spots are more common on the upper leaf surfaces but also occur on lower leaf surfaces. When
spots are sparse, there is not an obvious deleterious effect to the diseased leaf. Conversely, numerous spots tend to coalesce, which gives leaflet surfaces a "netted"
appearance and causes leaflets to die and defoliate. Perithecia are abundantly produced in detached diseased leaflets.
Leaflets with scorch symptoms become chlorotic, then necrotic at discrete points along the margins. Necrotic tissue becomes dark brown and has a chlorotic zone
along the edges of the discolored tissue. Lesions commonly develop from the tips of diseased leaflets along a wedgeshaped front toward the petiole. Pseudothecia
form abundantly in necrotic tissue. Necrotic tissue tends to fragment along the leaflet margins, which gives a tattered appearance to the leaf.
Management
Pestalotia Leaf Spot
Cause.
Pestalotia arachidicola.
Distribution.
Brazil.
Symptoms.
Circular (up to 12 mm in diameter) necrotic spots occur on diseased leaves.
Management.
Not reported.
Pestalotiopsis Leaf Spot
Cause.
Pestalotiopsis arachidis persists as saprophytic mycelia in infested residue. Conidia are produced in acervuli.
Distribution.
India.
Symptoms.
Diseased leaves have dark brown circular spots that are surrounded by yellow halos. Spots on the diseased lower leaf surfaces are marked by concentric rings and
have prominent black acervuli scattered throughout the spots.
Management.
Not necessary.

Page 419
Phanerochaete omnivorum Association
Cause.
Phanerochaete omnivorum.
Distribution.
Symptoms.
An orange resupinate fruiting body is produced on the lower stems and prostrate branches of diseased peanut plants.
Management.
Not reported.
Phomopsis Foliar Blight
Phomopsis foliar blight is also called Phomopsis blight.
Cause.
Phomopsis phaseoli (syn. P. sojae) survives as pycnidia or mycelia in infested residue.
Distribution.
Symptoms.
Diseased leaflet margins have necrotic lesions that are brown to black and have a chlorotic zone between the healthy and necrotic tissue. Lesions start at leaflet tips
and grow to the petioles in a Vshaped pattern. Pycnidia appear as small, black, pimplelike structures in rows parallel to midribs and smaller veins.
Discrete lesions have occurred in the center of leaflets. Such lesions are small (110 mm in diameter), circular to irregularshaped, and surrounded by a redbrown
margin. The centers of the lesions are white to tan, have a papery texture, and contain pycnidia.
Diseased stems become blackened.
Management.
Since Phomopsis foliar blight is not considered to be a serious disease, disease management is not necessary.
Cause.
Phyllosticta arachidishypogaea and P. sojicola survive as pycnidia and saprophytic mycelia in infested residue. Phyllosticta leaf spot is most prevalent early in the
growing season. Other causal organisms may also be involved.
Distribution.
Wherever peanut is grown. Phyllosticta leaf spot is not considered to be an important disease.
Symptoms.
Different types of symptoms may occur. Lesions are circular to oval (1.55.0 mm in diameter) with gray to tan centers and definite borders surrounded by redbrown
margins. Sometimes the centers of lesions fall out, which gives diseased leaflets a "shothole" appearance.
Other symptom descriptions note that lesions are tan to redbrown

Page 420
with a dark brown margin surrounded by a chlorotic halo. Such lesions are found predominantly near the tips of diseased leaflets and extend along the leaflet midribs.
Management.
Management measures are generally not considered necessary.
Phymatotrichum root rot is also called cotton root rot, Ozonium root rot, and Texas root rot.
Cause.
Phymatotrichopsis omnivora (syn. Phymatotrichum omnivorum) survives for several years as sclerotia at depths of 30 to 75 cm in soil and on weeds; however,
P. omnivora is very susceptible to freezing temperatures. Dissemination of P. omnivora is primarily by machinery moving infested soil within a field and from field to
field. Phymatotrichum root rot is most severe in alkaline, poorly aerated black clay soils.
Distribution.
The southwestern United States. Phymatotrichum root rot is not an important disease of peanut.
Symptoms.
Diseased plants are stunted, chlorotic, and die. Diseased roots become tan and have strands of whitish to tan mycelia on the outside of the root.
Management.
Disease management is generally not necessary, the following are aids to reduce disease:
1. Plow under green manure crops. Crop residues can also be plowed under if nitrogen is applied to promote rapid decay.
2. Rotate peanut with cereals or grasses.
3. Plow deeply during hot, dry weather to expose and kill the fungus.
4. Provide adequate fertility to ensure vigorous peanut growth.
Pod Wart
Pod wart may be the same disease syndrome as net blotch.
Cause.
Streptomyces spp. that occur in warted tissue, soil, and the rhizosphere.
Distribution.
Israel.
Symptoms.
Dark brown, necrotic, wartlike lesions occur on diseased pods.
Management.
Not reported.
Powdery Mildew
Cause.
Oidium arachidis. Development of powdery mildew is optimum at a temperature of 25°C.
Distribution.
Israel, Mauritius, Portugal, and Tanganyika.

Page 421
Symptoms.
Symptoms first occur in midsummer. Portions of the diseased upper leaflet surfaces are covered with a white, powdery growth consisting of the mycelium, conidia,
and conidiophores of the fungus. As the disease progresses, upper leaflet surfaces become covered with large spots that have brown, necrotic centers.
Management.
Pythium Damping Off
Cause.
Pythium aphanidermatum, P. debaryanum, P. irregulare, P. myriotylum, and P. ultimum. Pythium spp. survive as oospores and mycelia in soil and infested
residue. Oospores germinate and produce mycelia that may either infect plants directly by producing a germ tube or indirectly by forming sporangia. Zoospores form
within sporangia, are released, and "swim" through moist soil to a host root, where they encyst. The encysted zoospores germinate and produce hyphae that infect host
plants. Dissemination is by any means that moves soil, such as water and cultivation equipment.
In Oklahoma, greater populations of Pythium spp. were found in field soil containing peanut roots and pods than in soil without roots and pods.
Peanut diseases caused by Pythium spp. are more severe under high soil moisture and temperature conditions.
Distribution.
Pythium damping off has been reported from several countries and likely occurs wherever peanut is grown.
Symptoms.
Initially, diseased plants wilt. Watersoaked, necrotic tissue can be observed on hypocotyls and lateral branches near the soil line. Elongate, sunken, tan lesions may
partially or completely encircle stems and extend upward for 2 to 4 cm above the soil line. Diseased seedlings frequently topple over at the soil line.
Management
1. Reduce irrigation water and allow topsoil to dry.
3. Treat soil with a combined fungicide/nematicide.
4. Gypsum has been applied to soil with varying success. Deep plow to bury infested organic matter along with a gypsum application. The disparity in control may be
due to differences in soils, with some soils retaining more calcium under irrigation. Another factor may be the inoculum potential of different soils.
Pythiurn Pod Rot
Cause.
Pythium myriotylum is considered the major podrotting organism in the United States, but other Pythium spp. are also likely involved, often in combination with
Rhizoctonia solani and Fusarium spp. Pythium spp. sur

Page 422
vive as oospores and mycelia in soil and residue. Oospores germinate and produce mycelia that may infect plants directly by forming a germ tube or indirectly by
forming sporangia. Zoospores form within sporangia, are released, and ''swim" through soil water to a plant host, where they encyst. The encysted zoospores
germinate and produce hyphae that infect plants. Dissemination is by any means that moves soil, such as water and cultivation equipment.
The mite Caloglyphus rodionovi is associated with pod rot by enhancing the spread of the pathogen to adjacent healthy pods, and by introducing fungal propagules
to the pod surface or the pod interior. However, it is thought the primary role of mites is as a disseminating agent, not a wounding agent. Colonization of pods may be
regulated by pod development. Most commonly, Pythium populations peak several weeks after pegging, then rapidly decline by harvest time.
Distribution.
Most peanutgrowing areas.
Symptoms.
Initially, diseased pods have a light brown discoloration and extensive watersoaking of the tissue. Eventually, entire pods appear watery and have a brown to black
necrosis. Immature pods are usually completely destroyed. Seeds in mature fruit show various degrees of watersoaking and brown to black necrosis. Pegs may
become infected as they contact wet soil, causing peg tips to become rotted and blackened.
Management
1. Reduce irrigation water and allow topsoil to dry.
3. Treat soil with a combined fungicide/nematicide.
4. Gypsum has been applied to soil with varying success. Deep plow to bury infested organic matter along with the gypsum application. The disparity in control may
be due to differences in soils, with some soils retaining more calcium under irrigation. Another factor may be the inoculum potential of different soils.
Pythiurn Wilt
Cause.
Pythium myriotylum survives as oospores and mycelia in soil and residue. Oospores germinate and produce mycelia that may infect plants either directly by
producing a germ tube or indirectly by forming sporangia. Zoospores form within sporangia, are released, and "swim" through moist soil to a host root, where they
encyst. The encysted zoospores germinate and produce hyphae that infect plants. Dissemination is by any means that moves soil, such as water and cultivation
equipment.
Distribution.
Widespread.
Symptoms.
Initially, one or more branches may wilt, but the entire diseased

Page 423
plant seldom wilts. Soon, foliage on wilted branches becomes chlorotic and scorched, beginning at the leaflet margins and extending inward until entire leaflets and,
eventually, entire leaves are dry and crinkled. Petioles often remain green even if petiolules become dry. Vascular systems in the taproothypocotyl region show a
brown to black discoloration.
Management.
Not specifically reported but likely the same as for Pythium damping off.
Rhizoctonia Diseases
A portion of the disease syndrome is also called Rhizoctonia limb rot.
Cause.
Rhizoctonia solani, teleomorph Thanatephorus cucumeris, is seedborne and survives as sclerotia in soil or infested residue and saprophytically as mycelia in infested
residue. In a greenhouse study, peanut pods left in soil for 22 weeks after harvest contained R. solani AG4, which infected and killed soybean and peanut seedlings.
However, recovery of R. solani AG4 was greater from infested shells placed on the soil surface than from infested shells buried in the soil. Most R. solani isolates
that infect peanut are in anastomosis group AG4 and rarely in AG2.
Dissemination is by any means that moves soil containing sclerotia and mycelia. Basidiospores are disseminated by water and wind to host plants and infect either
through wounds or directly through the epidermis. Disease development is favored by temperatures of 19° to 36°C and moderate soil moisture. Disease incidence is
increased by tractor traffic.
Distribution.
Symptoms.
Seedlings may damp off before emergence. Lesions on the hypocotyls of emerged plants are sunken, elongated (23 cm), dark brown areas. A rapid browning of
diseased hypocotyls sometimes occurs. Similar lesions develop on taproots and lateral roots. Infection of hypocotyls also results in an increase in total and individual
lipid components.
Pods are subject to infection during all stages of development. Pegs and small pods first become discolored brown or black at the tips, then rot, and wither. Older
pods have slight superficial russeting to browning of entire pods and a decay of their contents. Lesions on older pegs are discolored brown to black and vary from
having a slight to an extensive sunken area. Diseased seed have discolored, faded, or stained seed coats. Cultivars with pink testae have a light brown to gray
discoloration.
Older diseased plants have sunken, dark brown cankers on primary roots and browning of secondary roots. Stems have dry, sunken, dark brown lesions several
centimeters long near the soil line. Stems are eventually girdled and diseased areas are thinner than "healthy" areas. With excess moisture, branches may become
infected and appear brown and shredded. Lower diseased leaves have temporary brown speckled or

Page 424
blotchy areas that disappear as the leaves die. Diseased plants become wilted and have one to several branches that die.
Management
1. Plow under infested residue. Burial of peanut pods 20 to 25 cm deep with a moldboard plow could effectively reduce the inoculum from the root zone of the
following crop.
2. Direct soil away from the plants during cultivation.
3. Do not rotate peanut with common bean, soybean, cotton, or southern pea.
5. Apply fungicide to soil where disease potential is great.
6. Trace elements, especially copper, reduce root rot.
Rhizopus Seed and Preemergence Seedling Rot
Cause.
Rhizopus arrhizus (syn. R. oryzae) and R. stolonifer are seedborne and survive in infested residue and soil, with the highest populations in the upper 15 cm of the soil
profile. The fungi are heterothallic and may go through one of two life cycles. One cycle entails sexual reproduction and requires compatible and physiologically distinct
mycelia. When compatible mycelia fuse, zygospores are formed that are capable of survival in soil for lengthy periods of time. Each zygospore germinates and forms a
sporangium in which sporangiospores (chlamydospores) are formed.
The second life cycle involves sporangiospores that either survive for periods of time in soil or each one germinates and forms a sporangium in which more
sporangiospores are formed. Sporangiospores may be disseminated a great distance by wind. Peanut seed and seedlings are infected by mycelia from germinating
sporangiospores. Physiologic strains of R. arrhizus and R. stolonifer vary considerably in their responses to different temperatures.
Distribution.
Symptoms.
When infected seeds are sown, decay of seeds is very rapid. In 36 to 96 hours after sowing, the cotyledons are invaded first, followed by destruction of primary
roots. A partial destruction of plumules and cotyledonary laterals results in stunted seedlings. Seed and emerged seedlings are reduced to a discolored dark brown to
black, rotted, pulpy mass. Frequently, a mat of mycelium, with adhering soil particles, envelops each seed. In about 5 days, seeds are indistinguishable from the
surrounding soil.
Management
2. Plow deeply to bury infested organic litter 7.5 to 15.0 cm in the soil.
3. Control soilborne insects to prevent pod damage.

Page 425
4. Harvest before pods and fruits become overly mature.
5. Cure peanuts as rapidly as possible after harvest and store in cool, dry storage facilities.
Rust
Rust is also known as peanut leaf rust.
Cause.
Puccinia arachidis is a rust fungus in which only the uredinial and telia stages are known. However, some researchers do not consider the fungus to be a Puccinia
sp. Hennen and Buritica (1993) propose the name Peridipes arachidis for the uredinia (conidiomata) of the peanut rust fungus. The telial stage is uncommon in most
areas but is common on wild Arachis spp. in Brazil. Urediniospores do not survive long in infested residue; therefore, overseasoning occurs on plants in continuous
cultivation and on volunteer plants. In North America, P. arachidis overwinters in the West Indies and tropics and is disseminated as windborne urediniospores to the
southern United States. Other longrange dissemination includes movement of residue, pods, and seeds that are externally contaminated with urediniospores. Short
range dissemination is by wind, splashing water, and insects.
Plants of all ages are susceptible. Infection occurs at temperatures of 20° to 30°C and in the presence of moisture. Dew provides sufficient moisture to promote
infection.
Distribution.
Most peanutgrowing areas of the world.
Symptoms.
Pustules develop on all aerial plant parts except flowers. Uredinia are most common on diseased lower leaflet surfaces. Initially, whitish flecks appear on diseased
lower leaflet surfaces 8 to 10 days after inoculation. A few hours later, yellowgreen flecks appear on upper leaflet surfaces opposite the lower leaflet pustules.
Uredinial pustules become visible in the whitish flecks on the lower leaf surface. At first, the pustules are yellow, then change to orange, then to tan, then to brown, and
enlarge and rupture within 2 days. Uredinia are 0.51.4 mm in diameter, circular, and often surrounded by a light green to tan margin. Infection sites may coalesce and
cause irregularshaped patches of uredinia. Eventually, tissue surrounding infection sites becomes necrotic and dries up in irregular patches. Diseased leaflets may curl
but tend to remain attached to plants. On highly susceptible genotypes, the original pustules may be surrounded by secondary pustules.
Management
3. Do not grow successive peanut crops in fields where viable urediniospores are present.

Page 426
4. Eradicate volunteer peanut plants in a field.
5. Sow at times that avoid infection from outside sources and environmental conditions conducive to rust buildup.
Scab
Cause.
Sphaceloma arachidis persists as mycelia in infested residue. Conidia are produced in acervuli and presumably function as primary inoculum. Scab may occur under
both dry and humid conditions.
Distribution.
Argentina and Brazil.
Symptoms.
Small, round to irregularshaped spots (approximately 1 mm in diameter) with sunken centers and raised margins occur beside the principal vein on both diseased leaf
surfaces. On the upper leaf surface, spots are tan with narrow brown margins. During humid conditions, lesions are covered with a gray, velvety growth consisting of
mycelium, conidia, and conidiophores. After conidia fall away, acervuli become evident as small brown to black objects within lesions. Spots on lower leaf surfaces
are pinkbrown to red and may have brown margins.
Petioles and branches have numerous spots that are a maximum of 3 mm long. Lesions coalesce and cover extensive areas and appear as cankerous growths that
cause distortion of branches and petioles, making them appear wavy or sinuous. Diseased plants have a general "burned" appearance and look as if they are covered
with "scabs."
Management.
Sclerotinia Blight
Cause.
Sclerotinia minor and rarely S. sclerotiorum. When S. sclerotiorum is found, it is in conjunction with S. minor. Sclerotinia minor overwinters as sclerotia in soil
and is occasionally seedborne. Dissemination from field to field and from one geographic area to another is by several means, including infested residue, hay, irrigation,
water, manure, sclerotia on surfaces of seed, windborne ascospores, and soil adhering to farm equipment, animals, or humans. Sclerotia in infested debris fed to
animals remain viable after passing through their digestive tracts. Approximately 2% of the sclerotia of S. sclerotiorum remain viable after passing through the digestive
tract of sheep.
During periods of cool temperatures and high relative humidity, sclerotia at or near the soil surface initiate infection directly. Sclerotia germinate myceliogenically and
form fastgrowing white mycelia that infect plant tissue near or in contact with soil. The reported optimum temperature for germination varies. Some researchers report
the optimum temperatures to be from 20° to 25°C. Others report a temperature range of 6° to 30°C for germination, with 18°C being the optimum temperature.
Relative humid

Page 427
ity for germination is from 95% to 100% for more than 12 hours; however, some report relative humidity need only be greater than 94%.
Germination of sclerotia is favored by a soil pH 6.0 to 6.5 and the presence of infested residue in the canopy. At 6.0 to 6.5 pH in the presence of remoistened leaves,
mycelia from sclerotia may be capable of direct infection without an exogenous food base.
Apothecia of S. minor are rarely observed during the growing season but are common on the soil surface in the spring and autumn. Sclerotia germinate and form
mushroomlike structures called apothecia. Asci are formed in a layer on the apothecial surface. The ascospores liberated from the asci are disseminated by wind to
nearby host plants and germinate under moist conditions. All parts of the plant, including branches, leaves, roots, pegs, and pods, can be infected, but infection of
aerial parts is uncommon. Senescing or mechanically injured leaflets are easily colonized by S. minor, but they are not prerequisites for infection. Disease development
is low when plants are small and are without a dense canopy or complete ground cover.
Distribution.
Sclerotinia blight occurs in most peanutgrowing countries of the world.
Symptoms.
The initial symptom is a rapid wilting of branch tips. Cankers approximately 2.5 cm wide may girdle stems at the soil line. Diseased areas become sunken and dry and
have a white, cottonlike, mycelial growth on them. Large, black sclerotia develop in mycelium on stem surfaces or inside stems. Diseased branch and peg tissue
becomes shredded, which resuits in pod losses.
Management
2. Apply foliar fungicides to give partial control.
3. Pruning peanut canopies to alter microclimate or enhance fungicide penetration may reduce disease and increase yield when S. minor damage is yieldlimiting.
Sclerotinia Leaf Spot
Cause.
Sclerotinia homoeocarpa.
Distribution.
The United States (Florida) on perennial peanut, Arachis glabrata.
Symptoms.
Circular, semicircular, or elliptical (1.31.9 cm) leaf spots are tan in the center and surrounded by a brown to purple ring. Leaf spots were reported to be associated
with weak and dying plants in a thin stand.
Management.
Not necessary because the disease is of little economic consequence when forage is harvested at recommended intervals.

Page 428
Southern Blight or Stem Rot
Southern blight is also called foot rot, root rot, Sclerotium blight, Sclerotium rot, Sclerotium wilt, and white mold.
Cause.
Sclerotium rolfsii survives as sclerotia in soil and saprophytically as mycelia in infested residue. Sclerotium rolfsii is most active near the soil surface because of an
adequate food base and absence of competitive or antagonistic fungi. Antagonism may be increased by high soil moisture.
Infection of host plants occurs either by sclerotia germinating under low relative humidity and producing infection hyphae or by mycelia growing through soil from a
precolonized substrate. Sclerotia may not have sufficient reserve energy to establish mycelia in a living host. A precolonized substrate is utilized as an energy source or
food base from which mycelia can grow to and infect a healthy host plant. Growth of mycelia from these food bases may be an important mode of infection.
Eventually, sclerotia form in mycelia on diseased tissue. Temperatures of2°C to 10°C kill mycelia and germinating sclerotia, but do not kill dormant mature sclerotia.
Disease is favored by warm and moist environmental conditions, which may be accentuated under a dense foliar canopy.
Distribution.
Symptoms.
Symptoms caused by infection of stems at the soil line are most common. Stem bases are covered with elongated, eroded lesions that are tan to reddish in color.
During dry weather, brown lenticular lesions may occur on stems just below the soil surface. Diseased stems are overgrown with white mycelium near the soil line,
particularly if a leaf canopy is present to maintain high humidity. Diseased areas of stems become shredded and numerous sclerotia are produced in the mycelium
growing over the stems. Excessive moisture may prevent mycelium from growing on the outside of diseased stems. Sclerotia are spherical, velvetyappearing, soft, and
initially white but eventually become light brown to brown. Mycelium also grows over the soil surface and organic debris.
Initially, branches suddenly wilt and leaves become chlorotic, then brown as they dry up. Branches adjacent to the first diseased branches then wilt and die. Eventually,
all branches on a plant will wilt, but dead plants tend to remain upright.
Pegs have light to dark brown lesions (0.5 to 2.0 cm long) that eventually cause tissue shredding and pod loss. Lesions on young pods of 'Spanish' peanuts are
orangeyellow to light tan. Older pods have light brown to black discolored zonate lesions. Severely decayed kernels are shriveled and lightly covered with mycelium.
Management
2. Bury surface residue by deep plowing.

Page 429
3. Sow seed in a flat or slightly raised bed area.
4. Move soil away from the row during cultivation to prevent accumulation of debris around the bases of plants.
5. Manage early leaf spot and late leaf spot to prevent leaf drop and subsequent accumulation of dead leaves at the bases of plants.
6. Apply fungicides to soil before planting.
7. Rotate peanut with cotton, small grains, or maize.
8. Apply transparent polyethylene sheets to soil in the offseason to raise the soil temperature, where practical.
Verticillium Wilt
Verticillium wilt is also called Verticillium pod rot.
Cause.
Verticillium dahliae and V. alboatrum. Verticillium dahliae is considered the primary causal agent and survives as microsclerotia on infested residue and possibly
on weeds. When residue decomposes, microsclerotia are released into the soil or remain imbedded in bits of residue in the upper soil profile for several years. Root
exudates stimulate microsclerotia to germinate and produce mycelia that infect the root system of host plants. Mycelium then grows into the xylem tissue of the infected
plant and blocks water from moving up the plant. Sclerotia are disseminated by being moved in soil and residue by machinery, water, and wind and possibly by seed.
Distribution.
Verticillium wilt occurs in all peanutgrowing countries, but the disease is not considered a serious problem.
Symptoms.
Symptoms occur at flowering time as a dull green or chlorotic discoloration of the lower leaflets. Eventually, many leaflets over an entire diseased plant become
withered, brown, and defoliate. If adequate moisture is present, diseased plants remain alive but are stunted, have sparse foliage, and become relatively unproductive.
In the advanced stages of the disease, the vascular system of roots, stems, and petioles has a brown to black discoloration. Diseased pods are black, rotted, and
sprinkled with white powdery patches that consist primarily of conidia.
Management
1. Grow resistant cultivars in areas where they are adapted. Bunchtype peanuts are more resistant than 'Valencia' and 'Spanish' types.
2. Rotate infested soil to grass, grain, sorghum, or alfalfa.
3. Practice clean fallow with occasional plowing during dry periods to deplete the amount of soilborne inoculum.
4. Practice field sanitation, such as burning or removing infested residue, to reduce inoculum.
5. Irrigate infested fields frequently to reduce stress.
6. Practice good weed control.

Page 430
Web Blotch
Web blotch is also called Ascochyta, leaf spot, muddy spot, net blotch, Phoma leaf spot, and spatselviek.
Cause.
Phoma arachidicola, teleomorph Didymosphaeria arachidicola, overwinters as pycnidia, pseudothecia, chlamydospores, and clusters of chlamydospores called
microsclerotia. Ascospores and pycnidiospores serve as primary inoculum. Under experimental conditions, chlamydospores have also been reported to serve as
primary inoculum. Disease is most severe during cool temperatures and high relative humidity.
Distribution.
Africa, Asia, Australia, North America, and South America.
Symptoms.
Several different symptoms may be present. The most distinct symptom is a webbing or netting pattern caused by brown fungal strands that radiate beneath the waxy
cuticle of leaf surfaces from different points of infection. Webbing may occur without blotch symptoms, but this symptom occurs more commonly when blotches are
present.
Circular, dark brown blotches have a lightercolored, irregular margin. Under moist conditions, blotches are surrounded by a grayish margin. Varying degrees of
webbing may surround blotches.
Another symptom develops during conditions favorable for rapid disease development. Tan spots are surrounded by gray margins made up of fungal strands growing
from the dark centers of spots.
Management
1. Apply a foliar fungicide during the growing season.
2. Plow under crop residue.
Yellow Mold
This disease may be similar to "Aflaroot" as described by Chohan and Gupta (1968).
Cause.
Aspergillus flavus and A. parasiticus survive as conidia and hyphal fragments in soil or infested residue. The fungi are seedborne and also are disseminated by wind,
water, and any means that moves soil. The fungi grow on most plant material below or above the soil surface and in most soil types.
Infection by Aspergillus flavus and A. parasiticus is optimum over a wide range of soil moistures at a temperature of 32°C. Aspergillus flavus and A. parasiticus
infect through wounds or other injuries made during harvest when the moisture content of peanuts is 12% to 35%. The fungi produce the toxin called aflatoxin. When
peanut follows maize in a rotation, fungal populations increase in the lower half of the plow layer.

Page 431
Distribution.
Symptoms.
Cotyledons of germinating seed are invaded first, then the emerging radicle and hypocotyl are infected and rapidly decay. Seed and seedlings that have not emerged
are shriveled and dried and become a brown to black "mass" 4 to 8 days after sowing. Diseased plant parts may be covered with a yellowgreen growth consisting of
fungal conidia, conidiophores, and mycelium.
Management
1. Use an inverter during the digging operation. Inverting allows peanuts to dry faster and minimizes fruit contact with the soil.
2. Dry peanuts to a 12% or less moisture content after harvest. Do not allow a container full of peanuts to stand without proper drying.
3. Minimize injury to pods during harvest.
4. Store peanuts in cool, dry facilities.
Zonate Leaf Spot
Cause.
Cristulariella moricola (syn. C. pyramidalis). The sclerotial stage is Sclerotium cinnamomi. Cristulariella moricola has been associated with leaf spots on
several deciduous trees.
Distribution.
The United States (Georgia). Zonate leaf spot is considered to be of minor importance.
Symptoms.
Symptoms occur late in the season. Necrotic spots (113 mm in diameter) occur on diseased leaves. Small spots have a light brown center surrounded by a darker
brown ring of necrotic tissue. Large spots have a zonate appearance on both diseased leaf surfaces.
Management.
Not reported.
Aphasmatylenchus straturatus
Cause.
Aphasmatylenchus straturatus is a migratory endoparasite and ectoparasite. The nematode survives the dry season adjacent to roots of the karite tree,
Butyrospermum parkii.
Distribution.
Burkina Faso.
Symptoms.
Diseased plants are generally stunted and have chlorotic foliage and reduced root development. Rhizobium nodulation and yields are reduced.
Management.
Not reported.

Page 432
Dagger
Cause.
Xiphinema americanum and X. diversicaudatum.
Distribution.
Widespread, but populations in peanut fields tend to be low.
Symptoms.
Galls and curly tips are produced on diseased roots.
Management.
Not necessary.
Pod Lesion or Kalahasti Malady
Cause.
Tylenchorhynchus brevilineatus (syn. T. brevicadatus).
Distribution.
India.
Symptoms.
Small brownyellow lesions occur on diseased pegs, pod stalks, and young developing pods. The margins of the lesions are slightly elevated. Pod stalks are greatly
reduced in length, and in advanced stages of disease, the pod surface is completely discolored. Diseased plants are stunted and root growth is reduced at maturity.
Pods are reduced in size, but kernels from such pods are apparently healthy.
Management.
Application of a nematicide in research plots has been effective.
Ring
Cause.
Criconemella ornata is thought to be ectoparasitic.
Distribution.
The United States.
Symptoms.
Diseased plants are chlorotic. Roots, pods, and pegs are discolored and have brown necrotic lesions that are superficial if small but extend deep into tissue if they are
large. Young roots and root primordia may be killed. Pod yields are reduced.
Management
1. Rotate peanut with nonhost crops.
Root Knot
Cause.
The peanut root knot nematode, Meloidogyne arenaria, and the northern root knot nematode, M. hapla. The Javanese root knot nematode, M. javanica, also has
been reported to attack peanut. Meloidogyne arenaria and M. javanica do not survive if the temperature averages below 3°C during the coldest month.
Meloidogyne hapla is limited by temperatures at or greater than 24° to 27°C.
Larvae are produced from eggs in infested soil and move through the

Page 433
soil to penetrate root tips. Larvae migrate through the root to vascular tissues, become sedentary, and commence feeding. Excretions of larvae stimulate cell
proliferation, which results in development of syncythia from which food is derived. Females lay eggs that are pushed out of roots into the soil.
Distribution.
The United States.
Symptoms.
Mild symptoms caused by M. arenaria are a slight yellowing of foliage and the imperceptible stunting of diseased plants. Severe disease symptoms consist of stunted
plants that are chlorotic, wilt, and die during dry weather. Along their length, roots and pegs have differentsized galls that may be several times the diameter of a
normal root or peg. Pods develop galls that appear as knobs, protuberances, or small warts. Galls on roots, pegs, and pods sometimes begin to deteriorate by
maturity and the resulting necrotic tissue is colonized by a number of fungi.
The northern root knot nematode causes similar aboveground symptoms, but galls are usually smaller than those caused by M. arenaria. Diseased roots tend to
branch near the point of invasion, resulting in a dense, bushy root system. Total crop loss may occur when disease caused by both nematodes is severe.
Management
1. Rotate peanut with a nonlegume crop for 2 to 3 years.
2. Apply nematicides either banded at time of planting or as a fumigant, using plowsole method during deep plowing of soil prior to sowing.
Root Lesion
The root lesion is also called the meadow nematode.
Cause.
Pratylenchus brachyurus, P. coffeae, and P. scribneri. Both adults and larvae infect roots, pegs, and pods, but higher nematode populations are present on the
pegs and pods. The nematodes directly penetrate plant tissues and feed on the parenchyma tissue.
Nematode numbers may increase on roots of other plants, especially rye, during winter months.
Distribution.
The United States.
Symptoms.
Symptoms appear on plants in circular areas within fields. Diseased plants are stunted and chlorotic because of small, discolored roots. Pegs have brown lesions, and
pods initially have small, tan spots with dark centers that eventually become discolored brown to black, angularshaped lesions. Lesions may become so numerous
that the entire pod is discolored. Damage caused by nematodes allows secondary fungi to enter and cause further discoloration and decomposition of roots, pods, and
pegs.

Page 434
Management
1. Apply nematicides that are either banded at time of sowing or as a fumigant, using plowsole method during deep plowing of soil prior to planting.
2. Fallowing reduces the nematode population.
Seed and Pod
Cause.
Ditylenchus africanus is a migratory endoparasite that completes its life cycle from egg to adult in 8 days at 30°C. The nematode enters the pods soon after pegging.
Nematodes have been observed in the exocarp, endocarp, testa, and embryo and on cotyledons. Eggs have been observed in all invaded tissues.
Distribution.
South Africa (Transvaal).
Symptoms.
Diseased hulls have a black discoloration that first appears along longitudinal veins. Kernels are shrunken, testae are brown to black, and embryos are brown. Early
germination may occur and seed weight may be greatly reduced.
Management.
Not reported.
Spiral
Cause.
Scutellonema cavenessi is active during the rainy season. The nematode goes into anhydrobiosis when soil moisture drops to 0.2%.
Distribution.
Mali, Nigeria, and Senegal.
Symptoms.
Foliage of diseased plants is chlorotic. Roots have reduced growth and Rhizobium nodulation.
Management
2. Leave fields fallow between crops.
Sting
Cause.
Belonolaimus longicaudatus and B. gracilis are nematodes with a wide host range. Nematodes feed at root tips and along sides of succulent roots and other
belowground parts without becoming attached to the roots. The nematodes are restricted to soils with 84% to 94% sand and occur in the top 30 cm of the soil profile.
The nematodes are most active at temperatures of 20° to 34°C.
Distribution.
The United States.
Symptoms.
Diseased plants are stunted and chlorotic and have stubby, sparse roots. Roots and pods may have small, dark, necrotic spots.

Page 435
Management
1. Rotate peanut with a nonlegume crop for 2 to 3 years.
2. Apply nematicides that are either banded at the time of sowing or a fumigant, using the plowsole method during deep plowing of soil prior to sowing.
Testa
Cause.
Aphelenchoides arachidis is a facultative endoparasite found primarily in the parenchymatous tissue and around the tracheids of the seed, testae, shells, roots, and
hypocotyls. Aphelenchoides arachidis is disseminated in infected seed and can survive desiccation in stored pods for up to 12 months. Volunteer plants may also
serve as a source of inoculum. Seed is predisposed to invasion by soilborne fungi.
Distribution.
Nigeria.
Symptoms.
Seed coats are discolored and translucent and have dark vascular strands. Seed coats may become unevenly thickened.
Management
1. Immerse seed in water at a temperature of 60°C.
2. Sundry pods after harvest.
Peanut Yellows
Peanut yellows is sometimes referred as peanut yellows diseases.
Cause.
Aster yellows phytoplasmalike organism is transmitted by the leafhopper Macrosteles quadrilineatus and possibly other leafhoppers.
Distribution.
Asia.
Symptoms.
Diseased plants are chlorotic.
Management.
Not reported.
Witches' Broom
Cause.
A phytoplasmalike organism.
Distribution.
China, India, Indonesia, Japan, Taiwan, and Thailand.
Symptoms.
Diseased plants are bushy due to the excessive proliferation of axillary shoots. Leaflets are chlorotic and smaller than normal. Pegs tend to grow upward. Yields may
be greatly reduced.
Management.
Not reported.

Page 436
Disease Caused by Rickettsia
Rugose Leaf Curl
Cause.
A rickettsialike organism that is transmitted by leafhoppers.
Distribution.
Australia.
Symptoms.
Leaflets are distorted and puckered.
Management.
Not reported.
Bean Yellow Mosaic
Cause.
Bean yellow mosaic virus (BYMV) is in the potyvirus group. BYMV is transmitted mechanically and by the cowpea aphid, Aphis craccivora, in a nonpersistent
manner. Arrowleaf clover, Trifolium vesiculosum, is a reservoir for BYMV.
Distribution.
The United States (Georgia and Texas).
Symptoms.
Initial symptoms are chlorotic rings and spots on diseased leaves. After 2 to 3 weeks, the symptoms disappear.
Management.
Not reported.
Cowpea Chlorotic Mottle
Cause.
Cowpea chlorotic mottle virus (CCMV) is in the bromovirus group.
Distribution.
Symptoms.
Infected plants are symptomless. However, CCMV is reported to have significant disease potential when it is in mixed infections with other viruses.
Management.
Not reported.
Cowpea Mild Mottle
Cause.
Cowpea mild mottle virus (CPMMV) is in the carlavirus group. CPMMV is transmitted by sap and by the whitefly, Bemisia tabaci.
Distribution.
India. Cowpea mild mottle is not considered to be a serious disease.
Symptoms.
The youngest leaves show a vein clearing followed by a downward rolling. Later, diseased leaves and petioles become necrotic and defoliation occurs. Diseased
plants are severely stunted and rarely produce pods.

Page 437
Management.
Avoid growing peanut near soybean or cowpea fields.
Cucumber Mosaic
Cause.
A strain of cucumber mosaic virus (CMVCA). CMV is in the cucumovirus group and is transmitted by seed and by the aphid Macrosiphum euphorbiae. CMV
infects 31 species of plants in six families.
Distribution.
China.
Symptoms.
Chlorotic spots occur on young emerging leaves. Other symptoms include young expanded leaves that are small, rolled, and generally chlorotic. A mosaic or mottling
occurs on some leaves. Diseased plants are stunted to onehalf to twothirds the size of a healthy plant.
Management.
Not reported.
Eyespot
Eyespot may be similar to or the same disease as groundnut eyespot, although the symptoms reported in the literature appear to be different.
Cause.
Peanut eyespot virus (PEV) is in the potyvirus group. PEV is transmitted by sap and by the cowpea aphid, Aphis craccivora, in a nonpersistent manner.
Distribution.
Ivory Coast.
Symptoms.
Dark green spots on diseased leaves are surrounded by chlorotic spots, which give an eyespot symptom consisting of concentric colored rings.
Management.
Not reported.
Groundnut Crinkle
Cause.
Groundnut crinkle virus is transmitted mechanically and possibly by whiteflies.
Distribution.
Ivory Coast.
Symptoms.
Plants are slightly stunted and have a slight reduction in leaf size. Leaves are faintly mottled and display a crinkling of the lamia.
Management.
Not reported.
Groundnut Eyespot
Groundnut eyespot may be similar to or the same disease as eyespot, although the symptoms reported in the literature appear to be different.
Cause.
Groundnut eyespot virus.

Page 438
Distribution.
West Africa. Groundnut eyespot is not considered a serious disease.
Symptoms.
Yellow eyespots occur on diseased leaves. Banding along the main veins may occur.
Management.
Not reported.
Groundnut Rosette
Groundnut rosette is also called rosette.
Cause.
Groundnut rosette virus (GRV) is an umbravirus and is transmitted mechanically. GRV depends on the groundnut rosette assistor virus (GRAV), a luteovirus, for
transmission by the black cowpea aphid, Aphis craccivora, in a persistent or circulative manner. However, GRAV causes no symptoms in peanut on its own. Neither
virus is seedborne. Variants of the satellite RNA, which differ in different parts of Africa, are responsible for the different symptoms.
Two forms of GRV exist: chlorotic rosette (GRVC) and green rosette (GRVG). Aphids acquire GRVC within 4 hours and GRVG within 8 hours. Median latent
periods are 26.4 and 38.4 hours for GRVC and GRVG, respectively. After a 24hour latent period, both viruses are transmitted within 10 minutes. Multiple plant
infections occur more frequently with GRVC than with GRVG. Maximum retention time for both viruses is the lifetime of aphids or about 14 days.
Peanut is the main source of inoculum. Diseased plants survive longer than healthy plants and are not normally harvested. Aphids colonize diseased plants, then rainy
fronts are responsible for the dissemination of the aphids.
Distribution.
Gambia, Java, Madagascar, Nigeria, Senegal, Sierra Leone, Tanganyika, and Uganda. Chlorotic rosette occurs throughout Africa south of the Sahara Desert. Green
rosette disease occurs in western Africa and Uganda, and mosaic rosette occurs only in eastern and central Africa. Groundnut rosette has also been reported from
Argentina, India, Indonesia, and the Philippines.
Symptoms.
There are three basic types of symptoms: chlorotic rosette, green rosette, and mosaic rosette.
Chlorotic rosette symptoms, which are caused by GRVC, initially occur on young leaflets as a faint mottling with a few green islands. Later, leaflets are pale yellow
with green veins. Diseased plants infected when they are young produce progressively smaller, chlorotic, curled, and distorted leaflets. Symptoms on older infected
plants may be restricted to a few branches or to the apical portion of the plants. Plants infected when they are young are severely stunted and have thickened stems
and a severe reduction in the number and size of pods.

Page 439
Green rosette symptoms, which are caused by GRVG, occur on young leaflets as a mild chlorotic mottling and isolated flecks. Although symptoms are masked in
older leaflets, the older leaflets are reduced in size and display outward rolling but are not distorted. Plants infected while young are severely stunted and are a darker
green than healthy plants.
Mosaic rosette symptoms occur on young leaflets as conspicuous mosaic symptoms that resemble those of chlorotic rosette except stunting is less severe.
Management
1. Destroy volunteer and unharvested diseased plants.
2. Sow early in the season at a high seeding rate.
3. Apply insecticides.
4. Sources of resistance are available in peanut germplasm.
Groundnut Streak
Cause.
Groundnut streak virus (GSV).
Distribution.
Ivory Coast.
Symptoms.
Necrotic streaks along leaflet veins in seedlings disappear as diseased plants mature.
Management.
Not reported.
Indian Peanut Clump
Indian peanut clump is also called peanut clump.
Cause.
Indian peanut clump virus (IPCV) is in the furovirus group. Two different isolates have been identified: the West African and the Indian. However, the Indian virus is
serologically unrelated to the West African virus and is considered by some researchers to cause a separate disease. The soil fungus Polymyxa graminis transmits the
West African IPCV and is thought to transmit the Indian isolate also. Both isolates are seedtransmitted.
Polymyxa graminis survives in field soil as cystosori. Cysts give rise to zoospores, which ''swim" through free soil water until they contact a host root and encyst.
Encysted zoospores produce a structure called a stachel through which zoosporic cytoplasm enters the host cell and becomes a plasmodium. Only primary root tissue
of young roots is infected; optimum infection occurs at a temperature of about 25°C. The host cell then becomes infected with IPCV if P. graminis is viruliferous.
After a period of time, the plasmodium develops into a zoosporangium, which releases additional zoospores that repeat the infection cycle. However, some plasmodia
develop into cysts and often nearly every cell in the small feeder roots will contain a cyst. As root cells senesce, cysts are eventually released into the soil, where they
can remain viable for years without loss of virulence.

Page 440
IPCV is considered by some researchers to cause a different disease than peanut clump virus.
Distribution.
India and West Africa.
Symptoms.
Symptoms are areas of diseased plants within fields that enlarge in succeeding years. Diseased plants are stunted and quadrifoliates are small initially and have mosaic
mottling and chlorotic rings but subsequently become dark green and have faint mottling. Plants eventually become bushy and have small, dark green leaves. Several
flowers are produced on erect petioles. The number and size of pods is reduced, resulting in smallersized seeds. Root systems are small and diseased roots darken
with an epidermal layer that easily peels off. However, isolates from different locations in India caused different symptoms on five different host range plants.
Management
2. Grow resistant cultivars in India.
Marginal Necrosis
Cause.
Possibly a virus. The disease agent is seedtransmitted.
Distribution.
Papua New Guinea.
Symptoms.
Diseased leaflets have marginal necrosis and crinkling.
Management.
Not reported.
Peanut Bud Necrosis
Peanut bud necrosis is also called peanut ringspot, spotted wilt, tomato spotted wilt, and tomato ringspot.
Cause.
Peanut bud necrosis is caused by both the peanut bud necrosis virus (PBNV) and the tomato spotted wilt virus (TSWV). PBNV and TSWV are in the tospovirus
group. In Louisiana, virus inoculum originates from noncultivated areas. TSWV overwinters in several species of perennial plants in areas that have cold winter
temperatures and in annual plants where winters are not cold enough to kill plants.
The presence of TSWV has been reported in spiny amaranthus, Amaranthus spinosus; blackseed plaintain, Plantago rugelii; buttercup, Ranunculus spp., with R.
sardous being the species most often associated with natural TSWV infection; coneflower, Rudbeckia amplexicaulis; horsenettle, Solanum carolinense; dandelion,
Taraxacum officinale; spiny sowthistle, Sonchus asper; blue vervain, Verben brasiliensis; and Lactucua spp., with L. floridana as an important overwintering
host.

Page 441
TSWV is transmitted mechanically and by several species of thrips, including potato or onion thrips, Thrips tabaci; blossom or cotton thrips, Frankliniella schultzei;
western flower thrips, F. occidentalis; and tobacco thrips, F. fusca. The chili thrip, T. setosus, has been shown to transmit the virus in Japan. TSWV must first be
acquired by the larval stage; the subsequent adults are able to transmit TSWV. TSWV persists in insects as long as the insect lives, but the virus is not transmitted
through insect eggs. Disease is more severe during high temperatures and abundant moisture.
Distribution.
Australia, Brazil, India, Nigeria, South Africa, Sri Lanka, and the United States (Alabama, Florida, and Georgia).
Symptoms.
Symptoms caused by TSWV and PBNV are similar. Young diseased leaflets have chlorotic spots or a mild mottle that develops into necrotic and chlorotic rings and
streaks. The bud necrosis symptom occurs when temperatures are above 30°C during the day, when petioles bearing fully expanded leaflets with initial symptoms
usually become flaccid and droop. This symptom is followed by a necrosis of the terminal bud. When a young plant is infected, the necrosis spreads toward the base
of the plant, resulting in plant death.
Other symptoms include stunting and proliferation of axillary shoots. Leaflets produced on the axillary shoots are reduced in size and show puckering, mosaic mottling,
and general chlorosis. These symptoms are most common on earlyinfected plants and give them a stunted and bushy appearance. Plants infected later may also be
stunted but the symptoms may be restricted to a few branches or to the apical parts of the plants.
Similar symptoms are reported for the bud necrosis disease from India. The quadrifoliate leaf below the terminal bud displays distinct chlorotic ring spots or chlorotic
speckling and often becomes flaccid. Terminal buds become necrotic, followed by a proliferation of small shoots with mottled leaves of a much reduced size. In
advanced stages of the disease, the whole plant becomes bushy and stunted and often dies. Pods are distorted and reduced in size. Early infection results in a greater
yield loss than that caused by a later infection.
Seed from earlyinfected plants are small and shriveled, and the seed coats are discolored red, brown, or purple and are mottled. Lateinfected plants produce seed
of normal size that has mottled and cracked seed coats.
Management
1. Good sources of resistance have been identified.
2. Sow early in the growing season to avoid thrips.
3. Use highquality seed treated with a fungicide seed protectant.
4. Sow at the recommended rate and spacing to give optimum plant populations.

Page 442
Peanut Chlorotic Ringspot
Peanut chlorotic ringspot is also called chlorotic spot or peanut chlorotic spot.
Cause.
Peanut chlorotic ringspot virus is transmitted mechanically.
Distribution.
India.
Symptoms.
Yellow spots (0.51.0 mm in diameter) first occur on young terminal leaves of the side branches. Spots enlarge and become irregularshaped. Some of the spots
develop rings around them, giving the appearance of ring spots.
Management.
Not reported.
Peanut Chlorotic Streak
Cause.
Peanut chlorotic streak virus (PCISV) is in the caulimovirus group. PCISV is mechanically transmissible to several plants in the Leguminosae and Solanaceae. Disease
is favored by the very high temperatures of the semiarid tropics.
Distribution.
India.
Symptoms.
Young diseased leaflets have oval, chlorotic streaks along the veins 3 to 4 weeks after inoculation. Streaks are not distinct in older leaflets and can be seen only when
viewed against light. In field infections, diseased plants are stunted and have chlorotic streaks on the younger leaflets.
Management.
Not reported.
Peanut Green Mosaic
Cause.
Peanut green mosaic virus (PGMV) is in the potyvirus group. PGMV can be mechanically transmitted.
Distribution.
India.
Symptoms.
Initially, chlorotic spots and vein clearing occur on young quadrifoliates, but later a severe mosaic occurs. The number of pegs, pods, and leaves, the amount of leaf
area, and the dry weight of shoots, roots, and pods are reduced. Premature leaf drop also occurs.
Management.
Bavistin (50% w/w Carbendazim) applied as a foliar spray reduced severity of symptoms in research trials.
Peanut Mild Mottle
Cause.
Virus producing mild mottle (VPMM); the virus sometimes is referred to as peanut mild mottle virus. It has been proposed that this virus should

Page 443
be considered the same as the peanut stripe virus. VPMM is transmitted mechanically and in a nonpersistent manner by the black cowpea aphid, Aphis craccivora,
and the green peach aphid, Myzus persicae.
Distribution.
China.
Symptoms.
Leaves are mildly mottled. Top leaflets frequently have distinct chlorotic spots or ring spots that disappear after several days and become mottled with dark green
islands on a light green background. Most leaf symptoms disappear during high temperatures. Diseased plants are not stunted but yields are reduced.
Management.
Not reported.
Peanut Mottle
Cause.
Peanut mottle virus (PMoV) is a potyvirus that is disseminated mechanically and in a nonpersistent manner by several aphid species. Another important means of
dissemination is by seed. PMoV is found at a low rate in embryos but not in seed coats or cotyledons. Wild peanut, Arachis chacoense, serves as a reservoir for
PMoV. Different strains of PMoV exist.
Distribution.
Worldwide.
Symptoms.
Diseased plants have a leaf mottling, leaflets that curl upward, and depressed interveinal tissue. A mild mottle that occurs on the youngest leaves is best observed by
transmitted light. Symptoms tend to become obscure during hot, dry weather as diseased plants mature. Seeds are discolored, and diseased pods are smaller than
healthy pods and have gray to brown patches. Yield and nodulation is reduced.
Symptom expression varies with the strains of Rhizobium that produce nodules on the diseased plant. Plants harboring an ineffective Rhizobium strain show more
severe symptoms than plants harboring an effective strain.
Management.
Grow the most tolerant cultivar.
Peanut Stripe
Cause.
Peanut stripe virus (PStV) is in the potyvirus group. Two symptom variants of peanut stripe virus occur: stripe (PStVS) and blotch (PStVB). It has been proposed
that the virus producing mild mottle, peanut mild mottle virus, and peanut chlorotic ring mottle virus, a virus found on peanut in Thailand, should also be considered as
PStV. Two different strains of PStV have also been identified in Taiwan and identified as PStVTs and PStVTc. The two strains are indistinguishable serologically.
Peptide profile data suggest that PStV is a strain of bean common mosaic virus.

Page 444
PStV is transmitted mechanically, in a nonpersistent manner by aphids, and is seedborne in cotyledons and embryos.
Distribution.
China, India, Indonesia, Malaysia, the Philippines, Taiwan, Thailand, and the United States, primarily in research areas of Florida, Georgia, North Carolina,
Oklahoma, Texas, and Virginia.
Symptoms.
PStVS causes dark green stripes along the lateral leaf veins. Initially, there is a discontinuous dark striping or banding along lateral veins of diseased leaves that
resembles a sergeant's stripes. Later, on older leaves, the striping fades and a mild oakleaf pattern occurs and becomes the predominant symptom expression.
On diseased leaves, PStVB infrequently causes large, dark green, circular areas or blotches that are not associated with veins. This is called peanut blotch.
PStVTs induces severe mosaic and systemic necrotic symptoms. PStVTc causes stripe symptoms.
Management.
The University of Georgia has issued the following guidelines for managing PStV in Georgia:
1. Only Georgiacertified seed shall be sown in research plots with the exception of breeding and variety performance tests.
2. Seed from research plots shall not be processed through commercial cleaning and shelling operations.
3. Peanuts from experimental plots shall be processed or sold for processing only and are not to be used for seed except in breeding tests.
4. All residual peanut seed and debris shall be removed from harvesting, handling, and transporting equipment before such items are removed from areas contaminated
with PStV to clean areas.
5. All research plots containing plants inoculated with virus shall be grown under screen cages with proper precautions to prevent spread and shall be planted only on
experiment station land.
6. Breeders shall release only seed that is free from PStV.
7. Virusfree seed to be retained for future seed production shall not be sown in areas where PStVinfected peanuts have been grown previously.
8. Virusfree seed shall not be sown in proximity to leguminous crops or other hosts, and rigid weed control shall be practiced in and around virusfree plots.
9. Researchers shall not import peanuts unless they are either tested for PStV before sowing or grown in screened isolation for one growing season to allow for visual
inspection and serological assay if necessary.
10. Peanut breeding plots shall be isolated from other research plots.
11. The Uniform Peanut Performance Trial shall be sown exclusively at one university farm.

Page 445
12. Other legume cropbreeding nurseries shall be separated from peanut research plots.
13. All seed shall be removed from PStVinfected research plots and plots shall be fumigated.
14. Infected seed, except breeders' seed, shall be destroyed.
Other:
15. Some wild peanut accessions are resistant.
Peanut Stunt
Cause.
Peanut stunt virus (PSV) is in the cucumovirus group. PSV overwinters primarily in white clover, Trifolium repens; crown vetch, Coronella varia; and other
legumes. PSV is transmitted by mechanical means, grafting, dodder, and three species of aphids in a nonpersistent manner. PSV is rarely seedborne and this is not a
factor in transmission. PSV has a wide host range.
Distribution.
Europe, Japan, Morocco, Sudan, and the United States.
Symptoms.
Diseased plants are severely dwarfed, but stunting may involve the entire vine or only a portion of the plant. Foliage is malformed and only a few to half of the leaves
on a stem are normal. Apical to normal leaves are stiff and erect, and pointed leaves have light green leaflets that are less than half normal size. Discoloration is
variable; the entire leaf or plant part may be slightly chlorotic, severely chlorotic, or mildly mottled or may be chlorotic and have dark green vein banding. Affected
leaves also may be curled upward. Fruits are small and poorly shaped and have split pericarps.
Management
1. Do not grow peanut in the vicinity of legumes.
2. Rogue out infected plants.
Peanut Yellow Mottle
Cause.
Peanut yellow mottle virus.
Distribution.
Nigeria.
Symptoms.
Young diseased plants have a bright yellow mottle. Yields are reduced.
Management.
Not reported.
Unnamed Virus Disease
Cause.
Virus isolated from an Erectoides peanut hybrid growing in a greenhouse in Stillwater, Oklahoma. The virus is transmitted mechanically and by grafting.

Page 446
Distribution.
The United States (Oklahoma).
Symptoms.
A wide chlorotic ringspot is associated with a chlorotic line pattern and mottling on diseased leaves. The virus causes a mosaic in peas, a severe malformation and
reduction in the leaf area of the lupine cultivar 'Tiftwhite,' and necrotic local lesions and chlorotic ringspot of the bean cultivars 'Topcrop' and 'Chenopodium,'
respectively.
Management.
Not reported.
Selected References
Adams, D. B., and Kuhn, C. W. 1977. Seed transmission of peanut mottle virus in peanuts. Phytopathology 67:11261129.
Alderman, S. C., and Nutter, F. W., Jr. 1994. Effect of temperature and relative humidity on development of Cercosporidium personatum on peanut in Georgia.
Plant Dis. 78:690694.
Baard, S. W., and Laubscher, C. 1985. Histopathology of blackhull incited by Thielaviopsis basicola in groundnuts. Phytophylactica 17:8588.
Baard, S. W., and Van Wyk, P.S. 1985. Neocosmospora vasinfecta pathogenic to groundnuts in South Africa. Phytophylactica 17:4950.
Bailey, J. E., and Brune, P. D. 1997. Effect of crop pruning on Sclerotinia blight of peanut. Plant Dis. 81:990995.
Baird, R. E., Bell, D. K., Sumner, D. R., Mullinix, B. G., and Culbreath, A. K. 1993. Survival of Rhizoctonia solani AG4 in residual peanut shells in soil. Plant Dis.
77:973975.
Balasubramanian, R. 1979. A new type of alternariosis in Arachis hypogaea L. Curr. Sci. 48:7677.
Bays, D.C., and Demski, J. W. 1986. Bean yellow mosaic virus isolate that infects peanut (Arachis hypogaea). Plant Dis. 70:667669.
Behncken, G. M. 1970. The occurrence of peanut mottle virus in Queensland. Aust. J. Agric. Res. 21:465492.
Bell, D. K., and Sobers, E. K. 1966. A peg pod and root necrosis of peanuts caused by a species of Calonectria. Phytopathology 56:13611364.
Bell, D. K., Locke, B.J., and Thompson, S.S. 1973. The status of Cylindrocladium black rot of peanut in Georgia since its discovery in 1965. Plant Dis. Rptr. 57:90
94.
BenYephet, Y., Mhameed, S., Frank, Z. R., and Katan, J. 1991. Effect of the herbicide ethalfluralin on net blotch disease of peanut pods. Plant Dis. 75:11231126.
Bhowmik, T. P., Sharma, R. C., and Singh, A. 1985. Effect of gypsum, row spacing, and groundnut varieties on the incidence of root rot disease caused by
Macrophomina phaseolina. Int. J. Tropical Plant Dis. 3:6972.
Black, M. C., and Beute, M. K. 1984. Relationships among inoculum density, microsclerotium size, and inoculum efficiency of Cylindrocladium crotalariae causing
root rot of peanuts. Phytopathology 74:11281132.
Brenneman, T. B., and Sumner, D. R. 1989. Effects of chemigated and conventionally sprayed tebuconazole and tractor traffic on peanut diseases and pod yields.
Plant Dis. 73:843846.

Page 447
Chang, C. A., Purcefull, D. E., and Zettler, F. W. 1990. Comparison of two strains of peanut stripe virus in Taiwan. Plant Dis. 74:593596.
Chohan, H. S., and Gupta, V. K. 1968. Aflaroot, a new disease of groundnut caused by Aspergillus flavus. Indian J. Agric. Sci. 38:568570.
Clinton, P. K. S. 1962. The control of soilborne pests and diseases of groundnuts in the Sudan central rainlands. Emp. J. Exp. Agric. 30:145154.
Culbreath, A. K., Beute, M. K., and Campbell, C. L. 1991. Spatial and temporal aspects of epidemics of Cylindrocladium black rot in resistant and susceptible
peanut genotypes. Phytopathology 81:144150.
Culver, J. N., Sherwood, J. L., and Melouk, H. A. 1987. Resistance to peanut stripe virus in Arachis germplasm. Plant Dis. 71:10801082.
de Klerk, A., McLeod, A., and Faurie, R. 1997. Net blotch and necrotic warts caused by Streptomyces scabies on pods of peanut (Arachis hypogaea). Plant Dis.
81:958.
Demski, J. W., and Lovell, G. R. 1985. Peanut stripe virus and the distribution of peanut seed. Phytopathology 69:734738.
Demski, J. W., Reddy, D. V. R., and Lowell, G., Jr. 1984. Peanut stripe, a new virus disease of peanut. (Abstr.) Phytopathology 74:627.
Demski, J. W., Reddy, D. V. R., Wongkaew, S., KameyaIwaki, M., Saleh, N., and Xu Z. 1988. Naming of peanut stripe virus. Phytopathology 78:631632.
Diener, U. L. et al. 1965. Invasion of peanut pods in the soil by Aspergillus flavus. Plant Dis. Rptr. 49:931935.
Dow, R. L., Porter, D. M., and Powell, N. L. 1988. Effect of environmental factors on Sclerotinia minor and Sclerotinia blight of peanut. Phytopathology 78:672
676.
Dubern, J., and Dollett, M. 1979. Groundnut crinkle, a new virus disease observed in Ivory Coast. Phytopathol. Zeitschr. 95:279283.
Garren, K. H., and Jackson, C. R. 1973. Peanut diseases. in Peanuts: Culture and Uses, pp. 429494. Peanut Research and Education Association, Stillwater, OK.
Germani, G. 1981. Pathogenicity of the nematode Scutellonema cavenessi on peanut and soybean. Rev. Nematol. 4:203208.
Gopal, K., and Upadhyaya, H. D. 1991. Effect of bud necrosis disease on yield of groundnut under field conditions. Indian Phytopathol. 44:221223.
Griffin, G. J., Garren, K. H., and Taylor, J. D. 1981. Influence of crop rotation and minimum tillage on the population of Aspergillus flavus group in peanut field soil.
Plant Dis. 65:898900.
Grinstein, A., Katan, J., Abdul Razik, A., Zeydan, O., and Elad, Y. 1979. Control of Sclerotium rolfsii and weeds in peanuts by solar heating of soil. Plant Dis.
Rptr. 63:10561059.
Halliwell, R. S., and Philley, G. 1974. Spotted wilt of peanut in Texas. Plant Dis. Rptr. 58:2325.
Hau, F. C., Beute, M. K., and Smith, T. 1982. Effect of soil pH and volatile stimulants from remoistened peanut leaves on germination of sclerotia of Sclerotinia
minor. Plant Dis. 66:223224.
Hennen, J. F., and Buritica, P. 1993. Peridipes arachidis, a conidial anamorph of the peanut rust fungus (Uredinales). (Abstr.) 1993 Annual Meeting of the
Mycological Society of America.

Page 448
Hoover, R. J., and Kucharek, T. A. 1995. First report of a leaf spot on perennial peanut caused by Sclerotinia homoeocarpa. Plant Dis. 79:1249.
Hull, R., and Adams, A. N. 1968. Groundnut rosette and its assistor virus. Ann. Appl. Biol. 62:139145.
Jackson, C. R. 1962. Aspergillus crown rot in Georgia. Plant Dis. Reptr. 46:888892.
Johnson, G. I. 1985. Occurrence of Cylindrocladium crotalariae on peanut (Arachis hypogaea) seed. Plant Dis. 69:434436.
Jones, B. L., and De Waele, D. 1988. First report of Ditylenchus destructor in pods and seeds of peanut. Plant Dis. 72:453.
KokalisBurelle, N., Porter, D. M., RodriguezKabana, R., Smith, D. H., and Subrahmanyam, P. (eds.). 1997. Compendium of Peanut Diseases, Second Edition.
American Phytopathological Society, St. Paul, MN. 94 pp.
Kolte, S.J. 1984. Diseases of Annual Edible Oilseed Crops. Volume I: Peanut Diseases. CRC Press, Inc., Boca Raton, FL. 143 pp.
Kucharek, T. A, 1975. Reduction of Cercospora leaf spots of peanut with crop rotation. Plant Dis. Rptr. 59:822823.
Kucharek, T. A. 1991. Unusual occurrence of lesions caused by Diplodia sp. in upper stems of peanuts in Florida. (Abstr.). Phytopathology 81:812.
Kuhn, C. W., and Demski, J. W. 1987. Latent virus in peanut in Georgia identified as cowpea chlorotic mottle virus. Plant Dis. 71:101.
Lana, A. F. 1980. Properties of a virus occurring in Arachis hypogaea in Nigeria. Phytopathol. Zeitschr. 97:169178.
Lutterell, E. S. 1981. Peanut web blotch: Symptoms and field production of inoculum. (Abstr.) Phytopathology 71:892.
McDonald, D., Bos, W. W., and Gumel, M. H. 1979. Effects of infestation of peanut (groundnut) seed by the testa nematode Aphelenchoides arachidis on seed
infection by fungi and on seedling emergence. Plant Dis. Rptr. 63:464467.
Minton, N. A, and Baujard, P. 1990. Nematode parasites of peanut, pp. 285320. In Plant Parasitic Nematodes in Tropical and Subtropical Agriculture, M. Luc, R.
A. Sikora, and J. Bridge (eds.). C.A.B. International, Wallingford, England.
Misari, S. M., Abraham, J. M., Demski, J. W., Ansa, O. A., Kuhn, C. W., Casper, R., and Breyel, E. 1988. Aphid transmission of the viruses causing chlorotic
rosette and green rosette diseases of peanut in Nigeria. Plant Dis. 72:250253.
Mullen, J. M, Hagan, A. K., Nelson, P. E. 1996. A new stem canker of peanut in Alabama caused by Fusarium oxysporum: A wounddependent disease. Plant
Dis. 80: 1301.
Nelson, P. E., Toussoun, T. A., and Marasas, W. F. O. 1983. Fusarium Species: An Illustrated Manual for Identification. The Pennsylvania State Univ. Press,
University Park, PA. 193 pp.
Nolt, B. L., Rajeshwari, R., Reddy, D. V. R., Bharathan, N., and Manohar, S. K. 1988. Indian peanut clump virus isolates: Host range, symptomatology, serological
relationships, and some physical properties. Phytopathology 78:310313.
Olorunju, P. E., Kuhn, C. W., Demski, J. W., Misari, S. M., and Ansa, O. A. 1992. Inheritance or resistance in peanut to mixed infections of groundnut rosette virus
(GRV) and groundnut rosette assistor virus and a single infection of GRV. Plant Dis. 76:95100.
Pataky J. K., and Beute, M. K. 1983. Effects of inoculum burial, temperature, and soil moisture on survival of Cylindrocladium crotalariae microsclerotia in North
Carolina. Plant Dis. 67:13791382.

Page 449
Phipps, P.M., and Beute, M. K. 1977. Influence of soil temperature and moisture on severity of Cylindrocladium black rot in peanut. Phytopathology 67:11041107.
Porter, D. M. 1970. Peanut wilt caused by Pythium myriotylum. Phytopathology 60:393394.
Porter, D. M., and Adamsen, F. J. 1993. Effect of sodic water and irrigation on sodium levels and the development of early leaf spot in peanuts. Plant Dis. 77:480
483.
Porter, D. M., Garren, K. H., Mozingo, R. W., and Van Schaik, P. H. 1971. Susceptibility of peanuts to Leptosphaerulina crassiasca under field conditions. Plant
Dis. Rptr. 55:530532.
Porter, D. M., Smith, D. H., and RodriguezKabana, R. (eds.). 1984. Compendium of Peanut Diseases. American Phytopathological Society, St. Paul, MN. 73 pp.
Porter, D. M., Wright, F. S., Taber, R. A., and Smith, D. H. 1991. Colonization of peanut seed by Cylindrocladium crotalariae. Phytopathology 81:896900.
Purss, G. S. 1962. Peanut diseases in Queensland. Queensland Agric. J. 88:540543.
Recheigl, N. A., Tolin, S. A., Grayson, R. L., and Hooper, G. R. 1989. Ultrastructural comparison of peanut infected with stripe and blotch variants of peanut stripe
virus. Phytopathology 79:156161.
Reddy, D. V. R., Wongkaew, S., and Santos, R. 1985. Peanut mottle and peanut stripe virus diseases in Thailand and the Philippines. Plant Dis. 69:1101.
Reddy, D. V. R., Subrahmanyam, P., Sankara Reddy, G. H., Raja Reddy, C., and Siva Rao, D. V. 1984. A nematode disease of peanut caused by
Tylenchorhynchus brevilineatus. Plant Dis. 68:526529.
Reddy, D. V. R., Richins, R. D., Rajeshwari, R., Iizuka, N., Manohar, S. K., and Shepherd, R. J. 1993. Peanut chlorotic streak virus, a new caulimovirus infecting
peanuts (Arachis hypogaea) in India. Phytopathology 83:129133.
Rothwell, A. 1962. Diseases of groundnuts in southern Rhodesia. Rhodesia Agric. J. 59:199201.
Rowe, R. C., and Beute, M. K. 1973. Susceptibility of peanut rotational crops (tobacco, cotton, and corn) to Cylindrocladium crotalariae. Plant Dis. Rptr.
57:10351039.
Rowe, R. C., Johnston, S. A., and Beute, M. K. 1974. Formation and dispersal of Cylindrocladium crotalariae microsclerotia in infected peanut roots.
Sai Gopal, D. V. R., Siva Prasad, V., Gopinath, K., Satyanarayana, T., Sreenivasulu, P., and Nayudu, M. V. 1987. Chemical suppression of peanut green mosaic
disease in peanut. (Abstr.) Phytopathology 77:1728.
Sanborn, M. R., and Melouk, H. A. 1983. Isolation and characterization of mottle virus from wild peanut. Plant Dis. 67:819821.
Sharma, N. D. 1974. A previously unrecorded leaf spot of peanut caused by Phomopsis sp. Plant Dis. Rptr. 58:640.
Shew, B. B., Beute, M. K., and Wynne, J. C. 1988. Effects of temperature and relative humidity on expression of resistance to Cercosporidium personatum in
peanut. Phytopathology 78:493498.
Shew, H. D., and Beute, M. K. 1979. Evidence for the involvement of soilborne mites in Pythium pod rot of peanut. Phytopathology 69:204207.
Sidebottom, J. R., and Beute, M. K. 1989. Control of Cylindrocladium black rot of peanut with cultural practices that modify soil temperature. Plant Dis. 73:672
676.
Sidebottom, J. R., and Beute, M. K. 1989. Inducing soil suppression to Cylindrocladium black rot of peanut through crop rotations with soybean. Plant Dis. 73:679
685.

Page 450
Singh, B., and Hussain, S. M. 1991. Bacterial wilt of groundnut: A new record for India. Indian Phytopathol. 44:369370.
Smith, D. H. 1972. Arachis hypogaea, a new host of Cristulariella pyramidalis. Plant Dis. Rptr. 56:796797.
Smith, D. H., Burdsall, H. H., Jr., Black, M. C., and Crumley, C. R. 1990. Association of Phanerochaete with peanut in Texas. (Abstr.). Phytopathology 80:438.
Sobers, E. K., and Littrell, R. H. 1974. Pathogenicity of three species of Cylindrocladium to select hosts. Plant Dis. Rptr. 58:10171019.
Soufi, R. K., and Filonow, A. B. 1992. Population dynamics of Pythium spp. in soil planted with peanut. Plant Dis. 12031209.
Sreenivasulu, P., and Demski, J. W. 1988. Transmission of peanut mottle and peanut stripe viruses by Aphis craccivora and Myzus persicae. Plant Dis. 72:722
723.
Subrahmanyam, P., Reddy, L. J., Gibbons, R. W., and McDonald, D. 1985. Peanut rust: A major threat to peanut production in the semiarid tropics. Phytopathology
69:813819.
Wadsworth, D. F., and Melouk, H. A. 1985. Potential for transmission and spread of Sclerotinia minor by infected peanut seed and debris. Plant Dis. 69:379381.
Wagih, E. E., and Melouk, H. A. 1987. A virus causing chlorotic ringspot of peanut. (Abstr.) Phytopathology 77: 1731.
Warwick, D., and Demski, J. W. 1988. Susceptibility and resistance of soybean to peanut stripe virus. Plant Dis. 72:1921.
Wills, W. H., and Moore, L. D. 1973. Pathogenicity of Rhizoctonia solani and Pythium myriotylum from rotted pods to peanut seedlings. Plant Dis. Rptr. 57:578
582.
Wongkaew, S., and Peterson, J. F. 1983. Peanut mottle virus symptoms in peanuts inoculated with different Rhizobium strains. Plant Dis. 67:601603.
Woodard, K. E., and Jones, B. L. 1983. Soil populations and anastomosis groups of Rhizoctonia solani associated with peanut in Texas and New Mexico. Plant
Dis. 67:385387.
Xu, Z., and Barnett, O. W. 1984. Identification of a cucumber mosaic virus strain from naturally infected peanuts in China. Plant Dis. 68:386389.
Xu, Z., Yu, Z., Liu, J., and Barnett, O. W. 1983. A virus causing peanut mild mottle in Hubei Province, China. Plant Dis. 67:10291032.
Yung, C. H., Wernsman, E. A., and Gooding, G. V., Jr. 1991. Characterization of potato virus Y resistance from gametoclonal variation in fluecured tobacco.

Page 451
13.
Diseases of Red Clover (Trifolium pratense)
Bacterial Leaf Spot
Bacterial leaf spot is also called bacterial blight and bacterial leaf blight.
Cause.
Pseudomonas syringae survives in infested residue. During cool, wet weather at any time of the growing season, bacteria are disseminated by splashing rain and enter
leaves through wounds or natural openings.
Distribution.
Symptoms.
Bacterial leaf spot affects stems, petioles, petiolules, stipules, and flower pedicels, but symptoms are most conspicuous on diseased leaflets. At first, tiny, translucent
dots appear on the lower leaf surfaces. The spots become black and have watersoaked margins and chlorotic halos that enlarge to fill the area between the leaf veins.
During wet weather, milky, white bacterial exudate develops in spots and appears as drops or a thin film on the spot. When the exudate dries, it forms a thin, crusty
film that glistens in the light. Leaves may become tattered and frayed by wind tearing out the dead portions. Lesions on petioles and stems are dark, elongated, and
slightly sunken.
Management.
None is recommended since bacterial leaf spot is not considered an important disease.
Anther Mold
Cause.
Botrytis anthophila, teleomorph Sclerotinia spermophila.
Distribution.
Not known.

Page 452
Symptoms.
A gray to black fungal growth occurs on diseased flowers.
Management.
Not reported.
Cause.
Aphanomyces euteiches. Oneweekold red clover is most susceptible to infection. Seedlings that are 2 and 3 weeks old are significantly less susceptible to infection.
Distribution.
The United States, but it is likely common wherever red clover is grown.
Symptoms.
A necrosis of diseased roots, hypocotyls, and cotyledons occurs. Surviving plants are stunted.
Management.
Low levels of resistance occur in some cultivars.
Black Patch Disease
Cause.
Rhizoctonia leguminicola is seedborne and survives as mycelia in infested residue.
Distribution.
The southern United States.
Symptoms.
Black patch occurs on scattered plants and in scattered groups of plants within a field. Seedlings are often blighted and overgrown with black mycelium. Leaves,
stems, flowers, and seeds become diseased. Leaf symptoms are lesions that vary in color from brown to grayblack and have concentric rings. Often all the bottom
leaves of diseased plants are killed. Black, coarse, aerial mycelial growth occurs on petioles and on stems, which frequently are girdled. Dark lesions and dark, coarse
mycelia occur on flowers and seeds.
Management
2. Cut hay earlier than normal to reduce foliage loss.
3. Rotate red clover with resistant crops.
Black Root Rot
Cause.
Thielaviopsis basicola, synamorph Chalara elegans, survives as chlamydospores in infested residue and soil. Chlamydospores germinate during moist soil conditions
and produce mycelia that directly infect host roots. Chlamydospores are formed in diseased tissues and returned to the soil when tissues decay.
Distribution.
Not known.
Symptoms.
The cortex of the hypocotyl below the soil line and taproots and

Page 453
fibrous roots become dark brown and necrotic. A severe root rot may develop, with subsequent wilting of foliage or plant death.
Management.
Not reported.
Brown Root Rot
Cause.
Phoma sclerotioides (syn. Plenodomus meliloti) overwinters in infested residue as pycnidia and saprophytic mycelia. It is not known for certain what the source of
primary inoculum is, but it is presumed to be conidia produced in pycnidia.
Distribution.
Canada.
Symptoms.
Diseased plants are observed in the spring as chlorotic, stunted plants that frequently die after beginning to grow. Circular, brown, necrotic areas occur on diseased
roots and eventually spread into the crown. Numerous pycnidia occur on diseased areas.
Management.
Rotate red clover with nonlegumes.
Common Leaf Spot
Common leaf spot is also called Pseudopeziza leaf spot.
Cause.
Pseudopeziza trifolii survives either as apothecia within leaf spots or as saprophytic mycelia in infested residue. During cool, wet weather, ascospores produced in
apothecia are disseminated by wind to host leaves.
Distribution.
Wherever red clover is grown.
Symptoms.
Very small, dark spots that vary in color from olive to redbrown, purple, or black develop on both diseased leaf surfaces. The angular to round spots with portions of
their margins jutting out like a finger or branch give spots a starlike appearance. Under magnification, an apothecium, which resembles a raised cushion, is observed in
the center of spots on the undersides of leaves during wet weather. Later, apothecia dry up and become dark, making them difficult to observe. While common leaf
spot is confined mostly to leaves, small, elongated, dark streaks may occasionally occur on petioles.
Management.
Not reported.
Curvularia Leaf Blight
Cause.
Curvularia trifolii. Curvularia leaf blight is most severe during warm, moist weather.
Distribution.
Worldwide. Curvularia leaf blight is considered to be of minor importance.

Page 454
Symptoms.
Watersoaked, angular, yellow to brown lesions develop on diseased leaflets. Lesions often develop on petioles, resulting in necrotic leaves that remain attached to the
plant.
Management.
Not necessary since Curvularia leaf blight is considered to be of minor importance.
Cylindrocarpon Root Rot
Cause.
Cylindrocarpon magnusianum (syn. C. ehrenbergii).
Distribution.
The United States.
Symptoms.
Similar to symptoms caused by C. crotalariae. Diseased roots have black lesions.
Management.
Not reported.
Cylindrocladium Root and Crown Rot
Cause.
Cylindrocladium crotalariae.
Distribution.
Symptoms.
Black lesions occur in crowns and roots of diseased plants. Diseased plants normally die.
Management.
Not reported.
Downy Mildew
Cause.
Peronospora trifoliorum survives in crown buds and infested leaves. Disease occurs during wet or humid weather.
Distribution.
Distribution is not known for certain, but downy mildew likely occurs wherever red clover is grown.
Symptoms.
The leaves at the tops of diseased plants are light green. A gray ''fuzzy" mycelial growth consisting of mycelium, conidia, and conidiophores is present on the underside
of diseased leaves during wet or humid weather. Leaves of severely diseased plants are twisted, and stem growth is retarded.
Management
1. Harvest early.
2. Rotate red clover with nonlegumes.
Fusarium Root Rot
Fusarium root rot is also called common root rot.

Page 455
Cause.
Several Fusarium spp., including F. acuminatum, F. avenaceum, F. oxysporum, F. roseum, and F. solani, are the fungi most commonly isolated from the
diseased roots and crowns of red clover. However, several other fungi are also associated with root rot of red clover. Fusarium are usually present in soil and persist
as chlamydospores and as saprophytic mycelia in infested residue.
Fusarium are generally considered to be weak pathogens and infect a plant after it has been weakened by some other cause, such as drought, low fertility, insects,
other diseases, improper management, or winter injury. Wounding of roots results in localized increases in incidence and severity of necrosis caused by F.
acuminatum and F. avenaceum. The main effect of wounding is not to provide an opening through which the fungus enters the host plant but to accelerate fungal
penetration and increased disease development by altering the hostpathogen interaction. This is done, following fungal penetration into the plant, by favoring the
formation of distributive hyphae throughout roots rather than the formation of chlamydospores.
Distribution.
Symptoms.
Diseased red clover plants may be killed in all stages of plant development, but stand loss is most conspicuous during the second year of stand establishment. Diseased
plants appear unthrifty, stunted, and yellowish and will wilt during hot, dry weather. Roots and crowns are spongy or soft and are discolored from light brown to red
brown to dark brown. Lesions develop on the surface of larger roots and subsequently cause feeder roots to be pruned off. The inner core of the taproot may be
decomposed.
Management.
In general, practice management that promotes vigorous plant growth. This includes the following practices:
1. Sow certified diseasefree seed of adapted cultivars. Some cultivars tend to be less affected by root rot than others.
2. Avoid overgrazing, particularly late in the growing season.
3. Get a soil test to determine the deficiencies or excesses of nutrients.
4. Soil should have a pH of 6.2 to 7.0.
Gray Stem Canker
Cause.
Ascochyta lethalis (syn. A. caulicola).
Distribution.
Canada. Gray stem canker is not considered a serious disease.
Symptoms.
Silverwhite cankers, which occur on midribs, leaf stalks, and diseased stems, sometimes girdle the lower stems. Fruiting bodies of A. lethalis are in the center of
cankers and resemble small, black dots. Severely dis

Page 456
eased stems may be stunted, swollen, and twisted and have a few small leaves.
Management.
Not reported.
Leaf Gall
Leaf gall is also called crown wart.
Cause.
Physoderma trifolii (syn. Urophlyctis trifolii) survives in soil and infested residue as resting sporangia. During wet soil conditions, sporangia liberate zoospores that
"swim" through moist soil to the developing buds of crown branches on host plants. Zoospores germinate and form infection hyphae that penetrate the host plants.
Distribution.
A minor disease found primarily in warmer red clovergrowing areas of Europe, North America, and South America.
Symptoms.
Irregularshaped galls form around the crowns of diseased plants just below the soil level. Galls are first produced in late spring and continue to increase in size during
the summer. Diseased plants wilt in hot weather.
Management.
Not reported.
Midvein Spot
Cause.
Mycosphaerella carinthiaca overseasons as perithecia and mycelia or sporodochia. It is not known for certain, but primary infection is presumed to be either
ascospores liberated from perithecia or conidia produced on sporodochia.
Distribution.
In warmer red clovergrowing areas of the world.
Symptoms.
Small, chlorotic spots occur on the veins of diseased leaves. The spots enlarge slightly and become dark brown. Infrequently, spots have gray centers.
Management.
Not reported.
Mycoleptodiscus Crown and Root Rot
Cause.
Mycoleptodiscus terrestris (syn. Leptodiscus terrestris) overwinters as sclerotia in infested residue and soil, and presumably as mycelia and acervuli in infested
residue. Most primary inoculum likely originates from sclerotia that germinate and directly infect roots and crowns. Conidia are formed in summer and disseminated by
being forcibly ejected from the acervulus by setae that unfold as the acervulus mucilage dries out. Disease is favored by warm, humid weather.

Page 457
Distribution.
The central and eastern United States. Mycoleptodiscus crown and root rot is not considered a serious disease of red clover.
Symptoms.
A brown to black rot occurs in diseased lateral roots, taproots, and crowns of older plants. Numerous sclerotia form in decayed tissue. Small spots develop on
diseased leaves, and reddishbrown lesions occur on stems. Spots on the lower stems expand and develop into crown rot.
Management.
Not reported.
Cause.
Myrothecium roridum and M. verrucaria are soil inhabitants and widespread facultative parasites. Myrothecium leaf spot is favored by wounds and hot, humid
weather.
Distribution.
The United States (Pennsylvania).
Symptoms.
Initially, small, dark, watersoaked lesions occur on both leaf surfaces and become dark brown to black. Sporodochia develop in lesions, often in concentric circles in
alternating light and dark brown rings that give the spot a "targetlike" effect. A slight chlorosis sometimes occurs around lesions. At first, lesions are circular, but as
they enlarge, they become irregularshaped and coalesce, which causes a necrosis of petioles and subsequent wilting of the leaves. If humid conditions persist for
several days, diseased leaves curl and die. Some lesions may be restricted by leaf veins. Symptoms appear most rapidly at wound sites but also may develop on
nonwounded tissue.
Management.
Not reported.
Myrothecium Root Rot
Cause.
Myrothecium roridum and M. verrucaria are soil inhabitants and widespread facultative parasites. Both fungi are thought to be primary pathogens rather than
secondary wound parasites.
Distribution.
The United States (Pennsylvania and Wisconsin).
Symptoms.
In slantboard evaluations, brown, watersoaked rots with poorly delineated margins occurred 3 days after inoculation. Foliage symptoms were chlorosis, purpling of
leaflet margins, and, finally, the death of diseased leaves and petioles. Foliar symptoms also included stunting.
In greenhouse evaluations, dark brown rots occurred across the entire root and had occasional streaks that extended upward in the vascular system. Decayed
portions of diseased roots remained firm and were not watersoaked.
Management.
Not reported.

Page 458
Northern Anthracnose
Northern anthracnose is also called clover scorch.
Cause.
Aureobasidium caulivorum (syn. Kabatiella caulivora) overwinters as mycelia and acervuli in infested residue and may be seedborne. Temperatures of 20° to 25°
C and wet weather are optimum for the production of conidia in acervuli and from mycelia; conidia are disseminated by wind or splashing water to host plants.
Distribution.
The cooler red clovergrowing areas of Asia, Europe, and North America.
Symptoms.
From a distance, a field of diseased plants will appear "scorched" as if by fire. The first symptom is the presence of elongated, dark brown to black lesions that split in
the middle and become light colored with dark margins on diseased leaf petioles and stems. Lesions may girdle and kill stems, causing leaves to become brown, wilt,
and die. Leaves and flower heads droop like shepherd's crooks. Diseased plant parts dry out rapidly and become so brittle that leaflets are easily broken off.
Small, irregularshaped, colorless acervuli that lack setae and white masses of conidia and conidiophores occur in deeper cracks and depressions.
Management.
Powdery Mildew
Cause.
Erysiphe polygoni overwinters as cleistothecia scattered on the surfaces of infested residue. Primary inoculum is provided by ascospores that are produced in asci
within cleistothecia and disseminated by wind to host leaves. Infection may occur any time during the growing season but is most common during cool nights and warm
days in the late summer and early autumn. Long periods of dry weather favor disease development. Conidia are subsequently produced on diseased leaf surfaces and
are the primary source of secondary inoculum throughout the remainder of the growing season. In the autumn, cleistothecia form on the surfaces of diseased plant
tissues.
Erysiphe polygoni is possibly an aggregate species consisting of several physiologic races. Erysiphe polygoni infects at least 359 species of plants in 154 different
genera.
Distribution.
Wherever red clover is grown in the temperate zones of the world.
Symptoms.
Powdery mildew is not serious early in the growing season but can cause reductions in yield and hay quality later in the growing season. Initially, patches of fine, barely
visible white mycelium develop on diseased upper leaf surfaces. The patches enlarge and merge, which gives the appearance of white flour or powder covering the
diseased leaf surfaces. If

Page 459
disease is severe, an entire field may look white. Diseased leaves remain green but a few turn yellow and wither prematurely.
Management.
Pseudoplea Leaf Spot
Pseudoplea leaf spot is also called pepper spot and burn.
Cause.
Pseudoplea trifolii (syn. Leptosphaerulina trifolii) overwinters as perithecia or mycelia in infested leaf residue. Ascospores are released during cool, wet weather
and disseminated by wind to host plants.
Distribution.
Wherever red clover is grown, but Pseudoplea leaf spot is most common in temperate, humid areas.
Symptoms.
Pseudoplea leaf spot occurs throughout the growing season but is most common during cool, wet weather in the spring or autumn. Tiny, sunken, black spots that
develop on both leaf surfaces and petioles eventually become gray and have a redbrown border. Although spots do not enlarge (they grow to a diameter of only a
few millimeters), they may become very numerous. Severely diseased leaves and petioles are chlorotic, then become brown, and wither, forming a mass of dead
leaves. Parts of flowers and flower stalks become diseased and die.
Management.
Cut hay before Pseudoplea leaf spot becomes too severe.
Rust
Cause.
Uromyces trifoliirepentis var. fallens (syn. U. trifolii var. fallens) is an autoecious longcycled rust fungus that overwinters as teliospores on red clover in the
southern United States and northern Mexico. Each summer, urediniospores are disseminated by wind to the northern United States and Canada. Although infection
occurs in the spring in warm red clovergrowing areas, infection does not occur until late summer or autumn in the northern United States and Canada. Rust
development is optimum during moist conditions at temperatures of 16° to 22°C.
Distribution.
Wherever red clover is grown in humid or semihumid areas.
Symptoms.
Rust is most important in new seedings and in stands left for seed instead of cut for hay purposes. When rust becomes severe, it is usually in fields where the cutting of
plants has been delayed.
The uredinial stage is the most obvious symptom and appears as small, redbrown pustules on diseased petioles, stems, and leaves, especially on the undersides of
leaves. When a pustule is rubbed, a red to brown dust or powder consisting of urediniospores is evident. Seriously rusted leaves may become chlorotic and defoliate.
Telia occur either in old uredinia or independently on the diseased leaf and are darker than uredinia. The ae

Page 460
cial stage develops as swollen, white to yellow pustules on stems, petioles, and leaves that appear under magnification to be clusters of tiny cuplike structures. Aecia
may cause distortion of diseased leaves and petioles.
Management.
Grow the most resistant cultivars.
Sclerotinia Crown and Root Rot
Sclerotinia root rot and crown rot is also called Sclerotinia crown and stem rot.
Cause.
Sclerotinia trifoliorum survives for several years in the soil as sclerotia. Sclerotia germinate in the autumn and form apothecia in which ascospores are produced and
disseminated by wind to host leaves. Disease development is optimum during wet weather at temperatures of 13° to 18°C.
Distribution.
In regions with mild winters or heavy snow cover. Sclerotinia crown and root rot is most important in the southern red clovergrowing areas of the United States.
Symptoms.
Sclerotinia root rot and crown rot occurs in patches within a field that may merge and form large areas of dead plants. Symptoms first appear in the autumn as small,
brown spots on diseased leaves and petioles. Leaves turn light brown, wither, and become overgrown with white mycelium that spreads to the crowns and roots. By
late winter or early spring, crowns and basal portions of young stems have a brown, soft rot that extends into the roots. As stems and petioles are killed, they are also
overgrown with white mycelium. Black sclerotia of various sizes form in mycelium and are imbedded or attached to the surface of diseased red clover tissue. When
infected tissue decomposes, the sclerotia are released into the soil.
Management.
Rotate red clover with a nonsusceptible host. The sclerotia will eventually decompose or the causal fungus will die out in the absence of a susceptible host.
Seed Mold
Cause.
Distribution.
Widespread.
Symptoms.
Diseased seed is shriveled and discolored and, when moistened, gray mycelium will grow from the seed. Diseased seed will damp off when sown.
Management
1. Do not sow diseased seed.

Page 461
Seed Rot and Damping Off
Seed rot and damping off is also called Pythium blight.
Cause.
Pythium spp., particularly P. debaryanum. Most Pythium spp. survive in soil as oospores. Under moist soil conditions, oospores germinate and form sporangia in
which zoospores are produced. Zoospores are released and "swim" through free water in the soil to the root tips or seeds of host plants and germinate. Usually, only
young plants are infected. Seedlings more than 5 days old apparently are almost immune, and older plants are rarely infected.
Distribution.
Symptoms.
Symptoms are not obvious because preemergence damping off is the most common form of Pythium blight. Seeds and seedlings become soft and are overgrown with
white mycelia when they are placed in a moist chamber. Emerged seedlings that become diseased have a soft, brown rot on the hypocotyl and roots.
Management.
Sooty Blotch
Sooty blotch is also called black blotch.
Cause.
Cymadothea trifolii, anamorph Polythrincium trifolii, overwinters as a stroma. Sometime during the growing season, perithecia form within the overwintered
stroma and ascospores are produced, liberated, and disseminated by wind to host leaves. Infection occurs in spring in the southern United States and during late
summer and autumn in the northern United States and Canada.
Distribution.
The temperate zones of the world.
Symptoms.
The first symptom occurs on lower leaf surfaces as tiny, olivegreen dots. The dots enlarge, become thicker and darker, and eventually resemble a velvety, black,
elevated cushion. In the autumn, the cushions are replaced by other black areas that have a shiny surface. Chlorotic spots that become necrotic appear on the upper
leaf surfaces opposite a cushion. Severe disease causes the entire leaf to turn brown, die, and defoliate.
Management.
Not known.
Southern Anthracnose
Cause.
Colletotrichum trifolii overwinters as acervuli on diseased stems, crowns, and roots. In some literature, Colletotrichum destructivum has been reported to be the
causal fungus of southern anthracnose. Conidia production is optimum during wet weather at a temperature of 28°C; conidia are splashed by rain or blown by wind to
host plants.

Page 462
Distribution.
Africa, southern Europe, and the southern United States.
Symptoms.
Symptoms closely resemble those of northern anthracnose except southern anthracnose is frequently found on the upper part of taproots and crowns, while northern
anthracnose is not. Southern anthracnose also is more likely than northern anthracnose to be present on the new growth of the second crop in the northern and
midwestern United States.
In the southern United States, southern anthracnose is present in the spring on the young, succulent parts of stems and petioles of the first crop. Dark brown, irregular
shaped spots develop on diseased leaves. These vary in size from barely visible dots to a general necrosis of entire leaves. Disease commonly develops on young
tissue but may also occur on older plant tissue.
The first symptoms on petioles and stems are watersoaked spots that become elongated and dark brown to black with a gray or light brown center. When viewed
under magnification, small, black setae that resemble tiny black spines can be seen in the centers of older, sunken lesions. Diseased petioles cause the attached leaflets
to droop. Stems may be killed when girdled by a lesion.
Diseased crowns are blueblack and attached stems are brittle, causing plants to break off at the ground level. Normally, the entire plant wilts and dies when the
crown is diseased.
Management
1. Grow adapted, resistant cultivars.
2. Use clean, certified seed from diseasefree plants.
Southern Blight
Cause.
Sclerotium rolfsii, teleomorph Athelia rolfsii, survives for several years in the soil or in plant residue as small, brown sclerotia that are disseminated by water and
wind. Sclerotia germinate under hot, humid conditions and form mycelial strands that infect plants.
Distribution.
In the warmer red clovergrowing areas of the United States and possibly Europe.
Symptoms.
Diseased plants are "bleached" to light tan and have a white, cottonlike mycelial growth on stems near the soil surface. Numerous small, tan to brown sclerotia that
resemble "seeds" form in mycelia growing on the stems, crowns, and residue on the soil surface.
Management
2. Practice proper mowing or grazing. The causal fungus does not grow well when exposed to direct sunlight and air movement.

Page 463
3. Grow a resistant plant host in the crop rotation. Avoid growing crops such as alfalfa and soybean in a rotation with red clover.
Spring Black Stem and Leaf Spot
Cause.
Phoma pinodella (syn. P. trifolii) overwinters as pycnidia in infested residue and may be seedborne. Spores are produced in pycnidia and are disseminated by wind
to host plants. Plants are infected during cool, wet weather in the autumn and spring.
Distribution.
Europe, North America, and South America.
Symptoms.
The most conspicuous symptom is on diseased stems. Initially, small, brown to black spots that vary in size and shape occur on stems. Spots merge and form large
black areas, especially on the lower stems. Young shoots may be girdled and killed. The black discoloration increases when clover is not cut at the proper time or is
left for seed.
Leaves have dark brown to black spots that are irregular in size and shape. Some spots may have gray centers. Diseased leaves, together with diseased stems, may
result in severe defoliation.
Management
3. Cut hay before defoliation becomes too severe.
Stagonospora Leaf Spot
Stagonospora leaf spot is also called gray leaf spot.
Cause.
Stagonospora recedens. However, S. meliloti, teleomorph Leptosphaeria pratensis, has also been reported to be a causal fungus. Stagonospora recedens
overwinters as mycelia and pycnidia in infested residue. Leptosphaeria pratensis overwinters as perithecia in infested residue. The fungi are poor soil saprophytes
and do not survive in the absence of residue colonized during their parasitic phase. During wet weather in the spring, both conidia and ascospores are produced. The
conidia are primarily disseminated to plant hosts by splashing rain and irrigation, and the ascospores by wind. Secondary inoculum is conidia produced in pycnidia
during wet conditions and disseminated by splashing rain or irrigation to plant hosts.
Distribution.
Generally distributed but most common in warm, humid areas or where red clover is grown under irrigation.
Symptoms.
Spots are circular to irregular (36 mm in diameter). The centers of spots are pale buff to almost white and have light to dark brown margins. In some instances, spots
have faint concentric zones that are the

Page 464
same color as the margins. Pycnidia appear as small, dark dots scattered throughout the older spots.
Management.
Rotate red clover with a resistant crop for 2 to 3 years. Many legumes, including alfalfa and other clovers, are susceptible.
Summer Black Stem
Summer black stem is also called angular leaf spot and Cercospora leaf and stem spot.
Cause.
Cercospora zebrina is seedborne and overwinters as mycelia in infested residue.
Distribution.
Europe, central and eastern North America.
Symptoms.
Summer black stem occurs in late summer and early autumn. Leaf spots are dark brown, angular, and somewhat limited by leaf veins. Older spots may appear ash
gray due to the sporulation of C. zebrina in the spot. Sunken, dark brown lesions occur on stems and petioles. Lesions may merge and form extensive dark areas on
the lower parts of stems. Seeds are also diseased.
Management
1. Treat seeds with a seedprotectant fungicide.
2. Harvest before defoliation becomes severe. This also helps to reduce inoculum.
Target Spot
Target spot is also called ring spot, Stemphylium leaf spot, and zonate leaf spot.
Cause.
Stemphylium sarciniforme and S. botryosum overwinter as mycelia in infested residue. The teleomorph of S. botryosum, Pleospora tarda, may survive as
perithecia in which ascospores are produced. At any time during the growing season, conidia are produced and disseminated by wind to host plant leaves. Diseased
leaves fall to the soil surface at harvest and provide inoculum for infection the following year. Disease development is optimum during moist weather and temperatures
of 20° to 24°C.
Distribution.
Symptoms.
Symptoms are confined to leaflets of plants growing in dense stands and are most severe in the late summer and autumn. The initial small, dark brown spots enlarge
and develop into targetlike spots with alternate light and dark brown rings. Entire leaves become wrinkled and dark brown and have a sooty appearance but remain
attached to diseased plants. Sunken brown lesions infrequently appear on the stems, petioles, and pods.

Page 465
Management.
No satisfactory disease management is known, but selection of resistant cultivars may be possible. Harvest early to reduce losses.
Violet Root Rot
Cause.
Helicobasidium brebissonii, anamorph Rhizoctonia crocorum (syn. R. violaceae), survives in soil as sclerotia or as saprophytic mycelia in residue. Disease is most
severe under wet soil conditions.
Distribution.
Symptoms.
Plants in a diseased area (which usually corresponds to a wet area of a field) are brown in contrast to surrounding green plants. Diseased roots have a brown to dark
brown or black discoloration and are covered with thick mats of violet mycelia that extend below the soil surface. Later, roots are rotted and shredded and have a
brown to dark violet discoloration. Barely visible tiny, black sclerotia are seen on diseased roots.
Management
1. Grow red clover in welldrained soil.
2. Harvest hay in the prebloom stage.
3. Rotate red clover with resistant crops, such as small grains and maize.
Winter Crown Rot
Winter crown rot is also called snow mold.
Cause.
Coprinus psychromorbidus, Phoma sclerotioides (syn. Plenodomus meliloti) and Typhula spp. Coprinus psychromorbidus was previously called the low
temperature basidiomycete (LTB). Disease occurs at temperatures near O°C at the soil surface and under a snow cover.
Distribution.
Canada.
Symptoms.
Young stands have irregularshaped areas of dead plants. Older stands have scattered plants with rotted crowns. White fungal threads are present at the edge of
melting snow.
Management.
Rotate with nonlegume plants.
Bulb and Stem
Cause.
Ditylenchus dipsaci survives for years as larvae in dry stems, plant crowns, soil, and other plant hosts. Larvae feed and reproduce in shoots near the crown, moving
over the plant surface in a film of water and infecting plants through stomates. A female nematode lays 75 to 100 eggs with optimum reproduction and infection in
heavy, wet soils at soil tem

Page 466
peratures of 15° to 21°C. Dissemination is by machinery, rain, and irrigation water.
Distribution.
Worldwide, but it is not considered a serious disease of red clover.
Symptoms.
Diseased plants are stunted and have a bushy appearance due to swollen nodes and shortened internodes, which result in abnormal proliferation and swollen, short
stems. White to light brown stems are scattered throughout a field. Shoots from infected buds are severely dwarfed and have swollen and spongy buds that are easily
detached from the plant.
Management
1. Plow under diseased stands.
2. Do not grow red clover in a rotation with alfalfa or other clovers.
Clover Cyst
Cause.
Clover cyst nematode, Heterodera trifolii.
Distribution.
Europe and probably other red clovergrowing areas.
Symptoms.
Diseased plants are stunted.
Management.
Follow general nematode management practices.
Dagger
Cause.
Distribution.
Widely distributed.
Symptoms.
Root growth of diseased plants is reduced. Necrotic areas form where feeding has occurred. Cells next to necrotic tissue may enlarge, causing a galllike growth.
Management.
Not known.
Lance
Cause.
Hoplolaimus spp. are ectoparasites that feed in the cortex area.
Distribution.
Symptoms.
Diseased plants are stunted and chlorotic. The taproot becomes necrotic and large numbers of secondary and tertiary roots are produced.
Management.
Not reported.
Lesion
Cause.
Pratylenchus penetrans. Not much information is known about P. penetrans on red clover, but the life cycle is assumed to be similar to that on

Page 467
other legumes. The preferred area of infection is root hairs on feeder roots, where nematodes force their way through or between epidermal and cortical cells. Gravid
females deposit eggs in infected root tissue or soil. The secondstage larvae emerge. Injury is most severe in sandy and sandy loam soils.
Distribution.
Widespread.
Symptoms.
Initially, a lesion appears on the affected root as a watersoaked area that becomes yellow and ellipticalshaped. Dark brown cells later appear in the center of the
lesion. Secondary infection by saprophytic fungi is thought to occur.
Management.
Nematicides are effective but impractical.
Pin
Cause.
Paratylenchus spp.
Distribution.
Not know for certain but assumed to be widespread.
Symptoms.
Necrotic areas occur on diseased roots.
Management.
Not known.
Ring
Cause.
Criconemella spp. are thought to be ectoparasitic.
Distribution.
The United States.
Symptoms.
Diseased plants are chlorotic. Roots are discolored with brown, necrotic lesions.
Management.
Not reported.
Root Knot
Cause.
Meloidogyne arenaria, M. hapla, M. incognita, and M. Javanica. Meloidogyne arenaria, M. incognita, and M. javanica do not survive if the temperature
averages below 3°C during the coldest month. Meloidogyne hapla is limited by temperatures above 26°C.
Distribution.
Symptoms.
Diseased plants are stunted and wilt during moisture stress. Leaves frequently have purple undersides. Roots have galls, which causes them to be excessively branched
and brittle.
Management
1. Rotate red clover with nonhosts.
2. Apply nematicides if practical.

Page 468
Spiral
Cause.
Distribution.
Widely distributed.
Symptoms.
Necrotic spots occur at the feeding sites on the roots. Roots may be severely damaged when high nematode populations are present.
Management.
Nematicides control nematodes on some crops.
Phyllocly
Cause.
Phytoplasmalike organism that survives in biennial and perennial plants. The organism is disseminated by leafhoppers.
Distribution.
Canada and Europe.
Symptoms.
Floral parts are turned into leaflike organs. Leaves are reduced in size and have a mild chlorosis. Newly emerged leaves are slightly deformed and old leaves may
have a bronze color.
Management.
Not reported.
Proliferation
Cause.
Phytoplasmalike organism that probably overwinters in biennial and perennial plants. Vectors are not known for certain, but leafhoppers may be involved.
Distribution.
Canada (Alberta).
Symptoms.
Foliar growth is profuse, giving the plant a witches' broom appearance. Flowers may be transformed into leaflike appendages.
Management.
Not reported.
Witches' Broom
Cause.
Phytoplasmalike organism.
Distribution.
Western Canada.
Symptoms.
Diseased plants are severely dwarfed and the numerous short, spindly shoots that originate from crown and axillary buds along the stem give plants an overall bunchy
appearance. Leaves are small and chlorotic.
Management.
Not reported.

Page 469
Yellow Edge
Cause.
Phytoplasmalike organism that overwinters in biennial and perennial plants. Dissemination is by leafhoppers.
Distribution.
Canada (Ontario and Quebec).
Symptoms.
New growth has a mild chlorosis that later becomes more pronounced along the leaf margins. Chlorosis may eventually become a redbrown discoloration. Clusters of
small leaves with short petioles and chlorotic margins develop at the nodes of creeping stems. Some plants do not have creeping stems; their numerous small leaves on
upright stems give the plant a witches' broom appearance. Flower size and production may be reduced. The entire diseased plant is stunted.
Management.
Not reported.
Alfalfa Mosaic
Cause.
Alfalfa mosaic virus is disseminated by several species of aphids.
Distribution.
Canada and the United States. Alfalfa mosaic is possibly distributed wherever alfalfa and red clover are grown.
Symptoms.
Diseased leaves are distorted and have a green and yellow mosaic pattern.
Management
2. Control aphids where possible.
Alsike Clover Mosaic
Alsike clover mosaic virus is possibly a strain of bean yellow mosaic virus. However, because their symptoms are different in the literature, both viruses are described
here.
Cause.
Alsike clover mosaic virus (ACMV) is in the potyvirus group. ACMV overwinters in perennial plants, such as wild sweet clover, and is transmitted mechanically and
by several species of aphids. ACMV is not thought to be seedborne.
Distribution.
Widespread.
Symptoms.
Symptoms are more prevalent along the borders of fields. The initial drooping of leaflets at the point of attachment to the stem is followed

Page 470
by development of angular, pale yellow spots. Diseased leaves become malformed and distorted.
Management.
Not reported.
Bean Yellow Mosaic
Alsike clover mosaic virus may be a strain of bean yellow mosaic virus. However, because their symptoms are different in the literature, both viruses are described
here.
Cause.
Bean Yellow mosaic virus (BYMV) is in the potyvirus group. BYMV overwinters in diseased legumes and is transmitted by aphids, especially the pea aphid,
Macrosiphum pisi. Arrowleaf clover, Trifolium vesiculosum, is reported to be a reservoir for BYMV. BYMV probably interacts with Fusarium spp. to increase
root rot and cause premature stand decline.
Distribution.
Africa, Asia, Europe, North America, and South America.
Symptoms.
A systemic mottling of diseased leaves is the most common symptom. Other symptoms include vein yellowing, distortion, vein necrosis, and systemic necrosis.
Management
1. Grow the least susceptible cultivar. There is some evidence that resistant cultivars can be developed.
2. Avoid growing red clover near garden peas and beans.
Clover Yellow Mosaic
Cause.
Clover yellow mosaic virus (CIYMV) is in the potexvirus group. CIYMV is seedborne.
Distribution.
Canada and probably other red clovergrowing areas.
Symptoms.
Diseased plants are frequently stunted and bushy. Leaves have a mosaic appearance and the veins are yellowed.
Management.
Sow diseasefree seed. Other general management measures may be useful.
Common Pea Mosaic
Common pea mosaic is also called Pea common mosaic, red clover mosaic, and pea mosaic virus.
Cause.
Common pea mosaic virus (CPMV) is reservoired in several legumes and transmitted by aphids, particularly the pea aphid, Macrosiphum pisi, but also by the aphids
Myzus persicae and Aphis rumicis. The aphids acquire CPMV after feeding 5 or more minutes on diseased plants. CPMV is not seedborne.

Page 471
Distribution.
Symptoms.
A yellow mottling consisting of various kinds of chlorotic streaks and spots is located on and between the veins of diseased leaves.
Management
Cowpea Mosaic
Cause.
Cowpea mosaic virus (CPMV) is in the comovirus group. CPMV is transmitted by sap and the bean leaf beetle, Cerotoma ruficornis.
Distribution.
Central America and the United States (including Puerto Rico).
Symptoms.
Diseased leaves have chlorotic and necrotic lesions. A systemic light green mosaic occurs on some diseased leaves.
Management.
Not reported.
Cucumber Mosaic
Cause.
Cucumber mosaic virus (CMV) is in the cucumovirus group. CMV is seedborne.
Distribution.
Symptoms.
Diseased leaves have a mosaic appearance.
Management.
Not reported.
Dwarf
Cause.
Soybean dwarf virus (SDV) is in the luteovirus group. SDV is transmitted by grafting and in a persistent manner by the aphids Aulacorthum solani and
Acyrthosiphon pisum. SDV is not seed or saptransmitted. The optimum temperature for transmission is 20°C.
Distribution.
Japan. SDV may also occur in Australia and New Zealand.
Symptoms.
Diseased plants are generally stunted. Leaves are rugose, curl down, and may have interveinal yellowing.
Management.
Not reported.
Red Clover Vein Mosaic
Cause.
Red clover vein mosaic virus (RCVMV) is in the carlavirus group. RCVMV overwinters in red clover and other legumes and is transmitted by the pea aphid,
Macrosiphum pisi, and other aphids. The pea aphid can ac

Page 472
quire the virus in 1 hour of feeding but loses infectivity in 24 hours. Seed transmission is suspected but has not been demonstrated. Diseased red clover plants serve as
reservoirs for RCVMV, which also causes pea stunt.
Distribution.
United States, particularly the eastern and north central states.
Symptoms.
Symptoms are most conspicuous on leaves of new growth. The first symptom is a faint yellowing of the leaf veins. Gradually the yellowing becomes more chlorotic
until veins and adjacent tissue become white. Yields are reduced and plants become more susceptible to root rot organisms, particularly Fusarium spp. Symptoms
become masked during warm weather.
Management
Ringspot
Cause.
Tobacco ringspot virus is in the nepovirus group.
Distribution.
Not known.
Symptoms.
Symptom description is obscure but is thought to be a mild mottling of leaves that occasionally results in necrotic spots on diseased leaves.
Management.
Not known.
Streak
Cause.
Tobacco streak virus is in the ilarvirus group.
Distribution.
Brazil and the United States.
Symptoms.
Necrotic areas occur in the stem pith, especially near nodes. Axillary buds develop and leaves are dwarfed.
Management.
Not reported.
Wilt
Cause.
Broadbean wilt virus is in the fabavirus group.
Distribution.
Not known.
Symptoms.
Diseased plants are distorted and have a yellow mosaic. Plants eventually wilt during severe disease conditions.
Management.
Not known.

Page 473
Selected References
Blain, F., Bernstein, M., Khanizadeh, S., and Sparace, S. A. 1991. Phytotoxicity and pathogenicity of Fusarium roseum to red clover. Phytopathology 81:105108.
Cunfer, B. M., Grahan, J. H., and Lukezic, F. L. 1969. Studies on the biology of Myrothecium roridum and M. verrucaria pathogenic on red clover.
Dickson, J. G. 1956. Diseases of Field Crops, Second Edition. McGrawHill Book Co. Inc., New York.
Engelke, M. C., Smith, R. R., and Maxwell, D. P. 1975. Evaluation of red clover germplasm for resistance to leaf rust. Plant Dis. Rptr. 59:959963.
Farr, D. F, Bills, G. R., Chamuris, G. P., and Rossman, A. Y. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society,
Hanson, E. W. 1959. Relative susceptibility of seven varieties of red clover to diseases common in Wisconsin. Plant Dis. Rptr. 43:782786.
Hanson, E. W., and Kreitlow, K. W. 1953. The many ailments of clover, pp. 217228. USDA Yearbook, Washington, D.C.
Kahn, M. A., Maxwell, D. P., and Smith, R. R, 1978. Inheritance of resistance to red clover vein mosaic virus in red clover. Phytopathology 68:10841086.
Leath, K. T, and Barnett, O. W. 1981. Viruses infecting red clover in Pennsylvania. Plant Dis. 65:10161017.
Leath, K. T, and Kendall, W. A. 1983. Myrothecium roridum and M. verrucaria pathogenic to roots of red clover and alfalfa. Plant Dis. 67:11541155.
Leath, K. T., Bloom, J. R., Hill, R. R, Kaufman, T. D., and Byers, R. A. 1983. Clover cyst nematode on red clover in Pennsylvania. Phytopathology 73:369.
Martens, J. W., Seaman, W. L., and Atkinson, T. G. (ed.). 1984. Diseases of Field Crops in Canada. Canadian Phytopathological Society, Ottawa, Canada. 160
pp.
McVey, D. V., and Gerdemann, J. W. 1960. Hostparasite relations of Leptodiscus terrestris on alfalfa, red clover and birdsfoot trefoil. Phytopathology 50:416
421.
Murray, G. M., Maxwell, D. P., and Smith, R. R. 1976. Screening Trifolium species for resistance to Stemphylium sarcinaeforme. Plant Dis. Rptr. 60:3537.
Rao, A. L. N., and Hiruki, C. 1985. Clover primary leaf necrosis virus, a strain of red clover necrotic mosaic virus. Plant Dis. 69:959961.
Roberts, D. A., and Kucharek, T. A. 1983. Cylindrocladium crotalariae associated with crown and root rots of alfalfa and red clover in Florida. (Abstr.)
Smith, O. F. 1940. Stemphylium leaf spot of red clover and alfalfa. J. Agric. Res. 61:831846.
Stutz, J. C., Leath, K. T., and Kendall, W. A. 1985. Woundrelated modifications of penetration, development, and root rot by Fusarium roseum in forage legumes.
Tofte, J. E., Smith, R. R., and Grau, C. R. 1992. Reaction of red clover to Aphanomyces euteiches. Plant Dis. 76:3942.

Page 475
14.
Diseases of Rice (Oryzae Sativa)
Bacterial Blight
Bacterial blight is also called kresek.
Cause.
Xanthomonas oryzae pv. oryzae (syn. X. campestris pv. oryzae) survives in the temperate regions of the world in the rhizospheres of weeds, in straw piles, and at
the bases of stems and on roots of rice stubble. In the tropics, X. oryzae pv. oryzae survives on weeds, on secondary growth from rice stubble, and in irrigation water
in canals and rice fields.
Xanthomonas oryzae pv. oryzae is seedborne, although the extent to which it is transmitted through emerging rice seedlings is questionable. Glumes are readily
infected, but recovery from infected seed is difficult because of the slow growth of X. oryzae pv. oryzae on media. Some evidence suggests that infected seed harbors
viable bacteria for only 2 months, indicating seeds may not be an important source of inoculum.
Bacteria are disseminated locally by wind and water, particularly during a storm. Longrange dissemination is by irrigation water. Bacteria enter plants through
hydathodes, growth cracks caused by the emergence of roots at the bases of leaf sheaths, and leaf wounds made by wind during storms. Bacteria do not enter through
stomates. Seedlings are more susceptible to infection than are older plants. Infection at the tillering stage can lead to a total crop loss; however, plants are most
commonly infected at the maximum tillering stage.
Disease is also associated with root and leaf wounds made when seedlings are pulled from seedbeds. This form of bacterial blight is called kresek, and plants less than
21 days old are the most susceptible. Kresek is favored by high temperatures (28° to 34°c).
Once inside a plant, bacteria affect the vascular tissue by cutting off water and causing infected plants to wilt. Bacteria ooze from lesions when

Page 476
ever moisture is present. The bacterial ooze dries and falls into the paddy water.
Bacterial blight became increasingly important when semidwarf, highyielding cultivars were adopted. Six races of X. campestris pv. oryzae have been characterized
in the Philippines. The races 1, 2, 3, and 5 are commonly detected in the Philippines, with race 2 being the most common. Race 1 is detected in lowlands where
traditional cultivars are sown or in areas where cultivars with gene Xa4 have been extensively cultivated. Race 3 is infrequently found. Race 4 is found only in
Palawan. Race 5 is in the highlands and dominates the bacterial population in Banaue, the mountain terraces more 1500 m above sea level. Race 6 is a minute
population. Bacterial blight is particularly destructive in Asia during the heavy rains of the monsoon season.
Distribution.
Africa, Asia, Caribbean, Central and South America, and the United States (Louisiana and Texas).
Symptoms.
Disease incidence increases with plant growth and is the highest at the flowering stage. Diseased seed may be discolored and poorly filled. However, symptomless
seed may harbor low populations of X. oryzae pv. oryzae that later serve as an inoculum source for introducing the pathogen into diseasefree fields.
Foliar symptoms are usually observed at the tillering stage. Watersoaked stripes, which occur along one or both margins of the upper portions of diseased leaf
blades, enlarge and become yellow. Eventually, the lesions cover entire leaf blades and may extend to the lower ends of leaf sheaths, turning them white, then gray due
to the growth of saprophytic fungi. Lesion development increases as the temperature increases and the relative humidity is greater than 70%. Discolored spots
surrounded by watersoaked areas appear on the glumes of green grain; spots on mature grain are gray or light yellow.
The most severe form of bacterial blight is kresek, or wilting. Symptoms appear 2 to 3 weeks after transplanting but only in the tropics due to the practice of cutting off
leaf tips before transplanting seedlings. Diseased leaves become graygreen, roll along the midrib, and eventually completely wither. Bacteria reach the growing point
through the vascular system and infect the bases of other leaves and eventually kill the plant.
Another symptom in the tropics is the production of pale yellow leaves on older plants. The oldest leaves on these older plants remain green, but the youngest leaves
are a uniformly pale yellow or whitish. Sometimes a broad greenyellow stripe may occur on leaves, and diseased tillers do not grow.
Epiphytotics that begin before flowering significantly reduce yield. Epiphytotics that occur after flowering have no effect on grain yield or yield components.

Page 477
Management.
Grow resistant cultivars. Resistance varies according to age of the plant and race of the causal bacterium. Genes Xa3, Xa4, Xa5, and Xa10 have been identified
as resistant genes. Reactions caused by these genes have been divided into seedling and adult plant resistances. Seedling resistance is stable over the entire growth
cycle and results, in adult plants, in lesions up to 15% the length of the lesions on the most susceptible cultivar. Cultivars with adult plant resistance based on the gene
Xa3 are similarly resistant in the adult plant stage but are susceptible in the seedling stage. Both resistances are race specific.
Seedling resistance increases with plant age; the fastest increase in resistance occurs 30 to 50 days after sowing. This differs from that of adult plant resistance, where
immature leaves that are still extending are more susceptible than mature, fully extended leaves.
Bacterial Glume Blotch
Bacterial glume blotch is also called bacterial sheath rot. In several Asian countries and in Hungary, Pseudomonas syringae pv. syringae also has been reported as
the cause of bacterial sheath brown rot.
Cause.
Pseudomonas syringae pv. syringae (syn. P. oryzicola).
Distribution.
Asia and Australia.
Symptoms.
Symptoms vary from dark brown areas (12 mm in diameter) surrounded by green to light brown tissue on scattered florets in a panicle to a dark brown discoloration
of complete florets. In severe disease, 75% of the panicle can be affected, but florets at the base of the diseased panicles rarely are completely discolored. Lesions
also occur on florets just emerging from the boot.
Light green to dark brown lesions without definite margins occur on flag leaf sheaths. Veins of flag leaf sheaths also are darker than interveinal tissue. The stems of
severely diseased plants may collapse at this point, but disease generally does not extend to the stem tissue. Bacterial ooze occurs on diseased tissue during warm,
moist conditions.
Management.
Bacterial glume blotch is not an economically important disease; therefore, management is not warranted.
Bacterial Halo Blight
Cause.
Pseudomonas syringae pv. oryzae. The causal bacterium is also pathogenic to barley, oat, and common bean.
Distribution.
Japan.
Symptoms.
Disease symptoms develop in the tillering stage and disappear in the boot stage. Diseased leaves have small brown lesions that are surrounded by large yellow halos.
Management.
Not reported.

Page 478
Cause.
Xanthomonas oryzae pv. oryzicola (syn. X. campestris pv. oryzicola). The bacterium is a gramnegative, nonsporeforming rod (1.2 × 0.30.5 m) with a single
flagellum. The bacterium survives on infested residue, seed, and possibly in irrigation water. Dissemination is by splashing and windborne rain, irrigation water, and
wind moving diseased leaves back and forth against healthy leaves. Bacteria enter plants through stomates but do not enter the xylem vessels until the later stages of
infection, when bacterial multiplication becomes limited.
After lesions develop, bacterial exudate develops on the surface of lesions during moist conditions at night but dries up and falls into the water when dry conditions
occur during the day. Disease development is favored by rain, high humidity, and temperatures of 28° to 30°C.
Distribution.
Tropical Asia.
Symptoms.
Initially, watery, dark green, translucent streaks (35 mm long) are confined between larger veins. The streaks enlarge into lesions and, under moist conditions, yellow
beads of bacterial exudate appear on lesion surfaces. When conditions become dry, the bacterial exudate dries and forms numerous small yellow beads on the lesion
surface. Susceptible cultivars may have yellow halos around lesions. Older lesions become light brown and translucent, and entire leaves die, become brown, then
graywhite and are colonized by saprophytic organisms.
Bacterial streak can be distinguished from bacterial blight by their thinner, translucent lesions with the yellow bacterial ooze.
Management.
Bacterial Sheath Brown Rot
Bacterial sheath brown rot is also called dirty panicle disease and manchado de grano.
Cause.
Pseudomonas fuscovaginae survives in infested straw, on grain crops, and on wild grasses. The bacterium is also seedborne and seedtransmitted. Disease is most
severe following early infection of the boots. Infection and disease development is favored by relatively cool (17°C and below), wet weather or high relative humidity
at the booting and heading stages.
Distribution.
Widespread. Bacterial sheath brown rot is an important disease in the highaltitude, highrainfall environments of Nepal. The disease is also economically important in
the mid to highaltitude regions of Burundi, Japan, Latin American, Rwanda, and Zaire.
Symptoms.
Symptoms of severe infections first appear at the heading stage and cause total spikelet sterility by preventing normal emergence of the

Page 479
panicle from the boot. Together with poor emergence, panicles and grain are partially to totally discolored. Grain discoloration may also be due to virus infection,
especially rice hoja blanca virus, before flowering, or severe soil stress. Highly acid upland soils or flooded acid soils with high iron content cause grain discoloration if
the rice lines are not adapted to these conditions. Several pathogenic fungi may also cause grain discoloration.
The flag leaf becomes rotted and has a brown discoloration. The disease can eventually lead to the death of the entire plant.
In mild infections, adult plants have characteristic graybrown to brown lesions on the flag leaf sheaths from the booting to heading stages of plant growth. Although
panicles still emerge, a reduced grain yield is produced.
Management.
Resistance has been reported.
Bacterial Sheath Stripe
Bacterial sheath stripe is sometimes called bacterial brown stripe and bacterial stripe. There appear to be some similarities between bacterial sheath stripe and
bacterial stripe in the literature and the two diseases may be the same. However, because symptoms appear to be dissimilar and the causal organisms are identified
differently in the literature, bacterial sheath stripe and bacterial stripe are treated as two separate diseases here.
Cause.
Pseudomonas syringae pv. panici (syn. P. panici). Disease is more severe under wet or humid conditions. Only immature plants become infected.
Distribution.
Japan, the Philippines, and Taiwan.
Symptoms.
Initially, watersoaked, longitudinal stripes form on the lower portions of leaf sheaths. Lesions enlarge (1100 mm), coalesce, and cover entire diseased leaf sheaths.
Bacterial exudate may form on lesion surfaces during humid conditions. Disease may progress into the unfolding leaves and cause a bud rot. Diseased plants may be
stunted or killed.
Management.
Not reported.
Bacterial Stripe
Bacterial stripe is also called bacterial brown stripe and brown stripe.
Cause.
Acidovorax avenae subsp. avenae (syn. Pseudomonas avenae, P. alboprecipitans and P. setariae) is seedborne and survives up to 8 years in seed.
Distribution.
Africa, Asia, Central America, Portugal, and South America.
Symptoms.
Symptoms occur only on seedlings grown in nursery boxes. Leaves and leaf sheaths develop watersoaked, brown, longitudinal stripes. Growth of seedlings with only
brown stripes is not affected in nursery boxes. However, seedlings with more severe symptoms of curving of leaf

Page 480
sheaths and abnormal elongation of mesocotyls, which cause leaves not to open, are generally stunted or curved.
Severely diseased seedlings are dwarfed and often turn yellow, wilt, and die. A heavy bacterial ooze occurs at cuts across brown lesions. Diseased seedlings die
shortly after transplanting. Grain is discolored.
Management.
Not reported.
Foot Rot
Foot rot is also called bacterial foot rot.
Cause.
A bacterium similar to Erwinia chrysanthemi. Iris plants commonly found along canals, ponds, or irrigated rice fields, particularly in Japan, serve as overwintering
hosts and sources of infection. Bacteria from diseased irises are liberated into the water and spread to rice plants by irrigation water. Other annual or perennial plants
may also serve as sources of inoculum.
Distribution.
Asia and the United States (Louisiana).
Symptoms.
Diseased tillers display symptoms of either sheath rot or a wilting of the younger leaves. Sometimes decay is found on plants without detectable sheath rot symptoms.
A dark brown rot occurs in diseased culms, which are soft and easily pulled apart, and bacterial ooze is present in the internodes. A black discoloration indicative of
decay occurs at the nodes, but when the decay is restricted to the lower nodes, new roots that may develop from noninfected nodes above the decayed area allow
new leaves to develop and panicles to keep growing.
Systemic crown infections occur at early tillering stages; sheath rot and restricted culm decay result from infections later than the maximum tillering stage.
Management.
Not reported.
Grain Rot
This disease is also known as glume blight.
Cause.
Burkholderia glumae (syn. Pseudomonas glumae). Bacteria are 1.0 × 1.5 m and have multiple polar flagella. Emerging rice panicles were inoculated at 100%
relative humidity for 24 hours.
Distribution.
Asia, Central America, and South America.
Symptoms.
A brown discoloration occurs on the diseased flag leaf sheath. Grain has a grayish discoloration.
Management.
A dry heat treatment of 65°C for 6 days eradicated bacteria from small seed samples.

Page 481
Seedling Blight
Cause.
Burkholderia plantarii (syn. Pseudomonas plantarii).
Distribution.
Japan.
Symptoms.
Diseased seedlings damp off.
Management.
Not reported.
Sheath Brown Rot
Sheath brown rot is also called bacterial sheath brown rot, bacteria brown rot, and sheath rot. The causal bacterium may be the principal causal agent of dirty panicle
disease. The following symptoms may also be similar to those of dirty panicle disease.
Cause.
Pseudomonas fuscovaginae is present on several grass hosts and is seedborne. Grain discoloration is more severe under high humidity and rainfall and in fields with
soil nutrient imbalances.
Pseudomonas syringae pv. syringae (syn. P. oryzicola) has been found to be associated with bacterial sheath rot in Hungary and Australia.
Distribution.
Africa, Asia, Australia, Europe, Central America, and South America. The disease is found in highland swamps at 1450 to 1600 m in Burundi, Latin America,
Madagascar, Rwanda, and Zaire.
Symptoms.
Longitudinal, redbrown, necrotic stripes extend the full length of diseased sheaths and often the entire length of leaf laminae. Other sheath symptoms are small (15
mm), brown, elongated spots that expand and coalesce to form indistinct blotches on sheaths and, sometimes, on culms.
Symptoms on seedlings are limited to a watersoaked, brown necrosis of sheaths and occasional brown necrotic stripes on leaves. However, black stripes have been
reported as a symptom on seedlings in Burundi. Seedlings often die.
When older sheaths are diseased, flag leaf sheaths enclosing emerging panicles sometimes have watersoaking, blotching, and brown necrosis. Severely diseased flag
leaf sheaths and collars are necrotic and dry. Developing florets are brown, and panicles partially emerge from the boots. Florets that do emerge frequently do not fill
with grain, are spotted or totally discolored, and are sterile. Seed has been described as ''rustyappearing." Roots may also have a brown discoloration.
Inoculated seedlings initially have watersoaked spots that evolve into dark brown streaks (510 cm long) on sheaths and laminae. Three to 5 days after inoculation,
symptoms appear on flag leaf sheaths as watersoaked spots that enlarge to form dark to grayishbrown blotches. Florets are darkto grayish brown.
Management.
Not reported.

Page 482
Aggregate Sheath Spot
Aggregate sheath spot is also called brown sclerotial disease. Aggregate sheath spot and sheath spot may be the same disease, but descriptions of the symptoms
appear to be sufficiently different to consider these as two different diseases.
Cause.
Ceratobasidium oryzaesativae, anamorph Rhizoctonia oryzaesativae. Some researchers consider R. oryzae and R. oryzaesativae to be synonymous. The
causal fungi survive as sclerotia in residue and soil. Initial infections occur by sclerotia floating on paddy water to plants. Ceratobasidium oryzaesativae causes
disease under warm weather conditions. Generally, disease is more severe at low soil nitrogen levels.
Distribution.
China, Japan, India, Iran, Thailand, the United States (California), and Vietnam.
Symptoms.
Lesions first appear at the waterline on lower leaf sheaths during the tillering stage. Lesions (0.5 to 4.0 cm long) are circular to ellipticalshaped and have graygreen to
strawcolored centers that are surrounded by distinct brown margins. A strip of necrotic cells runs down the middle of the lesion center. Frequently additional margins
that form around the initial lesion produce a series of concentric bands.
Disease progresses to upper leaf sheaths and sometimes to the lower portions of leaf blades. Lesions may coalesce and cover entire leaf sheaths, causing leaves to
turn bright yellow, then die. During favorable disease conditions, culms, flag leaves, and panicle rachises may become diseased and cause the death of entire tillers.
As leaf sheaths become rotted, abundant brown sclerotia are produced in and on diseased tissue. Sclerotia inside sheaths are cylindrical to rectangular and visible
through the diseased tissue. Sclerotia produced on the plant surface are irregularly globose.
Management.
Grow tall cultivars. These are more resistant than semidwarf cultivars.
Bakanae Disease
Bakanae disease is also called white stalk and palay lalake (man rice).
Cause.
Fusarium moniliforme survives between growing seasons as mycelia and conidia on or in seed. Fusarium moniliforme is also soilborne, but this is not considered
to be an important source of inoculum.
When seed is sown, F. moniliforme infects seedlings and grows systemically within the xylem tissue as microconidia and mycelium. Diseased plants will either be
stunted or elongated, depending on soil moisture con

Page 483
ditions. Fusarium moniliforme produces fusaric acid, which stunts plants in dry soil conditions, and gibberellin, which causes plants to elongate abnormally under
moist soil conditions. At flowering time, conidia are produced on diseased or dead culms and disseminated by wind to flowers of plant hosts or to developing grain,
which becomes either infected or contaminated.
Distribution.
Wherever rice is grown.
Symptoms.
Plants may be either elongated or stunted, but the most common symptom is abnormal elongation of diseased plants in seedbeds or fields. Diseased seedlings are thin,
chlorotic, and several centimeters taller than healthy plants. Severely diseased seedlings may die before or after transplanting.
In the field, diseased plants are taller than normal and have few tillers and chlorotic flag leaves. Leaves on a diseased plant die in a relatively short time. Diseased plants
that live have empty panicles. A white or pink fungus growth may appear on the lower parts of diseased plants.
Management
3. Experimentally, disease was reduced 1.9% to 77.0% when seeds were soaked in suspensions of antagonistic bacteria.
Basal Node Rot
Cause.
Fusarium oxysporum. Basal node rot is prevalent under two conditions: in fields where rice is grown in rotation with pasture grass, and in the second and third year
of successive rice cultivation.
Distribution.
Brazil.
Symptoms.
Areas of stunted plants with dull green leaves occur in fields. A black discoloration occurs at the point on underground basal nodes where adventitious roots are
initiated and often extends to mesocotyls and adventitious roots. Severely diseased plants have poorly developed roots and few tillers. Plant death is rare.
Management.
Not reported.
Black Kernel
Cause.
Curvularia lunata, teleomorph Cochliobolus lunatus. Disease is favored by excess moisture in the form of rain, dew, or high humidity and temperatures of 24° to
30°C.
Distribution.
Not reported, but likely common in warm, humid ricegrowing areas.

Page 484
Symptoms.
At maturity, diseased kernels are covered with a dense, velvety, dark fungal growth consisting of conidia and conidiophores.
Management.
Not reported.
Blast
Blast is also called Pyricularia blight and rotten neck.
Cause.
Pyricularia grisea (syn. P. oryzae), teleomorph Magnaporthe grisea, overwinters for at least 4 years as mycelia in infested residue, and for 1 or more years as
conidia on residue and seed in the temperate ricegrowing regions and, likely, in the tropical ricegrowing regions of the world. Although Rossman (1990) considered
Pyricularia grisea and P. oryzae to be synonymous, past literature reported that P. oryzae also survives in the temperate regions as chlamydospores, perithecia, and
sclerotia in soil, on winter cereals, diseased rice plants, and weed hosts. Survival is not important for P. oryzae in the tropics since airborne conidia are present
throughout the year.
Conidia are produced from mycelium and become windborne at night in the presence of dew or rain. High humidity favors subsequent disease development. At
temperatures of 18° to 20°C, rice cultivars adapted to temperate climates generally are more predisposed to infection than are tropical cultivars. Secondary inoculum
is conidia that are produced on lesions when there has been more than 93% relative humidity for 6 days and are disseminated by wind, water, infested residue, or seed
to other host plants.
Although plants of all ages are susceptible, blast is essentially a disease of young host tissues. For example, fully extended leaves are more resistant than partially
extended leaves, leaves on older plants are more resistant to infection, and panicle resistance is reported to increase with age. Rice plants also tend to be most
susceptible when they are grown in dry soil and are relatively resistant when they are grown under flooded conditions. Physical conditions tend to affect resistance;
plant susceptibility increases when plants are grown too close together and excessive nitrogen is applied to soil. Several physiologic races of P. oryzae are thought to
exist.
Distribution.
Generally distributed wherever rice is grown.
Symptoms.
Blast generally is more destructive in temperate environments than in the tropics. Symptoms of blast can be divided into two general phases, depending on when the
plant was infected. The leaf blast phase, which occurs between the seedling and late tillering stage, frequently causes the death of plants. The panicle blast phase, or
neck blast phase, occurs after flowering. Spots are produced on leaves, nodes, panicles, and grains, but seldom on leaf sheaths.
Spots on leaves begin as small, watersoaked, whitish, grayish, or bluish dots but quickly enlarge (0.30.5 × 1015 mm) under moist conditions.

Page 485
Mature leaf spots are elliptical and pointed at both ends and have a gray to whitish center surrounded by a brown to redbrown margin. Spots vary in shape and color
depending on cultivar, environment, and age. Resistant cultivars have only brown specks, while moderately resistant cultivars have small, roundish lesions with necrotic
centers and brown margins.
Later in the growing season, some cultivars are diseased where the flag leaf attaches to the sheath. The lesion enlarges downward on the sheath and upward on the
leaf, becoming gray at the point of attachment. The flag leaf may break off and become detached from the plant.
Nodes at or near flood level, which generally are the second or third node from the soil line may be infected. The base of the sheath turns black due to production of
conidia and the node eventually breaks apart and remains connected by a few vascular strands. The plant above the infected node dies.
Any portion of the panicle, panicle branches, and glumes may become diseased and have brown lesions. If the base of the panicle is diseased, rotten neck (or neck
rot) symptoms occur, causing the stem below the panicle to snap.
Management
1. Grow resistant cultivars; however, a cultivar may not be resistant to all races of P. oryzae. Some cultivars display adultplant resistance to leaf blast and panicle
blast. It is uncertain if vegetativestage resistance to leaf blast is correlated with resistance to neck blast.
2. Sow only clean, healthy seed treated with a seedprotectant fungicide.
3. Apply small increments of nitrogen at any one time.
4. Manage floodwater to maintain adequate but not excessive depth. Flooding is an effective way of managing blast.
5. Avoid excessive plant populations.
6. Apply a foliar fungicide if disease conditions warrant its use.
7. Destroy previous crop residue as soon after harvest as feasible.
8. Rotate rice with other crops.
9. Control grasses and other weeds.
10. Experimentally, silicon has been shown to lower disease intensity.
Brown Blotch
Cause.
Cercospora oryzae. Symptom development is aided by the secretion of a red toxin, cercosporin, by the mycelium of some pathovars. Cercosporin is excited upon
illumination and generates free radicals that damage cell membranes and cause cell death.
Distribution.
The United States (Louisiana and Texas).
Symptoms.
Initially, small, irregularshaped, brown blotches occur on the diseased leaf sheath approximately 3 to 4 cm below the ligule. Eventually,

Page 486
the blotch spreads to cover the entire leaf sheath. Leaves are prematurely desiccated and yields are reduced.
Management
1. Grow resistant cultivars. Resistant cells have a mechanism for excluding, exporting, or destroying cercosporin.
2. Sow earlymaturing cultivars early in the growing season to escape the disease.
Brown Spot
Brown spot is also called brown leaf spot, rice brown spot, and sesame leaf spot.
Cause.
Cochliobolus miyabeanus, anamorph Bipolaris oryzae, (syn. Drechslera oryzae and Helminthosporium oryzae). Some researchers consider the causal fungus to
be Exserohilum oryzae, but this name is not listed in Farr et al. (1989) as a synonym for B. oryzae. Cochliobolus miyabeanus overwinters primarily as mycelium in
seed. The following spring, infected seeds give rise to seedlings with spots on roots and coleoptiles. Leaves are usually not infected by seedborne inoculum because of
their rapid growth at this time. Most leaf spots originate from secondary infections that occur when conidia produced on spots that developed on coleoptiles are
disseminated by wind to leaves. Plants that grow in soils with nutritional deficiencies or poorly drained soils where nutrient uptake is hindered are more susceptible to
infection. Disease development is favored by relative humidities of 86% to 100% and temperatures of 20° to 25°C. Leaves must be wet for 8 to 24 hours for infection
and disease to occur. Bipolaris oryzae produces a toxin that induces disease symptoms.
Distribution.
Generally distributed in ricegrowing areas of Africa, Asia, and the Western Hemisphere.
Symptoms.
The first symptoms on coleoptiles are pale, yellowbrown spots or streaks. Young roots have blackish lesions. Young spots on leaves are small, circular, and dark
brown or purplebrown. Typical spots are oval, about the size and shape of sesame seeds, and evenly distributed over leaf surfaces. Spots may become numerous
enough to kill leaves. When fully developed, spots are brown with a gray or whitish center surrounded by a bright yellow halo. On very susceptible cultivars, spots
may be larger (1 cm long).
Black or dark brown spots appear on glumes and may cover entire surfaces of glumes. During humid weather, conidia are produced in spots, giving them a velvetlike
appearance. Grain has dark spots on endosperms.
Management
1. Balance soil fertility. Plants grown in silicondeficient soils are more prone to disease than plants grown in soils with adequate silicon. In de

Page 487
ficient soils, the addition of silicon decreases disease severity and increases yields.
2. Rotate rice with other crops.
5. Grow the most resistant and adapted cultivar.
Collar Rot (Ascochyta oryzae)
Collar rot is also called rice collar rot.
Cause.
Ascochyta oryzae.
Distribution.
India.
Symptoms.
Small, brown lesions expand to cover the whole collar region. Lesions extend down the diseased leaf sheath and blade, turning them dark brown to black. Leaf blades
separate from leaf sheaths and defoliate.
Management.
Not reported.
Collar Rot (Pestalotiopsis versicolor)
Collar rot is also called rice collar rot.
Cause.
Pestalotiopsis versicolor.
Distribution.
India.
Symptoms.
Symptoms first appear at the collar joining the leaf blade and leaf sheath and consist of small, brown lesions that expand to cover the whole collar region. Lesions
sometimes extend down the diseased leaf sheath and the blade, turning them dark brown to black. Subsequent rotting causes the leaf blade to separate from the
sheath and drop off. In severe cases, several leaves on the same plant dry up and defoliate.
Management.
Not reported.
Crown Sheath Rot
Crown sheath rot is also called Arkansas foot rot, black sheath, black sheath rot, and brown sheath rot.
Cause.
Gaeumannomyces graminis vat. graminis likely overseasons as perithecia and mycelia in infested residue and is seedborne to a slight extent. Ascospores are
disseminated by wind to host plants and initiate primary infection when moisture is present later in the growing season. Gaeumannomyces graminis var. graminis
also survives on St. Augustine grass and bermudagrass in Florida.
Distribution.
Africa, India, Japan, the Philippines, and the United States.

Page 488
Symptoms.
Symptoms appear late in the growing season. A brown discoloration occurs on diseased sheaths from the crown to the waterline or above. Leaf blades die when
sheaths are severely diseased. Numerous black perithecia are produced in the discolored areas but are not easily seen because only the perithecial peaks protrude
above the surface of the epidermis. Redbrown mycelial mats may be found on the inner surface of the diseased sheaths. At maturity, straw has a dull brownish cast.
Culms may also be infected, but perithecia are not produced. Few panicles—frequently only one—are produced on diseased plants. Lodging usually occurs at one of
the nodes rather than from the internode area.
Management
3. Sow early in the growing season.
4. Delay permanent flood.
Dead Tiller Syndrome
Cause.
An unidentified fungus is thought to be the cause.
Distribution.
The United States (Arkansas).
Symptoms.
Symptoms first appear 6 to 10 days after the permanent flood and progress from 8 to 14 days until the floodwater equilibrates to ambient soil and air temperatures.
The initial symptom is a slight discoloration of plants and some wilting, but advanced symptoms include severe wilting. Occasional plants have yellow to orange
chlorosis along older leaf tips or leaf margins. Diseased plants have a rotting culm (usually the main culm in a hill), which frequently produces a distinct odor when
crushed. Tillers or nearby plants are not affected. Decay begins internally at a node and can be well advanced before this symptom can be observed; plants then die in
24 to 48 hours. Dead tiller syndrome continues to develop throughout the growing season in areas where cold floodwater is added to the field.
Management.
Not reported.
Downy Mildew
Downy mildew is also called yellow wilt.
Cause.
Sclerophthora macrospora survives as oospores in infested leaf residue. Oospores germinate in the spring by forming sporangia. Sporangia, in turn, germinate by
their cell contents dividing into zoospores that are liberated into water and "swim" to a nearby rice seed that is germinating. Infection is optimum at temperatures of 18°
to 20°C. Oospores and sporangia are produced on diseased plants throughout the growing season and provide secondary inoculum.

Page 489
Distribution.
Australia, China, India, Italy, Japan, and the United States (Arkansas). Downy mildew is not considered a serious disease.
Symptoms.
Symptoms are most obvious at flowering time. Initially, the youngest leaves have chlorotic or whitish spots, and leaf sheaths may be distorted and twisted. Particles are
also distorted due to their failure to emerge from the distorted and twisted sheaths. These panicles also are smaller than normal and remain green, while the floral parts
are either bare or have a "hairy" appearance.
Management.
Eyespot
Eyespot has also been called brown spottype disease.
Cause.
Drechslera gigantea (syn. Helminthosporium giganteum). Grasses such as Cynodon dacytlon and Eleusine indica may be alternate hosts. Prolonged leaf
wetness favors disease.
Distribution.
Colombia, Guatemala, Guyana, Honduras, Mexico, Panama, and Peru.
Symptoms.
Initially, spots on leaves are small, watersoaked, olivaceous dots or rings. A yellow halo frequently appears around young spots but later disappears. Later, spots
develop into minute, longitudinally elongated, oval lesions (0.51.0 × 1.04.0 mm) with white to strawcolored necrotic centers and surrounded by narrow, dark
brown margins.
Under favorable disease conditions, successive development and coalescence of lesions produces a characteristic zonation, which is more irregularshaped than the
regular wavy pattern characteristic of leaf scald.
Management.
False Smut
False smut is also called green smut.
Cause.
Ustilaginoidea virens overwinters in temperate regions as sclerotia and chlamydospores. Most primary inoculum comes from sclerotia germinating and producing
stromata on tips of stalks. Ascospores are produced in perithecia within stromata and disseminated by wind to host flowers. Rice is infected either at very early
flowering or when grain is mature.
Individual grains are transformed into spore balls in which one to four sclerotia are produced. Secondary infection is by chlamydospores formed on spore balls that are
disseminated by wind to rice plants, where they germinate and form germ tubes on which conidia are borne. Chlamydospores do not free easily from smut balls
because of a sticky material that holds them in place. Optimum germination occurs at 28°C and, later, disease development is favored by high moisture.

Page 490
Distribution.
Most ricegrowing areas, but false smut causes little damage.
Symptoms.
A few to many grains of the panicle are transformed into balllike objects that have a velvety appearance. Balls are small and visible between glumes at first but
continue to grow and enclose the floral parts, reaching a diameter of 1.0 cm or more. Young balls are slightly flattened, smooth, yellow, and covered by a membrane.
With continued growth, ball membranes burst and expose mycelium and spores, and the color of the ball changes to orange and still later to yellowgreen or green
black. At this stage of disease development, the surface of the balls crack. When the balls are cut open, their white interior consists of mycelium together with floral
parts and other host parts.
Management.
Apply a foliar fungicide a few days before heading.
Fusarium Diseases
Cause.
Fusarium equiseti, F. semitectum (syn. F. pallidoroseum), F. nivale (syn. Microdochium nivale), and F. culmorum.
Distribution.
Symptoms.
Fusarium culmorum causes brown, necrotic leaf tips and spots on seedling leaves ranging from minute, irregularshaped spots to rectangular spots (12 × 46 mm)
that cover 3% to 5% of the leaf blade. Adult plants are usually not diseased.
Fusarium equiseti causes discoloration of vascular tissues of culms that extends from the seedling base to the third node. Diseased culms are initially reddish but later
become brown to black.
Fusarium semitectum causes disease of panicles and culms. Particles in the developing sheath at boot stage have irregularshaped lesions that are yellowish but later
become dark brown. Diseased culms have a reddish to brownish vascular discoloration that extends from the base of the plant to the third or fourth internode. A
necrosis develops during flowering and continues until ripening to partially or totally cover diseased kernel surfaces.
Fusarium nivale causes a necrosis of panicles and leaves.
Management.
Not reported.
Fusarium Leaf Blotch
Cause.
Fusarium solani.
Distribution.
India.
Symptoms.
Symptoms on diseased leaves are irregularshaped, oblong, brown necrotic areas (56 × 1420 cm) with watersoaked margins that eventually

Page 491
coalesce and result in a blight of the leaf blade. Disease usually appears a few centimeters from the leaf tip during the boot stage of plant development or later.
Management.
Not reported.
Fusarium Sheath Rot
Cause.
Fusarium moniliforme and F. proliferatum.
Distribution.
Fusarium moniliforme occurs in India and F. proliferatum occurs in the United States (Arkansas and Texas).
Symptoms.
Dark brown lesions occur on the flag leaf sheath, and there is a blanking/discoloration of the panicle. Young tillers of inoculated plants are sometimes killed. The
mycotoxins beauvericin, fumonisin, and moniliformin are produced by cultures of F. proliferatum. The fumonsins FB 1, FB 2, and FB 3 have been detected in
naturally contaminated rice in the United States.
Management.
Not reported.
The original name of the disease has been retained although the nomenclature of the causal organism has changed.
Cause.
Exserohilum rostratum (syn. Helminthosporium rostratum).
Distribution.
India.
Symptoms.
Symptoms are most prevalent in August. Small, lightcolored, oval to linear spots (1.0 × 2.03.0 mm) occur on diseased leaves.
Management.
Not reported.
Kernel Smut
Kernel smut is also called black smut and bunt.
Cause.
Tilletia barclayana (syn. Neovossia barclayana, N. horrida, and T. horrida). Tilletia barclayana survives as chlamydospores in endosperms, on the surface of
seeds, and in soil. Chlamydospores germinate in the presence of moisture and produce a promycelium on which several sporidia are borne in a whorl. Secondary
sporidia are produced either directly by budding from primary sporidia, or from mycelium produced by primary sporidia. The secondary sporidia are disseminated by
wind to host plants and infect flowers that are just opening. After infection occurs, only the endosperms, not the embryos, are destroyed. Tilletia barclayana
apparently does not become systemic in diseased seedlings.

Page 492
Abundant moisture during flowering increases disease incidence and severity. Moisture in the form of rain or dew at harvest time causes chlamydospores to swell and
break through the hull of the diseased seed and be released to infest soil and healthy seed. Diseased seed may also remain intact until sown the following spring.
Distribution.
Symptoms.
Symptoms are obvious only at maturity. Generally only a few grains in a panicle and often only a part of a grain—usually the endospermare diseased. After a rain or
dew, the mass of chlamydospores swells and bursts through a glume, appearing as tiny, black pustules or streaks. Severe disease causes a short, beaklike outgrowth
to be produced by ruptured glumes. Chlamydospores look like a black powder has been scattered onto the leaves and grains of surrounding plants. Chlamydospores
that do not break out of a glume can be seen through the wet hulls. Seeds that are not severely diseased may germinate, but the resulting seedlings are stunted. Smut
spores give milled rice a grayish color.
Management
2. Sow earlymaturing cultivars as early as feasible in the growing season.
3. Avoid high rates of nitrogen fertilizer.
Leaf Scald
Cause.
Microdochium oryzae (syn. Rhynchosporium oryzae) overseasons in and on seeds. Although Gerlachia oryzae is reported as the causal organism in some
literature, it is possibly a synonym of M. oryzae even though it is not listed as such by Fart et al. (1989). Microdochium oryzae is a weak pathogen that infects plants
either predisposed by other factors or through wounds. Seeds are the primary source of inoculum. Disease development is favored by wet weather.
Distribution.
West Africa, Central America, Southeast Asia, and the United States.
Symptoms.
Symptoms most commonly occur near tips of mature leaves but may also occur on leaves, leaf sheaths, culms, and grains in all stages of development. Oblong or
diamondshaped, watersoaked blotches that are somewhat restricted by veins develop into large olivecolored areas encircled by alternate dark and light brown
halos. Later, blotches become grayolive and have a characteristic zonation of light and dark brown rings. When large portions of leaves are diseased, they are killed
and become tan.
Management
3. Apply a seedtreatment fungicide.

Page 493
Leaf Smut
Cause.
Entyloma oryzae overwinters as chlamydospores in the sori on leaves. The following summer the presence of moisture and temperatures of 28° to 30°C is optimum
for chlamydospores to germinate and produce a promycelium on which sporidia are formed. The sporidia bud and form secondary sporidia that are disseminated by
wind to leaves, where they germinate in the presence of water.
Distribution.
Wherever rice is grown, but leaf smut is considered a minor disease.
Symptoms.
Leaf smut symptoms occur late in the growing season. On both sides of diseased leaves, sori occur as small, black, slightly raised, rectangular spots that may become
numerous but still remain distinct from each other. Sori have been mistaken for sclerotia. The chlamydospores in sori are held tightly together and are covered by the
leaf epidermis. After soaking in water for a few minutes, the epidermis ruptures and reveals a black mass of chlamydospores beneath the epidermis surface. Severely
diseased leaves may turn yellow, split, and sometimes die.
Management.
No management is necessary since leaf smut is not considered a serious disease.
Narrow Brown Leaf Spot
Narrow brown leaf spot is also called Cercospora leaf spot.
Cause.
Cercospora janseana (syn. C. oryzae), teleomorph Sphaerulina oryzina. Little is known of the life cycle of C. janseana as it relates to causing narrow brown leaf
spot on rice. Several physiologic races exist.
Distribution.
Generally distributed wherever rice is grown except in Europe.
Symptoms.
Disease usually does not become severe until rice approaches maturity. Symptoms are most common on leaves but may occur on leaf sheaths, glumes, and pedicels.
Tan or brown leaf spots (1.53.0 × 3.013.0 mm) occur only in interveinal areas of the diseased leaf.
Spots on glumes and pedicels are smaller and darker than the spots on leaves. Spots on leaf sheaths (750 mm long) are light to dark brown and have indefinite
borders that may encircle the plant.
Management
2. Sow earlymaturing cultivars early in the growing season to escape the disease.
Pecky Rice
Pecky rice is also called kernel spotting.

Page 494
Cause.
Cochliobolus miyabeanus, Curvularia spp., Fusarium spp., Microdochium oryzae, Sarocladium oryzae, and other fungi.
Distribution.
Widespread.
Symptoms.
Several or all florets per panicle are shriveled and discolored a light to dark brown, reddishbrown, purple, or white.
Management.
Normally not practiced.
Phoma Seedling Blight
Cause.
Phoma glomerata is seedborne.
Distribution.
Ghana.
Symptoms.
Diseased seed is covered with a pale brown to brown mycelium. Pycnidia are produced singly or in groups. Seedlings that rise from diseased seed damp off within 7
days after germination. Brown lesions occur on diseased coleoptiles, leaves, and culms of emerged seedlings. Roots show different degrees of root rot; pycnida
develop in the diseased areas of the root. Eventually, seedlings are killed.
Management.
Not reported.
Pithomyces Glume Blotch
Cause.
Pithomyces chartarum.
Distribution.
India.
Symptoms.
Diseased plants occur in patches within a field. Although all glumes on a head may be diseased, the terminal seeds are diseased most frequently. Initially, light brown
lesions occur on glumes of individual grains. In cases, lesions develop toward the tip of the grain rather than the base. Lesions become gray in the center and are
surrounded by a dark brown ring. Lesions enlarge and sometimes cover the whole surface of grains. Diseased glumes are grayer than healthy glumes. Grains enclosed
by infected glumes remain small, have an undeveloped endosperm, and germinate poorly. Diseased grains also are shriveled, discolored, and light in weight. Short,
dark conidiophores bearing conidia may be observed on diseased plant parts.
Management.
Not reported.
Pythium Damping Off
Cause.
Pythium irregulare, P. spinosum, and P. sylvaticum are the main causal agents of damping off of rice seedlings in nursery flats. Other Pythium spp. that contribute
to early damping off are P. aphanidermatum, P. myriotylum, P. splendens, P. ultimum, and P. vexans. Disease is favored by low tempera

Page 495
tures and a soil pH of 6.0. The main causal agents are pathogenic to rice seedlings at emergence but are no longer pathogenic to seedlings older than the firstleaf stage
of plant development. Pythium graminicola, however, is reported to cause damping off of rice seedlings at the two to threeleaf stage.
Distribution.
Damping off tends to be more of a problem in the temperate ricegrowing areas of the world than in the tropics.
Symptoms.
Diseased seedlings at the four to fiveleaf stage are chlorotic and stunted. Roots are necrotic and undeveloped. Severely diseased plants are killed.
Management.
Treat seed with a fungicide.
Rust
Cause.
Puccinia graminis f. sp. oryzae. The life cycle and symptoms are similar to those caused by P. graminis on other cereals. Rust is a minor disease on rice and causes
no economic loss.
Sheath Blight
Cause.
Rhizoctonia solani AG1 IA, teleomorph Thanatephorus cucumeris. Rhizoctonia solani survives as sclerotia in the top 1 cm of soil for up to 21 months in dry soil
but for less than 7 months in watersaturated soils. As soil depth increases, the number of viable sclerotia decreases. Survival also occurs as mycelia in infested
residue, and as sclerotia and the basidial stage of T. cucumeris on weeds. Thus weeds are hosts of the causal fungi and a potential source of inoculum to infect rice.
Primary inoculum likely consists of buoyant sclerotia; disease incidence is directly related to the number of these sclerotia. Sclerotia float on top of the water and tend
to accumulate around plants at the waterplant interface. There, sclerotia germinate and form infection hyphae that penetrate plants at the waterline.
The fungus then forms infection cushions and/or lobate appressoria on the plant surface. Mycelium grows rapidly on or inside the diseased plant tissues, spreading by
means of runner hyphae to the upper plant parts and initiating secondary infections that become spots. Eventually, sclerotia formed in the center of the spots are easily
detached and reinfest soil and water.
Infection and disease development are optimum at temperatures of 28° to 32°C and a 95% or higher relative humidity. Sheath blight is associated with intensive and
highinput production systems. Disease has been reported to be more severe under high nitrogen than low nitrogen conditions. Close sowing and heavy fertilization
increases the crop canopy, thereby raising humidity and increasing disease incidence and severity. In

Page 496
the United States, disease develops more extensively in semidwarf cultivars than in closely related standard height cultivars because of the shorter distance between the
waterline and panicles.
Distribution.
Wherever rice is grown. Sheath blight is considered by many researchers to be the most important disease of rice in the southern United States.
Symptoms.
Symptoms usually occur as lesions on lower leaf sheaths after diseased plants have reached the late tillering or early internode elongation stage of plant growth, but
symptoms may also occur on young plants. Spots or lesions appear mainly on diseased leaf sheaths but may extend into the leaf blades if environmental conditions are
favorable for disease development.
Symptoms appear near the waterline as greengray, elliptical spots that are about 1 cm long. Eventually, spots enlarge to 2 to 3 cm long, become gray, and have
irregular purplebrown margins. Lesions on the upper plant coalesce and encompass the entire diseased leaf sheaths and stems. Brown sclerotia in the center of spots
are easily detached. During humid conditions, mycelium may grow upward to infect higher leaf sheaths on the plant. With severe disease, all leaves of a plant may be
blighted, allowing increased sunlight penetration and decreased humidity. Lesions then dry up and become white, tan, or gray with brown borders.
Yields are reduced primarily from reduction in mean seed weight and a lower percentage of filled spikelets. Additional losses result from increased lodging or reduced
ratoon production.
Management
1. Apply fungicides and other chemicals that are effective in managing sheath blight.
2. Sow the recommended population. In the Philippines, a wider plant spacing generally decreased disease incidence and increased yield in BR1 rice.
3. Grow tolerant cultivars. Indica types are more tolerant than Japonica types. In the United States, semidwarf lines are more susceptible than standard height lines.
Most longgrain cultivars of rice in the United States are susceptible or very susceptible to sheath blight, whereas medium and shortgrain cultivars tend to be
moderately susceptible to moderately resistant. Resistance in plants is associated with two factors: a reduction in numbers of infection cushions and the production of
oxidized phenolic compounds, which slow the spread of R. solani within a plant. The phenolic compound factor is manifested as a dark zone around the lesion.
4. Apply proper fertility rates. High nitrogen applications increase disease incidence.
5. A suspension of Bacillus subtilis or an antibiotic substance from B. subtilis has been reported to limit size of lesions.

Page 497
Sheath Blotch
Cause.
Pyrenochaeta oryzae. Survival occurs as pycnidia in infested residue. Conidia are the primary inoculum.
Distribution.
Worldwide in all ricegrowing areas. In the United States, sheath blotch has been reported from Arkansas, Florida, and Texas.
Symptoms.
Oval, reddishbrown, blotchlike symptoms occur near the middle of the outer leaf sheaths of rice tillers. Lesions start from the margin of a sheath as dark reddish
brown, oblong blotches that enlarge, become bluish gray, and may cover the entire sheath. Lesions may grow to 10 cm and often appear at the junction of the sheath
and leaf blade, just below the leaf collar, without causing the collar to break. When dry, the affected part of the sheath turns graybrown and may or may not have
distinct redbrown to brown margins. As diseased plants mature, lesions enlarge to eventually cover the whole sheath and kill the leaf. Occasionally, P. oryzae infects
the leaf blade and glumes. Pycnidia may be seen embedded in diseased tissue.
Management.
Not reported.
Sheath Rot
Cause.
Sarocladium oryzae (syn. Acrocylindrium oryzae) is seedborne and survives as mycelia in infested residue. Conidia are produced from mycelia and disseminated by
wind to leaf sheaths, where entry is gained through stomata and injuries. Insect wounding is especially important in the infection process. High insect populations injure
the leaf sheaths enclosing panicles, thereby retarding emergence of panicles and facilitating development and spread of disease. Mycelium then grows intercellularly in
vascular bundles and sheath mesophyll tissues. Midribs of leaf blades and grains are also infected.
In the Philippines, rice is infected at all stages of growth but sheath rot is reported to be most destructive when plants are infected after booting. Maximum disease
occurs when minimum temperatures are 17° to 20°C and minimum relative humidity is 40% to 56% at flowering time. However, other reports from the Philippines
state the optimum temperature and relative humidity for infection and disease development of seedlings are 25° to 35°C and 70%, respectively. Heavy nitrogen
application and other fertility programs that result in poor growth favor disease development.
Distribution.
Southeast Asia and the United States.
Symptoms.
Symptoms vary with cultivar and the diseased plant part. Generally, sheath rot occurs on the top leaf sheaths, especially the flag leaf sheath enclosing the young
panicles. Initially, lesions start as oblong or somewhat irregularshaped spots (515 mm long) that either have gray

Page 498
centers with brown margins or are entirely graybrown. Lesions enlarge, coalesce, and cover most of the leaf sheath. Panicles fail to emerge or partially emerge, then
rot. A whitish, powdery growth consisting of mycelium, conidiophores, and conidia may be found inside diseased sheaths.
It has been reported that a large reduction in yield is due to a synergistic effect between S. oryzae and rice tungro virus.
Management
2. Balance soil fertility. Excessive nitrogen increases disease incidence and severity and increased potassium decreases it.
Sheath Spot
Sheath spot is also called bordered leaf spot, brown bordered leaf spot, red sclerotial disease, Rhizoctonia sheath spot, and sheath blight. Aggregate sheath spot and
sheath spot may be the same disease. However, descriptions of the symptoms appear to be sufficiently different to consider these as two separate diseases.
Cause.
Rhizoctonia oryzae. It is also reported that R. oryzaesativae (syn. Sclerotium oryzaesativae) is a causal organism. Although it is not known for certain how the
fungi survive, it is presumed that R. oryzae overwinters as mycelia or sclerotia in infested residue and possibly in soil. Wild grasses have also been observed to act as
overwintering hosts.
Dissemination is likely by wind or waterborne soil and residue. Sheath spot is most severe along levees and other places where rice growth is dense, and high humidity
and temperatures of 29° to 32°C commonly occur.
Distribution.
Japan, the United States, and Vietnam.
Symptoms.
Symptoms, in the form of spots, first appear during the late tillering or early heading stage of plant growth. Spots are confined almost entirely to leaf sheaths and do
occasionally occur on leaves but not on stems. Spots first appear on the lower leaf sheaths near the waterline but may occur on other sheaths of the diseased plant.
Spots initially are elliptical and have a redbrown discoloration. As spots mature, they have a bleached, strawcolored center with a wide, redbrown margin and
average 1 to 3 cm in length but may become as long as 10 cm. Lesions may enlarge and coalesce to form large discolored areas that kill diseased leaves and cause
plant lodging.
Management
2. Avoid excessive seeding rates.
3. Use proper timing of nitrogen topdress applications.
4. Control grasses and other weeds.

Page 499
Stackburn Disease
Cause.
Alternaria padwickii is seedborne and overwinters in soil and infested residue as sclerotia and saprophytic mycelia. Conidia produced on mycelia are disseminated
by wind to leaves, where infection is most likely to occur through a wound because A. padwickii is a weak pathogen.
Distribution.
Symptoms.
A few oval or circular spots occur on leaves and vary in size from 3 to 10 mm long. Initially, the centers of spots are tan, then become white and encircled by one or
two narrow, dark brown rings. The white spot is speckled with sclerotia that look like black dots scattered over the spot.
Glumes have tan to whitish spots that are surrounded by a relatively wide, dark brown margin. These spots also have sclerotia scattered over them. Diseased kernels
are discolored, shriveled, and brittle.
Roots and coleoptiles of germinating seedlings may have dark brown to black lesions with sclerotia scattered over them. Seedlings may either outgrow the disease or
wither and die.
Management.
Not reported.
Stem Rot
Cause.
Magnaporthe salvinii, synamorph Sclerotium oryzae (the sclerotial stage), anamorph Nakataea sigmoidea (syn. Helminthosporium sigmoideum and
Vakrabeeja sigmoidea). A similar fungus, H. sigmoideum var. irregulare, also was reported to cause the same disease, but it may be the same as N. sigrnoidea.
The fungi overwinter for up to 6 years as sclerotia in the top 5 to 10 cm of soil and on infested residue. Sclerotia are the primary inoculum. During tillage operations,
sclerotia float on the water surface, germinate, and infect plants through wounds. Conidia and ascospores are produced approximately 60 and 100 days after sowing,
respectively, but apparently do not cause severe enough disease to reduce yield. However, they may initiate secondary infections that, in turn, may increase the level of
overwintering sclerotia.
Sclerotia develop between the leaf sheath and culm. After harvest, S. oryzae continues to grow saprophytically on infested residue and produce large numbers of
sclerotia. Rice tissue parasitized by S. oryzae remains the most important source of sclerotia. Colonization of uninfected rice residue by mycelia from sclerotia is not an
important source of new sclerotia. Inoculum levels are greatest where large amounts of infested residues are left on or near the soil surface. High nitrogen levels
increase the incidence and severity of stem rot.
Distribution.
Burma, India, Japan, the Philippines, Sri Lanka, the United States (Arkansas, California, Louisiana, and Texas), and Vietnam.

Page 500
Symptoms.
Symptoms appear late in the growing season, generally within a week after a field has been drained of water. Symptom development occurs rapidly only after plants
are in the reproductive stage and is the most rapid at physiologic maturity.
Small, blackish, irregularshaped lesions occur on outer leaf sheaths near the waterline. Lesions enlarge as the disease progresses. Eventually, leaf sheaths are rotted
and numerous sclerotia form as S. oryzae grows between the diseased inner leaf sheaths and culms. One or two internodes of diseased stems rot and collapse, with
only the epidermis remaining intact. Dark gray mycelium may be seen in the hollowed stems and numerous, small, black sclerotia occur on inner stem surfaces. The
next internodes may appear to be healthy. Diseased stems lodge.
Occasionally in the tropics, leaf sheaths of transplanted seedlings rot at the waterline and cause the leaves above them to die.
Management
1. Sow earlymaturing cultivars early to escape disease injury.
2. Application of potassium fertilizer reduces stem rot severity.
3. Drain water at the early stages of infection and keep soil saturated but not covered with water until rice has almost matured.
4. Rotate a field out of rice for 6 years or more.
6. Destroy or remove infested rice straw.
Water Mold Disease
Cause.
Several aquatic Phycomycetes, including Achlya conspicua, A. klebsiana, Pythium dissotocum, and P. spinosum. Fusarium spp. also have been implicated as
causal organisms. The disease occurs in waterseeded rice.
Distribution.
Widely distributed.
Symptoms.
Germinating seed is rotted and diseased seedlings are weakened or killed, resulting in losses through reduced density, irregular stands, and poor growth of diseased
seedlings.
Management.
Apply a seedtreatment fungicide.
White Leaf Streak
Cause.
Ramularia oryzae.
Distribution.
Africa and Asia.
Symptoms.
White to gray lesions (0.5 × 1.02.5 mm) with narrow, brown borders develop on both leaf surfaces. However, lesions on diseased upper leaf surfaces may be
entirely white and have no borders, while lesions on lower leaf surfaces may be entirely brown.
Management.
Not reported.

Page 501
Lesion
Cause.
Pratylenchus zeae and probably other Pratylenchus spp. Pratylenchus zeae is an endoparasite that feeds and reproduces in the root cortex.
Distribution.
Temperate climates of the world.
Symptoms.
Aboveground symptoms include plant stunting. Diseased leaves are chlorotic and a purple to reddish discoloration may occur. Diseased roots have reduced growth
and few fibrous roots. Brown lesions may be present on roots and a general brown to blackish root decay may occur.
Management.
Pratylenchus zeae on upland rice can be controlled by crop rotation with at least two crops of cowpea or mung bean.
Rice Root
Cause.
Hirschmanniella oryzae is an endoparasite found in aquatic environments. The nematode is associated with lowland rice and is adapted to flooded paddies and
marshes. Hirschmanniella oryzae infects and reproduces on sedges and grasses but remains dormant when paddies are dry. It occurs in parenchyma tissue but not in
thin lateral roots where there are no air channels. Hirschmanniella oryzae moves out of roots into soil soon after seed forms or plant growth ceases.
A total of seven species of Hirschmanniella are reported to infect rice.
Distribution.
Symptoms.
Diseased roots become necrotic and discolored. Plants are stunted and the number of tillers, panicles, top growth, and yield are reduced. There is also a delay in
tillering and flowering.
Management.
Not reported.
Root Knot
Root knot is sometimes called the rice rootknot nematode.
Cause.
Meloidogyne spp., including M. arenaria, M. incognita, M. javanica, M. graminicola, M. oryzae, and M. salasi. Meloidogyne arenaria, M. incognita, and M.
javanica do not survive if the air temperature averages below 3°C during the coldest month and do not survive continuous flooding. Meloidogyne graminicola does
not invade roots in flooded soils but does survive inside roots for 5 weeks and in flooded soil for 5 months or more. Nematodes survive as eggs in soil or reproduce
on other plants. Sandy or coarsetextured soils favor reproduction.
The nematodes are obligate endoparasites. Secondstage juveniles infect the apical meristem of young seedling roots before flooding. Nematode se

Page 502
cretions stimulate development of giant cells and root galls in 4 days. Females lay eggs inside the galls and juveniles hatch and reinfect the same root. A life cycle is
completed in 19 days in welldrained soils at temperatures of 22° to 29°C.
Distribution.
Meloidogyne arenaria, M. incognita, M. javanica are found throughout Asia. Meloidogyne graminicola is found in Bangladesh, India, Laos, Thailand, and the
United States (Georgia, Louisiana, and Mississippi). Meloidogyne oryzae is found in Surinam, and M. salasi is found in Costa Rica and Panama.
Symptoms.
Aboveground symptoms on diseased plants are chlorosis, wilting, late maturation, and reduced plant growth and tillering. The characteristic root galls that are formed
prevent root elongation. Yield of upland rice is reduced. Deepwater rice infected by M. graminicola may not grow above the water.
Management
1. Continuous flooding of fields controls M. arenaria, M. incognita, and M. javanica.
2. Leave soil fallow or rotate to a nonhost plant, such as peanut, sweet potato, maize, and soybean.
3. Grow resistant cultivars where appropriate.
4. Apply nematicides in nurseries.
Stem
This disease is also called ufra or ufra disease.
Cause.
Ditylenchus augustus survives as adults in dry soil and infested residue. Nematodes migrate from diseased to healthy plants through water and by stem and leaf
contact at more than 75% relative humidity. Nematodes can also survive on and be dispersed in freshly harvested rice grain.
During periods of high humidity, active nematodes climb up seedlings, enter young growing tissue, and in 1 hour burrow between leaves and leaf sheaths, where they
feed as ectoparasites. As diseased plants grow, the nematodes move up to new tissue. All reproduction occurs only on rice plants. Younger plants are more likely to
become infected than older plants.
Distribution.
Bangladesh, Egypt, India, and Southeast Asia.
Symptoms.
Chlorosis and malformation of leaves occur 2 months after sowing. A few brown spots on diseased leaves and sheaths later become a darker brown, as do the upper
stem internodes.
The most obvious symptoms are panicles that have few or no filled spikelets toward the base and, together with leaves, are crinkled, twisted, corrugated, or otherwise
distorted. In some instances, two or three dis

Page 503
torted ears may be surrounded by one sheath. There may also be more than the normal number of branches on a diseased stem.
Diseased plants may or may not be killed; however, panicles from surviving plants either emerge or remain enclosed within the flag leaf sheaths. In both cases, kernels
usually are not produced.
Management
2. Dry rice grains to a moisture content of 14% or below before storage to eliminate the nematodes from grain.
Summer Crimp
Summer crimp is also called white tip.
Cause.
Aphelenchoides besseyi survives on seed for up to 2 years. Infested seed provides the major source of inoculum for nematode infection. Aphelenchoides besseyi
does not overwinter in soil but is disseminated by water through the soil. The nematode is mostly an ectoparasite, occurring within folded leaves in the early stages of
plant growth, then entering spikelets and finally the glumes. The optimum conditions for nematode development are a temperature of 28°C and a relative humidity of
70% or higher.
Distribution.
Africa, Australia, Cuba, Japan, Southeast Asia, and the United States.
Symptoms.
Diseased leaves are darker green than leaves of healthy plants. However, the most obvious symptom is chlorotic or white leaf tips (up to 5 cm long) that are evident at
the beginning of elongation and later become brown and tattered. Diseased plants are stunted, lack vigor, and give rise to tillers at the higher nodes of the plants.
Panicles of severely diseased tillers mature late. The length and number of spikelets are reduced and there is a high percentage of sterile, small, distorted glumes and
grains. Upper leaves, particularly flag leaves, are twisted so particle emergence from boots is often incomplete.
Management
2. Sow in water and keep fields flooded.
Diseases Caused By Phytoplasmas
Rice Orange Leaf Disease
Cause.
Possibly phytoplasmalike organisms (PLO) that are disseminated by the leafhoppers Recilia dorsalis and Inazuma dorsalis. The incubation pe

Page 504
riod in R. dorsalis nymphs is 15 to 33 days but has been reported to be as short as 2 to 15 days. The causal organism(s), which is persistent in the vectors, has an
average incubation period of 22 days in R. dorsalis and 10 to 28 days in rice plants. Some leafhoppers transmit the agent continuously and others transmit
intermittently until they die. PLO have been reported to be bounded by a unit membrane and to contain ribosome particles and DNAlike fibrils. Shapes of PLO vary
and range from 50 to 1100 nm in diameter.
Distribution.
Malaysia, the Philippines, Sri Lanka, Thailand, and probably other countries in Southeast Asia.
Symptoms.
Diseased plants are generally distributed sporadically within a field. Leaves become orange, roll inward, and dry up. Plants display symptoms 10 to 28 days after
inoculation and die 2 to 4 weeks after symptoms appear. Inoculated seedlings are stunted and leaf emergence is delayed, leaves are short and often have chlorotic
stripes, tip twisting, and ragged blades similar to symptoms of rice ragged stunt virusinfected leaves. Rice orange leaf disease does not cause serious yield loss.
Tungro symptoms are similar in some aspects to those of orange leaf.
Management.
Not reported.
Rice Yellow Dwarf
Rice yellow dwarf is also called yellow dwarf.
Cause.
A phytoplasmalike organism. The causal agent may overwinter in leafhoppers and the wild grass Alopecurus aequalis. The causal agent is disseminated primarily by
the leafhopper Nephotettix cincticeps and also by N. apicalis and N. impicticeps. Leafhoppers acquire the causal agent by feeding on diseased plants for 1 to 3
hours. There is a 20 to 39 day incubation period, after which the inoculation feeding time is usually less than 1 hour. The latent period in rice is about 1 month in
''warm" weather and 3 months in "cool" weather.
Distribution.
Tropical Asia.
Symptoms.
Diseased plants are generally chlorotic and stunted and produce numerous tillers. The uniformly pale green or pale yellow chlorosis first appears on the newest leaves
and continues on the successive leaves. Sometimes only a faint mottling occurs. Plants infected early normally do not die but produce abnormal heads or no heads.
Management
2. Apply an insecticide to kill overwintering insects.

Page 505
Cause.
African cereal streak virus (ACSV) is transmitted only by the planthopper Toya catilina. The natural virus reservoir probably is native grasses. Disease development
is aided by high temperatures.
Distribution.
East Africa.
Symptoms.
ACSV is limited to the phloem of diseased plants, where it causes a necrosis. Initially, faint broken chlorotic streaks begin near the leaf base and extend upward.
Later, definite alternate yellow and green streaks develop along the entire leaf blade but are more broken than on other cereals, resulting in a mottled appearance.
Eventually, diseased leaves become almost completely yellow. Leaves formed after infection tend to develop a shoestring habit and die.
Young diseased plants become chlorotic and severely stunted, and die. Little or no seed is produced. Plants become soft, flaccid, and almost velvety to the touch.
Management.
Not reported.
Giallume Disease
Giallume disease is also called barley yellow dwarf.
Cause.
Barley yellow dwarf virus (BYDV).
Distribution.
Italy and Spain.
Symptoms.
Diseased plants are stunted and have fewer than normal tillers. Foliage is yellowed.
Management.
Delaying the sowing date eliminated the occurrence of BYDV in Spain. The effect was attributed to the timing of insect vector flights and to temperature.
Grassy Stunt B
Cause.
There is a question if the causal organism grassy stunt B (GSB) is a virus (perhaps a strain of rice grassy stunt virus) or a phytoplasmalike organism. GSB is
transmitted in a persistent manner by the rice brown planthopper Nilaparvata lugens.
Distribution.
Taiwan.
Symptoms.
Symptoms vary somewhat depending on cultivar. Characteristic symptoms are excessive tillering with or without stunting. Initially, young

Page 506
diseased leaves are narrower than healthy leaves and are green but have faint to conspicuous chlorotic stripes on both sides of the midribs. Later, diseased leaves
become pale green and have a conspicuous mottling. Still later, leaves become yellow and the stripes disappear. Mildly stunted plants live to maturity but produce few
filled panicles.
Management.
Not reported.
Grassy Stunt Y
Cause.
There is question if the causal organism (GSY) is a virus (perhaps a strain of rice grassy stunt virus) or a phytoplasmalike organism. GSY is transmitted in a persistent
manner by the rice brown planthopper Nilaparvata lugens.
Distribution.
Taiwan.
Symptoms.
Symptoms vary somewhat depending on cultivar. Tillering is reduced in the winter but increases in the summer. Plants are slightly to markedly stunted. Leaves initially
may be somewhat chlorotic, narrow, and stiff and have an erect growth habit. Small, dark brown spots may occur on leaves of some cultivars and conspicuous
yellowwhite stripes may occur along leaf veins of other cultivars. Diseased plants are not killed but produce empty panicles.
Management.
Not reported.
Rice Black Streak Dwarf
Rice black streak dwarf is also called blackstreaked dwarf disease.
Cause.
Rice black streak dwarf virus (RBSDV) is transmitted in a persistent manner by the planthoppers Laodelphax striatellus, Unkanodes sapporonus, and
Ribautodelphax albifascia. Several grasses are hosts for RBSDV.
Distribution.
Japan.
Symptoms.
Galls appear as waxy, elongated, irregularly shaped protuberances extending along major veins on diseased lower leaf surfaces, the outer surface of leaf sheaths, and
culms. Protuberances form gray to dark brown streaks of various lengths on older leaves. The proximal portion of leaf blades is often twisted.
Plants infected early in their growth are severely stunted and have more tillers than normal. Foliage is darker than normal and few or no panicles are formed. Grain
often has dark brown blotches.
Management.
Rice Dwarf
Rice dwarf is also called dwarf disease.

Page 507
Cause.
Rice dwarf virus (RDV) is in the reovirus group. RDV is transmitted by the planthopper Nephotettix nigropictus.
Distribution.
Japan and Nepal.
Symptoms.
Diseased plants are stunted to various degrees. Leaves are dark green and have large numbers of discrete translucent spots that often coalesce and form longitudinal
lines parallel to the midrib. Spots are also present on leaf sheaths. Plants infected at an early growth stage are the most severely stunted, while those infected at a later
growth stage are less stunted. Both root and shoot systems are reduced, and panicles are either absent or reduced in size.
Management.
Not reported.
Rice Gall Dwarf
Cause.
Rice gall dwarf virus (RGDV) is in the reovirus group. RGDV is transmitted in a persistent manner by the leafhopper Recilia dorsalis and the green rice leafhoppers
Nephotettix cincticeps, N. malayanus, N. nigropictus, and N. virenscens. Nephotettix spp. have about a 2week incubation period. RGDV is not known to be
seedtransmitted.
Distribution.
Thailand.
Symptoms.
Diseased plants are severely stunted. Galls are most abundant on earlyinfected plants. Leaves are dark green and have galls or vein swellings on the under surfaces of
diseased leaf blades and on the outer sides of leaf sheaths. Galls initially are light green and translucent but eventually become white. Most galls are less than 2 mm
long, but they can vary in size (0.40.5 × 0.48.0 mm). Leaf tips may be twisted.
Management.
Not reported.
Rice Grassy Stunt
Rice grassy stunt is also called grassy stunt.
Cause.
Rice grassy stunt virus (RGSV) is in the tenuivirus group, but there is some question as to whether the causal organism is a phytoplasmalike organism. RGSV survives
yearround in rice, Oryzae sativa, and several other species of rice. RGSV also persists in and is transmitted only by the rice brown planthopper Nilaparvata
lugens. At least two different strains of RGSV, designated as RGSV1 and RGSV2, are known to occur.
Distribution.
Ceylon, India, Malaysia, the Philippines, and Thailand.
Symptoms.
RGSV1 symptoms are severely stunted plants that have excessive tillers and an erect growth habit. Diseased leaves are short and narrow, chlorotic, and covered
with numerous rusty spots. Young leaves of some

Page 508
cultivars may be mottled or may have narrow yellow and white stripes with diffuse margins parallel to the midribs. Stripes may be located only at the basal portion of
leaves or extend the entire length of diseased leaves. Numerous small tillers give a diseased plant a grassy appearance. Diseased plants normally survive but produce
few or no panicles.
RGSV2 symptoms on diseased plants are stunting, a yellow to orange discoloration, rusty spotting of lower leaves, and a narrowing of leaf blades. Young emerging
leaves are pale green to almost entirely chlorotic and tend to have striping and mottling symptoms. Leaves remain yellow even when the plants are adequately fertilized,
but mature leaves of plants infected with RGSV1 turn dark green when nitrogen fertilizer is applied. Severely diseased seedlings produce few tillers and eventually
die.
Management.
Some cultivars show a degree of resistance. Resistance is governed by a single dominant gene. Experimentally. Neem (Azadirachta indica) seed oil has been found
to reduce survival of planthoppers and suppress transmission of grassy stunt.
Rice Hoja Blanca
Rice hoja blanca is also called chlorosis, cinta blanca (white band), hoja blanca, raya (stripe), raya blanca (white stripe), rayadilla (striped), and white leaf.
Cause.
Rice hoja blanca virus (RHBV) is in the tenuivirus group. RHBV is transmitted by the planthopper Sogatodes oryzicola, and once RHBV is acquired, it is transmitted
through eggs from infective females to their progenies for several generations. Little is known of how the virus overwinters, but since hoja blanca is most prevalent in
the tropics, it is likely diseased rice plants grow yearround. Jungle rice, Echinochloa colonum, also is a host.
Distribution.
Western Hemisphere. In the United States, rice hoja blanca has been reported from Florida, Louisiana, and Mississippi.
Symptoms.
Initially, one or more white stripes or white mottling may occur on a diseased leaf, or the entire leaf may turn white. Diseased and normal tillers may be produced by
the same plant. Often the second crop of tillers produced by a diseased plant displays no symptoms.
Diseased plants are stunted, and panicles may not reach their normal size or may not emerge from sheaths. Hulls, which often are distorted, turn brown and dry out.
Flower parts are sterile or absent; therefore, few seeds are produced and heads remain upright instead of bending over.
Management.
Rice Necrotic Mosaic
Rice necrotic mosaic is also called necrotic mosaic disease, yaikasho, and eso mosaic.

Page 509
Cause.
Rice necrotic mosaic virus (RNMV) is in the potyvirus group. RNMV is saptransmissible and is soilborne. Transmission is by soilborne fungi, possibly Polymyxa
graminis. The weeds Ludwigia perennis and Brachiaria ramosa are hosts and potential reservoirs for the virus. Diseased plants occur mostly in upland seedbeds.
Distribution.
India and Japan.
Symptoms.
Initially, a mosaic mottling occurs on diseased lower leaves at about the maximum tillering stage, after seeds have been transplanted in paddy fields. Mottling consists
of light green to yellow streaks that are oval to oblong (1 × 1100 mm). Later, streaks on diseased leaves coalesce and form irregularshaped patches that spread to
the upper leaves. When several patches are present, a leaf becomes yellow. Mottling may also occur on the culm.
Plants are slightly reduced in size, but this is not very noticeable. The number of tillers is reduced and tillers that are present tend to lie flat, resuiting in a spreading
growth habit. Later, a few elongated, necrotic lesions appear on the surfaces of leaf sheaths and the basal portions of culms. There is also a reduction in the number of
panicles, which produce only a few light grains.
Management.
Not reported.
Rice Ragged Stunt
Cause.
Rice ragged stunt virus (RRSV) is in the reovirus group. RRSV is transmitted by the brown leafhopper, Nilaparvata lugens, with an acquisition period of 24 hours or
longer. RRSV is not mechanically or seedtransmitted. Vectors are most efficient at transmitting RRSV 5 days after hatching and become less efficient as they grow
older. RRSV is systemic. Rice ragged stunt is more severe on deepwater rice cultivars when plants are infected at the seedling to early stem elongation growth stages
than at the late stem elongation and flowering growth stages.
Distribution.
The Philippines, India, Indonesia, and Sri Lanka.
Symptoms.
Diseased plants are variously stunted at all growth stages. Severe stunting of deepwater rice varieties may lead to plant death because of drowning.
During the early growth of diseased plants, leaves are ragged; irregular edges consisting of one to 17 notches or indentations occur before leaf blades unroll. The
ragged edges vary in length and usually occur only on a portion of one side of a leaf blade but occasionally occur on both sides of a leaf blade and the leaf sheaths.
The ragged area is chlorotic, becomes yellow to brownyellow, and eventually disintegrates. However, dark green leaves have also been reported as a symptom.
The top portion of leaf blades is often twisted, resulting in a spiral shape

Page 510
of one or more turns. Vein swellings caused by a proliferation of phloem cells occur on the upper portions of the outer surfaces of leaf sheaths near the collar and, less
often, on the lower surfaces of leaf blades and culms. Vein swellings (1 × 1100 mm) are pale yellow or, infrequently, brown.
At the boot stage of plant growth, the flag leaves are shortened and often are twisted, malformed, or ragged. Tillers often generate nodal branches, which are
secondary or tertiary tillers produced at the upper nodes. Nodal branches often bear small panicles that are more numerous than on healthy plants.
Diseased plants flower later than healthy plants, which results in empty or partially filled panicles. As a consequence, yield losses of 50% to 100% have been reported.
Management.
No acceptable management measure is reported. However, neem (Azadirachta indica) seed oil has been found to experimentally reduce the survival of planthoppers
and to suppress the transmission of virus.
Rice Stripe
Rice stripe is also called stripe disease.
Cause.
Rice stripe virus (RStV) is in the tenuivirus group. Transmission in a persistent and a transovarial manner is by the planthoppers Laodelphax striatellus,
Ribautodelphax albifascia, and Unkanodes sapporonus. RStV multiplies and persists in vectors; therefore, disease incidence is correlated to the percentage of
viruliferous insects. Several other plants are virus hosts.
Distribution.
Japan, Korea, and Taiwan. RStV has been reported to cause the most serious disease of rice in Japan.
Symptoms.
Plants infected while young will have more pronounced symptoms than plants infected at a later growth stage. Early infection may cause severe plant stunting or death,
but plants infected later may be only slightly stunted.
Diseased leaves will emerge without unfolding, then elongate, become twisted, and droop. Leaves are chlorotic and often have a wide chlorotic stripe with diffuse
margins. Frequently, a gray necrotic streak that appears in the chlorotic area enlarges and eventually kills the leaf.
Leaves that unfold properly have an irregular chlorotic mottling that appears as a stripe the length of the diseased leaf blade and on the leaf sheath. The number of
tillers and panicles is reduced, and diseased panicles have malformed spikelets that do not emerge properly from leaf sheaths. Grain may be malformed.
Management.

Page 511
Rice Stripe Necrosis
Rice stripe necrosis is called rice "entorchamiento" in Colombia.
Cause.
Rice stripe necrosis virus (RSNV) is in the furovirus group. RSNV is transmitted by the soilborne fungus Polymyxa graminis. Polymyxa graminis survives in field
soil as cystosori. Cysts give rise to zoospores that "swim" through free soil water until they contact a host root and encyst. Encysted zoospores produce a structure
called a stachel through which zoosporic cytoplasm enters the host cell and becomes a plasmodium. Only primary root tissue of young roots is infected; optimum
infection occurs at a temperature of about 25°C. The host cell then becomes infected with RSNV if P. graminis is viruliferous. After a period of time, the plasmodium
develops into a zoosporangium that releases additional zoospores, which repeats the infection cycle. However, some plasmodia develop into cysts and, often, nearly
every cell in the small feeder roots will contain a cyst. As root cells senesce, cysts are eventually released into the soil, where they can remain viable for years without
loss of virulence.
Distribution.
Colombia and the Ivory Coast.
Symptoms.
Marked mosaiclike discolorations occur on diseased leaves. Entire leaves may become twisted or severely malformed and exhibit chlorotic stripes and necrosis.
Management.
Not reported.
Rice Transitory Yellowing
Rice transitory yellowing is also called brown wilt, rice transitory yellowing disease, and yellow stunt.
Cause.
Rice transitory yellowing virus (RTYV) is in the rhabdovirus group. RTYV is transmitted by the leafhoppers Nephotettix apicalis, N. cincticeps, and N. impicticeps.
RTYV persists and multiplies in vectors; however, virus is not infective when the temperature is below 16°C or above 38°C.
Distribution.
China, Japan, Taiwan, and Thailand.
Symptoms.
Diseased leaves become yellow, beginning at the distal portion of lower leaves; therefore, discoloration is initially more intense in the lower diseased leaves than in the
upper ones. Brown, rusty flecks or patches may appear on discolored leaves. The yellow discoloration eventually becomes indistinct in lower leaves, which soon roll
and wither, leaving only a few live upper leaves. Diseased plants have a reduced root system and produce few or no panicles.
Diseased plants often recover under greenhouse conditions. Following approximately a month of yellow leaves, normal leaves may be produced at a later plant growth
stage. Consequently, the appearance of diseased plants may become normal after yellow leaves have fallen off.

Page 512
Management.
Not reported.
Rice Yellow Mottle
Rice yellow mottle is also called rice yellow mottle disease.
Cause.
Rice yellow mottle virus (RYMV) is in the sobemovirus group. Survival of RYMV is in volunteer rice and ratoons, or rice regrowths, from previously harvested crops.
RYMV is mechanically transmitted through sap and is spread by adult leaffeeding beetles in the Chrysomelidae, especially Sesselia pusilla. In Madagascar,
Dicladispa gestroi is considered the most important vector. RYMV is also possibly spread by irrigation water. RYMV is not known to be seedborne. Disease
development is more severe in plants infected during an early growth stage than in plants infected at a later growth stage. Different strains of RYMV exist.
Distribution.
Burkina Faso, Ivory Coast, Guinea, Kenya, Liberia, Madagascar, Mali, Niger, Nigeria, and Sierra Leone.
Symptoms.
Initially, scattered, orangeyellow spots occur either on the youngest leaves of recently transplanted rice or on mature rice. Eventually, the older leaves at the bottom of
diseased plants are yellow and the younger leaves at the top of plants are orange. Young leaves have a thin mottle ranging from yellow to dark green. Both artificially
and naturally infected plants may be dwarfed, and seedlings may be killed. Depending on the age of plants at infection, there is a reduced tillering and panicles are
sterile, malformed, and only partially emerge, which results in reduced yields. Losses of up to 90% have been reported from Madagascar.
Management.
Grow resistant cultivars. Resistant cultivars also possess horizontal resistance to blast.
Tungro
The following diseases are also thought to be tungro: accepta no pula (red disease), cadangcadang (yellowing), leaf yellowing, mentek disease, panyakit merah (red
disease), penyakit habang, rice dwarf, stunt disease, and yellow orange leaf. Tungro is also called rice tungro.
Cause.
Two types of tungro virus particles occur: spherical particles (RTSV) and bacilliform particles (RTBV). RTSV contains singlestranded RNA and two major proteins
of 24 and 23 kDa. RTBV contains circular doublestranded DNA and a single major protein of 32 kDa.
RTBV is transmitted only with the help of RTSV. RTBV causes tungro symptoms of plant stunting and yelloworange discoloration, and RTSV enhances them.
Infection by RTSV alone causes only very mild stunting. RTSV is known as a latent virus and acts as a helper or an RTSVrelated helper factor for the transmission of
RTBV by leafhoppers. Hence, RTBV is

Page 513
transmitted only when the virus source is infected with both RTBV and RTSV, or when leafhoppers first acquire RTSV, then RTBV.
Other evidence suggests RTSV may not be the helper or the only helper for RTBV transmission. When leafhoppers were placed on RTBVinfected plants, RTBV
transmission occurred 7 days after acquisition. The helper factor for RTBV is lost after molting. RTSV causes disease as an independent pathogen, is efficiently
transmitted from plants infected with RTSV alone, and is retained by adult leafhoppers 2 to 3 days after acquisition.
RTSV and RTBV survive yearround in diseased rice plants or when one rice crop only is grown a year: survival is in stubble of diseased plants that ratoon and in
numerous grassy weeds.
Both viruses are transmitted in a semipersistent manner by the leafhoppers Nephotettix virenscens, N. malayanus, N. nigropictus, N. parvus, and Recilia dorsalis.
Greater disease spread occurs in wet seasons due to the greater numbers of vectors. Insects feed at least 30 minutes to acquire the virus from diseased plants and
transmit the virus by feeding for 15 minutes on healthy plants. Viruses are retained for 2 to 3 days in leafhoppers, after which they must be reacquired. Nephotettix
virenscens is reported to be the most efficient vector of both viruses, with retention for 4 days after acquisition. Nephotettix nigropictus is the least efficient vector
but retained both viruses for 5 days after acquisition. Leafhoppers feed predominantly on the phloem of leafhoppersusceptible cultivars but feed on the xylem of
leafhopperresistant cultivars.
Tungro is severe only in areas where host plants and vectors multiply yearround. Disease incidence generally increases with an increase in plant spacing. A wide
spacing results in larger plants with a larger surface area for vectors to feed on and more tissue for virus multiplication than smaller plants grown in a closer spacing.
High tungro incidence is associated with the vector population and the proportion of viruliferous vectors.
Several strains, differentiated on the basis of their characteristic symptoms on rice cultivars, are reported to exist. At least three strains of tungro virus have been
identified and designated as S, M, and T.
Distribution.
Bangladesh, India, Indonesia, Malaysia, Thailand, and the Philippines. Tungro is considered the most important viral disease of rice and the major constraint to rice
production in south and southeastern Asia.
Symptoms.
Plants infected with both viruses show severe tungro symptoms, while plants infected only with RTBV display mild stunting and yellowing. Plants infected only with
RTSV have indistinct symptoms, including mild stunting.
The most obvious symptoms are stunting, reduction in the number of tillers, and a leaf discoloration that varies from shades of yellow to orange starting at the leaf tips
and extending to the lower parts of diseased leaves. Discoloration of leaves in moderately resistant cultivars may gradually dis

Page 514
appear at the later stages of plant growth. Young leaves may be mottled and older leaves have rustycolored specks of various sizes.
Susceptible cultivars may be severely stunted and discolored, and die. The three strains of tungro virus—S, M, and T—each produce distinct symptoms on certain
rice cultivars. On diseased leaves, the S strain causes an interveinal chlorosis that looks like yellow stripes. The M strain produces mottling. The T strain causes narrow
leaf blades in some cultivars and a striping of diseased leaves in other cultivars.
Management
1. Grow resistant cultivars. Resistance to RTSV infection in some cultivars may not be due to resistance to leafhoppers.
2. Treat seed with a systemic insecticide.
3. Apply foliar insecticides to reduce vector populations.
4. Adjust planting date to correspond to low numbers of vectors.
5. Neem, Azadirachta indica, applied as a seed oil and cake at 150 and 250 kg/ha prevented tungro virus transmission by N. virescens. The feeding behavior was
disrupted as it shifted from phloem to xylem feeding.
Unknown Virus—Caused Disease
This disease may be rice wilted stunt disease.
Cause.
Unknown, but transmitted by a brown planthopper. The causal agent is possibly a virus and persists in the vector for a lengthy time even after molting.
Distribution.
The Philippines, particularly where brown planthopper populations are high.
Symptoms.
Initial symptoms occur 7 to 14 days after inoculation. Diseased plants are stunted. Leaves are yellow, abnormally narrow, and erect, which gives diseased plants an
erect growth habit. Irregularshaped, brownish blotches and chlorotic streaks that resemble a mosaictype of mottling may be observed on the discolored leaves.
Diseased plants die prematurely.
Management.
Not reported.
Waika Disease
Cause.
Rice waika virus (RWV) is transmitted by the green rice leafhoppers Nephotettix cincticeps, N. malayanus, N. migropictus, and N. virenscens. Strains designated
C and S are present in nature. RWV may be related to or the same as rice tungro spherical virus. RWV overwinters in ratoons.
Distribution.
Japan.
Symptoms.
Symptoms caused by RWV somewhat resemble those caused by tungro virus. Symptoms of strain C occur after the booting stage of plant growth. Diseased plants
have a slight stunting, slight discoloration and

Page 515
drooping of leaf blades, poor root systems, and a delay in the flowering time.
Symptoms of strain S are leaf discoloration and irregularshaped brown blotches on diseased leaves. Plants are severely stunted and have few tillers, delayed
flowering, and a reduction in yield.
Management.
Wilted Stunt Disease
Cause.
There is question if the causal organism is a strain of rice grassy stunt virus or a phytoplasmalike organism. The causal organism is transmitted in a persistent manner
by the rice brown planthopper, Nilaparvata lugens.
Distribution.
Taiwan.
Symptoms.
Symptoms vary, depending on cultivar. Initially, rusty spotting and yellowing that later intensify occur on lower basal leaves. Diseased plants eventually wilt. The
central, newly unfolded leaves are pale. Diseased plants produce few tillers in winter and slightly more tillers in summer.
Leaf twisting and trapping of unfolded leaves also occur in some cultivars. In other cultivars, diseased leaves are pale green, shortened, narrow, curled inward, and
brittle. Tillering may increase during the summertime. In still other cultivars, young leaves are pale green to pale yellow and exhibit conspicuous mottling. Sometimes
vague, chlorotic stripes that eventually disappear form along veins. Plants may be severely stunted and have few tillers. Eventually, leaves dry up, beginning at the basal
portion.
Severely diseased plants die, and surviving plants produce no panicles or a few poorly developed panicles.
Management.
Not reported.
Diseases Caused by Unknown or Abiotic Factors
Panicle Blight
Cause.
Unknown.
Distribution.
Not reported.
Symptoms.
Aborted florets and poor yields occur on diseased plants.
Management.
Not reported.
Sekiguchi Lesion
Cause.
Sekiguchi lesion is conditioned by a single recessive gene, sl, and can be induced by a number of biotic and abiotic agents. Sekiguchi lesion is

Page 516
likely a manifestation of a flaw in the biological mechanisms that regulate the hypersensitive response of plants homozygous for the sl gene to pathogenic agents.
Distribution.
Japan and the United States.
Symptoms.
Initially, lesions (12 mm in diameter) are gray, watersoaked spots that enlarge rapidly into diurnally zonate orangebrown areas. Gradually, lesions coalesce until the
whole plant is affected.
Management.
Not reported.
Straighthead
Cause.
The exact cause is not known, but it may be due to unfavorable soil conditions aggravated by prolonged flooding. It is more severe on sandy loam soils and seldom
occurs on clay soils. It has often occurred when soil containing too much undecayed plant material had been plowed under. In some limited geographical areas, it has
been caused by an accumulation of arsenic as a result of repeated applications of cotton insecticides.
Distribution.
Colombia, Japan, Portugal, and the United States.
Symptoms.
Rice heads remain upright at maturity because the few grains that form are too light to bend the heads over. Diseased heads often contain no fertile seed and hulls are
distorted into a crescent or parrotbeak form, especially on longgrain cultivars. One or both hulls and other flower parts are missing. In severe cases, heads are
smaller than normal and emerge slowly or incompletely from the boot. Diseased plants remain green and may produce shoots from the lower nodes. Diseased seeds
may have a low or abnormal germination.
Management
1. Grow resistant cultivars. No cultivar is immune or highly resistant.
2. Drain fields just prior to the stem elongation stage.
Selected References
Abbas, H. K., Cartwright, R. D., Shier, W. T., Abouzied, M. M., Bird, C. B., Rice, L. G., Ross, P. F., Sciumbato, G. L., and Meredith, F. I. 1998. Natural
occurrence of fumonisins in rice with Fusarium sheath rot disease. Plant Dis. 82:2225.
Ahn, S. W. 1980. Eyespot of rice in Colombia, Panama, and Peru. Plant Dis. 64:878880.
Anjaneyulu, A., Shukla, V. D., Rao, G. M., and Singh, S. K. 1982. Experimental host range of rice tungro virus and its vectors. Plant Dis. 66:5456.
Atkins, J. G. 1972. Rice Diseases. USDA Farmers Bull. No. 2120.
Attere, A. F., and Fatokum, C. A. 1983. Reaction of Oryza glaberrima accessions to rice yellow mottle virus. Plant Dis. 67:420421.

Page 517
Bajet, N. B., Aguiero, V. M., Daquioag, R. D., Jonson, G. B., Cabunagan, R. C., Mesina, E. M., and Hibino, H. 1986. Occurrence and spread of rice tungro
spherical virus in the Philippines. Plant Dis. 70:971973.
Bakr, M. A., and Miah, S. A. 1975. Leaf scald of rice: A new disease in Bangladesh. Plant Dis. Rptr. 59:909.
Baravidan, M. R., Mew, T. W., and Aballa, T. 1982. Some studies on bacterial stripe of rice. (Abstr.) Philipp. Phytopathol. 18:9.
Batchvarova, R. B., Reddy, V. S., and Bennett, J. 1992. Cellular resistance in rice to cercosporin, a toxin of Cercospora. Phytopathology 82:642646.
Bockus, W. W., Webster, R. K., and Kosuge, T. 1978. The competitive saprophytic ability of Sclerotium oryzae derived from sclerotia. Phytopathology 68:417
421.
Bockus, W. W., Webster, R. K., Wick, C. M., and Jackson, L. F. 1979. Rice residue disposal influences overwintering inoculum level of Sclerotium oryzae and
stem rot severity. Phytopathology 69:862865.
Bonman, J. M., Estrada, B. A., and Bandong, J. M. 1987. Correlation between leaf and neck blast resistance in rice. (Abstr.) Phytopathology 77:1723.
Bradbury, J. F. 1986. Guide to Plant Pathogenic Bacteria. C.A.B. International, Farnham Royal, United Kingdom. 332 pp.
Cabauatan, P. Q. 1982. An unknown disease of rice transmitted by the brown planthopper Nilaparvata lugens in the Philippines. (Abstr.) Philipp. Phytopathol.
18:13.
Cabauatan, P. Q., and Hibino, H. 1985. Transmission of rice tungro bacilliform and spherical viruses by Nephotettix virenscens Distant. Philipp. Phytopathol.
21:103109.
Cabauatan, P. Q., Hibino, H., Labis, D. B., Omura, T., and Tsuchizaki, T. 1984. Rice grassy stunt virus 2: A new strain of rice grassy stunt in the Philippines. (Abstr.)
Philipp. Phytopathol. 20:9.
Cabauatan, P. Q., Cabunagan, R. C., and Koganezawa, H. 1995. Biological variants of rice tungro viruses in the Philippines. Phytopathology 85:7781.
Cartwright, R. D., Correl, J. C., and Crippen, D. L. 1995. Fusarium sheath rot of rice in Arkansas. (Abstr.). Phytopathology 85:1199.
Chattopadhyay, S. B., and Dasgyotam, C. 1959. Helminthosporium rostratum Drechs. on rice in India. Plant Dis. Rptr. 43:12411244.
Chen, C. C., and Chiu, R. J. 1982. Three symptomatologic types of rice virus diseases related to grassy stunt in Taiwan. Plant Dis. 66:1518.
ChoongHoe, K., Rush, M. C., and Mackenzie, D. R. 1985. Effect of water management on the epidemic development of rice blast. (Abstr.) Phytopathology
75:501.
Chuke, K. C. and Lapis, D. B. 1985. Pathogenicity of Sarocladium oryzae and factors affecting sheath rot development on rice. Philipp. Phytopath. 21:2833.
CorreaVictoria, F. J., and Carrillo, D. 1997. Confirmation of the transmission of rice ''entorchamiento" (stripe necrosis) by the fungus Polymyxa graminis in
Colombia. (Abstr.) Phytopathology 87:S21.
Cother, E. J. 1974. Bacterial glume blotch of rice. Plant Dis. Rptr. 58:11261129.
Cottyn, B., Cerez, M. T., Van Outryve, M. F., Barroga, J., Swings, J., and Mew, T. W. 1996. Bacterial diseases of rice. I. Pathogenic bacteria associated with
sheath rot complex and grain discoloration of rice in the Philippines. Plant Dis. 80:429437.
Cottyn, B., Van Outryve, M. F., Cerez, M. T., De Cleene, M., Swings, J., and Mew, T. W. 1996. Bacteria diseases of rice. II. Characterization of pathogenic
bacteria associated with sheath rot complex and grain discoloration of rice in the Philippines. Plant Dis. 80:438445.

Page 518
Damicone, J.P., Patel, M. V., and Moore, W. F. 1993. Density of sclerotia of Rhizoctonia solani and incidence of sheath blight in rice fields in Mississippi. Plant Dis.
77:257260.
Danquah, O. A. 1975. Occurrence of Phoma glomerata on rice (Oryza sativa): A first record in Ghana. Plant Dis. Rptr. 59:844845.
Datnoff, L. E., and Jones, D. B. 1992. Sheath blotch of rice: A disease new to the Americas. Plant Dis. 76:11821184.
Datnoff, L. E., Snyder, G. H., and Deren, C. W. 1991. Effect of silicon fertilizer grades on brown spot development and yield of rice. (Abstr.) Phytopathology
81:1201.
Datnoff, L. E., Elliott, M. L., and Jones, D. B. 1993. Black sheath rot caused by Gaeumannomyces graminis var. graminis on rice in Florida. Plant Dis. 77:210.
Datnoff, L. E., Elliott, M. L., and Krausz, J.P. 1997. Cross pathogenicity of Gaeumannomyces graminis var. graminis from bermudagrass, St. Augustinegrass, and
rice in Florida and Texas. Plant Dis. 81:11271131.
Deighton, F. C., and Shaw, D. 1960. White leaf streak of rice caused by Ramularia oryzae sp. nov. Brit. Mycol. Soc. Trans. 43:516518.
Disthaporn, S., Catling, H. D., Chettanachit, D., and Putta, M. 1985. Effect of time of infection of rice ragged stunt virus on deepwater rice. Int. J. Tropical Plant Dis.
3:1925.
Duveiller, E., Miyajima, K., Snacken, F., Autrique, A., and Maraite, H. 1988. Characterization of Pseudomonas fuscovaginae and differentiation from other
fluorescent pseudomonads occurring on rice in Burundi. J. Phytopathol. 122:97107.
Fauqet, C., and Thouvenel, J. C. 1977. Isolation of the rice yellow mottle virus in Ivory Coast. Plant Dis. Rptr. 61:443446.
Febellar, N. G., and Mew, T. W. 1985. Crown sheath rot of rice. (Abstr.) Philipp. Phytopathol. 21:16.
Fomba, S. N. 1988. Screening for seedling resistance to rice yellow mottle virus in some rice cultivars in Sierra Leona. Plant Dis. 72:641642.
Gangopadhyay, S., and Row, K. V. S. R. K. 1986. Perennation of Pyricularia oryzae Briosi et Cav. in sclerotial state. Int. J. Tropical Plant Dis. 4:187192.
Ghosh, S. K. 1981. Weed hosts of rice necrosis mosaic virus. Plant Dis. 65:602603.
Gnanamanickam, S. S., Shigaki, T., Medalla, E. S., Mew, T. W., and Alvarez, A.M. 1994. Problems in detection of Xanthomonas oryzae pv. oryzae in rice seed
and potential for improvement using monoclonal antibodies. Plant Dis. 78:173178.
Groth, D. E., and Nowick, E. M. 1992. Selection for resistance to rice sheath blight through number of infection cushions and lesion type. Plant Dis. 76: 721723.
Goto, M. 1979. Bacterial foot rot of rice caused by a strain of Erwinia chrysanthemi. Phytopathology 69:213216.
Goto, M. 1979. Dissemination of Erwinia chrysanthemi, the causal organism of bacterial foot rot of rice. Plant Dis. Rptr. 63:100103.
Gunnell, P.S., and Webster, R. K. 1983. Sheath blight of rice in California. (Abstr.) Phytopathology 73:796.
Gunnell, P.S., and Webster, R. K. 1984. Aggregate sheath spot of rice in California. Plant Dis. 68:529531.
Gunnell, P.S., and Webster, R. K. 1985. The effect of cultural practices on aggregate sheath spot of rice in California. (Abstr.) Phytopathology 75:1340.

Page 519
Gunnell, P.S., and Webster, R. K. 1985. The perfect state of Rhizoctonia oryzaesativae, causal organism of aggregate sheath spot of rice. (Abstr.) Phytopathology
75:1383.
Hibino, H. 1983. Transmission of two rice tungroassociated viruses and rice waika virus from doubly or singly infected source plants by leafhopper vectors. Plant
Dis. 67:774777.
Hibino, H., Roechan, M., and Sudarisman, S. 1978. Association of two types of virus particles with penyakit habang (tungro disease) of rice in Indonesia.
Hibino, H., Cabauatan, P. Q., Omura, T., and Tsuchizaki, T. 1985. Rice grassy stunt virus strain causing tungrolike symptoms in the Philippines. Plant Dis. 69:538
541.
Hibino, H., Jonson, G. B., and Sta. Cruz, F. C. 1987. Association of mycoplasmalike organisms with rice orange leaf in the Philippines. Plant Dis. 7:792794.
Hibino, H., Daquioag, R. D., Cabauatan, P. Q., and Dahal, G. 1988. Resistance to rice tungro spherical virus in rice. Plant Dis. 72:843847.
Hibino, H., Ishikawa, K., Omura, T., Cabauatan, P. Q., and Koganezawa, H. 1991. Characterization of rice tungro bacilliform and rice tungro spherical viruses.
Hwang, B. K., Koh, Y. J., and Chung, H. S. 1987. Effects of adultplant resistance on blast severity and yield of rice. Plant Dis. 71:10351038.
Iboton Singh, N., and Tombisana, R. K. 1995. First report of Fusarium leaf blotch of rice. Plant Dis. 79:1186.
Iboton Singh, N., and Tombisana, R. K. 1995. Pestalotiopsis versicolor: A causal agent of rice collar rot. Plant Dis. 79:1186.
Imolehin, E. D. 1983. Rice seedborne fungi and their effect on seed germination. Plant Dis. 67:13341336.
Inoue, H. 1978. Strain S: A new strain of leafhopperborne rice waika virus. Plant Dis. Rptr. 62:867871.
Inoue, H., and Omura, T. 1982. Transmission of rice gall dwarf virus by the green rice leafhopper. Plant Dis. 66:5759.
John, V. T., Heu, M. H., Freeman, W. H., and Manandhar, D. N. 1979. A note on dwarf disease of rice in Nepal. Plant Dis. Rptr. 63:784785.
Jonson, G. B., Sta. Cruz, F. C., and Hibino, H. 1985. Etiology of orange leaf. (Abstr.) Philipp. Phytopathol. 21:6.
Kato, S., Nakanishi, T., Takahi, Y., and Nakagami, K. 1985. Studies on Pythium dampingoff of rice seedlings: (1) Pythium species associated with dampingoff in
the early growth stage of rice seedlings in nursery flats. Phytopathol. Soc. Japan Ann. 51:159167.
Kato, S., Nakanishi, T., Takahi, Y., Nakagami, K., and Ogawa, M. 1985. Studies on Pythium dampingoff of rice seedlings: (2) Pythium species associated with
dampingoff at the middle and latter growth stages of rice seedlings in nursery flats. Phytopathol. Soc. Japan Ann. 51:168175.
Kauffman, H. E., and Reddy, A. P. K. 1975. Seed transmission studies of Xanthomonas oryzae in rice. Phytopathology 65:663666.
Koch, M. F., and Mew, T. W. 1991. Effect of plant age and leaf maturity on the quantitative resistance of rice cultivars to Xanthomonas campestris pv. oryzae.
Plant Dis. 75:901904.
Kondaiah, A., Rao, A. V., and Srinivasan, T. E. 1976. Factors favoring spread of rice "tun

Page 520
gro" disease under field conditions. Plant Dis. Rptr. 60:803806.
Krishna, P. G., and Rush, M. C. 1983. Role of Pythium spinosum in the fungal complex causing the watermold disease of waterseeded rice. (Abstr.)
Kuwata, H. 1985. Pseudomonas syringae pv. oryzae pv. nov., causal agent of bacterial halo blight of rice. Phytopathol. Soc. Japan Ann. 51:212218.
Lee, F. N. 1990. Rice dead tiller syndrome in Arkansas. (Abstr.). Phytopathology 80:1005.
Lee, F. N., and Rush, M. C. 1983. Rice sheath blight: A major rice disease. Plant Disease 67:829832.
Leu, L. S., and Yang, H. C. 1985. Distribution and survival of sclerotia of rice sheath blight fungus, Thanatephorus cucumeris, in Taiwan. Phytopathol. Soc. Japan
Ann. 51:17.
Lindberg, G. D. 1970. Loss of rice yield caused by stem rot. (Abstr.) Phytopathology 60:1300.
Ling, K. C. 1975. Rice Virus Diseases. International Rice Research Institute, Los Banos, Philippines.
Ling, K. C., Tiongco, E. R., and Aguiero, V. M. 1978. Rice ragged stunt: A new virus disease. Plant Dis. Rptr. 62:701705.
Lozano, J. C. 1977. Identification of bacterial leaf blight in rice caused by Xanthomonas oryzae in America. Plant Dis. Rptr. 61:644648.
Marchetti, M. A. 1983. Potential impact of sheath blight on yield and milling quality of shortstatured rice lines in the southern United States. Plant Dis. 67:162165.
Marchetti, M. A., Bollich, C. N., and Vecker, F. A. 1983. Spontaneous occurrence of the Sekiguchi lesion in two American rice lines: Its induction, inheritance and
utilization. Phytopathology 73:603606.
MarinSanchez, J.P., and JimenezDiaz, R. M. 1982. Two new Fusarium species infecting rice in southern Spain. Plant Dis. 66:332334.
Mew, T. W., and Rosario, M. B. 1980. Bacterial foot rot of rice. (Abstr.) Philipp. Phytopathol. 16:5.
Mew, T. W., Vera Cruz, C. M., and Medalla, E. S. 1992. Changes in race frequency of Xanthomonas oryzae pv. oryzae in response to rice cultivars planted in the
Philippines. Plant Dis. 76:10291032.
Mew, T. W., Alvarez, A.M., Leach, J. E., and Swings, J. 1993. Focus on bacterial blight of rice. Plant Dis. 77:512.
Morinaka, T., Putta, M., Chettanachit, D., Parejarearn, A., Disthaporn, S., Omura, T., and Inoue, H. 1982. Transmission of rice gall dwarf virus by cicadellid
leafhoppers Recilia dorsalis and Nephotettix nigropictus in Thailand. Plant Dis. 66:703704.
Mueller, K. E. 1974. Field Problems of Tropical Rice. International Rice Research Institute, Los Banos, Philippines.
Nuque, F. L., Aguiero, V. M., and Ou, S. H. 1982. Inheritance of resistance to grassy stunt virus in rice. Plant Dis. 66:6364.
Omura, T., Inoue, H., Morinaka, T., Saito, Y., Chettanachit, D., Putta, M., Parejarearn, A., and Disthaporn, S. 1980. Rice gall dwarf: A new virus disease. Plant
Dis. 64:795797.
Oster, J. J. 1992. Reaction of a resistant breeding line and susceptible California rice cultivars to Sclerotium oryzae. Plant Dis. 76:740744.
Ou, S. H. 1973. A Handbook of Rice Diseases in the Tropics. International Rice Research Institute, Los Banos, Philippines.
Ou, S. H. 1986. Rice Diseases, Second Edition. Commonwealth Mycological Institute,

Page 521
Kew, Surrey, England. Eastern Press Ltd., London. 391 pp.
Ou, S. H., Nuque, F. L., and Vergel de Dios, T. L 1978. Perfect stage of Rhynchosporium oryzae and the symptoms of rice leaf scald disease. Plant Dis. Rptr.
62:524528.
Padwick, W. 1950. Manual of Rice Diseases. Commonwealth Mycological Institute, Kew, Surrey, England. Oxford University Press, England.
Prabhu, A. A., and Bedendo, L P. 1983. Basal node of rice caused by Fusarium oxysporum in Brazil. Plant Dis. 67:228229.
Rahman, M. L., and Evans, A. A. F. 1987. Studies on hostparasite relationships of rice stem nematode, Ditylenchus angustus (Nematoda: Tylenchida), on rice,
Oryzae sativa. L Nematologica 33:451459.
Reddy, P. R., and Mohanty, S. K. 1981. Epidemiology of the kresek phase of bacterial blight of rice. Plant Dis. 65:578580.
Reddy, A. P. K., Mackenzie, D. R., Rouse, D. L, and Rao, A. V. 1979. Relationship of bacterial leaf blight severity to grain yield of rice. Phytopathology 79:967
969.
Rivera, C. T., Ou, S. H., and Pathak, M.D. 1963. Transmission studies on the orangeleaf disease of rice. Plant Dis. Rptr. 47:10451048.
Rosales, A.M., Nuque, F. L., and Mew, T. W. 1986. Biological control of bakanae disease of rice with antagonistic bacteria. Philipp. Phytopathol. 22:2935.
Rossman, A. Y. 1990. Pyricularia grisea: The correct name for the rice blast disease fungus. Mycologia 82:509512.
Sahu, R. K., and Khush, G. S. 1989. Inheritance of resistance to bacterial blight in seven cultivars of rice. Plant Dis. 73:688691.
Saito, Y., Chaimongkol, U., Singh, K. G., and Hino, T. 1976. Mycoplasmalike bodies associated with rice orange leaf disease. Plant Dis. Rptr. 60:649651.
Saxena, R. C., and Khan, Z. R. 1985. Effect of neem oil on survival of the rice brown planthopper, Nilaparvata lugens (Stal) (Homoptera: Delphacidae), and on
grassy stunt and ragged stunt virus transmission. Philipp. Phytopathol. 21:8087.
Shahjahan, A. K. M., and Mew, T. W. 1986. Sheath blotch of rice in the Philippines. (Abstr.) Philipp. Phytopath. 22:5.
Shahjahan, A. K. M., Harahap, Z., and Rush, M. C. 1977. Sheath rot of rice caused by Acrocylindrium oryzae in Louisiana. Plant Dis. Rptr. 61:307310.
Shahjahan, A. K. M., Ahmed, H. V., Sharma, N. R., and Miah, S. A. 1985. Spacings x rate of nitrogen effect on sheath blight disease severity in BRI rice. (Abstr.)
Philipp. Phytopathol. 21:3.
Shakya, D. D., Vinther, F., and Mathur, S. B. 1985. Worldwide distribution of a bacterial stripe pathogen of rice identified as Pseudomonas avenae. Phytopathol.
Zeitschr. 114:256259.
Shukla, V. D., and Anjaneyulu, A. 1981. Adjustment of planting date to reduce rice tungro disease. Plant Dis. 65:409411.
Shukla, V. D., and Anjaneyulu, A. 1981. Plant spacing to reduce rice tungro incidence. Plant Dis. 65:584586.
Singh, R. A., and Raju, C. A. 1981. Some observations on sheath rot of rice. (Abstr.) Philipp. Phytopathol. 17:5.
Sthapit, B. R., Pradhanang, P.M., and Witcombe, J. R. 1995. Inheritance and selection of field resistance to sheath brown rot disease in rice. Plant Dis. 79:1140
1144.
Thomas, M.D., Mayango, D., and Oberly, W. 1985. Suppressions and elimination of Rhynchosporium oryzae by benomyl in rice foliage and seed in Liberia. Plant
Dis. 69:884886.

Page 522
Tschen, J. S. M. 1987. Control of Rhizoctonia solani by Bacillus subtilis. Trans. Mycol. Soc. Japan 28:483493.
Venkataraman, S., Ghosh, A., and Mahajan, R. K. 1987. Synergistic effect of rice tungro virus and Sarocladium oryzae on sheath rot disease of rice. Int. J. Tropical
Plant Dis. 5:141145.
Walawala, J. J., and David, R. G. 1984. Pathogenicity, damage assessment, and field population pattern of Hirschmanniella oryzae in rice. Philipp. Phytopathol.
20:3944.
Webster, R. K., and Gunnell, P.S. 1992. Compendium of Rice Diseases. American Phytopathological Society, St. Paul, MN. 62 pp.
Whitney, N. G. 1980. Brown blotch: A new disease of rice. (Abstr.) Phytopathology 70:572.
Zaragoza, B. A., and Mew, T. W. 1979. Relationship of root injury to the "Kresek" phase of bacterial blight of rice. Plant Dis. Rptr. 63:10071011.
Zeigler, R. S., and Alvarez, E. 1987. Bacterial sheath brown rot of rice caused by Pseudomonas fuscovaginae in Latin America. Plant Dis. 71:592597.
Zeigler, R. S. and Alvarez, E. 1989. Grain discoloration of rice caused by Pseudomonas glumae in Latin America. Plant Dis. 73:368.
Zeigler, R. S., Aricapa, G, and Hoyos, E. 1987. Distribution of fluorescent Pseudomonas spp. causing grain and sheath discoloration of rice in Latin America. Plant
Dis. 71:896900.

Page 523
15.
Diseases of Rye (Secale cereale)
Bacterial Streak
Bacterial streak is called bacterial blight, black chaff, and bacterial leaf blight.
Cause.
Xanthomonas campestris pv. translucens (syn. X. translucens f. sp. secalls). The taxonomy of the causal organism(s) continues to be in flux. Bacterial streak
(which is called bacterial blight, bacterial leaf streak, or black chaff on other small grains) is considered to be caused by five of the former X. campestris pathovars:
pv. cerealis, pv. hordei, pv. secalis, pv. translucens, and pv. undulosa. These pathovars are often grouped together under the name "translucens group" or are
considered to be a single species (X. translucens) or pathovar (X. campestris pv. translucens). Bragard et al. (1997) agreed that X. translucens pv. translucens
and X. translucens pv. hordei are true synonyms. They also reported that when using restriction fragmentlength polymorphism and fatty acid methyl esters analysis,
the pathovars X. translucens pv. cerealis, X. translucens pv. translucens, and X. translucens pv. undulosa clustered in different groups and corresponded to true
biological entities.
Bacteria are seedborne and overwinter in infested residue. Initial infection comes from seedborne bacteria that are disseminated by leaftoleaf and planttoplant
contact, splashing rain, and possibly insects. Bacteria enter into plants through natural openings, such as stomates and wounds.
Distribution.
Australia and North America.
Symptoms.
Symptoms occur after several days of damp or rainy weather. Diseased plants may be stunted, but this is not usually noticed until plants mature. Small watersoaked
spots occur on the youngest leaves and sheaths of older plants and sometimes on seedlings. Spots enlarge and may

Page 524
coalesce, become glossy and translucent, and eventually turn yellow or brown and have an irregular margin. Spots, when coalesced, do not become as stripelike as
bacterial blight on barley. Severely diseased leaves die back from the tip. Under humid morning conditions, droplets of milky bacterial exudate may be seen on
surfaces of spots. Droplets dry into hard, yellowish flakes that are easily removed from leaf surfaces.
Watersoaked areas occur on heads but bacterial exudate is not common on heads. Grain is not destroyed but may be brown and shrunken and carry bacteria to
infect next year's crop. If flag leaves are infected, heads may not emerge from the boot but may break through the side of the sheath and be destroyed and blighted.
Bacterial blight on rye can be diagnosed in the field in the same manner as bacterial blight on barley. When a newly developed spot is cut crosswise, a bead of milky
ooze will exude from the cut edge.
Management
2. Treat seed with a fungicide as a precaution even though bacterial blight is not known to be present.
3. Rotate rye with other crops. The causal bacterium that infects rye does not infect barley.
Halo Blight
Cause.
Pseudomonas syringae pv. coronafaciens (syn. P. coronafaciens) may be seedborne. Development of halo blight is most severe under cool, moist conditions.
Distribution.
Wherever rye is grown; however, halo blight is rarely severe enough to be economically important.
Symptoms.
Initially, minute, brown spots occur on diseased leaf sheaths, leaf blades, and along leaf margins, often in association with frost injury. A few days later, yellow halos up
to 15 mm in diameter surround the spots. Eventually, the centers of spots become necrotic and have a narrow chlorotic halo. Lesions may coalesce and cause entire
leaves to turn brown and have a scalded appearance that is a common symptom from flowering to maturity.
Normally, entire florets are blighted, but during less severe disease conditions, only small halos may occur on glumes. On early tillers, individual florets on heads are
sterile and turn white. On later tillers, all florets of some heads are diseased and produce shriveled grain or no seed. As temperatures increase later in the season, few
or no new lesions are formed.
Atypical symptoms reported from Virginia are as follows: Plants were slightly to severely stunted, often with chlorotic veins in the diseased leaves. Diseased blades on
some plants had chlorotic and necrotic lesions

Page 525
but no halo blight was observed. On other diseased plants, entire blades were yellowed.
Management.
Not reported.
Anthracnose
Cause.
Colletotrichum graminicola, teleomorph Glomerella graminicola, is an excellent saprophyte and overwinters as mycelia and conidia on winter cereals and infested
residue. Conidia are produced during wet weather and disseminated by wind to host plants. Disease development is most severe when weather is wet and at a
temperature of 25°C. Anthracnose is most likely to occur when rye is grown on coarse soils with low fertility in rotation with another cereal. Rye is one of the most
susceptible cereals to infection by C. graminicola.
Distribution.
Wherever rye is grown.
Symptoms.
Symptoms become apparent toward plant maturity as a premature ripening or whitening of seed, a general reduction in plant vigor, and the eventual death of diseased
plants. Specific symptoms occur most often on the lower parts of diseased plants because primary infections are initiated there. The crown and bases of some stems
become bleached, then turn brown.
Later, acervuli, which appear as small, black, raised spots, develop on the surfaces of the diseased lower leaf sheaths and culms. Under magnification, acervuli will
look like a "clump of spines." When moisture is plentiful, acervuli may develop on the leaves of dead plants. Round to oblong lesions bearing acervuli may occur on
green leaves. If infection occurs early in the life of the diseased plant, diseased kernels may be shriveled. A seedling and crown infection may occur under severe
disease conditions.
Management
1. Rotate rye with a noncereal or grass because C. graminicola can infect a large number of grass and cereal species. Legumes are not susceptible and would be a
suitable crop in a rotation.
Bunt
Bunt is also called common bunt, covered smut, European bunt, hill bunt, and stinking smut.
Cause.
Tilletia caries (syn. T. tritici) and T. laevis (syn. T. foetida and T. foetens). The species name "laevis" is sometimes spelled "levis" in the literature. The

Page 526
two fungi are closely related and have similar life cycles that may occur together in the same diseased plant.
Both fungi overwinter as teliospores (chlamydospores) on seed and in soil. When rye is sown, teliospores on or near seed in the soil germinate in the presence of
moisture and cool temperatures of 5° to 15°C. A promycelium (basidium) is formed on which eight to 16 basidiospores (sporidia) are produced. Basidiospores fuse in
the middle with a compatible basidiospore and form an Hshaped structure that germinates and produces secondary sporidia. Secondary sporidia then germinate and
produce mycelia that infect seedlings. Mycelium grows behind the growing point or meristematic tissue of the infected plant, invades the developing head, and
displaces the grain. Eventually, teliospores are formed in seed. At harvest time, infected seed is broken and teliospores are released, become windborne, and
eventually contaminate host kernels or soil.
Distribution.
Tilletia caries is generally distributed wherever rye is grown but is most prevalent in the northwestern United States. Tilletia laevis is limited to areas of Europe and
North America, where it has been reported in the Midwest and the northwestern United States.
Symptoms.
Common bunt is more severe when soil temperatures become cool following sowing. Rye sown in the spring may be less severely diseased. Diseased plants are
somewhat stunted but cannot be readily distinguished from healthy ones until the heading stage of plant growth. Bunted heads are more slender than healthy ones and
glumes of spikelets may be spread apart. A bunted head will often stay green for a longer time than normal and have a bluish cast. Bunted kernels are about the same
size as healthy seed but are light brown and more round in shape. The pericarp ruptures at harvest and teliospores contaminate healthy seed, giving them a "fishlike"
odor; hence, the name stinking smut. When crushed, the smut balls and diseased kernels have an oily feeling.
Management
1. Treat seed with a systemic seedtreatment fungicide.
3. Sow early in the autumn. Seedlings may be far enough advanced and less susceptible to infection by the time secondary sporidia develop.
Cause.
Hymenula cerealis (syn. Cephalosporium gramineum) survives for up to 5 years as conidia and mycelia in residue and in the top 8 cm of soil. Conidia serve as
primary inoculum and infect roots during winter and early spring through mechanical injuries caused by soil heaving and insects. Infection is most severe when
increased fungal sporulation and root growth occur in wet and acid soils that have a pH of 5.0. The subcrown internode can also

Page 527
be infected just as seed is germinating.
After infection, conidia enter xylem vessels and are carried upward in the plant, where they lodge and multiply at the nodes and leaves. Normally, there is no further
injury to roots. The fungus prevents water movement up the plant and also produces metabolites that are harmful to the plant. At harvest time, C. gramineum is
returned to the soil in infested residue, where it is a successful saprophytic competitor with other soil organisms.
Winter rye is most severely diseased. Spring rye is susceptible but apparently escapes disease and usually does not show symptoms.
Distribution.
Great Britain, Japan, and in most winter ryegrowing areas of North America.
Symptoms.
Diseased stunted plants are scattered throughout a field but are most numerous in the lower and wetter areas. During jointing and heading stages of plant growth, one
to two, but sometimes up to four, distinct yellow stripes occur the length of the diseased plant on leaves, sheaths, and stems. Thin, brown lines consisting of diseased
veins occur in the middle of the stripes. Stripes eventually become brown, are highly visible on green leaves, and remain noticeable on yellow straw. Toward harvest,
culms at or below nodes may become dark due to fungus sporulation. Heads of diseased plants are white and contain shriveled seed or no seed.
Management
1. Grow tolerant cultivars. No cultivars are resistant.
2. Rotate rye with a noncereal for at least 2 years.
3. Sow later in the autumn or when the soil temperature 10 cm below the surface is less than 13°C. Such plants apparently have limited root growth, which reduces
the number of infection sites.
4. Residue should be plowed deeper than 8 cm.
Common Root Rot
Cause.
Bipolaris sorokiniana, teleomorph Cochliobolus sativus, and Fusarium spp. Both fungi survive in soil as saprophytes on infested residue. Conidia of B.
sorokiniana and chlamydospores of Fusarium spp. survive for several months in soil and are seedborne.
Primary infections occur on coleoptiles, primary roots, and subcrown internodes. Infection of subcrown internodes is usually caused by B. sorokiniana. Fusarium
spp. infect secondary roots as they emerge from the crown. Diseased plants normally do not die because new roots are continually being produced. Conidia are
produced when disease progresses above the soil line on the diseased plants.
Most secondary sporulation is conidia produced on diseased crowns, with the remainder occurring on crown roots, subcrown internodes, seed

Page 528
pieces, and seminal roots. Sporulation is greatest on mature rye plants; the highest numbers of conidia are present on necrotic or senescent tissue, such as coleoptiles
and the lower outside leaf sheaths.
Plants under stress due to drought, warm temperatures, lack of nutrition, and insect injury are most subject to infection. Moisture is initially required for infection, but
once infection is initiated, disease development requires warm temperatures and moisture stress on the infected plant.
Distribution.
Symptoms.
Diseased seedlings may be killed before or after emergence, particularly in dry soil when inoculum is seedborne. Surviving seedlings have brown lesions on coleoptiles,
roots, and culms. Infections of crowns usually kill plants. Diseased older plants, which occur in random patches throughout a field, are stunted and lighter green and
mature earlier than healthy plants. Diseased plants also have few tillers, and their heads are bronzed and bleached or whiteheaded and contain shriveled seed. There
may be a browning of root systems that is observable only when roots are washed. Fusarium spp. in particular cause roots, culm bases, and lower nodes to become
dry and dark brown or black. Diseased plants then become brittle and break off easily near the soil line.
Management
2. Soil should have proper fertility to ensure growth of vigorous plants that are able to produce new roots and overcome root rot.
3. Sow rye in late autumn.
Cottony Snow Mold
Cottony snow mold is also called winter crown rot.
Cause.
Coprinus psychromorbidus.
Distribution.
Canada.
Symptoms.
After snowmelt, patches of dead rye plants occur where the snow was deepest in the field. Sometimes a sparse mycelial growth gives diseased plants a gray sheen,
but often, little mycelium can be found. Irregularshaped, gray to black sclerotia up to 1 mm in length are loosely attached to the diseased host tissues inside leaf
sheaths and, infrequently, on roots and subcrown internodes.
Management.
Not reported.
Dilophospora Leaf Spot
Dilophospora leaf spot is also called twist.

Page 529
Cause.
Dilophospora alopecuri (syn. D. graminis) survives as mycelia and pycnidia in infested residue and as conidia on seed. Primary infection is by conidia produced in
pycnidia and disseminated by wind and splashing rain to seedlings during wet weather. Secondary infection is by conidia produced in pycnidia within the spots on
seedling leaves during moist weather. The twist phase of the disease is caused by secondary conidia disseminated into the whorls by larvae of the seed gall nematode,
Anguina tritici, as it moves up the plant in a film of water.
Distribution.
Canada, Europe, India, and the United States. Twist has not been observed for several years and is considered to be a rare disease on rye.
Symptoms.
Initially, small, elongated, yellow spots appear only on diseased leaves. Spots become light brown with black centers that consist of stromata and pycnidia of D.
alopecuri. Leaves may be killed if the spots become numerous. When the whorl is colonized, leaves do not emerge or emerge twisted, distorted, and covered with
gray mycelium. This phase of the disease rarely occurs in the absence of A. tritici. Dilophospora alopecuri dries as stromata that occur as dark streaks on leaves
and in which pycnidia are produced.
Management
1. Rotate rye with other crops. Both rye and wheat are susceptible.
4. Sow certified rye seed.
Downy Mildew
Cause.
Sclerophthora macrospora survives for years as oospores in infested residue and soil. Sclerophthora macrospora is an obligate parasite and cannot grow
saprophytically on dead plant tissue. Oospores are disseminated on seed and in infested residue carried by wind and water. Oospores germinate in wet soil and
produce sporangia in which zoospores are formed. Zoospores are then released, ''swim" through soil water to seedlings, and infect host plants by forming a germ tube
that directly penetrates the plant. Oospores may survive for months in dry soil, then germinate and form only a single germ tube that directly penetrates a host plant.
Infection occurs at temperatures from 7° to 31°C. Following infection, S. macrospora develops systemically within infected plants, particularly in xylem tissue.
Distribution.
Wherever rye is grown. The disease is most severe in the wetter areas of a field.
Symptoms.
Downy mildew occurs only in localized areas of fields where seedlings have been growing in flooded or waterlogged soil for 24 hours or longer. Diseased plants are
dwarfed, deformed, and twisted and have leath

Page 530
ery, stiff, thickened leaves, stems, and heads. Diseased plants tiller excessively, and severely diseased plants form no seeds. In less severely diseased plants, dwarfing
may be slight, one or more of the upper leaves may be stiff, upright, or variously curled and twisted, and heads and stems may not be deformed. Under magnification,
numerous round, yellowbrown oospores may be seen in diseased tissue.
Management
1. Provide proper soil drainage, where possible.
2. Control grassy weeds that may serve as collateral hosts.
3. Sow cleaned seed from diseasefree plants to ensure no infested residue is disseminated with the seed.
Dwarf Bunt
Cause.
Tilletia controversa survives as teliospores in soil for up to 10 years or on the surfaces of infested seed. When rye is sown in moist soil, teliospores on or close to the
seed germinate under warm, dry conditions and form promycelia on which eight to 16 basidiospores are borne. Basidiospores fuse in the middle with a compatible
basidiospore and form an Hshaped structure that, in turn, germinates and forms a structure called a secondary sporidium. The secondary sporidia germinate and
produce infective mycelia.
Optimum germination of T. controversa occurs at temperatures of 3° to 8°C; the incubation period is 3 to 10 weeks. Infection generally requires a heavy snow cover
over unfrozen ground, which provides suitable conditions of moisture and temperature at the soil surface for teliospore germination and infection of plants.
After infection, mycelium grows behind the meristematic tissue of growing points, invades developing heads, and displaces grain. Eventually, teliospores form in the
seed. At harvest time, diseased seed is broken and teliospores disseminated by wind contaminate healthy kernels and soil.
Distribution.
In Canada, Europe, and the United States where a heavy snow cover is likely to occur over unfrozen ground.
Symptoms.
Diseased plants are generally onefourth to onehalf normal size. Viable pollen does not develop, and the ovaries of diseased florets are larger than those in healthy
florets. There are more buntinfested kernels per spikelet of a diseased plant than seeds per spikelet on a healthy plant. Smut balls are smaller and rounder than
common bunt and the spore mass feels dry. Spores smell like rotten fish.
Management
1. Grow resistant cultivars in adapted areas.

Page 531
Ergot
Cause.
Claviceps purpurea, anamorph Sphacelia segetum, survives as sclerotia on and in soil. Immediately before blossoming of host plants, a sclerotium germinates and
produces one or many stipes (stalks), each bearing a stromatic head in which perithecia form. Eventually, ascospores produced in the perithecia are disseminated by
wind to flowers. The ascospore germinates and produces a germ tube that grows into the young ovary. Conidia are then produced from mycelium growing in the
ovary within a sweet, sticky liquid called honeydew. Secondary dissemination is by insects that are attracted to the honeydew and inadvertently carry conidia to
healthy flowers. Sclerotia usually occur after the conidial stage, but under some conditions, particularly in tropical areas, no sclerotia are produced. As sclerotia
enlarge, floral bracts spread apart and dark sclerotial bodies protrude beyond the floral bracts. Sclerotia eventually replace kernels in diseased flowers. Several
grasses and cereals are susceptible to C. purpurea, but ergot is usually most severe on rye. Rye is predisposed to ergot by barley yellow dwarf virus infection.
Distribution.
Symptoms.
Few to many sclerotia (ergot bodies) are produced on a spike or panicle and appear as hard, purpleblack, hornshaped structures in place of seed. Prior to sclerotial
formation, honeydew and conidia accumulate in liquid droplets or adhere to the surfaces of floral structures. Insects feeding on honeydew are conspicuous around
diseased flowers. Saprophytic fungi grow on honeydew and give infected flowers a black or sooty appearance.
Management
1. Plow infested residue deep in the soil to place sclerotia where they will not effectively germinate but will eventually decompose.
2. Control grassy weeds since they may be infected by C. purpurea and serve as a source of inoculum.
3. Rotate rye with crops, such as legumes or maize, that are not susceptible to C. purpurea.
4. Clean seed to remove sclerotia.
Eyespot
Eyespot is also called Cercosporella foot rot, culm rot, foot rot, stem break, strawbreaker, and strawbreaker foot rot.
Cause.
Tapesia yallundae, anamorph Pseudocercosporella herpotrichoides (syn. Cercosporella herpotrichoides). At least two distinct morphological types that
correspond to the two pathotypes of P. herpotrichoides are present. Daniels et al. (1991) reported the two pathotypes designated wheat (W) and rye (R) are
distinguished on the bases of pathogenicity to wheat

Page 532
seedlings, spore morphology and colony morphology, pigmentation on maize meal agar, and isoenzyme polymorphisms. The wheat type is more pathogenic to wheat
and barley than to rye and has fastergrowing, evenedged colonies. The rye type is as pathogenic to rye as to wheat and barley and is slower growing and has
featheryedged colonies and more profuse sporulation.
Tapesia yallundae survives for several years as mycelia in infested residue. Sporulation occurs on straw at the soil surface during cool, damp weather or when
humidity is near saturation and temperatures are 8° to 12°C in the autumn or spring. Dispersal or dissemination is by splashing rain.
Development of epiphytotics is dependent on production of primary inoculum on residue remaining from the previous rye crop. The coleoptile is most susceptible to
infection during the seedling stage, but with the decay of the coleoptile, the susceptibility of leaf sheaths increases.
Secondary inoculum is not important in the development of an epiphytotic since spores occur on developing lesions too late in the growing season to cause infection.
However, late infections do add to the amount of inoculum available to infect plants of succeeding crops.
Distribution.
Widespread where rye is grown in a cool, moist climate. Rye is less prone to disease than wheat.
Symptoms.
The most conspicuous symptom is near the end of the growing season when diseased plants lodge. Lodging caused by eyespot disease causes straw to fall in all
directions; lodging caused by wind or rain causes straw to fall primarily in one direction.
Eyeshaped or ovate lesions with white to tan centers and brown margins develop first on the basal leaf sheath. Similar spots that form on stems directly beneath those
on the sheath weaken the stems and eventually cause them to lodge.
Crown and basal culm tissue is diseased, but roots are not, although a necrosis occurs around roots in the upper crown nodes. Under moist conditions, lesions enlarge
and a black, stromalike mycelium that develops over the surface of crowns and the bases of culms gives tissues a charred appearance. Stems shrivel and collapse or
plants become yellowish to pale green and heads are reduced in size and number. When infected early in their growth, individual culms and weaker plants are killed
before maturity.
Management
1. Rotate rye with noncereals.
2. Grow the most resistant cultivars. However, resistant cultivars often become diseased under severe disease conditions.
3. Apply fungicides to residue to decrease primary inoculum. Under experimental conditions, foliar fungicides control eyespot.
4. Reduced tillage limits foot rot incidence.

Page 533
Fusarium head blight is also called scab.
Cause.
Gibberella zeae, anamorph Fusarium graminearum, overwinters as mycelia and spores on seed, and as mycelia and perithecia in infested residue. Ascospores
produced in perithecia and conidia produced from mycelia during warm, moist weather are disseminated by wind to plant hosts. Diseased seed causes seedling blight,
and soilborne inoculum causes seedling blight and root rot. Fusarium head blight develops in warm, humid weather during formation and ripening of the kernels.
Prolonged wet weather during and after anthesis favors infection and subsequent disease development. Conidia produced on infected heads serve as secondary
inoculum.
Grain that becomes wet in swaths favors Fusarium head blight development. Fusarium head blight is more severe when rye follows maize.
Distribution.
Symptoms.
Disease begins in flowers and spreads to other parts of the head to give the appearance of premature ripening. Initially, one or more spikelets of emerged immature
heads are watersoaked, die, and become light brown, bleached, or white, beginning at the spikelet base. Eventually, hulls change from light brown to dark brown.
When infection occurs late in the development of seed, only the base of hulls is brown, but in severe cases, the entire kernel may become shrunken and brown. If the
rachis is diseased, the entire head is dwarfed and compressed. All spikelets above that point are closed rather than spreading, bleached, and sterile or contain only a
partially filled seed. Diseased kernels are grayish and light in weight. The interior of the kernel is floury and discolored. During humid or wet weather, pink to pinkred
mycelium and spores grow on infected spikelets. Later, small, black perithecia grow in the same diseased area. As in Fusarium head blight of wheat, mycotoxins, such
as 3acetyldeoxynivalenol and deoxynivalenol (vomitoxin), are assumed to be produced in diseased heads. Therefore, diseased grain may be harmful when fed to
hogs, dogs, and humans.
Management
1. Rotate rye with other crops. Do not grow rye after barley, maize, or wheat. Do not grow rye next to maize.
2. Plow under infested residue to hasten decomposition of residue and prevent spores from being windborne.
3. Do not spread manure that contains infested straw or maize stalks on soil where rye is growing.
4. Sow early to allow rye to escape warm, moist weather.
6. The Food and Drug Administration recommends 2 ppm or less of de

Page 534
oxynivalenol in grain entering the milling process, 1 ppm for finished rye products for human consumption, and 4 ppm for animal feed.
Fusarium Root Rot
Cause.
Fusarium culmorum. Primary inoculum is soilborne chlamydospores and infested residue in the upper 10 cm of soil. Entry into the crown is gained 2 to 3 cm below
the soil surface through openings around crown roots or by the infection of newly emerging crown roots. Disease is severe under dry soil conditions.
Distribution.
The United States.
Symptoms.
Diseased plants rarely show outward symptoms until after heading. The crown and basal stem tissues are decayed and have a brown discoloration and spongy texture.
Internodes become chocolate brown; however, leaf sheaths remain symptomless. Pink or burgundy mycelium is seen in hollow stems. Diseased plants die prematurely,
resulting in white heads.
Management
1. Do not rotate rye with wheat and oat.
2. Till fields after harvest to improve water infiltration.
3. Establish a dust and stubble mulch in spring.
4. Apply the proper amount of nitrogen.
Halo Spot
Cause.
Pseudoseptoria donacis (syn. Selenophoma donacis) overwinters as pycnidiospores, pycnidia, and mycelia in infested residue, seed, and overwintering rye and
wheat. During cool, moist weather, pycnidiospores are exuded from pycnidia and disseminated by wind and splashing rain to hosts.
Distribution.
In cool, moist climates of Great Britain, northern Europe, and the United States. Halo spot rarely causes much damage to rye.
Symptoms.
Numerous elliptical or diamondshaped spots less than 4 mm long occur on leaves and sometimes the culms of winter rye in the spring after the snow has melted.
Spots have purplebrown margins that eventually fade as the spots age. In time, the centers of spots become gray from the presence of small, black pycnidia.
Sometimes spots become so numerous that much of the leaf surface is destroyed.
Management.
Not necessary.
Karnal Bunt
Karnal bunt is also called partial bunt.
Cause.
Neovossia indica (syn. Tilletia indica) survives as teliospores in soil for more than 2 years and on seed. Most primary inoculum is derived from

Page 535
seedborne inoculum, but soilborne teliospores also serve as a source of inoculum. Teliospores germinate in the spring within 2 mm of the soil surface and produce a
promycelium that grows to the soil surface. Sporidia are produced on promycelia and disseminated by wind to host plants, where florets are infected. Sporidia are
disseminated a long distance by air currents and survive up to 12 hours at relative humidities of 95% and above. Maximum germination of teliospores in vitro occurs at
temperatures of 15° to 20°C in continuous light. Infection is favored by cool, wet weather.
During the early stages of infection, intercellular hyphae are present among parenchyma and chlorenchyma cells in the distal to midportions, but not the basal portions,
of the glume, lemma, and palea. Hyphae are absent from the ovary, subovarian tissue, rachilla, and rachis. Hyphae later grow intercellularly toward the floret base to
the subovarian tissue and enter the pericarp of the ovary through the funiculus. Hyphae are found in the rachis only during the later stages of infection. The epidermis of
the ovary is not penetrated, even after prolonged contact with germinating secondary sporidia. Kernels are wholly or partially converted into chlamydospores that are
disseminated by wind at harvest time to healthy seeds and soil.
Distribution.
Afghanistan, India, Iraq, Lebanon, Mexico, Nepal, Pakistan, Syria, Sweden, Turkey, and the United States. Karnal bunt is uncommon on rye.
Symptoms.
Normally, only a few random kernels per head are diseased and become wholly or incompletely converted to smut sori. Symptoms first appear at the softdough
stage in the form of blackened areas surrounding the base of the diseased grain and extend upward on the kernel for various lengths. In the most severe symptoms,
glumes may be spread apart and expose the bunted grains; however, this is not a common symptom. Most kernels are broken or partially eroded at their embryo end.
On severely diseased plants, grain is reduced to a fragile black membranous sack of teliospores with a dead, shriveled embryo. A foul odor of trimethylamine
accompanies diseased kernels. Diseased seed has a lower survival rate in storage than healthy seed.
Management
3. Hot water (60°80°C) with the addition of NaOCl reduces seedborne teliospores and contamination in storage facilities.
Leaf Rust
Leaf rust is also called brown rust.
Cause.
Puccinia recondita (syn. P. rubigovera var. secalis), anamorph Aecidium clematidis, is a heteroecious longcycle rust that has species of alkanet (An

Page 536
chusa spp.) as alternate hosts to rye and other Secale spp. However, the pycnial and aecial stages are rarely found in the United States.
Puccinia recondita commonly overwinters as urediniospores and mycelium in leaf tissue. Because of this mode of overwintering, losses are greatest in southern rye
growing areas, where urediniospores overwinter in greater numbers. During warm, wet weather in the spring, urediniospores produced within uredinia are
disseminated by wind to host plants. If warm, moist weather conditions continue, new uredinia will be produced in 7 to 10 days. As plants mature, telia are formed in
which teliospores are produced. The teliospores either germinate upon maturity in the autumn and produce basidiospores or overwinter and germinate in the spring. In
the United States, Anchusa spp. have rarely been observed to be infected in nature. Therefore, the teliospore stage is not considered to be important in the life cycle
of the fungus, and mycelia and urediniospores perform the overwintering function.
In Europe, teliospores also either germinate in autumn and produce basidiospores or overwinter and germinate the following spring. Aecia are observed on Anchusa
spp. from spring until autumn. Therefore, pycnia and pycniospores are probably produced in autumn or, more likely, in the spring. The resulting aeciospores are
disseminated by wind to rye and uredinia are produced on diseased rye leaves. However, mycelia and urediniospores also overwinter in Europe and the aecial stage
also is not thought to be essential. Leaf rust is severe during moist conditions, such as cool nights with abundant dew or warm, wet days.
Distribution.
Symptoms.
Leaf rust of rye is similar in appearance to leaf rust of wheat and barley, and crown rust of oat. Uredinia are small, oval, orangebrown pustules on both leaf surfaces.
As uredinia rupture, powdery, redbrown urediniospores are exposed. Similar pustules that are more elongated also develop on leaf sheaths and stems. Severely
rusted plants may also have pustules on necks and glumes.
Telia appear toward plant maturity as small, elongated, dark gray pustules that do not immediately break through the epidermis. Several telia may form a circle on a
diseased leaf. The pycnial and aecial stages on Anchusa spp. resemble those found on the alternate hosts of other leaf rusts.
Management.
There is no satisfactory management. Some rye cultivars apparently have more resistance than others. However, since rye is crosspollinated, cultivars are not
uniformly pure and do not display a high amount of resistance.
Leaf Streak
Cause.
Cercosporidium graminis (syn. Scolicotrichum graminis) likely survives as mycelia in infested residue. During wet weather in the spring, conidia are

Page 537
produced and disseminated by wind to hosts. Sporulation ceases during dry weather.
Distribution.
Generally distributed in most ryegrowing areas, but leaf streak on rye is uncommon.
Symptoms.
Oblong to linear, redbrown to brownpurple blotches with definite margins develop on diseased leaves. The necrotic area is dry and sunken. A good diagnostic
characteristic is the rows or tufts of conidiophores that emerge through stomata. These structures can be seen with the aid of magnification.
Management.
Management measures ordinarily are not practiced, but sanitation will reduce inoculum.
Cause.
Phaeosphaeria herpotrichoides (syn. Leptosphaeria herpotrichoides) overwinters as mycelia in infested residue and as ascospores in asci of pseudothecia on
infested residue. Free water must occur on leaves for more than 48 hours for infection to proceed.
Distribution.
Canada, Europe, and the United States. Leptosphaeria leaf spot is considered a minor disease on rye.
Symptoms.
Irregularshaped, diffuse, yellow to tan spots occur on diseased leaves.
Management.
Some cultivars are more resistant than others.
Loose Smut
Cause.
Ustilago tritici is seedborne and survives as dormant mycelium in seed embryos. Smutted heads emerge from the boot 1 to 2 days earlier than healthy heads.
Chlamydospores are disseminated by wind to flowers of host plants and germinate during cool temperatures of 16° to 22°C and moisture provided by dews or light
rain showers. The resulting germ tubes penetrate flower ovaries and stigmas and the subsequent mycelial growth is in the embryos of developing seed. As grain
matures, U. tritici becomes dormant in the seed embryos until the following growing season. When infected seed germinates, mycelium grows systemically within
plants and replaces healthy kernels with smutted heads filled with chlamydospores.
Distribution.
Wherever rye is grown, but loose smut on rye is relatively uncommon.
Symptoms.
Diseased seed does not have external symptoms and germination is not affected. Diseased seed gives rise to plants with smutted heads, but only a few kernels, and
not the entire head, are usually diseased. Smutted heads emerge 1 to 2 days earlier than healthy heads. The brown to dark

Page 538
brown spore mass is enclosed within a fragile, gray membrane that soon ruptures and releases spores, leaving an erect, naked rachis. At maturity, the barren rachis
remains erect and protrudes above the reclining heads of healthy plants.
Management.
Loose smut of rye is uncommon and management usually is not necessary. However, treating seed with a systemic fungicide will destroy dormant mycelium in seed
ovaries.
Pink Snow Mold
Cause.
Microdochium nivale (syn. Fusarium nivale and Gerlachia nivalis), teleomorph Monographella nivalis. Microdochium nivale oversummers as perithecia on
diseased lower leaf sheaths. In the autumn, leaf sheaths and blades near the soil surface and roots are infected by ascospores from perithecia and by mycelium growing
from infested residue. During cool, wet periods, with or without snow cover, mycelia grow from diseased to healthy plants. In the spring, secondary infection may
occur from conidia or ascospores. Pink snow mold is most severe when host plants are grown under a heavy snow cover.
Distribution.
Central and northern Europe, and North America.
Symptoms.
Damage usually corresponds to the pattern of snow cover. At snowmelt, pink mycelia and sporodochia are visible on living and dead plant tissue and on the soil
surface. Somewhat rectangularshaped, brown lesions surrounded by a darker brown band on the first and second leaves cause leaves to be chlorotic, then necrotic.
Necrotic leaves remain intact and do not disintegrate. Unless crowns are diseased, plants recover during warm, dry weather despite extensive disease symptoms on
leaves.
Management
1. Sow winter rye later in the autumn. Winter rye sown late in the autumn and rye sown in the spring will develop plant growth under conditions unfavorable to
infection.
2. Rotate rye with noncereal crops such as legumes.
Platyspora Leaf Spot
Cause.
Platyspora pentamera (syn. Clathrospora pentamera) survives as perithecia in infested residue. During wet spring weather, ascospores are produced and
disseminated by wind to hosts. There must be 24 to 72 hours of continual moisture for infection to occur. New perithecia are produced on diseased leaves as rye
plants mature.
Distribution.

Page 539
Symptoms.
Nondescript yellowbrown spots are randomly produced on diseased leaves. As plants mature, dark perithecia are produced on diseased tissue.
Management.
No specific management is necessary.
Powdery Mildew
Cause.
Blumeria graminis f. sp. secalis (syn. Erysiphe graminis f. sp. secalis) overwinters as cleistothecia on infested residue. In areas where leaf tissue survives as green
tissue throughout the winter, the fungus may overwinter as mycelium. Ascospores formed within cleistothecia in the spring are disseminated by wind to host plants and
serve as primary inoculum in northern ryegrowing areas. Conidia are produced as mycelium becomes established on diseased leaf surfaces, especially during humid,
cool weather but not in the presence of free water. Conidia account for most of the secondary inoculum and spread of powdery mildew during the growing season.
Cleistothecia form on diseased leaf surfaces as plants approach maturity.
Powdery mildew ceases to be a problem when weather becomes dry and warm later in the growing season.
Distribution.
Symptoms.
Disease is most severe on tender, rankgrowing plants that have been heavily seeded or have had heavy applications of nitrogen fertilizer. Superficial mycelia and
conidia appear as light gray or white spots on the upper surface of diseased leaves, sheaths, and floral bracts. Diseased plant parts appear to be dusted with a gray
powder. Spots enlarge, yellow, and eventually darken in color as diseased plants mature. Fungal growth occurs most often on the upper leaf surfaces and infrequently
on lower surfaces. The numerous small, round, dark cleistothecia that develop on diseased areas are easily seen under magnification.
Management.
Most cultivars of rye are resistant to powdery mildew, but foliar fungicides can be applied in unusual cases where disease becomes severe. Rye is the most resistant
cereal to powdery mildew.
Scald
Scald is also called Rhynchosporium leaf scald.
Cause.
Rhynchosporium secalis overwinters as stroma in lesions on perennial grasses or winter rye infected in the autumn, and in infested residue. During cool, humid spring
or autumn weather, conidia produced on stroma are disseminated by wind to plant hosts. Secondary inoculum is conidia that are produced during cool, humid
weather.

Page 540
Distribution.
Scald occurs to some extent wherever rye is grown.
Symptoms.
Young spots are dark bluegray, watersoaked blotches that occur mainly on leaves but occasionally on leaf sheaths. Spots become oval or lensshaped and have a
light tan or white center surrounded by a strawcolored border that, in turn, is surrounded by a yellowgreen halo whose margin gradually fades into the normal green
of the leaf. Leaf spots enlarge in cool weather and may have a zonate appearance due to successive enlargements.
Spots at the base of a diseased leaf may extend across the blade and down into the sheath, causing death of the entire leaf. Elongated spots cause the entire leaf to
lose color and wide spots cause death of leaf tissue.
Management
1. Rotate rye with resistant crops.
3. Destroy perennial grasses along edges of fields.
Cause.
Septoria secalis survives as conidia within pycnidia and as mycelia in infested residue, in lesions on live diseased plants, and in seed. There is some question whether
or not S. secalis is the same as S. tritici. Symptoms are similar but some reports state no secondary infection occurs with S. tritici.
In the autumn, conidia are disseminated by wind and, under moist conditions, infect winter rye. During moist, cool conditions in the spring, rye is infected by conidia
from pycnidia produced the previous season or the current spring.
Distribution.
Generally distributed wherever rye is grown.
Symptoms.
The first symptoms are light green to yellow spots that occur mostly between diseased leaf veins. Eventually, spots become light brown, irregularshaped blotches with
a speckled appearance due to pycnidia that are sprinkled throughout the spot. Pycnidia are very small but visible to the naked eye as tiny black or dark brown specks.
After leaves die, blotches are lighter than the surrounding tissue. Under moist conditions, leaves may die and plant crowns become diseased, resulting in weakened or
dead plants.
Management
2. Plow under infested residue to aid in decomposition and prevent conidia from being placed on the soil surface, where they are easily windborne.
3. Rotate rye with a resistant crop, preferably a legume.

Page 541
4. Treat seed with a systemic seedprotectant fungicide to kill fungi on seed or any mycelium that has grown into the seed coat.
Septoria tritici Blotch
Septoria tritici blotch is also called speckled leaf blotch.
Cause.
Septoria tritici, teleomorph Mycosphaerella graminicola. The fungi survive as mycelia in live rye plants and as pycnidia on infested residue. Conidia
(pycnidiospores) from residue presumably are the primary source of inoculum. Septoria tritici is also seedborne; however, this is uncommon.
During temperatures of 15° to 25°C and 100% relative humidity in the autumn or spring, pycnidiospores are exuded from pycnidia in a gelatinous drop called a cirrhi
that protects spores from radiation and drying out. Pycnidiospores are disseminated to lower leaves by splashing and blowing rain.
Infection requires 6 or more hours of wetness and subsequent disease development is favored by temperatures of 18° to 25°C. New pycnidia and pycnidiospores are
eventually produced on diseased tissue.
As diseased rye matures, ascospores produced in pseudothecia are disseminated by wind to host plants. However, ascospores apparently do not cause much damage
because of the maturity of the host plants when infected. Mycosphaerella graminicola is readily found on residue in the United Kingdom.
Distribution.
Generally distributed wherever rye is produced.
Symptoms.
Initially, small, light green to yellow spots occur between veins of the diseased lower leaves of a host plant, especially if the leaves are in contact with soil. Spots
rapidly elongate and form tan to redbrown, irregularshaped lesions that are often partly surrounded by a yellow margin. Lesions age and become light brown to
almost white and have small, dark specks (pycnidia) in the lesion center. The presence of pycnidia is a good diagnostic characteristic.
Infection of stem nodes, leaf sheaths, and tips of glumes also occurs. Severely diseased leaves turn yellow and die prematurely. Occasionally an entire plant may be
killed. Pycnia are produced in all diseased areas. Autumn and winter infections cause a reduction in root weight and mass.
Management
1. Sow cleaned, certified, diseasefree seed treated with a seedprotectant fungicide.
4. Apply a foliar fungicide if environmental conditions favor disease development.
5. Rotate rye every 3 to 4 years with a resistant crop. Most small grains are susceptible.

Page 542
Sharp Eyespot and Rhizoctonia Root Rot
Cause.
Rhizoctonia cerealis, teleomorph Ceratobasidium cereale, survives as sclerotia in soil or as mycelium in infested residue. Some researchers also consider R. solani
as a causal agent. Rye may be infected any time during the growing season. Sclerotia germinate to form mycelium or mycelium grows from a precolonized substrate to
infect roots and culms, particularly in cool and dry soils with less than 20% moistureholding capacity. Only R. solani AG4 has been reported to be pathogenic to rye
seedlings.
Distribution.
Symptoms.
Diamondshaped lesions that resemble those of eyespot occur on lower leaf sheaths. Lesions are more superficial than eyespot lesions and have light tan centers with
dark brown margins. Dark mycelium frequently is visible on lesions. Dark sclerotia may develop in lesions and between culms and leaf sheaths.
Seedlings may be killed, but plants produce new roots to compensate for those rotted off. When roots are diseased, plants may lodge and produce white heads.
Diseased plants appear stiff, have a grayish cast, and are delayed in maturity.
Management.
No management is truly effective. Vigorous plants growing in wellfertilized soil are likely to become severely diseased.
Snow Scald
Snow scald is also called Sclerotinia snow mold.
Cause.
Myriosclerotinia borealis (syn. Sclerotinia borealis) oversummers as sclerotia. In autumn, the sclerotia germinate during damp, cool weather and form cupshaped
apothecia. Ascospores produced in a layer of asci on the upper portion of the apothecium are disseminated by wind to seedlings. Snow scald occurs when cool,
damp autumns are followed by a deep snow cover that lasts 5 or more months over unfrozen or slightly frozen soil.
Distribution.
Canada, Europe, Japan, Scandinavia, and the former USSR.
Symptoms.
Snow scald occurs in scattered patches throughout a field. Sparse, gray mycelia cover bleached, dead plants exposed after the snow has melted. Leaves wrinkle on
exposure to light and eventually turn dark because of saprophytic growth of secondary fungi, and crumble. Sclerotia are globular, elongated, or ''flakelike" (0.3 to 7.0
mm long) and black at maturity. Sclerotia are found only in and on leaves, leaf sheaths, and crowns of dead plants.
Management
1. Rotate rye with a legume to help reduce inoculum.

Page 543
2. Plowing under infested residue will bury inoculum and prevent sclerotia from germinating, hastening their decomposition.
Speckled Snow Mold
Cause.
Typhula incarnata, T. idahoensis, T. ishikariensis, and T. ishikariensis var. canadensis. Some researchers consider T. ishikariensis and T. idahoensis to be two
distinct causal fungi, while others consider these two fungi to be synonymous.
The causal fungi oversummer as sclerotia in infested residue and soil and as mycelia on live plants, but neither fungus survives well saprophytically on infested residue.
Optimum infection occurs at temperatures of 1° to 5°C. Sclerotia germinate during wet weather in the autumn and form either basidiocarps or mycelia. Infection
occurs either by mycelium growing from sclerotia to nearby host plants or by basidiospores formed on the basidiocarp that are disseminated by wind to hosts.
Sclerotia are formed within necrotic tissue or in mycelium. Further infection occurs by mycelial growth under the snow cover. Typhula spp. growth is more closely
associated with snow cover than with Microdochium nivale (syn. Fusarium nivale and Gerlachia nivalis), the cause of pink snow mold.
Distribution.
Symptoms.
Graywhite mycelia are present on plants and soil that was exposed to the air as the snow melts. Numerous sclerotia occur in living tissues and are scattered in
mycelium growing over diseased plant surfaces, giving plants a speckled appearance. Typhula incarnata can infect plants aboveground and below the soil surface.
Dead leaves are common, but unless the plant crowns are infected, diseased plants recover during warm, dry weather, although they may never be as vigorous as
healthy plants. Leaves killed by T. incarnata and M. nivale crumple easily. Leaves killed by T. incarnata are covered with gray to white mycelium, while leaves
killed by M. nivale are covered by pink mycelium.
Management.
Rotation with a legume will help to reduce soil inoculum.
Spot Blotch and Associated Seedling and Crown Rots
Cause.
Bipolaris sorokiniana (syn. Helminthosporium sativum and H. sorokinianum), teleomorph Cochliobolus sativus, is seedborne and overwinters as mycelia in
infested residue and on seedling leaves of winter rye. During moist spring weather, conidia are produced on infested residue and disseminated by wind to seedling
leaves. Spot blotch is more severe in the presence of pollen, possibly because causal fungi use pollen as an exogenous source of energy.

Page 544
Distribution.
Wherever rye is grown, but damage is usually not severe.
Symptoms.
The first symptoms occur after warm and moist weather. Round to oblong, dark brown to black spots of various sizes with definite margins appear on diseased lower
leaf sheaths near the soil line and eventually extend into green leaf blades. Spots coalesce and form lesions or blotches that cover large areas of leaves. Older lesions
are olivecolored due to sporulation of fungi. Severely diseased leaves will completely dry up.
Seedborne inoculum results in seedling blight, and root and crown rot in dry, warm soils. Seedlings are dwarfed and have excessive tillering; crowns and roots may be
dark brown and rotted. Disease may progress, causing seedlings to become yellow or killing them preemergence or postemergence. The heads of severely diseased
live plants either do not emerge completely or have kernels that are poorly filled. Early head blight causes sterility or death of individual kernels soon after pollination.
Lesions on floral bracts and kernels vary from small black spots to a dark brown discoloration of the entire surface, which results in blackened ends of kernels.
Management
2. Apply a foliar fungicide to manage the leaf blotch phase before disease becomes severe.
3. Rotate rye with a resistant crop.
Stagnospora Blotch
Stagonospora blotch is also called glume blotch.
Cause.
Stagonospora nodorum (syn. Septoria nodorum), teleomorph Phaeosphaeria nodorum (syn. Leptosphaeria nodorum), overwinters as mycelia in live plants and
seed and survives 2 to 3 years as pycnidia on infested residue. During wet weather at temperatures of 20° to 27°C in the autumn or spring, pycnidiospores are exuded
from pycnidia within a gelatinous drop called a cirrhi that protects the spores from radiation and drying up. Pycnidiospores are disseminated by splashing and blowing
rain to lower leaves of host plants. Leaves and stems, but not heads, become infected. Infection requires 6 or more hours of wetness. New spores are produced in 10
to 20 days. Ascospores are produced in perithecia as rye matures in late summer or early autumn and are disseminated by wind to plant hosts. However, ascospores
normally do not cause much damage due to the advanced maturity of plants when they are infected.
Distribution.
Symptoms.
Nodes turn brown, shrivel, and are speckled with black pycnidia. Straw bends over and lodges just above nodes. Light brown spots, similar in

Page 545
appearance to Septoria leaf blotch, occur on leaves. A brown margin may surround the leaf spots, and pycnidia are present on both surfaces of diseased leaves. If a
flag leaf is diseased, the head may be deformed. Infection of the leaf sheath causes a dark brown lesion that may include most of the sheath. Severely diseased plants
are stunted.
Management
1. Sow certified, diseasefree seed that has been cleaned and treated with a seedprotectant fungicide.
2. Grow resistant rye cultivars.
3. Plow under infected residue where this is feasible.
5. Rotate rye with a resistant crop, such as legumes, every 3 to 4 years.
Stalk Smut
Stalk smut is also called flag smut, leaf smut, stem smut, and stripe smut.
Cause.
Urocystis occulata overwinters as chlamydospores on seed, which provides most of the primary inoculum. Winter rye seed that is sown into dry soil may be infected
infrequently by soilborne chlamydospores. Chlamydospores on seed germinate and produce basidiospores that, in turn, germinate and infect seedlings. The resultant
mycelium grows along with the culm. Sori, which are composed of large numbers of chlamydospores, form in parenchyma tissue located between the veins of culms
and, infrequently, in leaf blades. At first, sori are covered by an epidermis that ruptures at harvest time, liberating chlamydospores that are disseminated by wind to
contaminate seed or soil. If soils are moist, chlamydospores in soil germinate and infect rye seedlings, but if no seedlings are present, the population of chlamydospores
in the soil decreases.
Distribution.
Symptoms.
Stalk smut is evident just before heading. Diseased plants are stunted and may be overlooked or hidden among the healthy plants. Diseased plants are darker green
than healthy plants and have light green streaks in the upper leaves. Shortly, the light green streaks extend along leaves, sheaths, and stems as long, leadcolored
stripes called sori, which contain the spore mass of chlamydospores. The stripes eventually become black and the epidermis splits to expose the mass of
chlamydospores, which resembles dark brown or black dust. Leaves eventually split along the stripes.
Rarely does a diseased plant head out. If heads are produced, sori may be found on the chaff. Normally, every stem of a diseased plant is smutted and the affected
parts are twisted and distorted.

Page 546
Management
1. Treat seed with a seedprotectant fungicide to kill chlamydospores that have contaminated the seed surface.
2. Rotate rye with another crop. If stalk smut is a problem, do not grow rye continuously in the same field.
Stem Rust
Cause.
Puccinia graminis (syn. P. graminis f. sp. secalis) is a heteroecious longcycle rust that has barberries (Berberis canadensis, B. fendleri, B. vulgaris, and
Mahonia spp.) as alternate hosts.
Puccinia graminis in North America causes stem rust of rye by one of two life cycles. Urediniospores, or the repeating spores, are produced in uredinia on rye
during spring and summer and disseminated by wind to rye plants, where they infect and produce new urediniospores under moist conditions and moderate
temperatures of 15° to 25°C. Secondary urediniospores are produced in 7 to 10 days. This cycle will continue indefinitely as long as growing rye plants are available.
Urediniospores produced in northern ryeproducing areas are blown south in summer and autumn to infect rye in southern ryegrowing areas. The urediniospores will
then recycle on rye in southern areas until they are disseminated by wind north during late winter and spring to reinfect host plants growing in the northern ryegrowing
areas.
The second life cycle is as follows: As rye ripens, teliospores form that survive through the winter. In the spring, teliospores germinate and form basidiospores
(sporidia) that are disseminated by wind to the young leaves of barberry. Pycnia (spermogonia) formed on the upper leaf surfaces of barberry function in the exchange
of genetic material, thereby creating new races of the fungus. Each pycnium produces pycniospores and special mycelia called receptive hyphae. Pycniospores are
exuded out of the pycnium in a thick, sticky, sweet liquid that is attractive to insects. Pycniospores are splashed by water or carried by insects from one pycnium to
another, where they become attached to receptive hyphae. The pycniospore germinates and the nucleus from the spore enters into the receptive hypha, which results
in the formation of an aecium on the lower leaf surface directly under the pycnium. Aeciospores, which differ genetically from both pycniospores and receptive hyphae,
are produced in the aecia and disseminated by wind to rye. Each infection gives rise to a uredinium in which urediniospores are formed. The urediniospores then serve
as the repeating stage and are windborne to rye, where new generations of urediniospores are formed. Telia are once again produced as rye matures, thus completing
the life cycle. Epiphytotics develop during moist weather, but disease is not severe during dry weather.
Distribution.

Page 547
Symptoms.
Uredinia and telia occur on stems, leaf sheaths, leaf blades, glumes, and beards of rye. Uredinia are redbrown and oblong. The epidermis of leaves and culms
becomes ruptured and pushed back around the pustule, giving it a jagged or ragged appearance and exposing the urediniospores.
Just prior to plant maturation, telia appear mostly on leaf sheaths and culms. Telia are oblong to linear and dark brown to black. Teliospores are exposed when the
epidermis ruptures.
Pycnia appear on barberry leaves in the spring as bright orange to yellow spots that in the middle sometimes have what appears to be a drop of moisture, which is the
liquid containing pycniospores. On the other side of the leaf, opposite the pycnial spots, are aecia, which resemble raised, orangecolored, bellshaped clusters.
Management
1. Grow resistant rye cultivars.
2. Eliminate the common barberry from ryeproducing areas. The common barberry should not be confused with the Japanese barberry, which is immune to stem rust.
There are several characteristics to differentiate between the two. The common barberry has a sawtoothed leaf edge, gray outer bark, bright yellow inner bark,
berries borne in bunches, and spines with usually three in a group. The Japanese barberry has a smooth leaf edge, redbrown outer bark, bright yellow inner bark,
berries borne in ones or twos, and usually a single spine.
Strawbreaker
Strawbreaker is also called Cercosporella foot rot, stem break, eyespot, foot rot, and culm rot.
Cause.
Pseudocercosporella herpotrichoides (syn. Cercosporella herpotrichoides) survives for several years as mycelia in infested residue. Conidia are produced during
cool, damp weather in the autumn or spring and infect crown and basal culm tissue but not roots. Winter rye is more likely to be infected than spring rye.
Distribution.
Where rye is grown in cool, moist climates.
Symptoms.
Eyespot is most conspicuous near the end of the growing season by the lodging of diseased plants and the presence of white heads. Initially, eye or ovateshaped
lesions with white to tan centers and brown margins develop on diseased basal leaf sheaths. Similar spots form on stems directly beneath those on sheaths and cause
lodging. Roots are not infected, but necrosis occurs around upper crown nodes. Under moist conditions, lesions enlarge and the black stromalike mycelium that
develops over crown surfaces and the bases of culms gives tissues a charred appearance. Stems shrivel and collapse or plants are yellowish or pale green and their

Page 548
heads are reduced in size and number. Early infection causes death of individual culms and of plants before maturity.
Management.
Rotate rye with noncereals, such as legumes, or grass crops.
Stripe Rust
Stripe rust is also called yellow rust.
Cause.
Puccinia striiformis, anamorph Uredo glumarum, is a rust fungus that is not known to have an alternate host. Puccinia striiformis oversummers between harvest
and emergence of autumnsown rye as urediniospores on residual green cereals and grasses. Mycelia and, infrequently, urediniospores overwinter on barley, grasses,
rye, and wheat. Urediniospores are formed during cool, wet weather and disseminated by wind to plant hosts. Little infection occurs above 15°C in the summer.
Teliospores are formed but are not known to function as overwintering spores.
Distribution.
In North America, stripe rust occurs at the higher elevations and cooler climates along the Pacific Coast and intermountain areas from Canada to Mexico. Stripe rust
also occurs in the same environment in South America and in the mountainous areas of central Europe and Asia. Stripe rust is not as common on rye as it is on wheat
and barley.
Symptoms.
The most severe symptoms occur during cool, wet weather in the early growth period of rye. Symptoms occur early in spring, before the symptoms of other rusts
appear, especially in areas with mild winters. Yellow uredinia appear on autumn foliage and new spring foliage. Uredinia coalesce and produce long stripes between
veins of diseased leaves and sheaths. Small linear lesions occur on floral bracts. Telia develop as narrow, linear, dark brown pustules covered by epidermis.
Management.
Grow resistant cultivars. Many rye cultivars have at least partial resistance.
TakeAll
Cause.
Gaeumannomyces graminis var. tritici survives as mycelia in live plants or as mycelia and perithecia in infested residue. However, ascospores are not considered
important in the life cycle of takeall. In the autumn or spring, seedlings become infected when their roots grow into the vicinity of precolonized residue. Planttoplant
spread of G. graminis var. tritici occurs when hyphae grow through soil from diseased to healthy plants or when healthy roots come in contact with diseased roots.
Ascospores are produced in perithecia during wet weather but are not disseminated very far by either splashing water or wind. Takeall is usually more severe on rye
grown in alkaline soils.

Page 549
Distribution.
Wherever rye is grown. Takeall is less severe on rye than on wheat and barley.
Symptoms.
Takeall becomes most obvious as plants approach heading. The first symptoms are light to dark brown necrotic lesions on roots. By the time diseased plants reach
the jointing stage of maturity, most roots are brown to blackened, sparse, brittle, and dead. When pulled from the soil, the crowns of diseased plants can easily be
broken off. A very dark discoloration of stems just above the soil line and a mat of dark brown fungus mycelium under lower sheaths between stems and inner leaf
sheaths are visible. At this point many plants die, or if plants are still alive, they are stunted and leaves are yellow.
Stands are uneven in height and plants appear to be in several stages of maturity. At heading, diseased plants have few tillers, ripen prematurely, and have bleached,
sterile heads.
Management.
Rotate rye with a nongrass crop since G. graminis var. tritici is not a good saprophyte and does not survive long in soil in the absence of a host. Maize roots can
become infected and carry over inoculum for subsequent crops of rye.
Tan Spot
Tan spot is also called blight, leaf spot, and yellow leaf spot.
Cause.
Pyrenophora triticirepentis, anamorph Drechslera triticirepentis (syn. Helminthosporium triticirepentis), overwinters as pseudothecia on infested residue.
During wet spring weather, ascospores are released and disseminated by wind to plant hosts and serve as primary inoculum. Conidia and hyphal fragments may also
serve as primary inoculum. During wet weather in the growing season, conidia produced in older lesions and disseminated by wind serve as secondary inoculum. In the
autumn, pseudothecia are produced on diseased culms and leaf sheaths. Symptom development is favored by frequent rains and cool, cloudy, humid weather early in
the growing season.
Distribution.
Wherever rye is grown, but rye is usually not severely affected.
Symptoms.
Symptoms first appear in the spring on lower leaves and continue throughout the early summer onto the upper leaves of diseased plants. Initially, tan flecks appear on
both sides of diseased leaves. The flecks eventually become tan, diamondshaped lesions up to 12 mm long surrounded by a yellow border with a dark brown spot in
the center caused by the sporulation of P. triticirepentis. Lesions may coalesce, starting from the leaf tips, and cause large areas of leaves to die. Pseudothecia will
eventually develop on infested residue as dark raised bumps.

Page 550
Management
1. Apply a foliar fungicide before disease becomes severe and if weather conditions favor development of the disease.
Cereal Cyst
Cause.
Heterodera avenae survives for a year or more as cysts in soil. Larvae emerge in spring from eggs contained in overwintered cysts and enter plant roots to begin
feeding. Female nematodes swell as eggs develop in their bodies and break through the root surface but remain attached by a thin neck. Males revert to a vermiform
shape. Eventually, females form cysts that detach from roots. Heterodera avenae is also a pathogen of barley, oat, wheat, and numerous annual and perennial
grasses. Populations of nematodes increase in sandy soils. Other soil characteristics, such as the death of nematodes, when roots die, and fungal parasites, also cause
fluctuations in nematode populations.
Distribution.
Africa, Australia, southeastern Canada, Europe, Japan, the United States (Oregon), and the former USSR.
Symptoms.
The first symptom is the general poor growth of diseased plants in areas within a field. Leaf tips of diseased plants are red or purple. The discolored leaves die off and
plants become yellow. The roots are thickened and more branched than those of healthy plants. Heavy infestations cause wilting (particularly during times of water
stress), stunted growth, poor root development, and early plant death. Lemonshaped cysts are white at first, then gradually become dark brown as they harden.
Cysts are visible to the naked eye.
Management
1. Rotate rye with a legume crop.
2. Apply a nematicide to soil before sowing.
3. Sow rye in the autumn.
Leaf and Stem
Cause.
Ditylenchus dipsaci. Occurrence is associated with heavy soils, high rainfall, cool growing seasons, and winter grains. Free moisture permits the nematode to migrate
to and feed on aerial plant parts. The nematode penetrates leaves and stems.
Distribution.

Page 551
Symptoms.
Cell hypertrophy and hyperplasia occur. Stunting, distortions, and swollen stems are common symptoms. In severely infested areas within a field, growing points of
diseased plants are destroyed and the plants may die. Other plants have reduced spike growth and reduced grain yields.
Management
1. Rotate with noncereal crops.
Root Gall
Cause.
Subanguina radicicola survives in roots. Larvae penetrate roots, develop in cortical tissue, and form root galls in 2 weeks. The mature females begin egg production
within a gall. Eventually, galls weaken and release larvae into the soil that establish secondary infections. Each generation is completed in about 60 days.
Distribution.
Symptoms.
Diseased seedlings frequently have reduced top growth and chlorosis. Galls on roots tend to be inconspicuous and vary in diameter from 0.5 to 6.0 mm. Roots may
be bent at the gall site. At the center of larger galls is a cavity filled with nematode larvae.
Management.
Rotate rye with noncereal crops.
Root Knot
Cause.
Meloidogyne spp.
Distribution.
Widespread.
Symptoms.
Plant growth and dry shoot weight is reduced.
Management.
Not reported.
Root Lesion
Cause.
Pratylenchus spp. overwinter as eggs, larvae, and adults in host tissue or soil. Both larvae and adults penetrate roots, where they move through cortical cells and the
females deposit eggs as they migrate. Older roots are abandoned and new roots sought as sites for penetration and feeding.
Distribution.
Symptoms.
Diseased plants in areas of a field will appear yellow and under moisture stress. Roots and crowns will rot when Rhizoctonia solani infects through nematode
wounds. New roots become dark and stunted, causing yield loss.

Page 552
Management
1. Sow in autumn when soil temperatures are below 13°C.
2. Soil fumigants could be used where their high costs are warranted.
Seed Gall
Cause.
Anguina tritici survives as larvae in seed galls for several years. When galls are sown along with rye seed, larvae are released into the moist soil and move upward on
plants in a water film to the flower primordia. Nematodes then mature, copulate, and produce eggs. The seed galls develop from undifferentiated flower tissue
interacting with the nematodes. If gall development is retarded, larvae may be present in healthyappearing seed. Galls are mixed with normal seed or fall to the soil,
where nematodes become dormant under dry conditions.
Distribution.
Eastern Asia, parts of Europe, India, and the southeastern United States. Seed gall nematode is not a common disease of rye.
Symptoms.
Prior to heading, diseased plants are swollen near the soil line and leaves will be twisted, wrinkled, or rolled. After heading, distortions are not as obvious but plants
are stunted and mature slowly. Heads are small and dark seedlike galls force glumes to spread apart. Galls are dark brown and do not have the brush or embryo
markings of normal seed.
Management
1. Sow clean seed.
2. Seed may be soaked in hot (54°C) water for 10 minutes.
3. Rotate rye with a nonhost crop for 2 years. Wheat is also susceptible.
Stubby Root
Cause.
Paratrichodorus spp. survive in soil or on roots as eggs, larvae, and adults. These nematodes feed only on the outside of roots and move relatively rapidly through
fine, sandy soil at a speed of 5 cm/hr. Rye sown early in autumn in sandy soils is most severely diseased.
Distribution.
Symptoms.
Diseased roots are thickened, short, and stubby and have brown lesions on the root tips. Tops of diseased plants grow poorly, and entire plants may be easily pulled
from the soil due to the lack of a fibrous root system.
Management.
Not reported.

Page 553
Aster Yellows
Cause.
Aster yellows phytoplasma survives in several dicotyledonous plants and leafhoppers. Aster yellows phytoplasma is transmitted primarily by the aster leafhopper,
Macrosteles fascifrons, and less commonly by Endria inimica and M. laevis. The leafhoppers acquire the phytoplasma by feeding on diseased plants, then fly to
healthy plants, where they transmit the phytoplasma by feeding. Symptoms become most obvious at temperatures of 25° to 30°C.
Distribution.
Eastern Europe, Japan, and North America.
Symptoms.
Diseased seedlings either die 2 to 3 weeks after infection or if they survive are stunted and have leaves that are completely yellowed or have yellow blotches on them
and heads that are sterile and distorted. Infection of older plants causes leaves to become somewhat stiff and discolored shades of yellow, red, or purple, starting from
the tip or margin inward. Root systems may not be well developed.
Management.
Not reported.
Cause.
African cereal streak virus (ACSV) is transmitted by the planthopper Toya catilina, but the virus is not mechanically or seedtransmitted. The natural virus reservoir
presumably is native grasses. ACSV is limited to the phloem. Disease development is aided by high temperatures.
Distribution.
East Africa.
Symptoms.
Initially, faint, broken, chlorotic streaks begin near leaf bases and extend upward on the leaves. Later, definite alternate yellow and green streaks develop along entire
leaf blades. Eventually, leaves become completely yellow. New leaves tend to develop a shoestring habit and die. ACSV induces a necrosis in the phloem.
Young diseased plants become chlorotic, are severely stunted, and die. Seed yield is almost completely suppressed. Plants become soft, flaccid, and velvety to the
touch.
Management.
Not reported.

Page 554
Barley Yellow Dwarf
Cause.
Barley yellow dwarf virus (BYDV) is in the luteovirus group. BYDV survives in autumnsown small grains, such as barley, oat, and wheat and in annual and perennial
grasses. In general, however, local grasses, winter wheat, and maize are of little importance as primary sources for BYDV.
BYDV is transmitted by several species of aphids but is not transmitted through eggs, newborn aphids, seed, or soil or by mechanical means. Once an aphid acquires
BYDV, it is capable of transmitting BYDV for the rest of its life. Some strains of BYDV are transmitted equally well by all species of aphids, but some strains display
a high degree of vector specificity. Aphid flights are local or, if assisted by wind, extend for hundreds of kilometers, carrying virus inoculum long distances. Thus, the
major source of aphids in spring may be from distant plants; however, in autumn, aphids are both distant and local.
Epiphytotics occur during cool temperatures (10° to 18°C) and moist seasons that favor grass and cereal growth together with aphid multiplication and migration.
Infections occur through the growing season but are most numerous in areas that support populations of aphids.
Distribution.
Africa, Asia, Australia, Europe, New Zealand, North America, and parts of South America. BYDV on rye is not considered to be a serious disease.
Symptoms.
Symptoms are not striking and tend to be confused with nutritional disorders or weatherrelated problems but become more pronounced at cool temperatures of 16°
to 20°C and cloudless days. Single plants or groups of plants within a field are yellow and stunted. Seedling infection slows plant maturity and causes older leaves to
turn bright yellow; however, these striking symptoms are considered unusual on rye. Leaves tend to be stiff and discolored various shades of yellow, red, or purple,
starting from the blade edge. A later infection causes the flag leaf to become discolored yellow or red. Frequently, the feeding of some vectors produces tiny, brown
black spots on leaves and culms; adjacent tissues first turn yellow, then tan. Roots are not well developed, and phloem tissues are darkened.
Management.
Not reported for rye. However, it is suggested that winter cereals be sown later in the autumn.
Soilborne Mosaic
Soilborne mosaic is also called wheat soilborne mosaic.
Cause.
Wheat soilborne mosaic virus (WSBMV) survives in soil in Polymyxa graminis, a soilborne plasmodiophoraceous fungus that is an obligate par

Page 555
asite of several higher plants. WSBMV is spread inside of P. graminis by any means that disseminates soil containing P. graminis. Polymyxa graminis enters root
hairs and epidermal cells of roots as motile zoospores that ''swim" through wet soil at temperatures of 10° to 20°C. Once inside plants, P. graminis replaces cell
contents with plasmodial bodies that either segment into additional zoospores or develop into thickwalled resting spores 2 to 4 weeks after infection. WSBMV is
most common in lowlying areas of fields that tend to be wet. Warm weather prevents development of disease symptoms. Wheat soilborne mosaic is most severe on
rye sown in the autumn, but symptoms are not as common on rye as on wheat.
Distribution.
Argentina, Brazil, Egypt, Italy, Japan, and the eastern and central United States.
Symptoms.
Symptoms, which are most prominent in the spring on older leaves, range from a light green to yellow mosaic on diseased leaves. The youngest leaves and sheaths are
mottled and develop parallel spots or streaks. Diseased plants may be severely to slightly stunted.
Management
1. Rotate rye with noncereal crops.
2. Sow rye later in autumn.
Wheat Streak Mosaic
Cause.
The wheat streak mosaic virus (WSMV) is in the potyvirus group. WSMV survives in live cereals and grasses and is transmitted in late summer or early autumn to
earlyplanted rye by feeding of the wheat curl mite, Aceria tulipae. Mites and WSMV cannot survive longer than 1 to 2 days in the absence of a living plant. Only
young mites acquire WSMV by feeding 15 or more minutes. Once a mite has picked up WSMV, it is carried internally for several weeks. As winter rye plants
mature, mites migrate to nearby cereals, grasses, or maize and infect those plants. However, some grasses are hosts for mites and not for WSMV, and vice versa;
some are susceptible to both; and some are resistant to both. WSMV has a wide host range that includes barley, maize, oat, rye, and several annual and perennial
grasses.
Distribution.
Eastern Europe, western and central North America.
Symptoms.
Initially, light green to light yellow blotches, dashes, or streaks occur parallel to leaf veins. Diseased plants become stunted, have a general yellow mottling, and
develop an abnormally large number of tillers that vary considerably in height. Stunted plants with sterile heads remain after harvest, standing at the same height or
shorter than stubble. As diseased plants mature, streaked leaves turn brown and die.
Heads may be sterile or be partially sterile but have shriveled kernels.

Page 556
With severe disease, plants die before maturity. Feeding mites often cause leaf edges to curl tightly in toward the upper midvein.
Management
1. Destroy all volunteer cereals and grasses in the subject field 3 to 4 weeks before sowing and in the adjacent fields 2 to 3 weeks before sowing the subject field.
2. Sow rye as late as practical after the Hessian flyfree date. Rye often escapes infection if it emerges in October or later.
Selected References
Boewe, G. H. 1960. Diseases of wheat, oats, barley, and rye. Illinois Nat. Hist. Surv. Circ. 48.
Brooks, F. T. 1953. Plant Diseases, Second Edition. Oxford University Press, London.
Cunfer, B. M., and Schaad, N. W. 1976. Halo blight of rye. Plant Dis. Rptr. 60:6164.
Cunfer, B. M., Schaad, N. W., and Morey, D. D. 1978. Halo blight of rye: Multiplicity of symptoms under field conditions. Phytopathology 68:15451548.
Daniels, A., Lucas, J. A., and Peberdy, J. F. 1991. Morphology and ultrastructure of W and R pathotypes of Pseudocercosporella herpotrichoides on wheat
seedlings. Mycol. Res. 95:385397.
Degenhardt, K. J., Harper, F. R., and Atkinson, T. G. 1982. Stem smut of fall rye in Alberta: Incidence, losses and control. Can. J. Plant Pathol. 4:375380.
Duczek, L.J. 1990. Sporulation of Cochliobolus sativus on crowns and underground parts of spring cereals in relation to weather and host species, cultivar, and
Hosford, R. M. 1978. Effects of wetting period on resistance to leaf spotting of wheat, barley, and rye by Leptosphaeria herpotrichoides. Phytopathology 68:591
594.
Jedlinski, H. 1983. Predisposition of winter rye (Secale cereale L.) to ergot (Claviceps purpurea (Fr.) Tui.) by barley yellow dwarf virus infection. (Abstr.)
Leukel, R. W., and Tapke, V. F. 1954. Cereal smuts and their control. USDA Farmers Bull. No. 2069.
Mains, E. B., and Jackson, H. S. 1924. Aecial stages of the leaf rusts of rye, Puccinia dispersa Eriks. and Henn. and of barley, P. anomala Rostr., in the United
States. J. Agric. Res. 28:11191126.
McBeath, J. H. 1985. Pink snow mold on winter cereals and lawn grasses in Alaska. Plant Dis. 69:722723.
McKay, R. 1957. Cereal Diseases in Ireland. Arthur Guiness Son & Co. Ltd. Dublin.

Page 557
Ploetz, R. C., Mitchell, D. J., and Gallaher, R. N. 1985. Characterization and pathogenicity of Rhizoctonia species from a reducedtillage experiment multicropped to
rye and soybeans in Florida. Phytopathology 75:833839.
Richardson, M. J., and Noble, M. 1970. Septoria species on cereals—A note to aid their identification. Plant Pathol. 19:159163.
Roane, C. W. 1984. Atypical symptoms in rye caused by Pseudomonas syringae pv. coronafaciens. (Abstr.) Phytopathology 74:792.
Simmonds, P. M. 1955. Root diseases of cereals. Canada Dept. Agric. Pub. 952.
Western, J. H. 1971 Diseases of Crop Plants. The Macmillan Press Ltd., London.

Page 559
16.
Diseases of Safflower (Carthamus tinctorius)
Bacterial Leaf Spot and Stem Blight
Bacterial leaf spot and stem blight is also called bacterial blight.
Cause.
Pseudomonas syringae survives in soil and infested residue and as a parasite and pathogen on several other plants. Seeds, weeds, residue, and soil are possible
sources of primary inoculum. Pseudomonas syringae is disseminated by seed, flowing water, and any means that moves soil. Bacteria are splashed or blown onto
plant surfaces. Bacterial blight is most severe during warm rain or under sprinkler irrigation.
Distribution.
Symptoms.
Dark, watersoaked lesions occur on diseased leaves, stems, and leaf petioles. Spots on leaves become redbrown necrotic spots with pale margins. Other
descriptions state tissue in the center of leaf spots becomes translucent and is surrounded by a dark brown to black margin. The terminal bud is often necrotic. Rotting
of interior tissues of petioles often extends below the soil line into roots.
Severely diseased plants die, but plants that are not severely diseased will recover during dry conditions. Loss of the initial stem and branches can be compensated for
by increased lateral branching.
Management.
Not reported.
Stem Soft Rot
Cause.
Erwinia carotovora pv. carotovora. Stem soft rot occurs during wet weather.
Distribution.
Mexico.

Page 560
Symptoms.
Diseased plants wilt. Stems have a soft internal rot.
Management.
Not reported.
Cause.
Alternaria carthami. Alternaria alternata has also been reported as a causal agent. Both fungi are seedborne and survive in residue for at least 2 years. Leaf spots
in the early stages of plant development have been reported to yield only A. carthami; whereas A. alternata was the predominant fungus isolated from leaf spots on
diseased plants that were nearing maturity. Under greenhouse conditions, A. carthami is pathogenic on safflower at all growth stages. Alternaria alternata also
infects healthy safflower plants, but infections remain dormant until leaf senescence. Alternaria solani is also reported to penetrate healthy leaves, but it does not
cause leaf spots and mycelia remain dormant until leaf senescence. Secondary spread is by windborne conidia. Disease development is favored by abundant moisture
from dew or rain and temperatures of 25° to 30°C.
Distribution.
Wherever safflower is grown.
Symptoms.
Aboveground symptoms first appear on seedling cotyledons as brown spots that reach a maximum size of 5 mm in diameter. On diseased leaves of older plants, small
brown to dark spots (1 to 2 mm in diameter) with concentric rings enlarge to about 1 cm and coalesce to form large lesions. The centers of these spots are light in
color and have alternate light and dark brown rings. Fully mature spots tend to develop holes, which cause a cracking of leaves. Conidia produced in the spots give
them a dusty appearance.
When stems of emerging seedlings are diseased, a brown discoloration appears on the stems just above the soil level. Stem infection may cause the complete collapse
of a plant.
Flower heads are first infected at the base of the calyx. Diseased buds shrink and dry up instead of opening. Seed coats may have brown, sunken lesions. Diseased
seeds that are sown may rot before germination; if seed does germinate, the resulting seedlings may damp off.
Management
3. Place seeds in water at 50°C for 30 minutes.

Page 561
Anthracnose
Cause.
Colletotrichum capsici and Gloeosporium carthami.
Distribution.
Colletotrichum capsici is reported from India and G. carthami from Australia, Japan, Kenya, and the United States.
Symptoms.
Colletotrichum capsici is reported to cause plant wilting. Gloeosporium carthami causes a dieback and premature death. Light brown, elongated lesions may occur
on diseased stems.
Management.
Not reported.
Botrytis Head Rot
Botrytis head rot is also called Botrytis flower blight, and gray mold.
Cause.
Botrytis cinerea, teleomorph Botryotinia fuckeliana, survives as sclerotia in soil and infested residue. Primary inoculum is sclerotia that either support conidiophores
and conidia on their surfaces or germinate and form mycelium. Conidia are disseminated by wind and water and sclerotia are disseminated by any means that moves
soil. Secondary inoculum is provided by conidia that are abundantly produced on diseased tissue during moist weather and disseminated by wind for long distances to
the flowers of plant hosts. Botrytis head rot is most severe in cool, wet weather during or after flowering.
Distribution.
Wherever safflower is grown in moist climates.
Symptoms.
Diseased seed heads initially change color from dark to light green, then become completely brown. During cool, wet weather, diseased floral parts are covered with a
gray, fuzzy mold consisting of mycelium, conidiophores, and conidia. The fungus progresses through the seed head and into the stem, causing diseased heads to be
easily detached from the stem. Infection at the early stage of bloom causes seed to be light in weight; later infection results in seed that is of almost normal weight.
Management.
Not reported, although anecdotal evidence suggests it is not advisable to grow safflower in moist areas where environmental conditions are conducive to Botrytis head
rot.
Cause.
Cercospora carthami survives in infested residue. Dew condensation early in the morning appears to be critical for spore germination and germ tube elongation.
Conidia require 3 to 4 days to penetrate leaves but are able to withstand three to four intervening 20hour dry periods. Spore germination, germ tube penetration, and
subsequent disease development are greatest under moist, humid conditions with little wind.

Page 562
Distribution.
Australia, Africa, India, Middle East, southern Russia, and the southern United States. Cercospora leaf spot is considered of minor importance and generally occurs in
warmer safflowergrowing areas.
Symptoms.
Symptoms can occur at almost any stage of growth. Round (310 mm in diameter) to irregularshaped brown spots occur mostly on the lower leaves of diseased
plants. Spots are slightly sunken and frequently have concentric rings and a yellowish margin. Diseased leaves become distorted and have interveinal necrosis. During
moist conditions, both sides of spots become grayish because of the sporulation of conidia. In Australia, leaf spots remain confined to older leaves and are reported to
have a whitish center with a graybrown margin.
Along with bracts, stems and nodes may become infected. Flower buds turn brown, wither, and die; no seed is produced.
Management.
Not necessary.
Charcoal Rot
Cause.
Macrophomina phaseolina (syn. Sclerotium bataticola and Rhizoctonia bataticola) is seedborne as pycnidia and sclerotia. Charcoal rot is most severe at high soil
temperatures (30°C and above) and low soil moisture.
Distribution.
Wherever safflower is grown in warmer climates. Charcoal rot rarely occurs in northern safflowergrowing areas.
Symptoms.
Symptoms usually occur after flowering. Diseased stalks ripen prematurely; the bases of the stalks become gray and only the vascular bundles or fibers remain, which
gives the inside of the stems a shredded appearance. Vascular fibers become covered with small, black sclerotia that resemble pepper or "flecks" of charcoal. Stems
infected with M. phaseolina and parasitized by stem weevil larvae have a brown to black discoloration that may be with or without typical gray areas on the stem
surface. Portions of the lower stems and upper taproots are hollow and contain mixtures of insect frass and fragments of pith tissue.
Flowers ripen prematurely, which results in small, poorly filled, distorted heads with a zone of aborted flowers. Infected seed that is sown either does not germinate or
if it does germinate, roots, hypocotyls, and cotyledons are discolored. Pycnidia and sclerotia eventually develop on diseased plant parts.
Management
1. Rotate safflower with a resistant crop, such as small grains. Soybean and sunflower also are susceptible.
3. Grow cultivars that have resistance.
4. Irrigate at flowering or at flowering and ripening stages of plant growth.

Page 563
Colletotrichum Stem Rot
Cause.
Colletotrichum orbiculare.
Distribution.
Australia.
Symptoms.
Brown, necrotic lesions occur on the bases of diseased stems. Diseased plants may die.
Management.
Not necessary.
Damping Off
Cause.
Several fungi, including Alternaria spp., Fusarium spp., Penicillium spp., Phytophthora spp., and Pythium spp.
Distribution.
Widespread. Wherever safflower is grown under moist soil conditions.
Symptoms.
Diseased plants fail to emerge or die shortly after emergence.
Management.
Downy Mildew
Cause.
Bremia lactucae f. carthami.
Distribution.
Cyprus, Iran, Israel, and the former USSR.
Symptoms.
Typical mildew symptoms characterized by the downy growth of mycelium, conidiophores, and conidia occur on leaves.
Management.
Not reported.
Fusarium Wilt
Cause.
Fusarium oxysporum f. sp. carthami, which survives as chlamydospores in soil and infested residue, is seedborne as internal mycelium and conidia contaminating the
outside of seeds. Mycelium and conidia may also survive in infested residue for a short period of time. Abundant conidia are produced on residue and disseminated by
wind to other areas. Some conidia are converted to chlamydospores when they fall to the soil. Mycelia from residue, germinating chlamydospores, and conidia
penetrate roots and enter into the waterconducting vascular tissue (xylem tissue). Microconidia and conidia move up the xylem tissue and microconidia lodge at
nodes, where they germinate. Eventually, water movement within a plant is inhibited by tyloses, gums, and physical blockage.
Fusarium wilt severity is greatest during high temperatures and moist weather in plants grown in acidic, lighttextured soils that are high in nitrogen. Different physiologic
races of F. oxysporum f. sp.carthami exist.

Page 564
Distribution.
Symptoms.
A typical symptom is the yellowing of leaves on one side of the diseased plant. Unilateral yellowing also occurs on leaves and some seed heads. Yellowing, which
begins on lower leaves, is followed by wilting that progresses up the plant. Plants infected when young are usually killed, and older plants that become infected may
also die but usually only branches on one side of the diseased plant are killed. Seed heads are frequently blighted and distorted due to the fungus growing up the
vascular system into the seed head. Diseased heads have aborted seed. The vascular system of the roots and stems has a brown discoloration.
Management
3. Rotate safflower with other crops.
4. Some safflower selections are resistant to race 4.
Cause.
Phyllosticta carthami.
Distribution.
The Philippines.
Symptoms.
Scattered tan spots occur on diseased leaves. Later, black specks, which are pycnidia, can be observed scattered throughout the spots.
Management.
Not reported.
Phytophthora Root and Stem Rot
Phytophthora root and stem rot is also called Phytophthora root rot.
Cause.
Phytophthora cactorum, P. cryptogea, P. drechsleri, and P. nicotianae var. parasitica (syn. P. parasitica) have been reported to cause disease of safflower. All
species are thought to survive in infested residue and soil. A general life cycle for all Phytophthora spp. is the sporangia are formed that germinate and produce either
mycelium or zoospores that "swim" to roots, then encyst and germinate. Plants may be infected at all stages of growth. Phytophthora root rot is most severe in wet
soils, particularly in surfaceirrigated fields or poorly drained areas, and at soil temperatures of 25° to 30°C. Water stress before infection predisposes plants to root
rot caused by P. cryptogea. Physiologic races of the different Phytophthora spp. are thought to exist.
Distribution.
Australia and the western United States.
Symptoms.
Lower stems of seedlings collapse, causing plant death. The first aboveground symptom on diseased older plants is that leaves become light

Page 565
green or yellow, then they wilt, die, and turn brown. In the early stages of wilting, roots become discolored reddish. As Phytophthora root and stem rot progresses,
the roots and lower stems become dark brown to black. This discoloration extends upward above the soil line on stems and is a diagnostic symptom.
Early inoculation of plants reduces the length of fine roots, which reduces their capacity to take up water. However, this has only a slight overall effect on water uptake
because of the increased water uptake by the remaining roots. Lesions that develop on stem bases or taproots greatly reduce water uptake by diseased plants.
Management
2. Provide good drainage. Where flood irrigation is used, avoid ponding of water.
3. Grow surfaceirrigated safflower on beds under furrow irrigation instead of flood irrigation.
Powdery Mildew
Cause.
Erysiphe cichoracearum (E. cichoracearum f. sp. carthami).
Distribution.
Afghanistan, India, Israel, and Russia.
Symptoms.
A gray, powdery mass of mycelium, conidia, and conidiophores occurs on diseased leaf surfaces.
Management.
Not reported.
Pythium Damping Off
Cause.
Several Pythium spp, including P. acanthicum, P. aphanidermatum, P. debaryanum, P. irregulare, P. myriotylum, P. oligandrum, P. splendens, P. ultimum,
and a divergent form of P. ultimum reported from Canada labeled as Pythium sp. "group G." Disease is favored by wet soil conditions.
Distribution.
Worldwide.
Symptoms.
The initial symptom is the hypocotyl becomes flaccid and discolored a light brown. Eventually, seedlings are killed.
Management.
Apply fungicide seed treatments.
Pythium Root Rot
Cause.
Pythium spp., particularly P. ultimum and P. splendens. The severity of Pythium root rot is greatest on safflower grown under irrigation. Only young plants are
susceptible. Susceptibility of host plants is related to the elongation of hypocotyls and the first internode tissue.

Page 566
Distribution.
Symptoms.
The hypocotyl and first internode become watersoaked, soft, and discolored a light brown. Plants topple over and tissues continue to rot and collapse.
Management
2. Plants do not become diseased when they are not grown under irrigation.
Ramularia Leaf Spot
Ramularia leaf spot is also called brown leaf spot.
Cause.
Ramularia carthami. Disease is favored by irrigation but does not occur on rainfed safflower crops.
Distribution.
France, India, Israel, and Russia.
Symptoms.
Round spots (210 mm in diameter) occur on both sides of diseased leaves. Spots are characterized by a whitish, dense mass of mycelium, conidiophores, and
conidia in their centers. Dried up and necrotic spots are discolored brown. Yields are reduced and seed quality is affected.
Management.
Rotate safflower with other crops.
Rhizoctonia Blight and Stem Canker
Rhizoctonia blight and stem canker is also called Rhizoctonia blight.
Cause.
Rhizoctonia solani, teleomorph Thanatephorus cucumeris. The optimum soil temperatures for disease development are 20° to 25°C.
Distribution.
The United States (New Mexico and Texas).
Symptoms.
Dark cortical lesions occur slightly below or at the soil line on diseased seedling stems. In the advanced stages of disease, lesions extend upward on stems beyond the
attachment point of the lowest leaves. Lesions frequently girdle stems. Root development is reduced.
Management.
Rust
Cause.
Puccinia calcitrapae var. centaureae (syn. P. carthami). Puccinia verruca is also reported to be a causal fungus. Puccinia calcitrapae var. centaureae is an
autoecious rust fungus whose five spore stages occur only on safflower. Teliospores are seedborne and overwinter on infested residue. In the spring, a teliospore
germinates and produces a promycelium on which

Page 567
four basidiospores form. The basidiospores, which are violently discharged upward from diseased or infested tissue, are disseminated by wind to nearby host plants.
Basidiospores germinate and pycnia are formed at the infection site. Most of each pycnium is submerged below the leaf surface. However, the opening of each
pycnium is above the epidermis surface of cotyledons, hypocotyls, tender stems, and true leaves. Aecia, which form in 4 to 7 days, are in close association or closely
grouped with pycnia. In gross morphology, an aecial pustule is similar to a uredinium and has been referred to as a primary uredinium and a uraecium. Uredinia are
scattered over host tissue and, unlike aecia, are not closely grouped. As uredinia pustules mature, telia form in the uredinia or in separate telia. Several physiologic
races occur.
Distribution.
Symptoms.
Puccinia calcitrapae var. centaureae, unlike most rust fungi, has two distinct pathological stages: a seedling phase and a foliage phase. The seedling phase results
from infection by basidiospores originating either from soil or from seedborne teliospores. The foliage phase occurs at any growth stage and results from infection by
windborne urediniospores.
Infection of seedling hypocotyls causes swelling and often the diseased stem bends and twists to one side. Chestnutbrown pustules, which commonly are aecia and
rarely uredinia, form on diseased hypocotyls and less often on cotyledons and young leaves. Aecia are grouped in clusters, but uredinia are scattered. Diseased
seedlings may collapse at or slightly below the soil surface and die. On older plants, a pronounced girdling and hypertrophy of stem bases occurs, which causes
diseased plants to break at this point during wind and rainstorms.
Aeciospores or urediniospores from seedling infections initiate foliar infections. Small, powdery, chestnutbrown pustules develop abundantly on the lower leaf
surfaces and less abundantly on the upper leaf surfaces, cotyledons, and flower bracts. On highly susceptible varieties, pustules may reach a diameter of 1 to 2 mm
and be surrounded by a secondary and frequently a tertiary ring of uredinia. Small chlorotic or necrotic flecks develop on resistant varieties, but no sporulation occurs.
Toward the end of the growing season, the chestnutbrown pustules become black from the formation of teliospores in them.
Management
2. Rotate safflower with other crops.
4. Flood soils for 7 days to reduce inoculum in soil.
5. Grow resistant cultivars; however, cultivars resistant to one race of P. calcitrapae var. centaureae may be susceptible to other races.

Page 568
Sclerotinia Stem Rot and Head Blight
Sclerotinia stem rot and head blight is also called Sclerotinia stem rot.
Cause.
Sclerotinia sclerotiorum survives in soil and infested residue as sclerotia. During wet weather, sclerotia germinate and form either several apothecia or mycelium.
Ascospores are formed in a layer of asci on the apothecium and are disseminated by wind to plant hosts. Disease is most severe during humid conditions around the
base of the host plant.
Distribution.
Symptoms.
Diseased leaves turn yellow, wilt, become brown, and shrivel. The entire plant may die, causing the top to curve downward. A white, cottony growth, which is the
fungus mycelium, occurs on the base of the diseased stem. Sclerotia appear as black, elongated objects (212 mm long) on and in stems, and on adjoining roots.
Cortical tissue of lower stems becomes shredded. Roots generally are not infected or discolored.
When head rot occurs, the diseased flower heads sometimes fall from the plant, leaving the outer bracts in place. Sclerotia also form in flower heads. At maturity,
diseased heads contain few or no seeds, which often are replaced by a dustyappearing residue.
Management
1. Do not include safflower in a rotation with other plants susceptible to S. sclerotiorum.
2. Use soil fumigation on small areas.
3. Fields may be flooded for 4 weeks, then dried up prior to planting.
Septoria Leaf Spot
Cause.
Septoria carthamicola and S. carthami. The fungi are presumably seedborne.
Distribution.
Australia, Bulgaria, Canada, Morocco, Turkey, and the former USSR.
Symptoms.
Tan to dark leaf spots occur on diseased leaves.
Management.
Not reported.
Verticillium Wilt
Cause.
Verticillium dahliae survives as microsclerotia in soil and infested residue. Microsclerotia germinate and produce mycelia that infect nearby host plants. Verticillium
wilt is more severe during cool, wet weather. Plants may be infected at any stage of growth.
Distribution.

Page 569
Symptoms.
Young plants are stunted. Diseased leaves are darker green than healthy leaves and may be crinkled between the veins. Cotyledons are yellowish, flaccid, and quickly
dry up.
Symptoms on plants infected at a later growth stage first occur on the lower leaves. Diseased leaves may display unilateral growth because the healthy half of the leaf
grows faster than the diseased half, causing the entire leaf to grow in a ''C" or comma shape. The "healthyappearing" half of a diseased leaf is a normal green, while
the diseased half is tan or light brown. A characteristic symptom is chlorotic areas on leaf margins and principal veins that give leaves a mottled appearance. As
diseased plants grow older, the chlorotic areas enlarge and become light tan or whitish. A dark discoloration occurs in vascular strands, particularly at the nodes,
petioles, and leaf traces. Plants may die prematurely and usually do not produce viable seed.
Management.
Verticillium wilt is ordinarily considered a minor disease. Do not rotate safflower with cotton, peanut, or other susceptible crops.
Disease Caused By Nematodes
Root Knot
Cause.
Meloidogyne arenaria, M. incognita, and M. javanica do not survive if the temperature averages below 3°C during the coldest month. Disease is favored by warm
soil temperatures.
Distribution.
The United States.
Symptoms.
Typical root galls form on diseased roots.
Management
1. Sources of resistance are available.
2. Do not rotate with cotton, sorghum, and sugar beet.
Disease Caused By Phytoplasmas
Phyllody
Phyllody is also called safflower phyllody.
Cause.
Phyllody phytoplasma is transmitted by the leafhopper Neoaliturus fenestratus. Other species in the family Compositae, including tricolor chrysanthemum,
Chrysanthemum carinatum; strawflower, Helichrysum bracteatum; common sunflower, Helianthus annuus; and cape marigold, Dimorphotheca sinuata, also
are susceptible to the phytoplasma. Periwinkle, Vinca rosea, is also susceptible.

Page 570
Distribution.
Israel.
Symptoms.
Initially, abnormal axillary budding occurs, starting when the diseased plant reaches a height of 20 to 30 cm. The main stem of a diseased plant produces numerous
secondary shoots, beginning at the top and spreading rapidly throughout the entire main stem. These secondary shoots are very thin and may produce new branchings.
Very small, yellowish leaves appear, and after several weeks, witches' broom symptoms develop. Many short stems appear on the infected flower heads instead of
the typical tubular flowers of healthy plants. Flowers on diseased plants either have no seeds or the seeds are sterile. In contrast, healthy plants produce one main stem
and few lateral ones on the upper part of the central stem and from one to five colored flower heads.
Management.
Keep safflower fields free of the weed Carthamus tenuis because the leafhopper breeds in this plant.
Alfalfa Mosaic
Cause.
Alfalfa mosaic virus (AMV).
Distribution.
The United States.
Symptoms.
Dark streaks occur on diseased roots and stems and eventually encircle the stem. Mosaic symptoms may occur on leaves.
Management.
Not reported.
Chilli Mosaic
Cause.
Chilli mosaic virus (CMV) is transmitted from diseased to healthy plants by several species of aphids.
Distribution.
India.
Symptoms.
Light and dark green patches are scattered over diseased leaves.
Management.
Not reported.
Cucumber Mosaic.
Cause.
Cucumber mosaic virus (CMV) is in the cucumovirus group. CMV is transmitted from diseased to healthy plants early in the growing season by the green peach
aphid, Myzus persicae. CMV has a wide host range.
Distribution.
Symptoms.
A light and dark green mosaic pattern occurs on diseased upper

Page 571
leaves and bracts. Some leaves may become blistered and distorted. The mosaic pattern is less distinct on lower leaves and becomes a scattering of light and dark
green flecks. Diseased plants may be stunted but usually develop to maturity.
Management.
Not reported.
Lettuce Mosaic and Necrosis
Cause.
Lettuce mosaic virus (LMV). LMV is mechanically transmissible through sap and by the aphid, Myzus persicae.
Distribution.
Symptoms.
Diseased plants have a terminal necrosis of stems, leaves, flower buds, and roots. Dark streaks that occur on roots and stems may eventually encircle the stem. A
transverse section through the stem reveals the necrosis of cortical, xylem parenchyma, and cambium tissues.
Inoculated safflower varieties have displayed local lesions due to the development of systemic mosaic symptoms. Inoculated young plants die from necrosis but the
systemic spread of the virus is delayed or does not occur in older, inoculated plants.
Management.
Resistance has been identified in some safflower cultivars.
Tobacco Mosaic
Cause.
Tobacco mosaic virus (TMV) is in the tobamovirus group.
Distribution.
Morocco.
Symptoms.
After being mechanically inoculated, small, reddish, local lesions occur on cotyledons. During temperatures of 28° to 32°C and high light intensity, necrotic ring and
line patterns appear on cotyledons. Later, typical blotchy light and dark green mosaic patterns occur on all subsequent leaves until flowering.
Management.
Not reported.
Turnip Mosaic and Necrosis Severe Mosaic
Turnip mosaic and necrosis is also called severe mosaic.
Cause.
Turnip mosaic virus (TuMV) is in the potyvirus group. TuMV is mechanically transmitted by the aphid, Myzus persicae. Species of Brassica serve as sources for
TuMV.
Distribution.
The United States (the Sacramento Valley in California).
Symptoms.
Diseased plants are stunted and their leaf and seed heads are reduced in size. Leaves and bracts of seed heads have small dark green and pale green areas, pale green
vein banding, distortion, and bronzing. Seed

Page 572
ovules rot, resulting in a reduction in seed yield. Some cultivars develop necrotic lesions and do not display mosaic symptoms.
Management.
Not reported.
Selected References
Ashri, A. 1961. The susceptibility of safflower varieties and species to several foliage diseases in Israel. Plant Dis. Rptr. 45:146150.
Beech, D. F. 1960. Safflower—An oil crop for the Kimberleys. Western Australia Dept. Agric., Perth, Bull. 2720.
Chakrabarti, D. D, and Basuchaudhary, K. C. 1978. Incidence of wilt of safflower caused by Fusarium oxysporum f. sp. carthami and its relationship with the age
of the host, soil and environmental factors. Plant Dis. Rptr. 62:776778.
Classen, C. E., Schuster, M. L., and Ray, W. W. 1949. New diseases observed in Nebraska on safflower, Plant Dis. Rptr. 33:7375.
Duniway, J. M. 1977. Predisposing effect of water stress on the severity of Phytophthora root rot in safflower. Phytopathology 67:884889.
Erwin, D.C., Starr, M. P., and Desjardins, P. R. 1964. Bacterial leaf spot and stem blight of safflower caused by Pseudomonas syringae. Phytopathology 54:1247
1250.
Heritage, A. D., and Harrigan, E. K. S. 1984. Environmental factors influencing safflower screening for resistance to Phytophthora cryptogea. Plant Dis. 68:767
769.
Howard, R. J., and Moskaluk, E. R. 1990. Seedling blight of safflower in southern Alberta. (Abstr.). Can. J. Plant Pathology 12:334.
Huang, H. C., Morrison, R. J., Nuendel, H.H., Barr, D. J. S., Klassen, G. R., and Buchko, J. 1992. Pythium ultimum "group G," a form of Pythium ultimum
causing dampingoff of safflower. Can. J. Plant Pathol. 14:229232.
Irwin, J. A. G., and Jackson, K. J. 197Z Safflower diseases in Queensland. Queensland Agric. J. 103:516520.
Jacobs, D. L., Bergman, J. W., and Sands, D. C. 1982. Etiology and epidemiology of bacterial leaf spot and stem blight of safflower in Montana. (Abstr.)
Klein, M. 1970. Safflower phyllody—A mycoplasma disease of Carthamus tinctorius in Israel. Plant Dis. Rptr. 54:735738.
Klisiewicz, J. M. 1974. Assay of Verticillium in safflower seed. Plant Dis. Rptr. 58:926927.
Klisiewicz, J. M. 1975. Survival and dissemination of Verticillium in infected safflower seed. Phytopathology 65:696698.
Klisiewicz, J. M. 1977. Effect of flooding and temperature on incidence and severity of safflower seedling rust and viability of Puccinia carthami teliospores.
Klisiewicz, J. M. 1977. Identity and relative virulence of some heterothallic Phytophthora species associated with root and stem rot of safflower. Phytopathology
67:11741177.
Klisiewicz, J. M. 1980. Safflower germplasm resistant to Fusarium wilt. Plant Dis. 64:876877.

Page 573
Klisiewicz, J. M. 1981. Isolation of turnip mosaic virus from safflower. (Abstr.) Phytopathology 71:886.
Klisiewicz, J. M. 1983. Etiology of severe mosaic and its effect on safflower. Plant Dis. 67:112114.
Klisiewicz, J. M., Houston, B. R., and Peterson, L. J. 1963. Bacterial blight of safflower. Plant Dis. Rptr. 47:964966.
Kolte, S.J. 1985. Diseases of Annual Edible Oilseed Crops. Volume II: Sunflower, Safflower, and Nigerseed Diseases. CRC Press Inc., Boca Raton, FL. 154 pp.
Liddell, C. M., and Duniway, J. M. 1987. Changes in water uptake and root distribution occurring during the development of Phytophthora root rot in safflower.
Lockhart, B. E. L., and Goethans, M. 1977. Natural infection of safflower by a tobamovirus. Plant Dis. Rptr. 61:10101012.
Lopez, C. J. A., and Fucikovsky, Z. L. 1986. Safflower Carthamus tinctorius L. stem soft rot at Chapingo, Mexico. (Abstr.) Phytopathology 76:374.
Mortensen, K., and Bergman, J. W. 1983. Cultural variance of Alternaria carthami isolates and their virulence on safflower. Plant Dis. 67:11911194.
Mortensen, K., Bergman, J. W., and Burns, E. E. 1983. Importance of Alternaria carthami and A. alternata in causing leaf spot diseases of safflower. Plant Dis.
67:11871190.
Raccah, B., and Klein, M. 1982. Transmission of the safflower phyllody mollicute by Neolaiturus fenestratus. Phytopathology 72:230232.
Rathaiah, Y., and Pavgi, M. S. 1971. Ability of germinated conidia of Cercospora carthami and Ramularia carthami to survive desiccation. Plant Dis. Rptr.
55:846847.
Sackston, W. E. 1953. Foot and root infection by safflower rust in Manitoba. Plant Dis. Rptr. 37:522523.
Sackston, W. E. 1960. Botrytis cinerea and Sclerotinia sclerotiorum in seed of safflower and sunflower. Plant Dis. Rptr. 44:664668.
Stovold, G. 1973. Phytophthora drechsleri Tucker and Pythium spp. as pathogens of safflower in New South Wales. Australian J. Exp. Agric. and Animal
Husbandry 13:455459.
Thomas, C. A. 1970. Effect of seedling age on Pythium root rot of safflower. Plant Dis Rptr. 54:10101011.
Thomas, C. A., Rubis, D. D., and Black, D. S. 1960. Development of safflower varieties resistant to Phytophthora root rot. Phytopathology 50:129130.
Thomas, C. A., Klisiewicz, J., and Zimmer, D. 1963. Safflower diseases. USDA Agric. Res. Serv. ARS 3452.
Weiss, E. A. 1971. Diseases of Safflower in Castor, Sesame and Safflower. Barnes and Noble Inc., New York.
Zazzerini, A., Cappelli, C., and Panattoni, L. 1985. Use of hotwater treatment as a means of controlling Alternaria spp. on safflower seeds. Plant Dis. 69:350351.
Zimmer, D. E. 1963. Spore stages and life cycle of Puccinia carthami. Phytopathology 53:316319.
Zimmer, D. E., and Thomas, C. A. 1967. Rhizoctonia blight of safflower and varietal resistance. Phytopathology 57:946949.
Zimmer, D. E., Klisiewicz, J. M., and Thomas, C. A. 1963. Alternaria leaf spot and other diseases of safflower in 1962. Plant Dis. Rptr. 47:643.

Page 575
17.
Diseases of Sorghum (Sorghum bicolor)
Cause.
Acidovorax avenae subsp. avenae (syn. Pseudomonas avenae and P. alboprecipitans) does not survive well in infested residue or soil. Vaseygrass, Paspalum
urvillei, is considered a primary source of inoculum in Florida. Warm, rainy weather favors disease development but leaf blight will occur below 18°C. Bacteria are
splashed or blown onto a host plant and enter the stalk through hail wounds or other injuries. Disease symptoms were severe following heavy rains in Illinois.
Distribution.
The central and southern United States.
Symptoms.
Symptoms occur on diseased leaves from late April to early June and are similar to symptoms on maize except that lesions on sorghum may be more reddish than
those found on maize. Watersoaked brown lesions occur on leaves as they emerge from whorls, then the diseased leaves become ellipticalshaped and are gray or
white until plant maturity. Lesions may coalesce during wet weather and form large necrotic areas that cause leaves to shred in the wind. Diseased plants may be
stunted.
Management.
Bacterial Leaf Spot
Bacterial leaf spot is also called bacterial spot.
Cause.
Pseudomonas syringae (syn. P. syringae pv. syringae) overwinters in soil, on seed, and presumably on infested residue, johnsongrass, and sorghum plants that
remain in the field after harvest. Bacteria are disseminated by wind, rain, and insects. Infection occurs through stomates and wounds. The optimum conditons for
bacterial leaf spot are wet weather and a temperature of 12°C.

Page 576
Distribution.
Wherever sorghum is grown.
Symptoms.
Spots first appear on lower leaves and progress upward as diseased plants approach maturity. Spots are circular to elliptical (110 mm in diameter). Spots are dark
green and watersoaked initially, but soon become tan with a red border. Small lesions may be entirely red and have somewhat sunken centers. Numerous spots
coalesce, form large diseased areas, and cause leaves to die. Lesions also occur on leaf sheaths and seeds.
Management
1. Sow healthy seed that has been treated with a seedprotectant fungicide.
2. Rotate sorghum with resistant crops.
4. Destroy johnsongrass and sorghum plants left after harvest.
Bacterial leaf streak is also called bacterial streak.
Cause.
Xanthomonas campestris pv. holcicola (syn. Bacterium holcicola, Phytomonas holcicola, Pseudomonas holcicola, and X. holcicola). Xanthomonas
campestris pv. holcicola overwinters in infested residue and standing plants left in a field after harvest. In Kansas, bacteria have been reported to survive up to 24
months in seed in an unheated building. Bacteria are disseminated locally by water and wind and over long distances by residue and seed.
Xanthomonas campestris pv. holcicola enters plants primarily through wounds and stomates. The bacterium is systemic in sorghum and is probably translocated in
xylem tissue. Development of bacterial leaf streak is favored by warm, wet weather.
Distribution.
Argentina, Australia, India, Mexico, Nigeria, New Zealand, the Philippines, Russia, South Africa, and the United States.
Symptoms.
Watersoaked, translucent streaks (3 × 25150 mm) occur on diseased leaves of all ages. Initially, light yellow drops of bacterial exudate present on translucent
streaks dry to thin white or creamcolored scales. Later, redbrown blotches enlarge and become red throughout the streaks, causing the watersoaked and
translucent areas to disappear. Portions of streaks may broaden into elongated oval spots with tan centers and narrow red margins. Numerous streaks may coalesce
and form long, irregularshaped areas that cover large portions of diseased leaves. Necrotic tissue between redbrown streaks is bordered by dark, narrow margins.
Management
1. Rotate sorghum with other crops.
3. Sow healthy seed treated with a fungicide.

Page 577
Bacterial Leaf Stripe
Bacterial leaf stripe is also called bacterial stripe.
Cause.
Pseudomonas andropogonis is seedborne and survives in infested residue and soil and on sorghum plants remaining in the field after harvest. Local dissemination is
by wind, water, and insects; longrange dissemination is by seed or residue. Infection occurs through stomates and injuries caused by wind and insects. Optimum
development of bacterial leaf stripe occurs at temperatures of 25° to 29°C and wet weather, such as cloudy, humid days following rain.
Distribution.
Argentina, Australia, China, Taiwan, Nigeria, and the United States.
Symptoms.
Initially, linear, interveinal lesions that are approximately 1 cm long develop on leaves. Later, the stripes that develop are restricted to interveinal areas of apical
portions of the lower leaves and leaf sheaths. Depending on the diseased cultivar, stripes are a continuous color that varies from tanred to brick red to dark purple
red. Stripes, which vary in length from 25 mm to the length of the leaf blade, sometimes coalesce and cover large areas of diseased leaves. Watersoaking of tissue
adjacent to lesions normally does not occur.
Bacterial exudate found on the underside of affected portions of leaves and along leaf margins dries and forms red crusts or thin scales that are washed off by rain.
Lesions also occur on kernels, peduncles, and rachis branches and in the interior of stalks.
Management
3. Delay sowing to avoid wet climatic conditions.
4. Control weeds, such as johnsongrass.
6. Grow resistant or tolerant sorghum cultivars.
Erwinia Soft Rot
Cause.
Erwinia chrysanthemi. Mode of entry is by contaminated water entering whorls of young, growing plants, a situation that occurs during mild flooding. Development
of Erwinia soft rot is favored by temperatures of 30°C and higher.
Distribution.
Symptoms.
Symptoms appear in about the fourthleaf stage of growth. Severe symptoms include death of the top four to five leaves, but the lower leaves appear normal. Dead
tissue can be easily pulled from whorls. The inside of whorls is composed of wet, necrotic tissue. An unpleasant odor is associ

Page 578
ated with this "wet" tissue. Less severe symptoms include necrotic stripes, pigmented stripes, or blotches on the upper leaves without stalk rot or top necrosis.
Management.
Not reported. Erwinia soft rot is not thought to pose a significant threat except in poorly drained fields where prolonged periods of high temperatures occur during the
early stages of seedling development.
Pseudomonas fuscovaginae Disease
Cause.
Pseudomonas fuscovaginae is an opportunistic pathogen whose development is favored by low temperatures above an altitude of 1300 m.
Distribution.
Burundi.
Symptoms.
Symptoms occur at the boot stage of plant development. Initially, brownblack watersoaked spots (2 mm in diameter) occur on the adaxial side of leaf sheaths; later
they coalesce and become as long as 20 cm. Inside the leaf sheaths, light brown patches with withered centers and sharp, reddishbrown borders occur on the
abaxial side. Occasionally there is an inhibition of the panicle emergence, and large grayish, watersoaked lesions occur on the diseased flag leaf sheath.
Management.
Not reported.
Yellow Leaf Blotch
Cause.
Pseudomonas sp. is seedborne.
Distribution.
West Africa.
Symptoms.
Scattered cream to yellow to beige lesions (810 × 2535 mm) occur on diseased leaves. Occasionally lesions are 30 mm wide by 200 mm long, slightly water
soaked, and have a tendency to follow leaf veins. Young plants infected at the two to threeleaf stages sometimes are severely stunted and killed.
Management.
Not reported.
Acremonium Wilt
Cause.
Acremonium strictum (syn. Cephalosporium acremonium). Infection occurs in the leaf blade or sheath, where systemic colonization occurs. Soilborne infection
has been reported from Egypt.
Distribution.
Argentina, Egypt, Honduras, India, and the United States.
Symptoms.
Diseased plants are stunted and chlorotic. The vascular system has a brownish discoloration that extends from the leaf sheaths into the

Page 579
vascular bundles of stalks. The lower leaves become chlorotic initially, then develop redbrown streaks and eventually die. Sometimes large areas of wilted tissue
develop along one axis of diseased leaves on either side of a midrib. In severely diseased plants, the upper leaves and shoots die and foliar wilting occurs.
Management.
Most cultivars are resistant.
Anthracnose Leaf Blight
Anthracnose is also called red leaf spot.
Cause.
Colletotrichum graminicola, teleomorph Glomerella graminicola, is seedborne, surviving as conidia and mycelia in seed. Diseased plants are produced from seed
with no visible symptoms, such as the presence of acervuli. Conidia and mycelia also survive in infested residue, soil, johnsongrass, and other weeds. In Texas,
sclerotia have been reported to survive for 18 months in stalk residue on the soil surface. Germination of sclerotia decreased faster in stalk residues buried at a depth
of 10 and 20 cm in soil than in infested residue placed on the soil surface, suggesting the sclerotia on the soil surface may act as a primary source of inoculum for
initiating anthracnose in the field.
Spores are produced during warm, wet weather in midsummer. During moist weather later in the growing season, conidia produced in lesions are disseminated by
wind to other plant hosts. In Africa, C. graminicola has been reported to rapidly destroy sorghum plants as the diseased plants approach maturity. Different
physiologic races or pathotypes exist.
Distribution.
Wherever sorghum is grown, but anthracnose is most severe in warm, humid climates.
Symptoms.
Symptoms occur on leaves at approximately midsummer as welldefined circular to ovalshaped spots that normally are 3 to 6 mm in diameter but may grow as large
as 25 mm in diameter. Spots develop small, circular, light tan centers with wide tan, orange, red, or blackpurple margins, depending upon the diseased cultivar.
During periods of high humidity, spots increase in number and cover much of the diseased leaf area; elliptical to elongate lesions may cover the entire length of the
midrib. Blackish growths that may be present in spots are setae, which under magnification appear to be short, stiff hairs. Pink spore masses may develop in these
blackish areas during humid weather.
Diseased plants may eventually become defoliated and, under severe disease conditions, die before maturity. Yield losses for susceptible cultivars have been reported
to be 50% in a severe anthracnose epiphytotic. On broomcorn, production of heads may be poor and the sugar content of sweet sorghum may be reduced.
The stalk rot phase is discussed in "Red Rot" later in this chapter.

Page 580
Management
1. Grow resistant cultivars. Dilatory resistance is identified in commercial sorghum hybrids
2. Sow healthy seed that has been treated with a seedprotectant fungicide.
3. Control weeds in a field.
Banded Leaf and Sheath Blight
Banded leaf and sheath blight is also called Rhizoctonia blight.
Cause.
Rhizoctonia solani AG1, teleomorph Thanatephorus cucumeris. The primary inoculum originates from mycelia and sclerotia in infested residue or soil. Secondary
spread of inoculum is by mycelia contacting host plant leaves or by mycelia and sclerotia disseminated by wind and splashing rain. Basidiospores may also be
important in initiating disease. Development of banded leaf and sheath blight occurs during moist conditions with high relative humidities and high temperatures.
Distribution.
Tropical areas of the world, but banded leaf and sheath blight is not considered an important disease.
Symptoms.
Leaves and sheaths initially develop watersoaked, graygreen lesions that eventually develop into irregular tan to redbrown lesions (28 mm wide) with white centers
and purple borders. One or several lesions form horizontal bands across diseased leaf blades and leaf sheaths. Lesions may be covered with fluffy, white mycelium or
brown mycelial mats of sclerotia. On older lesions, individual sclerotia look like white to dark brown objects that are 15 mm in diameter.
Management.
Do not rotate sorghum with rice or soybean.
Charcoal Rot
Cause.
Macrophomina phaseolina (syn. Botryodiplodia phaseoli, M. phaseoli, Rhizoctonia bataticola, and Sclerotium bataticola) survives primarily as sclerotia in
infested residue. Although pycnidia do not commonly occur, they serve as another means of overwintering. Macrophomina phaseolina is not a good soil saprophyte
and is inhibited in saprophytic growth in residue by other soil micro flora. However, growing successive crops of sorghum builds up inoculum, in the form of sclerotia,
in the soil. In India, sclerotia counts increased when sorghum was intercropped continuously with pigeon pea in rainy and dry seasons, and when sorghum followed
safflower and chickpea in the rainy season. Charcoal rot generally occurs in localized areas. Therefore, it is likely that inoculum is primarily sclerotia disseminated by
any means that moves soil or residue rather than propagules that may be disseminated a long distance by wind.

Page 581
During soil temperatures of 30°C and above and available soil moistures of 80% or less, sclerotia germinate and form infection hyphae that penetrate belowground
tissue of host plants. Stress created by drought is necessary for infection by M. phaseolina.
Disease severity increases during high nitrogen conditions and high plant populations growing in moisture stress conditions. A high plant population increases
competition for available soil moisture, while high nitrogen promotes luxuriant shoot growth relative to root development. Therefore, under moisture stress the lack of a
sufficient root system reduces the ability of plants to obtain moisture when the water requirement is increased by luxuriant shoot growth. However, in reports from the
Philippines, deep plowing and proper weeding limited the severity of infection regardless of nitrogen, phosphorous, or potassium levels and population density.
Distribution.
Wherever sorghum is grown under hot, dry conditions.
Symptoms.
Charcoal rot first occurs on host plants growing in the driest soil in a field. Diseased plants may be destroyed in 2 to 3 days from the onset of symptoms. Symptoms
move upward on a diseased stalk from the original infections on the crown. After the initial general watersoaking of piths, diseased stalk tissues turn bright red to
black, then die and the color fades. The lower stems dry up and shred and numerous small black sclerotia form on the remaining vascular bundles. Diseased plants
then lodge.
Management
1. Sweet sorghums and many forage sorghums are resistant, but grain sorghums tend to be susceptible. Resistance is associated with exodermis lignification.
3. Sow the recommended plant population.
4. Follow cultural practices that conserve soil moisture.
Cochliobolus Leaf Spot
Cause.
Cochliobolus bicolor.
Distribution.
India.
Symptoms.
Lesions on diseased leaves are circular and have alternating concentric strawcolored bands. In severe cases, spots coalesce and cover a large area of the leaf
surface.
Management.
Not reported.
Covered Kernel Smut
Cause.
Sporisorium sorghi (syn. Sphacelotheca sorghi) overwinters primarily as teliospores (chlamydospores) on the outside of infested seed. Teliospores

Page 582
germinate in two ways: (1) When contaminated seed is sown, teliospores germinate along with the seed and form a fourcelled promycelium that bears lateral sporidia.
Sporidia then germinate, infect developing seedlings, and form mycelia that grow systemically within the infected plants. (2) Teliospores germinate by directly
producing germ tubes that infect seedlings.
At the heading stage of plant development, kernels are replaced by teliospores enclosed in a membrane which ruptures at harvest time and releases teliospores that
contaminate seed or soil. Teliospores in soil are not important in the infection of seedlings. Smut incidence decreases when seed is planted in wet soils at temperatures
of 15.5° to 32.0°C. Several physiologic races of S. sorghi exist.
Distribution.
Symptoms.
Growth of plants is not affected and diseased plants appear normal until the heading stage of plant development. Although an occasional healthy kernel may occur,
usually all kernels are replaced by dark brown, powdery masses of teliospores enclosed in gray or brown membranes. The teliospores and membrane is called a
sorus. Sori vary in size from being small enough to be covered by glumes to being over 1 cm long. The membrane ordinarily remains intact until harvest time, when it is
ruptured by harvest equipment.
Management
1. Treat seed with a protectant fungicide.
2. Sow seed from smutfree plants.
3. All commercial cultivars of sorgo, kaffir, durra, sudangrass, and broomcorn are susceptible. Hegari, milo, gurno, and feterita types of sorghum are resistant to one
or more races.
Crazy Top
Cause.
Sclerophthora macrospora (syn. Sclerospora macrospora) survives as oospores in residue and other grasses. Oospores germinate in saturated soil in 24 to 48
hours and form sporangia in which zoospores are produced. Zoospores are then liberated from sporangia and ''swim" to preemergent or postemergent seedlings,
where they germinate, infect the host plant, and produce systemic mycelium inside the infected plant. Oospores are produced in and adjacent to the veins of diseased
leaves. Crazy top occurs over a wide range of temperatures.
Distribution.
Symptoms.
Diseased leaves are mottled, thickened, stiffened, and twisted or curled, and their surfaces are covered with bumps. Although sorghum heads usually are not
produced, some may have numerous leafy shoots.
Management.
Not necessary, since crazy top is not serious on sorghum.

Page 583
Curvularia Kernel Rot
Cause.
Curvularia lunata. Infection is favored by rain, high humidity, and temperatures of 24° to 30°C.
Distribution.
Mexico.
Symptoms.
Symptoms are observed on diseased spikelets at maturity. Kernels are covered with a dense, "velvetappearing" fungal growth consisting of mycelium, conidia, and
conidiophores.
Management.
Not reported. However, sources of resistance to general grain molds have been identified in some accessions.
Ergot
Ergot is also called honeydew and sugary disease.
Cause.
Claviceps sorghi and C. africana. Sphacelia sorghi is considered the anamorph of both C. sorghi and C. africana.
Sexual reproduction by C. africana, or the formation of sclerotia that produce stromatic heads, has only been observed in laboratory experiments and is believed to
be unimportant to its survival in nature. The dispersal of secondary conidia over long distances (300 km/day) is believed to be the primary reason for the rapid spread
of C. africana through the Western Hemisphere. In the absence of sclerotia, survival of C. africana in the United States may only occur in southern sorghum
producing areas, thereby reducing the incidence of ergot in the northern sorghumproducing areas.
Male sterility or fertility problems maximize susceptibility through lengthening the time a sorghum flower ovary remains unfertilized. Commercial grain sorghum hybrids
have negligible incidence because they are highly selffertile and rapid pollination prevents infection. Malesterile (female parent) sorghums are generally the sorghums
most heavily damaged by ergot because they require an external pollen source for fertilization. Pollen sterility due to causes such as cool temperatures encourages
infection.
Claviceps sorghi sclerotia are present but do not readily germinate in nature. Typically, most ergots germinate and produce stromatic heads at ends of stipes (stalks).
Perithecia form in stromatic heads, then ascospores produced in perithecia are disseminated by wind to host florets. However, because the ascospores are not readily
formed in nature, their role in ergot epidemiology is unknown. Development of the anamorph, S. sorghi also is little understood. It has been suggested that conidia
from alternate grass hosts and infested panicle debris in soil may serve as primary inoculum.
Infection occurs through unfertilized florets. Infection of florets is favored by temperatures of 20° to 25°C and high humidity from the time of panicle emergence
through the fertilization of ovaries. Conidia germinate

Page 584
and produce germ tubes that penetrate the stigma, grow down the style, and colonize the ovary. The ovary is converted into a fungal mass and stroma; approximately
7 to 10 days after infection, a sweet, sticky substance (honeydew) consisting of liquid and conidia exudes from diseased florets during rainy, cloudy weather.
Honeydew contains three types of conidia: macroconidia, secondary conidia, and microconidia. Macroconidia, which are ellipticalshaped, are the first to be released
in the honeydew. Under humid conditions some macroconidia on the surface of the honeydew germinate by germ tubes that enmesh and form a hyphal mat. Others
germinate and form erect conidiophores on which pyriform secondary conidia form outside the honeydew surface. Later, small obovate microconidia are found in the
honeydew. All three conidial forms germinate on and penetrate the stigma.
Stromata develop at temperatures of 14° to 35°C. Honeydew and conidial production occur at temperatures of 14° to 28°C and relative humidities above 90% for
12 to 16 hours a day. Sclerotia develop at temperatures of 28° to 35°C and relative humidities below 90% for 2 hours a day. Honeydew may be disseminated from
flower to flower by insects, rain, and wind. Later, the stroma is transformed into a hard sclerotium.
Honeydew also contaminates the grains, and above 90% relative humidity, stromata and honeydew become colonized by saprophytic fungi. Consequently, sclerotia
are not formed, but after honeydew dries, secondary conidia of S. sorghi are spread primarily by wind and germinate during rainy, cloudy weather.
Longrange spread possibly is by sclerotia mixed with seed.
Distribution.
Claviceps sorghi causes ergot in India. Claviceps africana causes ergot in Australia, Central America, North America, South Africa, and South America.
Symptoms.
Initially, drops of sticky, pinkish to brownish liquid (honeydew), which is sweet to the taste and attracts numerous insects, exudes from ovaries. The saprophytic fungus
Cerebella volkensii may grow over the honeydew and convert it into a sticky, matted, black mass. If the mycoparasite is not present, fungal tissue in ovaries grows
into hard, grayish, elongated and slightly curved, hornlike sclerotia.
Ergot is an ovary replacement disease that creates two major problems. First, infection of malesterile (Aline) ovaries precludes normal seedset or development.
Thus, infections are directly responsible for seed yield losses. Second, seeds developing adjacent to infected florets often become contaminated with the sugary,
sphacelial honeydew and support growth of saprophytic surface molds. Such seeds are of poor and downgraded quality and because of their stickiness may be
difficult to remove during harvesting.

Page 585
Management
1. Sow seed lots free of sclerotia.
2. Locate seed fields in areas not conducive to disease.
3. Apply a foliar fungicide from the flag leaf stage to the end of anthesis.
4. Practice pollen management techniques.
5. Ergotresistant lines from Ethiopia have been identified.
False Mildew
Cause.
Beniowskia sphaeroidea. Disease is favored by humid weather.
Distribution.
Malawi and Uganda.
Symptoms.
Typical white growth consisting of mycelium, conidia, and conidiophores occurs on diseased leaves.
Management.
Not reported.
Cause.
Fusarium moniliforme, teleomorph Gibberella fujikuroi. According to Nelson et al. (1983), F. subglutinans and F. proliferatum share many morphological
characteristics with F. moniliforme and may be involved in the same disease syndrome. Fusarium subglutinans is separated taxonomically from F. moniliforme
because F. subglutinans bears microconidia on polyphialides only in false heads and not on microconidial chains. Fusarium moniliforme bears microconidia both in
false heads and in long chains. Fusarium proliferatum is separated from F. moniliforme in that F. proliferatum also bears microconidia in chains of various lengths
and in false heads but it forms microconidia in chains on polyphialides, whereas F. moniliforme forms microconidia in chains on monophialides. It is likely these fungi
have been misidentified or confused with each other in the past. Some researchers still consider the three fungi synonymous, presumably on the basis of their
morphology. It has been reported that Fusarium napiforme also has been isolated from sorghum heads.
Gibberella fujikuroi consists of at least seven distinct mating populations, which are designated A through G. Populations of A, D, and E are the most common on
maize and correspond to the particular anamorph species. Both A and F mating populations are considered to be F. moniliforme; population A contains many prolific
fumonisinproducing strains, while members of the F population produce little or no fumonisin. Most strains of F. moniliforme found on maize are population A and
most found on sorghum are F. Population D is considered to be F. proliferatum and contains many strains that produce copious amounts of fumonisins. Fusarium
proliferatum was demonstrated to produce beauvericin, fumonisin B 1, and moniliformin in maize grown in Italy. Populations B and E are considered to be F.
subglutinans and produce little or no fumonisin. In maize grown in

Page 586
temperate regions, F. moniliforme and F. proliferatum represent the greatest threat for fumonisin production.
Although little is known of the survival or dissemination of F. moniliforme as it relates to head blight of sorghum, it is likely similar to Fusarium stalk rot of maize.
Therefore, F. moniliforme probably overwinters as mycelia in sorghum or maize residue. Conidia are then produced and disseminated by wind to peduncles, where
they enter through cracks or wounds in the peduncle, rachis, or panicle branches. Prolonged wet weather preceding anthesis favors Fusarium head blight.
Distribution.
Areas where sorghum is grown under warm, humid conditions. Fusarium napiforme has been reported from Namibia.
Symptoms.
Several to all the florets in a diseased seed head may be killed. Whole seed heads may be covered with a white to pinkish mycelial growth. When panicles are split, a
red, brown, or black discoloration occurring in the upper peduncles extends into branches of heads. Sometimes the discoloration extends into stalks and discolors the
rind. Peduncles may be necrotic and break over. The rachis and rachis branches may become necrotic or have an external red discoloration.
Management.
Grow resistant cultivars. Resistance to general grain molds has been identified in some accessions.
Fusarium Root and Stalk Rot
Cause.
Fusarium moniliforme is considered the dominant causal organism, but other Fusarium spp., specifically F. graminearum, also have been reported as causal fungi.
The fungi survive as chlamydospores, chlamydosporelike structures, and mycelia in maize or sorghum residue. Fusarium moniliforme is also seedborne. Conidia are
produced on residue and disseminated by wind to host plants. Mycelium also grows through soil to roots and enters through natural openings or wounds made by
insects, machinery, and other means.
Near plant maturity, host plants must be predisposed by insect wounds, disease injury, poor fertility, or hot, dry weather for Fusarium root and stalk rot to occur.
Usually disease is most severe during cool, wet weather following hot, dry weather as plants near maturity.
Fusarium root and stalk rot is more severe in conventional tillage than in ecofallow systems. High nitrogen to potassium ratios and high plant populations also increase
disease severity. In the Philippines, however, deep plowing and proper weeding limited disease severity regardless of nitrogen, phosphorous, or potassium levels and
population density.
Distribution.
Wherever sorghum is grown under hot, dry conditions. In the United States, the area from Kansas to Texas is most severely affected.
Symptoms.
Although stalk rot is ordinarily accompanied by root rot, symp

Page 587
toms may not be observed when irrigated plants are grown in soils with adequate fertility. Root cortical tissue, then the vascular tissue decompose. Older roots are
often totally destroyed, leaving diseased plants with little anchorage. Such plants are easily pulled from soil or toppled over by wind. Newly formed roots have lesions
of various sizes and shapes that vary in color from light tan to brick red to pink to black, depending on the diseased cultivar.
Stalk rot symptoms resemble those of maize. The fungi grow from diseased roots and crowns into the plant stalk. Initially, leaves turn brown and the outsides of nodes
have dark lesions. Inside the stalk, the pith is watersoaked initially and later disintegrates, leaving only pink, red, or redpurple vascular bundles intact. Eventually,
diseased interior stalk tissue becomes dark red. White to pink mycelia may grow on the outsides of nodes during damp weather. Stalks may break over near the soil
surface.
Management
1. Provide a full moisture profile at sowing and ensure adequate irrigation during the growing year.
2. Practice good weed and insect control.
3. Maintain a balanced soil fertility.
4. Grow recommended plant populations of hybrids that have good stalk strength.
5. Practice an ecofallow system, especially in a winter wheatgrain sorghumfallow rotation.
Fusarium thapsinum Infection
Cause.
Fusarium thapsinum, teleomorph Gibberella thapsina. Fusarium thapsinum and F. moniliforme are similar morphologically and may have been confused in the
literature. Distinguishing F. thapsinum from F. moniliforme is accomplished by crosses with standard femalefertile tester strains. Fusarium thapsinum produces a
yellow pigment in culture; F. moniliforme does not. Fusarium thapsinum does not produce fumonisins, but F. moniliforme does. Fusarium thapsinum produces
moniliformin, whereas F. moniliforme does only rarely. Fusarium thapsinum is sensitive to hygromycin; F. moniliforme is not. Therefore, the numerous reports in
the literature that assign the predominant Fusarium spp. associated with head blight of sorghum to F. moniliforme and consider this organism to be the same one
responsible for stalk and ear rot in maize may be erroneous.
The nonproduction of fumonisins or the production of large amounts of moniliformin by isolates of F. moniliforme from sorghum probably refers to strains of F.
thapsinum rather than to strains of F. moniliforme. This difference also suggests that sorghum is more likely to be naturally contaminated with moniliformin than with
fumonisins and maize is more likely to be naturally contaminated with fumonisins instead of moniliformin.

Page 588
Distribution.
Egypt, South Africa, the Philippines, Thailand, and the United States (Alabama, Arkansas, Georgia, Illinois, Kansas, Mississippi, Missouri, Ohio, and Texas).
Symptoms.
Gibberella thapsina has been reported to cause a seedling blight. Symptoms consisted primarily of the formation of reddishbrown lesions at the bases of root
laterals and, after 3 days, death of the infected lateral. On some plants the entire root system was necrotic.
Fusarium thapsinum was isolated from asymptomatic seeds, stems, roots, and crowns, which suggests F. thapsinum may be endophytic. The pathogenicity has not
been tested under field conditions, but under greenhouse conditions, some strains can cause lesions in stalks following toothpick inoculations.
Management.
Not reported.
Gray Leaf Spot
Gray leaf spot is also called angular leaf spot and cercosporiosis.
Cause.
Cercospora sorghi survives as mycelia in infested residue, in sorghum plants that remain standing after a field has been harvested, in grasses as a parasite and
saprophyte, and in infested seed. Primary inoculum is conidia produced during warm, wet weather and disseminated by wind and splashed by rain to plant hosts. Later
in the season, conidia produced in lesions provide inoculum for secondary infections.
Distribution.
Wherever sorghum is grown in warm, humid, or wet climates.
Symptoms.
Gray spot normally occurs too late in the growing season to cause injury, but if humid weather persists in midseason, considerable damage may occur. Initially, small,
circular to elliptical, dark purple or red spots occur on diseased leaves late in the growing season after plants are mature. Later, spots elongate to 30 mm until they are
limited by leaf veins and become rectangular. Spots may be light to dark red, purple, or tan. Thick, gray mycelia, together with numerous conidia, eventually cover the
spots; hence, the name gray leaf spot. Sporulation is more prevalent in spots on the diseased lower leaf surfaces. During periods of high humidity, large areas of leaves,
including the spots, are covered with a thick mycelial growth. In severe disease conditions, leaf sheaths and upper stems are also affected.
Management
2. Rotate sorghum with small grains.
4. Eliminate wild sorghum and grasses that act as pathogen hosts.

Page 589
Green Ear
Cause.
Sclerospora graminicola overwinters as oospores in soil and on seed. Oospores germinate and form germ tubes that infect new leaves. Temperatures of 24° to 32°
C for 2 days after sowing are conducive to heavy infection. Secondary spread is by the dissemination of sporangia that formed on diseased leaves by wind to host
plants. Sporangia germinate indirectly and release three or more zoospores, which then germinate and form germ tubes that penetrate host leaves. Sporangia
infrequently germinate directly and form a germ tube. Oospores eventually form in diseased tissue and return to the soil or contaminate seed when the diseased tissue
decays. Optimum development of green ear occurs with a high humidity and a temperature of 17°C.
Distribution.
Africa, Asia, Europe, and North America.
Symptoms.
The head is completely or partially transformed into a mass of small, twisted leaves; hence, the name green ear. The malformation is due to upper segments of the floral
axis that normally develop into grain being converted into small, leafy shoots. Sporangia that resemble a "fuzz" are produced on diseased leaves during periods of high
humidity.
Management.
Not necessary.
Head Smut
Head smut is also called ear and tassel smut.
Cause.
Sporisorium holcisorghi (syn. Sphacelotheca reiliana, Sorosporium reilianum, and Ustilago reiliana), according to Farr et al. (1989). Sporisorium holci
sorghi survives as chlamydospores in soil. When seed is sown, chlamydospores in the dry soil germinate at temperatures of 27° to 31°C and form fourcelled or
branched promycelia that bear sporidia terminally and near septa. Sporidia may then sprout and form secondary sporidia or germinate and form germ tubes that
penetrate meristematic tissue of seedlings. Sporisorium holcisorghi develops only in actively growing meristematic tissue. Seedborne chlamydospores apparently are
not important in infection. Physiologic races of S. holcisorghi are present.
Distribution.
Generally wherever sorghum is grown.
Symptoms.
Disease symptoms first appear when a young head enclosed in a boot is completely replaced by a large smut gall surrounded by a whitish membrane. The membrane
ruptures before the head emerges and exposes a mass of dark brown to black, powdery chlamydospores intermingled with a network of long, thin, dark, broomlike
structures. Sometimes chlamydospores are not present, but witches' brooms consisting of many small, rolled leaves protrude from heads of suckers at nodes or joints.

Page 590
All or part of the panicle becomes incorporated into a single sorus. Parts of a diseased panicle that are not included in a sorus usually are blasted or have a
proliferation of individual florets. Sori may develop on the foliage and culms in some sweet sorghums and sudangrass cultivars.
Management
1. Grow resistant cultivars and hybrids.
2. Rotate susceptible sorghum cultivars and hybrids with resistant crops. Grow susceptible sorghum in the same field every 4 years to genetically stabilize the race or
races of S. holcisorghi.
Ladder Leaf Spot
Confusion about the common name exists in the literature. It is sometimes referred to as "latter" leaf spot.
Cause.
Phaeoramularia fusimaculans (syn. Cercospora fusimaculans), according to Farr et al. (1989).
Distribution.
Brazil, Colombia, Cuba, El Salvador, Honduras, Malawi, Mexico, Rwanda, the United States (Georgia and Texas), Venezuela, and Zambia.
Symptoms.
Sclariform, or ladderlike, lesions occur on diseased leaves. Lesions are elliptical to rectangular, pale brown, and segmented by darkbordered markings that are
limited by secondary and tertiary veins and give lesions a "ladderlike" appearance.
Management.
Levels of resistance exist in Sorghum bicolor.
Leaf Blight
Leaf blight is also called Helminthosporium leaf blight, Helminthosporium blight, and northern leaf blight.
Cause.
Exserohilum turcicum (syn. Bipolaris turcica, Drechslera turcica, and Helminthosporium turcicum), teleomorph Setosphaeria turcica (syn.
Trichometasphaeria turcica). Exserohilum turcicum is seedborne and overwinters in infested residue and soil as mycelium and as conidia that may be converted
into chlamydospores. The optimum production of conidia on infested residue at the soil surface occurs during moist weather at temperatures of 18° to 27°C; conidia
are disseminated by wind to plant hosts. Heavy dews particularly favor development of leaf blight. Seed rot and seedling blight can occur in cold, wet soil. During
humid weather, secondary inoculum is conidia that are abundantly produced in lesions and disseminated by wind to other hosts.
Distribution.
Wherever sorghum is grown, but leaf blight is not common in drier climates.

Page 591
Symptoms.
Infected seedlings either die or develop into stunted plants. The small redpurple or yellowtan leaf spots that develop on leaves of diseased seedlings enlarge,
coalesce, and turn the leaves a purplegray color.
Spots on older leaves occur as yellowish, grayish, or tan, elliptical lesions several centimeters long. Lower leaves are infected first and the disease symptoms progress
up the plant. During humid conditions, lesions enlarge and kill and wither large parts of leaves, giving diseased plants the appearance of being injured by frost.
Depending on the cultivar, the centers of lesions are usually grayish to tan and have a redpurple or tan margin. In warm, humid weather, profuse sporulation gives
lesions a dark green or black appearance. Grain is not infected but yields are reduced.
When seedlings were inoculated, Setosphaeria turcica caused rot of roots, crowns, and stalks. Leaves eventually wilted and plants died.
Management
1. Grow resistant cultivars. Most grain and sweet sorghum cultivars have some resistance. In humid areas of the southern United States, most cultivars will sustain
some leaf blight. Two types of resistance are known: polygenic resistance is characterized by a few small lesions, and monogenic resistance is characterized by a
hypersensitive fleck with little or no lesion development.
2. Infested residue should be plowed into soil. Leaf blight is more severe under minimumtillage conditions.
Leaf Spot
Although both leaf spot and red spot are reported to be caused by Exserohilum rostratum; the descriptions of the symptoms are sufficiently different to warrant
describing them as two different diseases.
Cause.
Exserohilum rostratum (syn. Helminthosporium rostratum) survives as mycelium in infested residue and may be seedborne. The production of conidia on residue
is optimum during wet conditions at a temperature of 30°C; conidia are windborne to hosts. Conidia produced in spots during warm, wet conditions provide
secondary inoculum.
Distribution.
Africa and the United States, particularly in warm areas.
Symptoms.
Older leaves are more susceptible to infection than young leaves. Spots (12 × 25 mm) with tan centers and purple margins develop on diseased leaves. The spots
are limited laterally by leaf veins but may coalesce and form large necrotic areas.
Management.
Leaf spot is of minor importance on sorghum and no disease management is necessary.

Page 592
Long Smut
Cause.
Tolyposporium ehrenbergii survives as teliospores that are disseminated by seed, soil, and wind. However, infection only occurs from airborne spores during
flowering, and not from seed or soilborne spores or mycelium. Spores on the soil surface are the most important initial source of infection when they are picked up by
wind during dry periods, deposited on flag leaves, and then washed down behind the leaf sheaths. From boot to anthesis stages of plant growth, teliospores germinate
directly and produce germ tubes or germinate indirectly and produce sporidia that infect floral parts. Seed or seedling infection does not occur.
Distribution.
Asia, Botswana, Malawi, Tanzania, Zambia, and Zimbabwe.
Symptoms.
Sori in ovaries are irregularly distributed, somewhat cylindricalshaped (0.51.0 × 4.0 cm) with tapered ends, and surrounded by a firm false membrane of fungal
tissue.
Management.
Not practiced, but resistant germplasm for breeding programs exists.
Loose Kernel Smut
Cause.
Sporisorium cruentum (syn. Sphacelotheca cruenta) overwinters as teliospores on the outside of seed. Teliospores also survive in soil, but these are apparently not
important in seedling infection. When seed is sown, teliospores germinate, at the same time seed does, and form fourcelled promycelia that bear lateral sporidia. The
sporidia germinate and infect the developing seedling. Optimum infection occurs over a wide range of soil moistures and pHs at temperatures of 20° to 25°C.
Mycelium grows systemically in the plant. At heading, kernels are replaced by teliospores enclosed in a membrane that soon disintegrates and releases the spores.
Secondary infection may occur when the released teliospores infect latedeveloping heads, causing them to become smutted. Physiologic races exist.
Distribution.
Wherever sorghum is grown, but loose kernel smut is not a common disease.
Symptoms.
Diseased plants are stunted and head out early. Abundant side branches and tillers may develop. Normally all kernels in an infected panicle are smutted, but some
kernels may be transformed into leafy structures or escape infection completely. Individual kernels are replaced by smut galls that are 2.5 cm or longer, pointed, and
covered with a thin membrane that usually breaks when galls are full size. The powdery, dark brown to black teliospores are soon blown away, leaving a long, dark,
pointed, curved structure called a columella in the center of what was the gall. Sometimes the primary head is not smutted, but the tillers or the ratoon crop are.

Page 593
Management
1. Treat seed with a protectant fungicide.
2. Sow seed from smutfree plants.
3. All commercial cultivars of sorgo, kaffir, durra, sudangrass, and broomcorn are susceptible. Hegari, milo, gurno, and feterita types of sorghum are resistant to one
or more races.
Milo Disease
Milo disease is also called Periconia root rot and milo root rot.
Cause.
Periconia circinata survives as conidia in soil and as chlamydospores or thickwalled mycelial cells in roots and soil. Chlamydospores and conidia are disseminated
by any process that moves or transports soil. Chlamydospores germinate and produce both conidiophores, on which conidia are borne, and infection hyphae that
penetrate roots. Conidia also germinate and produce infection hyphae. Periconia circinata produces a toxin that kills plant tissue in advance of mycelial growth.
Chlamydospores are eventually produced in diseased tissue and returned to the soil during harvest and upon decomposition of infested plant tissue.
A pathogenic population of P. circinata depends on continuous growth of susceptible sorghum cultivars. The populations of toxinproducing isolates are higher in the
roots of diseased susceptible genotypes than in the soil. However, pathogenic toxinproducing isolates are not isolated from the roots of resistant genotypes.
Distribution.
Primarily the sorghumgrowing areas of the southern United States.
Symptoms.
The first symptoms occur 3 to 4 weeks after sowing susceptible sorghum seeds into heavily infested soil. Initially, plants are stunted and there is a slight rolling of
diseased leaves; the older leaves turn a light yellow at the tips and margins. Leaves continue to yellow and dry up until all leaves are affected and plants die at heading.
Sometimes symptoms do not appear until a rapid development of symptoms occurs at heading. A dark red color occurs in the centers of diseased stalks and extends
into roots. Roots may become severely rotted and slough from the rest of the plant. Diseased plants usually produce smaller heads.
Management.
Grow resistant cultivars and hybrids.
Oval Leaf Spot
Cause.
Ramulispora sorghicola survives as sclerotia associated with leaf residue on the soil surface. After periods of high humidity or rain, conidia are produced and
disseminated by wind or splashed by rain to host leaves. Plants are infected at all stages of growth.
Distribution.
Africa, Asia, the Caribbean, and Central America.

Page 594
Symptoms.
Initially, small, watersoaked spots with tan, brickred, or purple borders occur on diseased leaves. The small spots develop into roughly circularshaped lesions (1.5
4.0 × 3.08.0 mm) with pinkgray to yellowish centers and dark red or tan borders (1 mm wide). Sometimes a few scattered, small, black sclerotia appear in spots on
the underside of diseased leaves.
Oval leaf spot can be confused with anthracnose leaf blight. The diseases may be distinguished by the setae. In oval leaf spot, the setae are clear brown and arise from
sclerotia. In anthracnose leaf blight, setae are black and do not arise from sclerotia.
Management.
Rotate sorghum with resistant crops.
Panicle and Grain Anthracnose
Cause.
Colletotrichum graminicola, teleomorph Glomerella graminicola, is seedborne and survives in infested residue, soil, johnsongrass, and other weeds. Spores are
produced during warm, wet weather in midsummer. During moist weather later in the growing season, conidia are produced in lesions and disseminated by wind to
other plant hosts. Different physiologic races or pathotypes exist.
Panicle and grain anthracnose occurs on mature plants during cloudy, warm, and humid weather. Conidia are produced on leaves and washed behind leaf sheaths by
rain. Mycelia from germinating conidia enter the panicle.
Distribution.
Wherever sorghum is grown, but it is most severe in warm, humid climates.
Symptoms.
Normally only mature plants display disease symptoms. Initially, symptoms appear on diseased panicles as watersoaked, discolored lesions that become tan to
purpleblack. Young lesions appear as elliptic pockets or bars immediately beneath the epidermis. The interior of the panicle has a mottled appearance caused by red
brown tissue interspersed with white tissue. Diseased panicles are small and light in weight and mature early. Small black streaks (acervuli) may appear and extend to
the seed.
Diseased seeds have encircling dark brown to black streaks. Severely diseased seeds may be totally discolored and either germinate poorly or cause seedling blight
from seedborne inoculum. Diseased plants are produced from seed with visible symptoms, such as the presence of acervuli.
Management
2. Apply seedtreatment fungicides.
3. Grow resistant cultivars. Resistance to general grain molds has been identified in some accessions.

Page 595
Phoma Leaf Spot
Cause.
Phoma sorghina (syn. P. insidiosa) overwinters as pycnidia on infested residue and seed. Conidia are produced in pycnidia during warm, wet weather in the spring
and disseminated by wind and splashing rain to leaves. Secondary spread is by formation of pycnidia in infected tissue and subsequent production of conidia.
Distribution.
Wherever sorghum is grown in warm temperatures. Phoma leaf spot is considered a minor disease.
Symptoms.
Irregular or subcircular spots 1 cm or more in diameter develop on leaves. Spots are yellowbrown or tan to gray and may either be indefinite in outline or have a
narrow, redpurple margin. Pycnidia develop as small, black dots scattered over dead leaf tissue or in groups or lines between veins. Pycnidia also develop on glumes
and seed.
Management.
Phoma leaf spot is generally considered to be very minor, but the following aid in managing the disease.
1. Sow clean, healthy seed treated with a seedprotectant fungicide.
Pokkah Boeng
Pokkah boeng is also called top rot and twisted top.
Cause.
Fusarium subglutinans (syn. F. moniliforme var. subglutinans). Fusarium subglutinans overwinters as mycelia and perithecia in infested residue and is seedborne
as mycelia and conidia. Conidia produced from mycelia growing on residue during wet weather are disseminated by wind and splashing rain to plant hosts, where they
lodge in leaf sheaths or whorls and germinate. During wet weather, F. subglutinans also grows upward on the outside of stalks. Metabolites produced by F.
subglutinans cause distortions in plants.
Distribution.
Tropical or semitropical areas where humidity is high.
Symptoms.
Leaves near the top of plants are deformed and discolored and have wrinkled bases and numerous transverse cuts in the margins. Often leaves are so wrinkled that
they do not unfold properly, resulting in a plant with a ladderlike appearance. In severe cases, F. subglutinans may grow from whorls and sheaths into stalks,
causing the tops of diseased plants to die. Mild symptoms on leaves may be a mosaic that resembles a virus symptom.
Stalks may bend over at narrow, uniform, transverse cuts in the rind as if a knife had cut out portions. The latter symptom may be covered by leaf sheaths and may not
be apparent until stalks are broken over at the cut.

Page 596
Management.
Pokkah boeng is not considered a serious disease of sorghum and no management measures are necessary.
Pythium Root Rot
Cause.
Pythium arrhenomanes and P. graminicola are considered the primary causal organisms. Other Pythium spp. associated with root rot are P. periplocum and P.
myriotylum. Pythium root rot is favored by high soil temperatures and moisture throughout the growing season. However, infections increase at the boot stage and
later stages of plant growth; plant death normally occurs during stress conditions at and after plant maturity. Seedling blight caused by P. arrhenomanes has been
reported to be optimum at a soil temperature of 15°C.
Distribution.
Not known for certain, but Pythium root rot is thought to be widespread.
Symptoms.
Symptoms usually occur on larger adventitious roots. Redbrown to blackish, sunken lesions occur on diseased roots. Frequently, at root death, the entire root
becomes discolored.
Pythium arrhenomanes has been reported to cause preemergence and postemergence seedling death.
Management.
Highly susceptible genotypes have been identified.
Pythium Seed and Seedling Blight
Cause.
Several Pythium spp., including P. debaryanum, P. irregulare, P. paroecandrum, P. rostratum, P. splendens, P. ultimum, and P. vexans. The fungi survive as
oospores, sporangia, or mycelia in infested residue.
Disease is severest in wet soils at temperatures of 10° to 13°C. Under these conditions, seed germination and growth is slow, making plants more susceptible to
infection. Sporangia either germinate directly and form germ tubes or germinate indirectly by forming vesicles in which zoospores are formed. Similarly, oospores either
germinate directly and form germ tubes or germinate indirectly by forming zoosporangia in which zoospores are formed. Zoospores ''swim" by means of flagella
through soil water to host seeds and roots. Once in contact with a susceptible plant, a zoospore will encyst, germinate, and produce a germ tube that penetrates the
host plant. As mycelium grows through a plant, sporangia and oospores are produced on and in the diseased plant.
Distribution.
Symptoms.
Seeds may be rotted before germination, and seedlings may be infected before or after emergence. Seeds are brown, soft, and overgrown with mycelium. It is difficult
to find infected seeds in soil because of their rapid decomposition and the adhering soil that is bound to the seed by

Page 597
mycelia, making seeds indistinguishable from the surrounding soil. Roots are watersoaked, discolored brown, and have a sloughed appearance.
Aboveground symptoms are yellowing, wilting, and death of leaves. Lesions on mesocotyls initially are brown and sunken. Eventually, mesocotyls become soft and
watersoaked.
Management.
Resistance to P. arrhenomanes has been identified in a grain sorghum cultivar.
Red Rot
Red rot is also called anthracnose stalk rot, Colletotrichum rot, and red stalk rot. Although red rot is the stalk rot phase of anthracnose leaf blight, it is discussed as a
separate disease.
Cause.
Colletotrichum graminicola is discussed earlier in the chapter in "Anthracnose Leaf Blight." Conidia are washed down behind leaf sheaths, germinate, and infect
stalks any time after the jointing stage of plant growth.
Distribution.
Symptoms.
Red rot occurs primarily in the stalks of mature plants. The basal portion of a diseased stalk becomes reddened or purple. When a stalk is split lengthwise, the
alternate discolored and white areas in the pith give a marbled appearance throughout the diseased area. Depending on the cultivar, discolored areas range from tan to
purplish red. A similar symptom occurs when the peduncle or the upper stem below the head becomes diseased. Cankers on stalks are bleached and the surrounding
areas are reddish, orange, or purple.
Stalks frequently break near the middle of the stalk or just below the seed head. Diseased plants that do not break produce small heads which often have small seeds.
Management
1. Grow resistant cultivars and hybrids.
Red Spot
Although both leaf spot and red spot are reported to be caused by Exserohilum rostratum, the descriptions of the symptoms are sufficiently different to warrant
describing them as two different diseases.
Cause.
Distribution.
The United States (Mississippi).
Symptoms.
Symptoms resemble those of anthracnose leaf blight, but unlike anthracnose leaf blight, the lesions of red spot are not sunken into the diseased leaf. On sweet
sorghum, red spot lesions on the leaf midrib are red

Page 598
brown to black with tan or brown centers, irregularshaped, and longitudinal (812 × 50 mm).
Management.
Red spot is of little economic importance, but the symptoms could be mistaken for those of red rot in breeding programs that screen for anthracnose leaf blight.
Rhizoctonia Stalk Rot
Cause.
Rhizoctonia solani survives in soil and infested residue as sclerotia. Sclerotia are disseminated by any means that moves soil, such as wind and running water.
Sclerotia germinate and form infective hyphae that penetrate the plant host. Plants lacking in vigor are more susceptible to infection.
Distribution.
Widely distributed but of minor importance.
Symptoms.
Initially, the pith becomes reddish but vascular bundles remain as light streaks. Later, brown sclerotia (15 mm in diameter) form on the outside of stalks but under the
leaf sheaths.
Management.
Not necessary.
Rough Leaf Spot
Rough leaf spot is also called Ascochyta spot and rough spot.
Cause.
Ascochyta sorghi is seedborne and overwinters as pycnidia in soil and as pycnidia and mycelia in the infested residue of sorghum and perennial weeds. During wet
weather, conidia are produced in pycnidia and ooze out in a cirrhi, where they are disseminated by splashing rain and by wind to host plants. Later, pycnidia are
produced in spots and conidia are formed during wet weather and disseminated to other host plants as secondary inoculum.
Distribution.
Africa, Asia, southern Europe, and the United States, particularly the humid sorghumgrowing areas of the southeastern states. Rough leaf spot is generally considered
to cause minor losses.
Symptoms.
Initially, small, circular to oblong, lightcolored spots with welldefined margins develop near the ends of diseased leaves. The spots enlarge, coalesce, and form large
blotches which are covered by hard, black, raised pycnidia that give the spots a rough surface and appearance. Depending on the diseased cultivar, these lesions may
be grayish, yellowbrown, or purplered and elongated parallel to the veins. As diseased leaves mature, the pycnidia may fall off or be washed off by rain, leaving only
large areas of tan necrotic tissues that have either a reddish or tan border, or an indistinct border. Lesions may also occur on leaf sheaths and stalks. Sometimes,
pycnidia develop on healthyappearing, green parts of leaf surfaces and on glumes.

Page 599
Management
1. Grow resistant grain sorghum and sweet sorghum cultivars.
Rust
Cause.
Puccinia purpurea is a rust fungus that overwinters as urediniospores and mycelia in infested sorghum residue in warmer sorghumgrowing areas, or on johnsongrass.
However, spores are relatively shortlived in the absence of a living host but thrive on ratooned and successively planted sorghum. Oxalis corniculata may be an
alternate host and has been reported to become infected and produce abundant aecia. Infected perennial and collateral hosts and scattered diseased sorghum plants
serve as infection foci. Urediniospores are disseminated by wind to host plants, and during periods of high humidity, urediniospores produced within uredinia become
secondary inoculum. Light drizzles and heavy dew especially favor infection.
The function of teliospores is not considered important in the life cycle of P. purpurea. Twocelled teliospores, which develop as leaves mature, either germinate
immediately or overwinter before germinating to produce one basidiospore per cell.
Distribution.
Wherever sorghum is grown, but rust is most severe in areas of high humidity or rainfall.
Symptoms.
Rust symptoms normally appear on diseased plants nearing maturity. The first symptoms are small purple, red, or tan flecks or spots on both leaf surfaces. In
susceptible cultivars, the spots enlarge and may cover much of the leaf surface. Small, raised, brownish pustules (uredinia) develop in the spots. Uredinia are elliptical
(2 mm in length) and form in interveinal tissue parallel to veins. Often a purple, reddish, or tan area surrounds each uredinium. The epidermis of a uredinium ruptures
and exposes reddish to dark brown urediniospores.
Telia develop later in the season, frequently in old uredinia and commonly on the undersides of leaves. Telia are dark brown, elliptical to linearshaped and often
observed as streaks or stripes 1 to 3 mm in length. The epidermis may stay intact for a long time.
Management.
Forage sorghum types are usually more severely diseased than grain sorghums. Rust usually appears too late in the growing season to cause much injury to some
cultivars. Wilson et al. (1991) noted no consistent differences in yield or digestibility between diseasefree plots of susceptible and resistant cultivars. They further
observed that drymatter concentration was unaffected by disease but the rate of loss of digestible drymatter yield was greater at low rust severities than at higher rust
severities. Some accessions have resistance.

Page 600
Sooty Stripe
Cause.
Ramulispora sorghi survives for several years primarily as sclerotia in soil and residue. Sporodochia, the structures upon which conidia are produced, also are
important in survival when infested leaf residue is left on or above the soil surface throughout the winter.
During warm, moist conditions in the growing season, conidia are produced on the surface of sclerotia or on sporodochia and dispersed by wind and splashed by rain
to host plant leaves and sheaths. Ramulispora sorghi infects plants at all growth stages, but the oldest leaves and leaf sheaths are infected first. Eventually, conidia
produced from the stromata in lesions and disseminated by wind function as secondary inoculum. In time, sclerotia are produced on lesion surfaces, where they remain
attached to residue or are easily dislodged and fall into the soil.
Distribution.
Africa, Asia, South America, and the United States, particularly in warm, humid, sorghumgrowing areas.
Symptoms.
Initially, small, watersoaked, oblong, redpurple or tan spots with a yellow halo appear on diseased leaf laminae or leaf sheaths. The spots develop into elongated to
elliptical lesions with tan necrotic centers and redpurple to tan borders. Diseased leaves often turn bright yellow from the broad yellow margins that surround lesions.
Mature lesions average about 5 cm or longer in length. Lesion centers become grayish from the production of conidia during warm, wet weather and, later, appear
sooty due to the formation of numerous small, black, superficial sclerotia. Sclerotia are easily wiped off and cling to fingers like soot.
Management.
Generally, sooty stripe occurs too late in the growing season to cause severe plant damage.
1. Hybrids vary greatly in tolerance to sooty stripe. Plant resistance is the most practical means to manage this disease.
Sorghum Downy Mildew
Cause.
Peronosclerospora sorghi (syn. Sclerospora sorghi) survives for several years as oospores in infested residue and in soil after infested residue has decomposed.
Peronosclerospora sorghi is also seedborne as oospores on the surface of seeds and mycelium within seeds. Oospores germinate and infect young plant roots under
low soil moisture conditions to a minimum temperature of 10°C. Mycelium then grows systemically inside the infected plant and, eventually, oospores are formed
within the diseased tissue. Penetration of leaves occurs by germ tubes from oospores penetrating through stomatal openings. Conidia generally cause local lesions but
can

Page 601
also cause systemic infections if leaves are infected before they are fully developed.
Conidia are produced only at night on diseased leaf surfaces when dew periods of several hours are associated with cool nights at temperatures of 18° to 21°C.
Viable conidia may be carried several thousand meters by the wind, but most remain within a few centimeters or meters from where they were produced and play no
role in longdistance dissemination.
Disease severity increases more rapidly from year to year on plants grown on sandy soils rather than on clay soils. Optimum disease incidence apparently occurs at a
soil temperaturemoisture combination of 25°C and 0.2 bar, respectively, and a soil texture of 80% sand. Some herbicides and herbicide antidotes increase severity
of downy mildew damage in susceptible sorghum genotypes.
Three pathotypes of P. sorghi known in Texas are referred to as P1, P2, and P3.
Distribution.
Africa, southeastern Asia, India, and the United States, particularly the Texas Gulf Coast and midwestern states. P1, the original pathotype, is widely distributed in
Texas. P2 is rare and reported from just two locations. P3 is widely distributed along the upper coastal plains of southern Texas.
Symptoms.
Seedlings are infected at germination and display a chlorotic mottle or are generally chlorotic and stunted. Conidia and conidiophores, which look like white "fuzz," are
produced on the undersides of chlorotic leaves during humid weather.
As diseased plants grow, vivid green and white stripes appear on diseased leaves in the late spring or early summer. Sometimes whole leaves either become chlorotic
or have one or two narrow green stripes. Conidia are usually not produced on these leaves.
Local infections on diseased leaves appear as small, rectangular, chlorotic spots that soon become necrotic and give leaves a stippled or speckled appearance.
Conidia are also produced in these local lesions.
Systemically diseased plants that develop late in the season have striped or mottled leaves. Diseased plants (1) fail to head, (2) produce sterile heads, or (3) form
partially diseased heads. As interveinal tissue is destroyed, leaf shredding occurs and oospores are released.
Management
1. Apply a systemic fungicide seed treatment.
2. Grow resistant sweet and grain sorghum hybrids.
3. Do not grow grain sorghum after sudangrass.
4. Sow only highquality seed.
5. Do not grow sudangrass and sorghum sudan hybrids in areas where downy mildew is present because very susceptible hosts tend to increase the population of
oospores in the soil.

Page 602
6. Rotate sorghum with other crops not susceptible to P. sorghi.
7. Destroy sorghum stubble after harvest.
8. Deep plow to place oospores below seed depth.
9. Sow as early as possible in the growing season.
Southern Leaf Blight
Cause.
Cochliobolus heterostrophus, anamorph Bipolaris maydis (syn. Drechslera maydis and Helminthosporium maydis), overwinters as conidia and mycelia in
infested residue. In the spring, conidia are disseminated by wind and splashed by rain to growing plants, where infection occurs in free moisture and temperatures of
15.5° to 26.5°C. Bipolaris maydis does not sporulate readily on sorghum. Disease is most severe when susceptible cultivars are grown in continuous sorghum culture
in a minimumtillage system under overhead irrigation.
Distribution.
Symptoms.
Symptoms are primarily lesions on diseased leaves. Occasionally lesions merge and cover large areas of the leaves. Lesions are tan (26 × 322 mm) and have parallel
sides and buff to brown borders. Often lesions have dark reddishbrown borders. Lesions may coalesce and kill leaves.
Management.
Disease management measures are not necessary since southern leaf blight is generally not considered an important disease on sorghum.
Southern Sclerotial Rot
Cause.
Sclerotium rolfsii survives as sclerotia in soil and residue and as mycelia in residue. However, S. rolfsii only survives in warmer sorghumgrowing climates because
low winter temperatures kill both sclerotia and mycelia. Sclerotia germinate and form mycelia that infect seeds and roots. Under continuous wet soil conditions, S.
rolfsii is reported to grow saprophytically from soil to the lowest leaf sheath.
Distribution.
Warmer sorghumgrowing areas of the world. Southern sclerotial rot is not an important disease on sorghum.
Symptoms.
Typically one to three sheaths are affected on plants nearing the bloom stage or later stages of plant development. Occasionally all leaf sheaths may be diseased and
the plant killed. Initially, a watersoaked lesion that becomes red, purple, or brown forms at the base of the lowest leaf sheath that is in contact with soil. Leaf blades
eventually wilt, become necrotic, and may shred. Mats of white mycelium grow inside leaf sheaths to approximately 30 cm above the soil surface. Fans of mycelium
merge from sheaths and spread over the base of the leaf for approximately 13 mm. Young axillary shoots become blighted and covered with mycelium.
Numerous sclerotia (12 mm in diameter) that are white initially, then

Page 603
become brown are produced inside diseased leaf sheaths. Numerous sclerotia also are produced on dead shredded leaves at the base of a diseased plant.
Management.
Not necessary because southern sclerotial rot is of minor importance on sorghum.
Tar Spot
Cause.
Phyllachora sacchari (syn. P. sorghi) survives on weed hosts such as johnsongrass and wild sorghums. Ascospores are formed in stromata on leaf surfaces and
disseminated by wind to other leaf surfaces. Tar spot is most severe during warm, wet weather.
Distribution.
India, Madagascar, Malaysia, the Philippines, and Thailand.
Symptoms.
Small (1 mm or less in diameter), black, round to elongated, raised spots occur on diseased leaves. The spots, composed of hard stromatic masses of fungus, extend
through the diseased leaf to both leaf surfaces. The black stroma may be surrounded by a yellowish, reddish, or necrotic ring. Lesions may coalesce and become large
enough to harm the leaf.
Management.
Target Leaf Spot
Cause.
Bipolaris cookei (syn. Helminthosporium cookei) survives primarily as mycelia in infested residue, particularly in leaf veins within lesions, and on leaves as
chlamydospores formed from conidia. Sporulation occurs under humid conditions and conidia are disseminated by wind to host plants. Development of target leaf spot
is favored by moist, humid weather and temperatures of 19° to 33°C.
Distribution.
Cyprus, India, Israel, South America, Sudan, and the United States. Target leaf spot is of minor importance.
Symptoms.
Symptoms vary according to sorghum genotype. Initially, symptoms are red or gray dots that later develop into definite spots. The welldefined spots on diseased
leaves vary in size from small spots (23 mm in diameter) to larger elongated lesions (1015 mm wide) that are delimited by leaf veins. The shapes of spots vary from
rectangular to narrow and the colors can be brown, reddish with lightcolored centers, tan, purple, or light brown. There is a distinct circular center in each leaf spot
lesion. Spots coalesce and form large areas of necrotic tissue. Lesions of target leaf spot somewhat resemble those of gray leaf spot caused by Cercospora sorghi;
however, the two leaf spots can often be distinguished by the presence of the distinct circular center in each target leaf spot lesion.
Management.
Not necessary.

Page 604
Zonate Leaf Spot
Zonate leaf spot is also called Gloeocercospora leaf spot.
Cause.
Gloeocercospora sorghi overwinters as sclerotia in infested residue on or above the soil surface. Primary inoculum is sclerotia which germinate and produce conidia
that are disseminated by splashing rain and by wind to host plants. Both leaves and sheaths may be infected. Gloeocercospora sorghi is also seedborne as mycelium
and possibly sclerotia. During warm, wet weather, sporulation occurs in lesions as pink sporodochia that form above stomates. The conidia are borne in a pinkish,
gelatinous mass and are splashed to healthy host tissue. Sclerotia are eventually formed in lines parallel to veins in leaf lesions.
Distribution.
Africa, Asia, Central and South America, the United States, and the West Indies. Zonate leaf spot is most severe in warm, wet climates.
Symptoms.
Initially, small, redbrown, watersoaked spots that sometimes have a narrow chlorotic halo occur on leaves near the soil surface. Spots enlarge, elongate parallel to
the veins, and become dark red or tan. Eventually, the spots occur as circular areas on diseased leaves or semicircular patterns along the leaf margins. Typically,
circular redpurple bands alternate with tan areas in a concentric or zonate pattern with irregular borders. Spots vary in diameter from a few millimeters to several
centimeters and may cover the entire width of the diseased leaf.
During warm, wet weather, conidia are produced in lesions as a pinkish gelatinous spore mass that forms above a stomate. Sclerotia eventually appear as small, black,
raised bodies in lines parallel to the veins.
Plants that are severely diseased in the seedling stage may become defoliated or die. Plants infected when older may have their foliage destroyed before they mature,
which results in poorly filled seed.
Management
1. Grow resistant or tolerant cultivars or hybrids.
2. Sow only clean seed treated with a seedprotectant fungicide.
Awl
Cause.
Dolichodorus spp. are ectoparasitic nematodes that are limited to wet soils. Some dissemination occurs by water. Feeding is at the root tips.
Distribution.
The United States.
Symptoms.
The aboveground symptom of diseased plants is plant stunting.

Page 605
Belowground symptoms are stubby and thick roots with some lesions present.
Management.
Not reported.
Cereal Root Knot
Cause.
Meloidogyne naasi overwinters as eggs. Secondstage larvae emerge from eggs and penetrate the root epidermis just above the root cap. Nematode secretions
transform pericycle cells into giant cells. Two to three generations of nematodes are produced each growing season.
Distribution.
Thailand and the United States (Kansas).
Symptoms.
Plants in irregularshaped areas within a field are stunted and chlorotic. Root galls may be elongated swellings or discrete knots. These galls are normally smaller than
those caused by other rootknot nematodes. Roots are often curved in the shape of a hook, horseshoe, or a complete spiral.
Management.
Not reported.
Dagger
Cause.
Distribution.
Not known.
Symptoms.
An aboveground symptom on diseased plants is slight to moderate stunting. Belowground symptoms are a reduction in feeder roots accompanied by necrosis of a
portion of the root system.
Management.
Not reported.
Lesion
Cause.
Pratylenchus hexincisus and P. zeae are endoparasitic.
Distribution.
Worldwide.
Symptoms.
Diseased plants are stunted and chlorotic. Roots are poorly developed and have necrotic lesions. Pratylenchus hexincisus increases the severity of charcoal rot.
Management.
Not reported.
Needle
Cause.
Longidorus africanus and other Longidorus spp.
Distribution.
Not known for certain but likely the same as for maize: Sandy soils in temperate regions.
Symptoms.
Symptoms on sorghum have not been well described but are con

Page 606
sidered similar to those on maize. Diseased plants are severely stunted and chlorotic. Belowground symptoms include yellow discoloration, slightly swollen root tips,
stubby roots, pruning of lateral roots, and a scarcity of small feeder roots.
Management.
Not known.
Pin
Cause.
Paratylenchus spp.
Distribution.
Not known.
Symptoms.
Brown necrotic areas occur on roots. Large populations can kill roots of other crops.
Management.
Not reported.
Reniform
Cause.
Rotylenchulus spp.
Distribution.
Topics.
Symptoms.
Diseased roots are slightly swollen. Damage on sorghum is not thought to be severe.
Management.
Not reported.
Ring
Cause.
Criconemella spp. is an ectoparasite.
Distribution.
Symptoms.
The aboveground symptom for diseased plants is a mild stunting. Belowground symptoms are lesions on roots and some decay.
Management.
Not reported.
Root Knot
Cause.
Meloidogyne spp.
Distribution.
Not known for certain, but rootknot nematodes are presumably widely distributed on sorghum.
Symptoms.
Diseased plants in irregularshaped areas within a field are stunted and chlorotic and have delayed blooming and reduced yields. Roots have galls, elongated swellings,
or discrete knots or swellings. Root proliferation is common.
Management.
Not practiced. Certain grain sorghum cultivars have been reported to be highly susceptible to M. incognita.

Page 607
Spiral
Cause.
Helicotylenchus spp. are either ectoparasites, semiendoparasites, or endoparasites.
Distribution.
Likely wherever sorghum is grown.
Symptoms.
An aboveground symptom of diseased plants is plant stunting. Belowground symptoms are a reduction in the number of feeder roots and some root rot.
Management.
Not reported.
Sting
Cause.
Belonolaimus longicaudatus is an ectoparasite that produces a phytotoxic enzyme. The nematode is found only in sandy soils.
Distribution.
Generally wherever sorghum is grown.
Symptoms.
Symptoms on sorghum have not been well described but are thought to be similar to those on maize. Aboveground symptoms are stunting and chlorosis. Belowground
symptoms include deep necrotic lesions on roots. Root tips are frequently destroyed, which results in thick, stubby roots.
Management.
Not reported.
Stubby Root
Cause.
Paratrichodorus minor is an ectoparasite found primarily in sandy soils. Most nematode feeding is around root tips.
Distribution.
Not known.
Symptoms.
Aboveground symptoms of diseased plants include severe stunting and chlorosis. Diseased roots are stubby and sometimes appear thicker than normal.
Management.
Not reported.
Stunt
Cause.
Merlinius brevidens, Quinisulcius spp., and Tylenchorhynchus spp. are ectoparasites.
Distribution.
Not reported.
Symptoms.
Diseased plants may be stunted and chlorotic. The root system is poorly developed and has fewer than normal feeder roots. Numerous root tips may be short and
thickened.
Management.
Not reported.

Page 608
Yellow Sorghum Stunt
Cause.
A phytoplasma. It is not known how the causal agent overseasons or is transmitted.
Distribution.
The southern and midwestern United States, including Alabama, Georgia, Kentucky, Louisiana, Mississippi, Ohio, and Texas.
Symptoms.
Diseased plants are generally more prevalent at or near the edges of fields. Plants are stunted, about half of normal height, and leaves are bunched together at the tops.
Diseased leaves are rigid and curled adaxially about the blade axis. Leaves have pronounced puckering, resulting in undulating margins, and a yellowtinged cream
color that makes plants conspicuous from a distance.
Diseased plants seldom produce panicles; if particles are produced, they are normally barren. Plants infected early in the growing season when they are less than 0.3 m
tall remain at that height but stalks continue to increase in diameter. These plants usually also display other disease symptoms.
Management.
Australian Maize Stripe
Cause.
Australian maize stripe agent is thought to be a virus. The agent is vectored by the planthopper Peregrinus maidis. The major reservoir host is Sorghum
verticillifiorum. Acquisition and inoculation threshold periods were approximately 1 hour each.
Distribution.
Australia (Queensland). Incidence may be high in sweet maize grown in coastal districts where the vector and reservoir are common, but the disease is rare in the
major inland agricultural areas.
Symptoms.
Broad yellow stripes occur on diseased leaves.
Management.
Not reported.
Brome Mosaic
Cause.
Brome mosaic virus (BMV) is in the bromovirus group. BMV persists in cereal crops and perennial grasses and can survive for several months in dried infested tissue.
BMV is primarily saptransmitted. Local spread presumably occurs through plant contact and transfer of sap by machinery

Page 609
and wind. Soil transmission by the dagger nematodes Xiphinema coxi and X. paraelongatum has been reported from Europe.
Distribution.
Symptoms.
Diseased leaves display narrow, interveinal chlorotic streaks that appear mottled from a distance. Mechanically inoculated plants may be stunted.
Management.
Cucumber Mosaic
Cause.
Cucumber mosaic virus (CMV) is transmitted by the aphid Aphis gossypii.
Distribution.
The United States.
Symptoms.
Chlorotic lesions and stripes occur on diseased leaves.
Management.
Not reported.
Elephant Grass Mosaic
Cause.
Elephant grass mosaic virus (EGMV). EGMV has been tentatively identified as a potyvirus that causes a mosaic of elephant grass but has a very limited host range. In
greenhouse tests, the virus was transmitted mechanically but not by aphids.
Distribution.
Brazil.
Symptoms.
Chlorotic spots and streaks developed on leaves 1 to 2 weeks after inoculation.
Management.
Not reported.
Johnsongrass Mosaic
Cause.
Johnsongrass mosaic virus (JGMV) is in the potyvirus group. JGMV was formerly the sugarcane mosaic virus, strain JG, from Australia and the maize dwarf mosaic
virus, strain O, from the United States. JGMV is transmitted mechanically and nonpersistently by the corn leaf aphid, Rhopalosiphum maidis.
Distribution.
Presumably wherever sorghum is grown near johnsongrass.
Symptoms.
Initially, the youngest leaves of diseased plants have a stippled mottle or mosaic of light and dark green that develops into narrow streaks. Symptoms may occur on all
leaves, leaf sheaths, and husks that develop after infection. As diseased plants mature, the mosaic disappears and leaves become yellowish green and frequently show
blotches or streaks of red.

Page 610
Management
Maize Chlorotic Dwarf
Cause.
Maize chlorotic dwarf virus (MCDV) overwinters in johnsongrass and is transmitted in a semipersistent manner by the leafhoppers Graminella nigrifrons and G.
sonora.
Distribution.
The United States (Mississippi, Louisiana, and Texas).
Symptoms.
Slight stunting and tertiary veinal chlorosis occurs on diseased plants.
Management.
Maize chlorotic dwarf is not of economic importance at present; therefore, disease management is not warranted.
Maize Chlorotic Mottle
Cause.
Maize chlorotic mottle virus (MCMV) is in the sobemovirus group. MCMV survives in maize residue and is transmitted by six species of beeties: the cereal leaf
beetle, Oulema melanopa; the corn flea beetle, Chaetocnema pulicaria; the flea beetle, Systena frontalis; the southern corn rootworm, Diabrotica
undecimpunctata; the northern corn rootworm, D. longicornis; and the western corn rootworm, D. virgifera. MCMV is also transmitted mechanically and possibly
by soil.
Distribution.
Brazil, Peru, and the United States (Hawaii, Kansas, Nebraska, and Texas).
Symptoms.
Diseased leaves are chlorotic and mottled.
Management.
Not reported.
Maize Dwarf Mosaic
Cause.
Maize dwarf mosaic virus (MDMV) now consists of former MDMV strains A, D, E, and F; former sugarcane mosaic virus, strain J, infective to johnsongrass in the
United States; and maize mosaic virus, Europeantype, from Yugoslavia.
MDMV persists in several annual and perennial grasses. In the spring, aphids, particularly the corn leaf aphid, Rhopalosiphus maidis, and the greenbug, Schizaphis
graminum, feed on overwintering hosts and acquire the virus. Twentythree species of aphids are known to be vectors of strain A. Aphids can retain infective virus
for 20 minutes after feeding and transmit it in a styleborne nonpersistent manner during their movements between diseased and healthy plants. High aphid populations
often induce a high disease incidence through secondary infection.

Page 611
Increases in levels of natural infection by MDMV occur in insecticidetreated (carbofuran) sorghum in the field. In greenhouse tests, carbofurantreated plants
increased infection in S. graminum transmission tests. In mechanical inoculation tests, virus infection was reduced in carbofurantreated sorghum.
Distribution.
Potentially wherever sorghum is grown.
Symptoms.
Symptoms of MDMV infection can vary according to sorghum genotype, virus strain, and temperature. Plants infected as seedlings are more severely diseased than
plants infected later in the growing season. Symptoms are most evident on the upper two or three leaves as an irregular mottling of dark and light green areas
interspersed with longitudinal white or light yellow streaks. Some sorghums that have the gene for red pigmentation may have the mottling replaced by a red leaf
symptom, especially on abnormally cool nights. This causes a red leaf or a red stripe symptom that appears as elongated stripes with necrotic centers and reddish
margins or, infrequently, as round spots.
Severely diseased plants may die. Diseased plants that are still living may be stunted and have delayed flowering and subsequent failure to head or set seed.
Maize dwarf mosaic, strain A, causes pigmented necrotic lesions on panicle branches, followed by excessive shrinkage of seed. These symptoms occur when
temperatures of 16°C or less prevail for 4 or more consecutive days while seed is in mild to soft dough stage.
Management
1 No sorghum cultivar is resistant to all strains of MDMV; however some cultivars are resistant to some strains of MDMV.
2. Control grassy weeds, particularly johnsongrass, in a field.
Maize Dwarf Mosaic Head Blight
Cause.
Maize dwarf mosaic virus (MDMV) is discussed in ''Maize Dwarf Mosaic" in this chapter.
Distribution.
Potentially wherever sorghum is grown.
Symptoms.
Plants infected by MDMV at or near heading may fail to fill properly. Symptoms may be absent on vegetative parts. Normal and underdeveloped seed occur together
in the same spikelet or panicle. The small seed may be restricted to one side of a head or follow patterns of anthesis. Diseased seeds are light in weight, have chalky
endosperms, shatter easily, and may be black due to growth of fungi such as Alternaria spp. Pigmented, necrotic lesions appear on branches of panicles and are most
likely to develop on cool nights on sorghums that carry the gene for red pigmentation. Similar symptoms may occur from root or stalk rots except there are no lesions
on branches of panicles.

Page 612
Management
3. Sow sorghum early.
Maize Rough Dwarf
Cause.
Maize rough dwarf virus (MRDV) is in the fijivirus group. MRDV is disseminated only by the planthopper Laodelphax striatellus.
Distribution.
Southern and southeastern Europe.
Symptoms.
Symptoms on sorghum are not clearly understood. On maize, early infection results in severely stunted plants with numerous enations on the leaf underside and sheath.
Root systems are reduced in size and discolored. Ears either are not formed or tend to be small and malformed. Later infection does not result in any noticeable
stunting, but enations are still formed.
Management.
Not reported.
Maize Streak
Cause.
not seedborne or mechanically transmitted in maize and, presumably, not in sorghum.
Distribution.
Symptoms.
Chlorotic streaks and stripes occur on diseased leaves.
Management.
Some sorghum cultivars have levels of resistance.
Maize Stripe
Cause.
Maize stripe virus (MStpV) is in the tenuivirus group. MStpV is transmitted in a persistent manner by the planthopper Peregrinus maidis.
Distribution.
Australia and possibly India and Africa.
Symptoms.
Diseased plants are chlorotic, flower early, and tiller excessively.
Management.
Not reported.
Maize Yellow Stripe
Cause.
leafhopper Cicadulina chinai. Acquisition and inoculation

Page 613
threshold times are 30 minutes each, with a latent period of 4.5 to 8.0 days if temperatures remain between 14°C minimum and 25°C maximum for the time of the
latent period. The maximum retention period is 27 days.
Barley, wheat, and graminaceous weeds are winter hosts. Different strains of MYSV exist.
Distribution.
Egypt.
Symptoms.
Symptoms on sorghum are not well described. Three symptom types exist on maize: fine stripe, coarse stripe, and chlorotic stunt. Each type may represent different
MYSV strains. Experimentally, the fine stripes that appear on the first leaves are followed by coarse stripes on younger leaves; however, some leaves have both
symptom types.
Management.
Not reported.
Peanut Clump
Cause.
Peanut clump virus (PCV) is in the furovirus group. PCV is soilborne and the soil fungus Polymyxa graminis is the suspected vector. PCV is also mechanically
transmitted.
Distribution.
Upper Volta.
Symptoms.
Great millet, Sorghum arundinaceum, is a symptomless natural host.
Management.
Not reported.
Red Stripe Disease
Cause.
Johnsongrassinfecting strain of sugarcane mosaic virus (SCMV). SCMV is in the potyvirus group.
Distribution.
Australia (New South Wales).
Symptoms.
Symptoms vary with the diseased cultivar. An initial mosaic pattern that develops on diseased leaves eventually becomes interspersed with necrotic areas. Some
cultivars develop a severe necrosis. Systemically infected leaves may also become necrotic. Diseased plants may be stunted and have a severe yellow mosaic.
Management.
Control johnsongrass.
Rice Stripe
Cause.
Rice stripe virus (RStV) is in the tenuivirus group. Transmission is by the planthoppers Laodelphax striatellus, Ribautodelphax albifascia, and Unkanodes
sapporonus in a persistent and a transovarial manner. RStV multi

Page 614
plies and persists in vectors; disease incidence is correlated to percentage of viruliferous insects. Several other plants are virus hosts.
Distribution.
Japan, Korea, and Taiwan.
Symptoms.
Diseased leaves are chlorotic or have chlorotic striping.
Management.
Not reported.
Sorghum Mosaic
Cause.
Sorghum mosaic virus (SrMV), which is in the potyvirus group, consists of former sugarcane mosaic virus strains H, I, and M from the United States. SrMV is
soilborne but the actual mechanism of soil transmission is unknown. SrMV is transmitted in a nonpersistent manner by at least seven aphid species. Aphids that
normally acquire SrMV from sugarcane or perennial grasses may become widely dispersed by wind. SrMV is also mechanically transmitted.
Distribution.
Anywhere that sorghum and sugarcane are grown in the same area.
Symptoms.
Viruscaused symptoms are related to the distribution of aphid vectors. Edges of fields are frequently the first and only areas affected. Symptoms vary according to
sorghum cultivar, SCMV strain, and environment.
Diseased plants have a light green mottling or mosaic, often with red lesions that occur only at temperatures of 16°C or less. Diseased plants are stunted and the
number of heads and seeds and the head length are reduced. Flowering is delayed.
Management.
Grow tolerant or resistant cultivars.
Sorghum Stunt Mosaic
Cause.
Sorghum stunt mosaic virus (SSMV) is in the rhabdovirus group. SSMV is transmitted by the leafhopper Gramindla sonora, but is not mechanically transmitted.
Minimum acquisition and inoculation times are 6 and 1 hours, respectively. Transmission efficiency is highest at temperatures of 24° to 36°C.
Other hosts of SSMV include maize and wheat.
Distribution.
Symptoms.
Diseased plants are severely stunted. Leaves have chlorotic and necrotic mottling and streaking.
Management.
Not reported.

Page 615
Sorghum Yellow Banding
Cause.
Sorghum yellow banding virus (SYBV) is a saptransmissible, small isometric virus. A soilborne mechanism is the possible mode of transmission for SYBV.
Distribution.
The United States (California and Texas).
Symptoms.
The first symptoms are yellow streaks that coalesce into bands. Later, a severe stunting of diseased plants occurs. Naturally infected sudangrass, Sorghum
sudanense, displayed chlorotic streaks on the leaves.
Symptoms of inoculated plants in the greenhouse were similar and appeared 15 to 20 days after inoculation. In some cases, the plants continued to grow while older
leaves lost their symptoms and yellow streaks appeared on new leaves. In other cases, the plants became dwarfed and chlorotic and eventually died. Symptoms on
plants in the field occurred 20 to 25 days after inoculation.
Management.
Not reported.
Sugarcane Chlorotic Streak
Cause.
Sugarcane chlorotic streak virus is transmitted by the insect Draeculacephala portola.
Distribution.
Symptoms.
Pale yellow steaks less than 5 cm in length occur on the second and third leaves. Streaks are irregular in width and are not continuous.
Management.
Not reported.
Sugarcane Fiji Disease
Cause.
A virus that is transmitted by the leafhopper Perkinsiella saacharicida.
Distribution.
The Philippines and possibly Nigeria.
Symptoms.
Diseased leaves have galls and are stiff and malformed. Diseased plants have shortened stalks with poorly formed heads or no heads and become prematurely brown.
Management.
Not reported.
Wheat Streak Mosaic
Cause.
Wheat streak mosaic virus (WSMV). WSMV is vectored by the wheat curl mite, Aceria tosichella (syn. A. tulipae).
Distribution.

Page 616
Symptoms.
Symptoms on diseased leaves range from a mosaic with interveinal reddening to a mosaic with interveinal reddening that becomes necrotic.
Management.
Not reported.
Unknown Virus
Cause.
Unknown virus consisting of flexuous rods of approximately 10 nm in diameter and a modal length of 422 nm. The virus is mechanically transmitted.
Distribution.
Symptoms.
Severe mosaic symptoms occur on diseased leaves.
Management.
Not reported.
Disease Caused By Unknown Factors
Weak Neck
Cause.
Originally, weak neck was associated with physiologic disorders resuiting from inherent plant characteristics and environmental stresses in combine types of grain
sorghum. The peduncle and rachis do not develop sufficient thickwalled tissue to ripen and support the developing head. Secondary organisms invade such tissue and
further weaken it.
Distribution.
The United States.
Symptoms.
The culm breaks below the head, resulting in poorly developed heads with lightweight seed. The upper culm tissues dry out, become spongy, and bleach to a tan
color. Frequently the peduncle may be watersoaked and have an accumulation of a sticky exudate during wet weather.
Management.
Grow resistant cultivars in which grain ripens before the culm weakens.
Selected References
Ali, M, E. K., and Warren, H. L. 1987. Physical races of Colletotrichum graminicola on sorghum. Plant Dis. 71:402404.
Ali, M. E. K., Warren, H. L., and Latin, R. X. 1987. Relationship between anthracnose leaf blight and losses in grain yield of sorghum. Plant Dis. 71:803806.
Anonymous. 1975. Prevent and identify grain sorghum diseases. World Farming 17:1114
Bandyopadhyay, R., Mughogho, L. K., and Satyanarayana, M. V. 1987. Systemic infection of sorghum by Acremonium strictum and its transmission through seed.
Plant Dis 71:647650.

Page 617
Bandyopadhyay, R., Mughogho, L. K., and Prasada Rao, K. E. 1988. Sources of resistance to sorghum grain molds. Plant Dis. 72:504508.
Bandyopadhyay, R., Mughogho, L. K., Manohar, S. K., and Satyanarayana, M. V. 1990. Stroma development, honeydew formation, and conidial production in
Claviceps sorghi. Phytopathology 80:812818.
Bell, K. K., Harris, H., and Wells, H. D. 1973. Rhizoctonia blight of grain sorghum foliage. Plant Dis. Rptr. 57:549550.
Birchfield, W., and Anzalone, L., Jr. 1982. Grain sorghum rootknot and reniform nematode host reactions. (Abstr.) Phytopathology 72:355.
Borges, O. L. 1983. Pathogenicity of Drechslera sorghicola isolates on sorghum in Venezuela. Plant Dis. 67:996997.
Cardwell, K. F., Hepperly, P. R., and Frederiksen, R. A. 1989. Pathotypes of Colletotrichum graminicola and seed transmission of sorghum anthracnose. Plant
Dis. 73:255257.
Casela, C. R., and Frederiksen, R. A. 1993. Survival of Colletotrichum graminicola sclerotia in sorghum stalk residues. Plant Dis. 77:825827.
Castor, L. L., and Frederiksen, R. A. 1980. Fusarium head blight occurrence and effects on sorghum yield and grain characteristics in Texas. Plant Dis. 64:1017
1019.
Cook, G. E., Boosalis, M. G., Dunkle, L. D., and Odvody, G. N. 1973. Survival of Macrophomina phaseoli in corn and sorghum stalk residue. Plant Dis. Rptr.
57:873875.
Craig, J., Frederiksen, R. A., Odvody, G. N., and Szerszen, J. 1987. Effects of herbicide antidotes on sorghum downy mildew. Phytopathology 77:15301532.
Creamer, R., He, X., and Styer, W. E. 1997. Transmission of sorghum stunt mosaic rhabdovirus by the leafhopper vector Graminella sonora (Homoptera:
Cicadellidae). Plant Dis. 81:6365.
CuarezmaTeran, J. A., Trevathan, L. E., and Bost, S.C. 1984. Nematodes associated with sorghum in Mississippi. Plant Dis. 68:10831085.
Dean, J. L. 1968. Germination and overwintering of sclerotia of Gloeocercospora sorghi. Phytopathology 58:113114.
Doupnik, B., Jr., Boosalis, M. G., Wicks, G., and Smika, D. 1975. Ecofallow reduces stalk rot in grain sorghum. Phytopathology 65:10211022.
Duveiller, E., Snacken, F., Maraite, H., and Autrique, A. 1989. First detection of Pseudomonas fuscovaginae on maize and sorghum in Burundi. Plant Dis. 73:514
517.
Edmunds, L. K., and Niblett, C. L. 1973. Occurrence of panicle necrosis and small seed as manifestations of maize dwarf mosaic virus infection in otherwise
symptomless grain sorghum plants. Phytopathology 63:388392.
Edmunds, L. K., and Zummo, N. 1975. Sorghum Diseases in the United States and Their Control. USDA Agric. Res. Serv. Agric. Hdbk. No. 468.
Edmunds, L. K., Futrell, M. C., and Frederiksen, R. A. 1969. Sorghum diseases. In Sorghum Production and Utilization, J. S. Wall and W. M. Ross (eds.). AVI
Publishing Co., Westport, CT.
EIShafey, H. A., AbdElRahim, M. F., and Refaat, M. M. 1979. A new Cephalosporiumwilt disease of grain sorghum in Egypt. Egypt Phytopathol. Congr. 3rd.
Proc., pp. 514532.

Page 618
Forbes, G. A., and Collins, D.C. 1985. A seedling epiphytotic of sorghum in south Texas caused by Pythium arrhenomanes. Plant Dis. 69:726.
Forbes, G. A., Ziv, O., and Frederiksen, R. A. 1987. Resistance in sorghum to seedling disease caused by Pythium arrhenomanes. Plant Dis. 71:145148.
Frederiksen, D. E., and Leuschner, K. 1997. Potential use of benomyl for control of ergot (Claviceps africana) in sorghum Alines in Zimbabwe. Plant Dis. 81:761
765.
Frederiksen, R. A. 1980. Sorghum downy mildew in the United States: Overview and outlook. Plant Dis. 64:903908.
Frederiksen, R. A. (ed.). 1986. Compendium of Sorghum Diseases. American Phytopathological Society, St. Paul, MN. 82 pp.
Frederiksen, R. A., and Rosenow, D. T. 1971. Disease resistance in sorghum, pp. 7182.26th Ann. Corn and Sorghum Res. Conf. Proc. Chicago.
Janke, G. D., Pratt, R. G., Arnold, J. D., and Odvody, G. N. 1983. Effects of deep tillage and roguing of diseased plants on oospore populations of
Peronosclerospora sorghi in soil and on incidence of downy mildew in grain sorghum. Phytopathology 73:16741678.
Jardine, D.J. 1989. Seedling blight of grain sorghum caused by Gibberella thapsina. (Abstr.). Phytopathology 79:1193.
Jensen, S. G., Mayberry, W. R., and Obrigawitch, J. A. 1986. Identification of Erwinia chrysanthemi as a softrotinducing pathogen of grain sorghum. Plant Dis.
70:593596.
Jones, B. L. 1971. The mode of Sclerospora sorghi infection of Sorghum bicolor leaves. Phytopathology 61:406408.
Jones, B. L. 1978. The mode of systemic infection of sorghum and sudangrass by conidia of Sclerospora sorghi. Phytopathology 68:732735.
Klaassen, V. A., and Falk, B. W. 1989. Characterization of a California isolate of sorghum yellow banding virus. Phytopathology 79:646650.
Klittich, C.J.R., Leslie, J. F., Nelson, P. E., and Marasas, W. F. O. 1997. Fusarium thapsinum (Gibberella thapsina): A new species in section Liseola from
sorghum. Mycologia 89:643652.
Lakshmanan, P., Mohan, S., and Jeyarajan, R. 1987. A new leaf spot of sorghum caused by Cochliobolus bicolor in Tamil Nadu, India. Plant Dis. 71:651.
Langham, M. A., Toler, R. W., Alexander, J. D., and Miller, F. R. 1984. Evaluation of Sorghum bicolor (L.) Moench accessions under natural infection with yellow
sorghum stunt mycoplasma. (Abstr.) Phytopathology 74:868.
LeonoGallegos, H. M., and Sanchez Castro, M. A. 1977. The occurrence in Mexico of Curvularia Iunata on sorghum kernels. Plant Dis. Rptr. 61:10821083.
Mabry, J. E., and Lightfield, J. W. 1974. Long smut detected on imported sorghum seed. Plant Dis. Rptr. 58:810811.
Manzo, S. K. 1976. Studies on the mode of infection of sorghum by Tolyposporium ehrenbergii, the causal organism of long smut. Plant Dis. Rptr. 60:948952.
Marasas, W. F. O., Rabie, C. J., Lubben, A., Nelson, P. E., Toussoun, T. A., and Van Wyk, P. S. 1987. Fusarium napiforme, a new species from millet and
sorghum in southern Africa. Mycologia 79:910914.
Martins, C. R. F., and Kitajima, E. W. 1993. A unique virus isolated from elephant grass. Plant Dis. 77:726729.
Mayhew, D. E., and Flock, R. A. 1981. Sorghum stunt mosaic. Plant Dis. 65:8486.

Page 619
McLaren, N. W. 1992. Quantifying resistance of sorghum genotypes to the sugar disease pathogen (Claviceps africana). Plant Dis. 76:986988.
Munkvold, G. P., and Desjardins. A. E. 1997. Fumonisins in maize. Can we reduce their occurrence? Plant Dis. 81:556565.
Natural, M.P., Frederiksen, R. A., and Rosenow, D. T. 1982. Acremonium wilt of sorghum. Plant Dis. 66:863865.
Nelson, P. A., Toussoun, T. A., and Marasas, W. F. O. 1983. Fusarium Species: An Illustrated Manual for Identification. The Pennsylvania State University Press,
University Park. 193 pp.
Odvody, G. N., and Dunkle, L. D. 1973. Overwintering capacity of Ramulispora sorghi. Phytopathology 63:15301532.
Odvody, G. N., and Dunkle, L. D. 1975. Occurrence of Helminthosporium sorghicola and other minor pathogens of sorghum in Nebraska. Plant Dis. Rptr.
59:120122.
Odvody, G. N., and Dunkle, L. D. 1979. Charcoal stalk rot of sorghum: Effect of environment on hostparasite relations. Phytopathology 69:250254.
Odvody, G. N., and Forbes, G. 1984. Pythium root and seedling rots, pp 3135. In Sorghum Root and Stalk Rots: A Critical Review. L. K. Mughogho (ed.).
International Crops Research Institute for the SemiArid Tropics, Pantancheru, India.
Odvody, G. N., and Madden, D. B. 1984. Leaf sheath blights of Sorghum bicolor caused by Sclerotium rolfsii and Gloeocercospora sorghi in south Texas.
O'Neill, N. R., and Rush, M. C. 1982. Etiology of sorghum sheath blight and pathogen virulence on rice. Plant Dis. 66:11151118.
Pande, S., Mughogho, L. K. Seetharama, N. and Karunakar, R. I. 1989. Effects of nitrogen, plant density, moisture stress and artificial inoculation with
Macrophomina phaseolina on charcoal rot incidence in grain sorghum. J. Phytopathol. 126:343352.
Penrose, L.J. 1974. Identification of the cause of red stripe disease sorghum in New South Wales (Australia) and its relationship to mosaic virus in maize and
sugarcane. Plant Dis. Rptr. 58:832836.
Pratt, R. G., and Janke, G. D. 1978. Oospores of Sclerospora sorghi in soils of south Texas and their relationships to the incidence of downy mildew in grain
sorghum. Phytopathology 68:16001605.
Pratt, R. G., and Janke, G. D. 1980. Pathogenicity of three species of Pythium to seedlings and mature plants of grain sorghum. Phytopathology 70:766771.
Raghava Reddy, J., Claflin, L. E., and Ramundo, B. A. 1991. Systemic colonization of grain sorghum plants by Xanthomonas campestris pv. holcicola. (Abstr.)
Schuh, W., Jeger, M. J., and Frederiksen, R. A. 1987. The influence of soil temperature, soil moisture, soil texture, and inoculum density on the incidence of sorghum
downy mildew. Phytopathology 77:125128.
Seifers, D. L., and Harvey, T. L. 1989. Effect of carbofuran on transmission of maize dwarf mosaic virus in sorghum mechanically and by the aphid Schizaphis
graminum. Plant Dis. 73:6163.
Seifers, D. L., Harvey, T. L., Kofoid, K. D., and Stegmeier, W. D. 1996. Natural infection of pearl millet and sorghum by wheat streak mosaic virus in Kansas. Plant
Dis. 80:179185.

Page 620
Shafie, A. E., and Webster, J. 1979. Trichometasphaeria turcica as a root pathogen of Sorghum bicolor var. feterita. Plant Dis. Rptr. 63:464466.
Sifuentes, J., and Frederiksen, R. A. 1988. Inheritance of resistance to pathotypes 1, 2, and 3 of Peronosclerospora sorghi in sorghum. Plant Dis. 72:332333.
Singh, D. S., and Pavgi, M. S. 1982. Perpetuation of two foliicolous fungi parasitic on sorghum in India. Phytopathol. Medit. 21:4142.
Szerszen, J. B., Frederiksen, R. A., Craig, J., and Odvody, G. N. 1988. Interactions between and among grain sorghum, sorghum downy mildew, and the seed
herbicide antidotes Concep II, Concep, and Screen. Phytopathology 78:16481655.
Tangonan, N. G., and Quimio, T. H. 1986. Effects of various cultural management practices and weather factors on the development of sorghum stalk rot in
Mindanao. Philipp. Phytopathol. 22:4957.
Tarr, S. A. 1962. Diseases of Sorghum, Sudan Grass and Broom Corn. Commonwealth Mycological Institute, Kew, England. University Press, Oxford.
Tegegne, G., Bandyopadhyay, R., Mulatu, T., and Kebede, Y. 1994. Screening for ergot resistance in sorghum. Plant Dis. 78:873876.
Toler, R. W. 1985. Maize dwarf mosaic, the most important virus disease of sorghum. Plant Dis. 69:10111015.
Trimboli, D. S., and Burgess, L. W. 1983. Reproduction of Fusarium moniliforme basal stalk rot and root rot of grain sorghum in the greenhouse. Plant Dis.
67:891894.
Tuleen, D. M., Frederiksen, R. A., and Vudhivanich, P. 1980. Cultural practices and the incidence of sorghum downy mildew in grain sorghum. Phytopathology
70:905908.
Wall, G. C., Mughogho, L. K., Frederiksen, R. A., and Odvody, G. N. 1987. Foliar disease of sorghum species caused by Cercospora fusimaculans. Plant Dis.
71:759760.
Williams, R.J., Frederiksen, R. A., and Mughogho, L. K. (eds.). 1978. Proceedings of the International Workshop on Sorghum Diseases. ICRISAT, Patancheru,
India. 469 pp.
Wilson, J. M., and Frederiksen, R. A. 1970. Histopathology of the interaction of Sorghum bicolor and Sphacelotheca reiliana. Phytopathology 60:828832.
Wilson, J. P., Gates, R. N., and Hanna, W. W. 1991. Effect of rust on yield and digestibility of pearl millet forage. Phytopathology 81:233236.
Young, G. V., Lefebvre, C. L., and Johnson, A. G. 1947. Helminthosporium rostratum on corn, sorghum and pearl millet. Phytopathology 47:180183.
Zummo, N. 1986. Red spot (Helminthosporium rostratum) of sweet sorghum and sugarcane, a new disease resembling anthracnose and red rot. Plant Dis. 70:800.
Zummo, N., and Broadhead, D. M. 1984. Sources of resistance to rough leaf spot disease in sweet sorghum. Plant Dis. 68:10481049.
Zummo, N., Bradfute, O. E., Robertson, D. C., and Freeman, K. C. 1975. Yellow sorghum stunt: A disease symptom of sweet sorghum associated with a
mycoplasmalike body in the United States. Plant Dis. Rptr. 59:714716.
Zvoutete, P., Claflin, L. E., and Ramundo, B. A. 1991. Portal of entry of Xanthomonas campestris pv. holcicola into grain sorghum plants. (Abstr.) Phytopathology
81:1193.
Zvoutete, P., Claflin, L. E., and Ramundo, B. A. 1991. Seedborne role and longevity of Xanthomonas campestris pv. holcicola in grain sorghum. (Abstr.)

Page 621
18.
Diseases of Soybean (Glycine max)
Bacillus Seed Decay
Cause.
Bacillus subtilis is an aerobic, grampositive, sporeforming rod (0.7 × 1.02.0 m).
Seed losses are highest during moist and warm conditions at temperatures of 25° to 35°C in storage, in the field, and under experimental conditions.
Distribution.
Not known for certain, but likely occurs wherever soybean is grown under warm and wet conditions.
Symptoms.
Seeds have a soft, ''mushy" decay and are often covered with a slimy, rough to smooth, whitish to grayish bacterial growth.
Management.
Not reported.
Bacterial Blight
Cause.
Pseudomonas syringae pv. glycinea has several synonyms. The bacterium has straight or slightly curved gramnegative rods that occur either singly or in chains of a
few cells. Polar flagella are either monotrichous or multitrichous, rarely nonmotile. Levan is produced but gelatin and arbutin are not hydrolized.
Pseudomonas syringae pv. glycinea is seedborne and overwinters in infested residue and possibly directly in the soil. Bacteria associated with infested leaf tissue
overwinter on the soil surface if the weather is cold and dry. The major spread of bacteria occurs during windy, cool, and wet weather when wind and water spread
bacteria from soil, cotyledons, and leaves of diseased plants. Diseased cotyledons from seedborne infection may be a major source of secondary inoculum. Bacteria
are also spread by leaves rubbing together and during cultivation when foliage is wet. Bacte

Page 622
ria in the presence of free water enter plants through wounds and stomates.
Cool, rainy weather favors the development of bacterial blight. Optimum infection occurs at temperatures of 24° to 26°C. Because bacteria become dormant during
warm, dry weather, little or no disease development occurs during higher temperatures later in the growing season.
The incidence and severity of bacterial blight are greater in reduced tillage than in conventional tillage systems. However, a report from Missouri said bacterial blight
was less in notill soybeans. The yields from diseased plants were reported to be greater at a row spacing of 45 cm than at 60 or 90 cm. Several races of P. syringae
pv. glycinea exist.
Distribution.
Wherever soybean is grown.
Symptoms.
Symptoms may appear 5 to 7 days after a storm has occurred and are most common from early to midseason. Lesions first appear on cotyledon margins. As the
lesions enlarge, the entire cotyledon collapses and becomes discolored dark brown. Diseased seedlings are stunted, and if the growing point becomes diseased, the
seedling may be killed.
Leaf symptoms start as small, angular, watersoaked spots that become yellow. The centers dry out and become redbrown to black as the tissue dies. The spot is
usually surrounded by a watersoaked margin bordered by a yellow halo. As spots increase in size, wind and rain may cause large areas of the diseased leaf to fall out,
which gives a ragged appearance to diseased leaves. Severely diseased leaves may drop off plants.
Pod lesions, which are small and watersoaked initially, enlarge to cover much of the pod and become brown to black. Diseased seeds may be shriveled, sunken, and
discolored, or they may display no symptoms. Severely diseased seeds in the field may be covered with a "slimy" bacterial growth. Seed may also be infected during
harvest or storage.
Systemic symptoms have been reported to consist of chlorotic mottling; yellowing; the formation of narrow, elongated leaves; and a general plant stunting.
Management
2. Rotate soybean with other crops.
4. Do not cultivate soybeans when the foliage is wet because machinery may disseminate bacteria in a water film.
5. Apply a foliar fungicide during the growing season if conditions, such as growing soybeans for seed, warrant it. However, applying fungicides to control bacterial
blight normally is not a practical means of disease management.
7. Avoid growing highly susceptible cultivars.

Page 623
Bacterial Crinkle Leaf
Bacterial crinkle leaf is also known as bacterial crinkle leaf spot.
Cause.
The causal agent of bacterial crinkle leaf spot has been tentatively identified as Pseudomonas syringae pv. syringae.
Distribution.
The United States.
Symptoms.
Young diseased leaflets are severely distorted or crinkled and have a necrosis of the veins and interveinal tissues. Lesions are not watersoaked and do not develop
chlorosis or a halo around "spots."
Management.
Disease management normally is not practiced because bacterial crinkle leaf, to date, is not an economically important disease.
Bacterial Pustule
Cause.
Xanthomonas campestris pv. glycines (syn. X. phaseoli var. sojensis and several others). The species name sometimes appears in the literature as "glycinea."
Xanthomonas campestris pv. glycines is gramnegative, has single, straight rods (0.40.7 × 0.71.6 m), is motile by a single polar flagellum, and is obligately
aerobic. Colonies on nutrient media are smooth, circular, butyrous or viscid, and usually yellow. Gelatin, starch and casein are hydrolyzed.
Xanthomonas campestris pv. glycines overwinters in infested residue on the soil surface and buried in soil, on seeds, and in the rhizosphere of wheat roots. Some
weeds, such as redvine, Brunnichia cirrhosa, and hyacinth bean, Dolichos bifiorus, are also hosts.
Bacterial pustule develops during wet, warm weather (optimum temperatures are 30° to 33°c). New infections may occur throughout the growing season because
bacteria continue to be active at high temperatures, unlike bacterial blight, where the causal bacterium becomes dormant. Bacteria are disseminated by splashing
water, leaf contact, and machinery during cultivation when soybean foliage is wet. The bacteria disperse from a source equally in all directions and at the same rate on
resistant or susceptible soybeans. After 35 days, external bacterial populations are 20 to 50fold greater on susceptible than resistant plants. Bacteria enter plants
through leaf wounds or natural openings, such as stomates, and multiply intercellularly.
Distribution.
Wherever soybean is grown in a warm, wet climate.
Symptoms.
The first symptoms on diseased leaves are small, yellowgreen spots that have brown centers and are most conspicuous on the upper leaf surface. Spots lack the
watersoaked appearance typical of most bacterial infections. Spots may merge and form larger dead areas in which the diseased tissue falls out, giving leaves a
ragged appearance. In cases of severe

Page 624
disease, defoliation may occur. The best diagnostic symptom is the presence of small raised pustules that develop in the center of lesions on the lower leaf surfaces.
Pustules eventually rupture and dry. The presence of a pustule and the absence of a watersoaked appearance before the spot becomes yellow distinguishes bacterial
pustule from bacterial blight.
Management
1. Grow resistant cultivars. The rxp gene confers resistance by making it necessary to increase the number of bacteria cells necessary to infect a soybean plant.
3. Plow under infested soybean residue.
4. Grow diseasefree seed.
5. Do not cultivate when foliage is wet because machinery will spread the bacteria.
Bacterial Tan Spot
Cause.
Curtobacterium flaccumfaciens. Confusion surrounds the identity of the causal organism, which may be C. flaccumfaciens pv. flaccumfaciens (syn.
Corynebacterium flaccumfaciens pv. [or subsp.] flaccumfaciens). Curtobacterium flaccumfaciens is internally seedborne.
When infected seed is grown, bacteria may move up the vascular system of the diseased plant during temperatures of 25° to 30°C and infect the unifoliate and first
trifoliate leaves. Curtobacterium flaccumfaciens is spread throughout the growing season by windblown rain and infects plants through wounds resulting from leaf
toleaf contact caused by wind. Infection is reduced after flower set.
Distribution.
The United States (Iowa).
Symptoms.
An oval to elongated chlorotic pattern starts at the diseased leaf margins and progresses to the midribs. Symptoms continue on to petioles, leaving large necrotic areas
that fall out during high winds. Leaflets with large or multiple lesions defoliate from diseased plants.
Seedlings grown from diseased seed may be stunted and have fused leaflets. Plants that become infected when older will have empty pods and the diseased leaves
develop a marginal necrosis or necrotic spots on the interior portions of the laminae.
Plant damage is a function of the number of infected seedlings arising from diseased seed. Yield losses may occur with susceptible cultivars.
Management
2. Sow healthy seed.
3. Sow early in the growing season when temperatures are below 25°C to avoid leaf infection via the vascular system.

Page 625
Bacterial Wilt (Curtobacterium flaccurnfaciens)
Bacterial wilt may be the same disease as or a phase of bacterial tan spot. Because the symptoms have different descriptions in the literature, they are listed as two
separate diseases here.
Cause.
Curtobacterium flaccumfaciens (syn. Corynebacterium flaccumfaciens) is seedborne and may overwinter in infested crop residue.
Distribution.
Russia and Ukraine.
Symptoms.
Diseased leaves are yellowed and eventually wilt and dry out but remain attached to plants. The vascular system is discolored and diseased plants weaken, become
stunted, and eventually die.
Diseased seeds may either appear to be normal or will have a bright yellow discoloration caused by bacteria under the seed coat. Infrequently, a small amount of
yellow exudate may form on the hilum of a diseased seed.
Management.
No specific control measures are reported in the literature. However, it is suggested those disease management measures used for other bacterial diseases of soybean
may be useful in managing bacterial wilt.
3. Plow under residue because the bacterium does not survive well in soil.
4. Do not cultivate when foliage is wet because bacteria may be spread by machinery.
5. Apply a foliar fungicide during the growing season if conditions, such as growing soybean for seed, warrant it. However, applying fungicides to control bacterial wilt
normally is impractical.
Bacterial Wilt (Curtobacterium sp.)
Cause.
Curtobacterium sp. (syn. Corynebacterium sp.). Curtobacterium sp. resembles Curtobacterium flaccumfaciens; therefore, this bacterial wilt may be the same as
previously described. However, while there appears to be some similarity between the two diseases, the symptoms are dissimilar enough to treat them as different
diseases.
Distribution.
The United States (Iowa).
Symptoms.
Diseased plants are wilted and severely stunted. Pods are empty and abnormally formed. Lower leaves have marginal necrosis. Wilt does not occur after flower set.
Management.
Not necessary, but the following measures suggested for bacterial blight may apply.

Page 626
4. Do not cultivate when foliage is wet.
5. Apply a foliar fungicide during the growing season if conditions, such as growing plants for seed, warrant it. However, applying fungicides to control bacterial wilt
Bacterial Wilt (Pseudomonas solanacearum)
Cause.
Pseudomonas solanacearum has several synonyms. It is occasionally seedborne and overwinters in infested crop residue.
Distribution.
Ukraine and the United States (North Carolina).
Symptoms.
Diseased leaves become chlorotic and eventually develop small, dark brown spots that elongate into lesions with dark borders. Eventually, lesions dry up and
disintegrate, giving leaves a ragged appearance. The entire plant then progressively wilts. Young diseased plants may develop a rapid, severe wilt. Other diseased
plants wilt only slightly and are stunted.
Management
5. Apply a foliar fungicide during the growing season if conditions, such as growing plants for seed, warrant it. However, applying fungicides to control bacterial wilt
Pseudomonas Seed Decay
Cause.
Pseudomonas syringae pv. glycinea has several synonyms. Pseudomonas syringae pv. glycinea is seedborne and overwinters in infested residue and possibly
directly in the soil. Bacteria associated with infested leaf tissue overwinter on the soil surface if the weather is cold and dry. The major spread of bacteria occurs during
windy, cool, and wet weather when wind and water spread bacteria from soil, cotyledons, and leaves of diseased plants. Diseased cotyledons from seedborne
infection may be a major source of secondary inoculum. Bacteria are also spread by leaves rubbing together and during cultivation when foliage is wet. Bacteria in the
presence of free water enter plants through wounds and stomates.
Cool, rainy weather favors the development of Pseudomonas seed de

Page 627
cay. Optimum temperatures for infection are 24° to 26°C. Because bacteria become dormant during warm, dry weather, little or no disease development occurs
during higher temperatures later in the growing season.
Distribution.
Symptoms.
Seeds may be symptomless. If symptoms occur, seeds may be shriveled, develop raised or sunken lesions, and become slightly discolored. Under high moisture
conditions, seeds may be covered with a "slimy" growth.
Management
5. Apply a foliar fungicide during the growing season if conditions, such as growing plants for seed, warrant it. However, applying fungicides to control seed decay
Wildfire
Cause.
Pseudomonas syringae pv. tabaci (syn. P. tabaci and Bacterium tabacum.) Other synonyms are noted in the literature. Pseudomonas syringae pv. tabaci
overseasons in infested residue and seed and on the root surfaces of many plants, but alternate freezing and thawing kills the bacterium. Pseudomonas syringae pv.
tabaci is spread by wind and splashing water. Water congestion of plant tissues caused by beating rains is often required for invasion and infection by the bacteria.
Bacterial pustule lesions provide the entrance for P. syringae pv. tabaci; consequently wildfire is closely associated with bacterial pustule and a pustule can usually be
found in the center of a wildfire lesion.
Distribution.
Brazil and the southern United States.
Symptoms.
Light brown, necrotic spots, varying in size and shape, form on diseased leaves and are usually surrounded by a large yellow halo with a definite margin. Sometimes
smaller dark brown to black lesions form without the halo. Lesions may enlarge during wet weather and form large dead areas that eventually tear away. During severe
disease conditions of wet weather, almost complete defoliation of diseased plants may occur.
Management

Page 628
5. To prevent spread of bacteria, do not cultivate soybeans when the foliage is wet.
Acremonium Wilt
Cause.
Acremonium sp.
Distribution.
Not known for certain but presumed to be the same as for Phialophora gregata. (See "Brown Stem Rot.")
Symptoms.
Similar to those caused by P. gregata. A brown discoloration of vascular and pith tissues occurs. Often the browning occurs only at the nodes; internodal tissue may
be white. Later in the growing season, the lower part of the diseased stem may show external browning, wilting, and premature leaf drop. Severely diseased plants
may lodge, presumably because of extensive stem injury.
Leaf symptoms are not ordinarily a reliable diagnostic tool since they may be confused with other leaf disorders. Leaf symptoms develop about 3 weeks before
physiological maturity when diseased plants are subjected to high temperatures or drought stress following a period of cool weather. Leaves may wilt and tissue
between the veins turns brown and dries rapidly, but tissue adjacent to veins remains green. Eventually, the whole leaf dies.
Management.
Not reported.
Alternaria leaf spot is also called Alternaria leaf spot and pod necrosis.
Cause.
Alternaria spp. Alternaria atrans is known to be a weak parasite that infects leaves through wounds made by a mechanical injury such as aphid punctures and
sunburn injury. Alternaria tenuissima and A. alternata are frequently associated with seeds and with injury diseases caused by the bean leaf beetle, Ceratoma
trifurcata. Alternaria tenuissima has also been reported to cause a leaf spot of soybeans in India and a wilt of soybeans in Kenya.
Alternaria spp. are seedborne. Conidia produced on saprophytic mycelia are disseminated by wind to soybean plants. Infection occasionally occurs on young plants,
but Alternaria leaf spot is generally a disease of plants nearing maturity. High levels of seed infection have been associated with wet years, frost injury, and stink bug
and bean leaf beetle damage.

Page 629
Distribution.
Symptoms.
Spots on leaves and pods are brown and have concentric rings that are 6 mm or larger in diameter. Leaf spots may merge and form large dead areas that cause
diseased leaves to dry up and defoliate prematurely. Diseased seeds are shrunken, green to brown, and often fail to germinate. Seed infected by A. alternata is small
and shrunken and has light to dark brown lesions.
Management.
Alternaria leaf spot usually goes unnoticed, occurs too late in the growing season to cause yield reductions, and is not considered severe enough to warrant control
measures.
Anthracnose
Cause.
Colletotrichum truncatum (syn. C. dematium var. truncatum, C. glycines, C. caulicola, C. viciae, and Vermicularia polytricha). Colletotrichum
gloeosporioides has been reported from Spain as a cause of anthracnose, but C. gloeosporioides is not associated with most phases of the disease. Other fungi
mentioned as causal agents are Glomerella glycines (anamorph C. destructivum), C. capsici, C. caulivorum, C. graminicola, V. truncata, and G. singulata.
Colletotrichum capsici is reported to be weakly pathogenic to soybeans, but survival in soybeans may be a source of inoculum for infecting cotton bolls.
Colletotrichum truncatum overwinters as mycelia and microsclerotia in seeds, seed coats, infested residue, and weeds. Conidia produced from mycelia growing on
diseased cotyledons or in residue in soil during warm, wet weather are disseminated by wind to host plants. Isolates may be separated into microsclerotiaforming and
nonmicrosclerotiaforming types. Colletotrichum truncatum infects soybeans in all stages of development. Preemergence or postemergence damping off occurs
during wet springs. Infection occurs up to temperatures of 30°C, then infection declines as the temperature increases. Anthracnose tends to be more severe under
narrow row conditions when plants are irrigated. Roots may also be infected.
Distribution.
Wherever soybean is grown. Anthracnose tends to be economically important in the humid tropics and subtropics and is widespread and severe in the midwestern and
southeastern United States.
Symptoms.
Symptoms generally appear during growth stages V1V3 (early seedling), R7R8 (late reproductive), and senescence. Colletotrichum truncatum grows from
diseased cotyledons onto stems and causes either numerous small, shallow, elongated, redbrown lesions or a few large dark lesions, both of which kill the young
plant. In humid weather, cotyledons become watersoaked, wither, and fall off.
Stems, pods, and leaves of young plants may be infected without show

Page 630
ing external symptoms until environmental conditions become more favorable for disease development. Symptoms on stems, pods, and petioles are irregularshaped,
brown to black discolored areas that somewhat resemble symptoms of pod and stem blight. In advanced stages of disease, diseased tissue is covered with acervuli
that, under magnification, resemble tiny pincushions covered with black spines. Diseased plants may be stunted.
Foliar symptoms that develop after prolonged periods of high humidity include leaf rolling, necrosis of laminar veins, petiole cankering, and premature defoliation.
Diseased lower branches and leaves that may be killed during wet weather cause the death of mature plants.
When pods or pedicels are infected early, a few small seeds or no seeds develop and mycelium may completely fill the pod cavity. Diseased seeds are dark brown
and shriveled, or if less severely diseased, seeds may be symptomless. When sown, diseased seed results in reduced emergence.
Following inoculation in an aeroponic growth chamber, root symptoms initially were light yellow discolorations that developed into irregularshaped brown lesions.
Later, the lesions became watersoaked, dark brown to black, and extended above and below the point of inoculum introduction. Acervuli and sclerotia developed on
secondary roots misted for 1 second every 30 minutes, but neither acervuli or sclerotia formed on roots misted for 1 second every 5 minutes.
Management
3. Apply a foliar fungicide to plants during the growing season.
6. Resistance has been identified.
Ascochyta Leaf Spot
Cause.
Ascochyta phaseolorum, A. pinodella, A. sojae, and A. sojaecola. Ascochyta pinodella and A. sojaecola are reported to be seedborne. Ascochyta leaf spot is
favored by higher humidities and frequently begins in the lower canopy of older plants.
Distribution.
Europe, Iran, Japan, and Zambia.
Symptoms.
Seedling blight may occur, but the most common symptom is leaf spots that first occur on the lower leaves of older diseased plants. Leaf spots are round and
discolored brown and have a dark margin. Stems have brown elongated streaks. Pod symptoms vary from small spots to a general browning of poorly developed
pods.
Management.
Resistant cultivars have been developed in Russia.

Page 631
Aspergillus Seedling Blight
Cause.
Aspergillus melleus is seedborne.
Distribution.
The United States.
Symptoms.
Diseased seedlings are stunted and chlorotic. Cotyledons are curled and have deep necrotic lesions on the lower side. Russetting occurs on hypocotyls of a few plants.
Management.
Not reported.
Brown Spot
Brown spot is also called Septoria brown spot.
Cause.
Septoria glycines overwinters as pycnidia and mycelia in infested residue and as mycelium in diseased seeds. During warm, wet weather, conidia that are produced
on infested residue, cotyledons, and diseased unifoliate leaves infected by seedborne inoculum are disseminated by wind and splashing rain to host leaves. Disease
development is optimum at a temperature of 28°C and high relative humidity. Dry weather halts the spread of the disease.
Septoria glycines produces the hostspecific, macromolecular, uronic acidrich, polysaccharide pathotoxin, which causes typical brown spot symptoms on soybeans.
A report from Missouri suggested brown spot incidence was lower in soybeans grown in reduced tillage systems than in conventional tillage. Several other plants also
are susceptible to S. glycines.
Distribution.
Asia, Brazil, Canada, Europe, and the United States, particularly the Midwest.
Symptoms.
Two distinct types of lesions have been described. The most common type is associated with plants grown from yellow seeds. In the spring, angular, red to brown
spots that vary from the size of a pinpoint to 5 mm in diameter and are surrounded by a chlorotic halo appear on both surfaces of unifoliate leaves but are more
pronounced on the underleaf surface. Leaves become chlorotic and are prematurely defoliated.
The less common type of lesion, which is associated with plants grown from green seeds, has the typical angular, red to brown spots, but the spots do not have the
surrounding chlorotic halo.
Spores produced on the primary leaves may spread and infect the trifoliate leaves, stems, and pods. Trifoliate leaves have numerous irregular tan lesions that gradually
turn dark brown. Later in the growing season, entire leaves may become rusty brown and defoliate prematurely. Defoliation of diseased plants occurs from the bottom
up, causing the lower portions of diseased plants to be bare of leaves before plant maturation. Brown lesions without a characteristic size or shape form on pods,
stems, and petioles. Petioles that have fallen to the soil surface may be covered with pycnidia

Page 632
that appear as scattered tiny black spots. Seed weight is reduced by disease, but the number of pods per plant and the number of seeds per pod are not.
Management
2. Grow a less susceptible cultivar.
Brown Stem Rot
Brown stem rot is also called Phialophora stem rot.
Cause.
Phialophora gregata (syn. Cephalosporium gregatum) survives as mycelia in infested residue, particularly in woody stem tissue. The population density of P.
gregata is greater in infested residue on the soil surface than in buried residue. Phialophora gregata survives up to 30 months in residue on the soil surface, but the
fungus cannot be detected in buried residue after 11 to 17 months.
Conidia, the main source of primary inoculum, are produced from mycelia that precolonized residue buried to a depth of 30 cm in the soil. Phialophora gregata has
been reported to be seedborne as mycelium within the seed coat but has not been detected in the embryo or cotyledon.
Infections occur through roots and the lower stem early in the growing season. Mycelium then grows upward in the xylem vessels, producing conidia that are carried
along, and interrupts water and nutrient flow in the diseased plant.
Development of brown stem rot is greatest at temperatures of 15° to 27°C, but temperatures above 27°C suppress disease development. Adequate moisture early in
the growing season and moisture stress later in the growing season has been reported to increase disease severity. However, contradictory results suggest dry soil
conditions during the preflower period were associated with lower disease incidence, and postflower moisture deficits were associated with reduced internal stem
browning and foliar symptoms. The latter results are consistent with the hypothesis that fungal pathogens of the vascular system advance upward in the stem largely by
spores carried in the transpiration stream; therefore, symptom severity is greatest if soil water is readily available. There reportedly is a greater development of brown
stem rot symptoms in plants grown in lowfertility soils.
Two forms of P. gregata have been reported. Type I isolates cause both internal stem browning and foliar interveinal necrosis. Type II isolates cause only stem
symptoms. However, evidence suggests that physiologic specialization exists.

Page 633
Distribution.
Canada, Egypt, Mexico, and the United States.
Symptoms.
Internal pith and vascular tissue become brown. The browning often occurs only at the nodes and the internodal tissue remains white. Later in the growing season, the
lower part of the stem may show external browning, wilting, and premature leaf defoliation. Severely diseased plants may lodge, presumably because of extensive stem
injury.
Leaf symptoms are ordinarily not a reliable diagnostic tool because they may be confused with other leaf disorders. Leaf symptoms develop about 3 weeks before
physiological maturity when diseased plants are subjected to high temperatures or drought stress following a period of cool weather. Leaves may wilt and the tissue
between the veins becomes brown and dries rapidly, but tissue adjacent to veins remains green. Eventually, the entire leaf dies. In contrast to the yellowgreen color of
a normally maturing field, an entire field of diseased soybeans may turn brown, as if an early frost had occurred.
Pod and seed abortion is a major effect of brown stem rot. Usually the more extensive the internal stem browning is, the greater the yield reduction. However, some
results indicate that greater yield losses occur when both foliar and stem symptoms develop than when only internal stem browning develops. Both type I and type II
isolates cause browning of internal stem tissues, but they differ in their ability to cause foliar symptoms. Type I isolates cause chlorosis, necrosis, and wilt of foliage;
type II isolates do not cause foliar symptoms. Inoculation with type I isolates significantly reduces yields; inoculation with type II isolates does not affect yields.
Management
1. Do not grow soybean, alfalfa, or red clover in infested soil for 3 years. Infested residue decomposes within this time and P. gregata cannot survive in soil outside of
precolonized residue.
Cercospora Leaf Spot and Blight
Cause.
Cercospora kikuchii (see ''Purple Stain"). Cercospora leaf spot and blight is favored by extended periods of high humidity and temperatures of 28° to 30°C.
However, no germination occurs below 92% relative humidity, and disease does not occur with leaf wetness periods of less than 18 hours or at temperatures above
30°C.
Distribution.
Japan, Taiwan, Uganda, and the United States.
Symptoms.
Cercospora leaf spot and blight is more severe on earlymaturing than latematuring cultivars. In Arkansas, the initial symptoms were observed at the beginning of seed
set through full seed set stages of plant growth.

Page 634
Diseased upper leaves exposed to the sun have a light purple, leathery appearance. Later, redpurple, angular to irregularshaped lesions occur on the upper and
lower leaf surfaces. These lesions, which vary in size from a pinpoint to irregular patches up to 1 cm in diameter, may coalesce and form large necrotic areas. Veinal
necrosis also may occur. Severe disease may cause rapid chlorosis and necrosis that results in defoliation starting with the upper diseased leaves. Green leaves may
occur below the defoliated areas. This obvious blighting occurs over large geographic areas, including entire fields.
Redpurple, slightly sunken lesions several millimeters long occur on petioles and stems. On susceptible cultivars, redpurple lesions that later become purplish black
occur on pods.
Management
2. An increase in the amount of potassium in fertilizer decreased incidence and severity of Cercospora leaf spot and blight.
Cercospora Seed Decay
Cause.
Cercospora sojina (syn. C. daizu) overwinters as mycelium in seed, primarily in the parenchymatous region of the seed coat, and in infested residue. Conidia
produced in cotyledonary lesions when infected seed germinates and on residue during warm, moist conditions are disseminated by wind to young leaves, pods, stems,
and seeds. Disease severity is greatest under warm, humid conditions. Different races of C. sojina exist.
Distribution.
In warm, humid areas of the soybeangrowing areas of the world.
Symptoms.
Seeds have conspicuous light to dark gray and brown areas that vary from specks to large blotches covering the entire seed coat. Some lesions show alternating
bands of light and dark brown. Sometimes brown and gray lesions diffuse into each other. Normally the seed coat cracks or flakes.
Management
1. Grow cultivars resistant to frogeye leaf spot.
3. Rotate soybean with other crops. Leave fields out of soybean for at least 2 years.
4. Apply foliar fungicides at the R3R5 growth stages.
Charcoal Rot
Charcoal rot is also called dry weather wilt and summer wilt.

Page 635
Cause.
Macrophomina phaseolina (syn. Botryodiplodia phaseoli, M. phaseoli, Rhizoctonia bataticola, and Sclerotium bataticola) survives as sclerotia and mycelia in
infested residue and in dry soil, but the fungus does not survive longer than a few weeks in wet soil. The depth of burial in soil apparently has little effect on fungus
survival. Macrophomina phaseolina is a good colonizer of plant debris in soil but it cannot persist long in the presence of other soil microflora. Macrophomina
phaseolina is also seedborne as ectophytic and endophytic sclerotia and hyphae; the hyphae are found in the seed coats, endosperms, and embryos. Pycnidia are
rarely produced on soybeans.
Seedling disease is greatest at high temperatures (28° to 35°C optimum), and both sclerotia and mycelia are equally effective as infective propagules. Sclerotia
germinate on root surfaces and form several germ tubes that penetrate roots and grow as mycelium within xylem tissues. Disease development in older infected plants
is also associated with hot, dry weather, and when unfavorable environmental conditions stop plant growth. Charcoal rot occurs on irrigated soybeans when water is
withheld to promote plant maturity.
Both infected seedling and older plants wilt due to the physical plugging of the xylem by mycelium or by the production of toxins or enzymes by the fungus, which stops
the upward movement of water in the xylem tissue.
Infection by the soybean cyst nematode, Heterodera glycines, can increase root colonization by M. phaseolina. Charcoal rot becomes more severe when soybeans
are grown in the same field in successive years. Longterm tillage does not affect charcoal rot incidence and severity.
Distribution.
Symptoms.
Redbrown lesions that later become ashy gray to black occur on seedlings at the soil line and extend upward on diseased stems. Leaves of severely diseased plants
turn yellow, wilt, and remain attached to the plant. Diseased seedlings are more likely to die in warm and dry soils than in cool and moist soils.
The best diagnostic symptom occurs after midseason. When the epidermis of diseased stems is removed, small black sclerotia which can be observed under the
epidermis are so numerous that diseased tissues have a grayblack color resembling a "sprinkling" of powdered charcoal. When the lower portion of diseased plants is
split open, there are black streaks in the woody portion. Diseased seeds have indefinite black spots and blemishes on the seed coat.
Management
1. Rotate soybean with other crops. Soybeans should not be grown in the same soil for at least 2 years to significantly reduce the number of propagules.

Page 636
2. Do not oversow. Crowded seedlings are more subject to infection.
3. Follow a good fertility program.
Choanephora Leaf Blight
Cause.
Choanephora infundibulifera may survive in the infested residue of different host plants. Choanephora leaf blight is severe under humid conditions or abundant
rainfall.
Distribution.
Thailand and the United States (Louisiana and Mississippi).
Symptoms.
Disease symptoms first occur on the oldest leaves nearest the soil surface. Distal halves of diseased leaves initially develop a grayish color. In approximately 5 days,
the diseased areas become darkened and necrotic. Later, the diseased portion dries up and curls.
Sporangiophores and sporangioles may be observed on blighted leaves and the edges of necrotic areas during periods of high humidity. Defoliation of diseased leaves
also may occur during periods of high humidity. If humidity is low, only the diseased area of the leaf drops off, leaving the unaffected leaf portion intact. Severely
defoliated plants may be stunted and seeds may be smaller than normal.
Management.
Not reported.
Cotyledon Spot
Cotyledon spot is also called Curvularia cotyledon spot.
Cause.
Curvularia lunata var. aeria and C. lunata are seedborne.
Distribution.
Brazil, India, and the United States (Puerto Rico).
Symptoms.
Diseased seeds show a slight discoloration. Upon germination, seed coats have a reddish tint and the underlying cotyledonary tissue becomes light brown. Lesions,
which are superficial and irregularshaped, do not enlarge once cotyledons have expanded. Up to 70% of the surface of diseased cotyledons may be affected.
Management.
Not reported. Cotyledon spot is considered of minor importance.
Downy Mildew
Cause.
Peronospora manshurica (syn. P. sojae) overwinters as oospores in infested residue and on seed. When adverse dry conditions occur during seed maturation, P.
manshurica survives as thickwalled mycelium between the hourglass layer and the parenchymatous tissue of the seed coat and it may also survive on the seed
surface as resistant, thickwalled resting or sclerotized mycelium.

Page 637
Under cool conditions, diseased seeds give rise to systemically infected seedlings. Seedling hypocotyls may be infected by soilborne oospores, which also results in
systemically infected seedlings. Conidia produced on the undersides of diseased leaflets and disseminated by wind to other host plants serve as secondary inoculum.
Older leaves eventually become resistant to infection.
Development of downy mildew is favored by temperatures of 20° to 22°C and high humidity. Several physiologic races of P. manshurica exist.
Distribution.
Symptoms.
An early symptom is indefinite yellowgreen areas on the upper leaf surfaces. In time, diseased areas enlarge, become grayish to dark brown, and are surrounded by
yellowgreen margins. A gray "fuzz" consisting of mycelium and spores develops in the diseased areas on the undersides of leaves, usually during periods of frequent
dews or abundant rain. Severely diseased leaves become yellow, then brown, and defoliate prematurely.
Pod infections occur, but external symptoms may not be evident. The inside of the pod and diseased seeds are encrusted with a white "coating" that consists of thick
walled oospores and mycelium. Diseased seeds often are a dull white, have cracked seed coats, and may be smaller or lighter in weight than healthy seeds.
Systemically infected plants remain small and have mottled graygreen leaves that cuff downward at the edges. The undersides of diseased leaves are covered with the
typical gray fungal growth consisting of mycelium and spores. Diseased seeds and the seedlings that develop from them usually are not killed, but they may serve as
infection foci from which the disease spreads to other host plants.
Management
3. Plow under infested refuse.
Drechslera Blight
Cause.
Drechslera glycini.
Distribution.
India.
Symptoms.
Circular to angular brown spots form near diseased leaf margins. As the lesions enlarge, the centers turn gray and have a dark brown margin that is sometimes
surrounded by a chlorotic halo. Lesions may develop along the veins of diseased leaves and cause leaves to cuff and dry.
Management.
Not reported.

Page 638
Essex Disease
Essex disease has some similarities to soybean severe stunt. The two diseases may be part of the same disease syndrome.
Cause.
Fusarium oxysporum, F. solani, and possibly Rhizoctonia solani. Fusarium solani and F. oxysporum are isolated from the hypocotyl lesions of 'Essex' seedlings
at 0.01 MPa water potential and temperatures of 15% 20°, or 25°C. Fusarium oxysporum is also isolated, at a high incidence, from cotyledon lesions at a
temperature of 20°C.
Rhizoctonia solani is isolated from hypocotyl lesions at a temperature of 25°C; thus it may produce symptoms when soil temperatures are relatively high and soil
moisture is low at sowing time.
A soilborne viruslike agent also was found associated with Essex disease.
Distribution.
The United States (Delaware and Virginia). The cultivar 'Essex' is severely diseased, but other cultivars are also affected.
Symptoms.
Damping off and reduced seedling emergence occur but are not always observed. Symptoms have been reported to occur when the first true leaves appear bunched,
thickened, and darker green than healthy leaves. Diseased plants are stunted and have reduced numbers of flowers and pods.
Brown or reddishbrown, small, discrete lesions that occur on cotyledons, hypocotyls, and roots of seedlings are uncommon on the roots of older, stunted plants.
Brown, elongated lesions occur on the hypocotylroot transition zone. Fusarium oxysporum is isolated from small, light brown lesions on roots, and F. solani is
isolated from darker brown lesions, particularly on the lateral roots.
Stunting of diseased plants may be common. In low rainfall years, chlorosis and early plant death may occur.
Management.
Not reported.
Frogeye Leaf Spot
Frogeye leaf spot is also called Cercospora leaf spot and frogeye.
Cause.
Cercospora sojina (syn. C. daizu) overwinters as mycelium in seed, primarily in the parenchymatous region of the seed coat, and in infested residue. Conidia are
produced in cotyledonary lesions when infected seed germinates, and on infested residue during warm, moist conditions and disseminated by wind to young host
leaves. All leaves on a host plant may become infected together with pods, stems, and seeds. Severity of frogeye leaf spot is greatest under warm, humid conditions.
Different races of C. sojina exist.

Page 639
Distribution.
In warm, humid areas of the soybeangrowing areas of the world.
Symptoms.
Frogeye leaf spot is primarily a disease of the foliage, but stems, pods, and seeds may also become diseased. Small, circular to angular, redbrown spots form on
diseased upper leaf surfaces. On lower leaf surfaces, the centers of spots are a darker brown or gray because of clusters of dark gray conidiophores. Spots are
discrete, enlarge (15 mm in diameter), and become surrounded by a narrow redbrown border but do not have a chlorotic halo. Older leaf spots become thin,
"paperlike," and transparent. Several spots may coalesce and form large irregularshaped areas on diseased leaves. Severely diseased leaves defoliate prematurely.
Infection of stems and pods occurs later in the growing season. Initially, lesions on stems are elongated and reddish and have a black border. Lesions later become
brown, then light gray, and finally black when the causal fungus starts to sporulate. The circular pod lesions are brown to gray and have a narrow dark brown ring. The
fungus may grow through the pod wall to infect the seed. (See "Cercospora Seed Decay.")
Management
3. Rotate soybean with other crops. Leave field out of soybeans for at least 2 years.
4. Apply foliar fungicides at the R3R5 growth stages.
Fusarium graminearum Seed Infection
Cause.
Fusarium graminearum is reported to be a secondary colonist of oosporeencrusted seeds infected by Peronospora manshurica. Prolonged rainy weather and
mild temperatures during the autumn after soybeans have matured in the field apparently favors colonization.
Distribution.
The midwestern United States.
Symptoms.
Pericarps are stained pink to red. Diseased seeds are contaminated with deoxynivalenol (vomitoxin) and zearalenone.
Management.
Not reported.
Fusarium oxysporum Seed Infection
Cause.
Fusarium oxysporum. Fungus hyphae occur in all layers of the seed coat of diseased seeds but not in the endosperm or cotyledons. Terminal and intercalary
chlamydospores of F. oxysporum form in hyphae growing on the underside of seed coats.

Page 640
Distribution.
Presumably this disease is widespread.
Symptoms.
Diseased seeds become shrunken, are slightly irregularshaped, often have cracks in the seed coat, and have light to dark pink discolored areas over most of the seed
surface. Heavily diseased seeds do not germinate. Diseased seeds that do germinate damp off before and after emergence and seedlings may have a root rot.
Management.
Not reported.
Fusarium pallidoroseum Seed Infection
Cause.
Fusarium pallidoroseum (syn. F. semitectum). Disease occurs in warm and humid conditions. Frequently, the fungus Phomopsis longicolla is also isolated from
diseased tissue.
Distribution.
Where soybean is grown in tropical and subtropical conditions.
Symptoms.
Diseased seed is pink to reddish in color. Germination is somewhat reduced and there are reductions in the root weight and in the dry shoot weight of seedlings.
Management.
Apply a fungicide seed treatment.
Fusarium Root Rot
Cause.
Fusarium spp., including F. solani and F. oxysporum, are common soil fungi that survive as chlamydospores in soil and infested residue, and as saprophytic mycelia
in infested residue. Survival of Fusarium spp. is better at low soil moistures. Seeds and roots of seedlings are infected during dry soil conditions.
Fusarium spp. are also seedborne, infecting seeds under conditions such as insect injury, especially stink bug damage, and high amounts of precipitation before
harvest. A higher incidence of F. solani infection is associated with poorquality seeds than with healthy seeds, possibly because the growth of F. solani is enhanced
by the greater amount of exudation from poorquality seeds than from healthy seeds. Poor stands caused by Fusarium root rot are usually associated with poor seed
quality, heavy rains, soil compaction, or wet soil after sowing. Trifluralin predisposes soybean seedlings to infection by F. oxysporum.
Distribution.
Symptoms.
Infected seed may have poor germination, which results in preemergence or postemergence damping off, or lateemerging seedlings and stunted plants.
Fusarium solani has been reported to cause light to dark brown, sunken lesions on primary and secondary roots. Other Fusarium spp. may cause

Page 641
complete destruction of the root systems of severely diseased plants. Wilting is most frequently observed on seedlings or young plants when roots are rotted and soil
moisture is low. Older plants are seldom killed, but they wilt when soil moisture is low, then recover turgidity at night or when soil moisture again becomes adequate.
Management
1. Seedlings infected with Fusarium spp. and showing signs of wilting or death of lower leaves should not be cultivated until adequate soil moisture is available.
2. When plants are cultivated, soil should be ridged around the bases of the plants to promote development of roots from the stem above the diseased area. These
roots are not as easily infected by Fusarium spp. and help the plants to recover rapidly.
Fusarium Wilt
Fusarium wilt is also called Fusarium blight.
Cause.
Fusarium oxysporum f. sp. tracheiphilum race 1 (syn. F. tracheiphilum), F. oxysporum f. sp. vasinfectum race 2, and F. oxysporum f. sp. glycines. Fusarium
spp. survive as chlamydospores in soil and infested residue and as saprophytic mycelia in infested residue and weed hosts. Mycelium, regardless of its origin,
penetrates roots and grows up the xylem tissue, thereby inhibiting flow of water to the top of the diseased plant. Seedlings and young plants are predisposed to
infection by the soybean cyst, rootknot, and sting nematodes.
Distribution.
Symptoms.
Symptoms generally appear about midseason when the weather becomes warm (28°C has been reported as the optimum temperature) and is accompanied by
moisture stress. The best diagnostic characteristic is a browning or blackening of the vascular system. Wilting of stem tips and the presence of flaccid leaves are the
most common symptoms on young plants. Areas of diseased plants within a field are randomly scattered, round to elongated patches. Leaves on diseased plants may
either become chlorotic or wither and defoliate.
Management.
Some cultivars have a level of resistance.
Leptosphaerulina Leaf Spot
Cause.
Leptosphaerulina trifolii (syn. L. briosiana). Leptosphaerulina briosiana has also been reported to be a causal agent.
Distribution.
Leptosphaerulina trifolii has been reported from India, and L. briosiana from the United States (Maryland and Missouri).

Page 642
Symptoms.
Lesions on both young and old diseased leaves initially are circular, purplish spots whose centers eventually become graytan and contain black perithecia. Later,
lesions become irregularshaped and dull white to gray. In Maryland, small necrotic spots appear on leaves. Symptoms from Missouri were reported to be similar to
those described for soybean sudden death syndrome.
Management.
Not reported.
Mycoleptodiscus Root Rot
Cause.
Mycoleptodiscus terrestris (syn. Leptodiscus terrestris) survives as sclerotia in infested residue and soil. Infection occurs in warm, wet soils. Sclerotia presumably
germinate directly and form mycelia that penetrate roots. Acervuli and conidia are produced in foliar infections, but it is not known what function they perform in the
disease cycle.
Distribution.
The United States. Mycoleptodiscus terrestris is also a pathogen of alfalfa, red clover, and birdsfoot trefoil.
Symptoms.
Postemergence damping off of seedlings is characterized by a brown to black rotting of the roots. Older plants may also develop a root rot that is characterized by a
redbrown decay of the taproot cortical tissues and a destruction of the secondary root system. This symptom is similar to that caused by Rhizoctonia solani.
Because M. terrestris occurs in association with other root rot fungi, distinct symptoms are difficult to diagnose and Mycoleptodiscus root rot may be confused with
other rots.
Leaf infections have occurred in inoculation experiments. Leaf spots are red to light brown and up to 3 mm in diameter. Acervuli form on diseased leaves.
Management.
Not reported.
Myrothecium Disease
Cause.
Myrothecium roridum. Disease development is favored by high temperature and humidity.
Distribution.
Southeast Asia, Brazil, India, and the United States.
Symptoms.
Spots on diseased leaves initially are small (1 mm in diameter), round, and brownish. Spots enlarge (810 mm in diameter), become dark brown, and are surrounded
by translucent concentric zones. Sporodochia appear in the translucent areas as small white erumpent structures that gradually turn dark green and ultimately appear as
black dots surrounded by a slight chlorosis. The necrotic tissue in the center of the spots fails out and gives a shothole effect to the diseased leaves.
Small white dots, which later turn black due to the formation of

Page 643
sporodochia, appear on flowers. Diseased flowers turn brown and drop from the plant. Sporodochia on pods first appear as white dots, similar to those on leaves, but
later turn black and coalesce to form a black mass. Mature pods are less severely infected than young pods.
Management
1. Do not sow infected seed.
Neocosmospora Stem Rot
Neocosmospora stem rot is also called Neocosmospora wilt.
Cause.
Neocosmospora vasinfecta survives either as ascospores in perithecia or mycelium embedded in infested organic matter in soil with a low moisture content. Severity
of Neocosmospora stem rot is greater at higher air temperatures than at lower temperatures. There may be a relationship between Neocosmospora stem rot and soil
nematode infections.
Distribution.
Japan, Nigeria, and the southeastern United States. Neocosmospora stem rot is not considered to be of economical importance.
Symptoms.
Internal symptoms may resemble those of brown stem rot. The primary symptom of diseased stems is a redbrown to dark brown discoloration in the pith and xylem
that extends 20 to 25 cm upward from the soil surface. Redbrown lesions of 20 mm or less in length infrequently occur on the outsides of stems. Orange to red
perithecia may occur on the outsides of the lower stems of dead plants. Interveinal areas of diseased leaves are brown and have chlorotic margins, which results in the
infrequent yellowing and defoliation of lower leaves.
Management.
Not reported.
Phomopsis Seed Rot
Phomopsis seed rot is also called Phomopsis seed decay.
Cause.
Phomopsis longicolla is reported to be the predominant causal organism. However, Diaporthe phaseolorum (syn. D. phaseolorum var. caulivora, D.
phaseolorum var. sojae, and D. sojae), anamorph P. phaseoli (syn. P. batatae, P. glycines, P. sojae, and Phoma subcircinata) also is reported to be a causal
fungus and may well be the dominant causal organism. Other reported names for causal fungi are P. phaseolorum f. sp. sojae and P. phaseoli f. sp. caulivora;
however, these names are not listed in Farr et al. (1989). The nomenclature of the causal fungi remains somewhat unclear, but the causal fungi likely may be the same
fungi that are attributed to being the cause of pod and stem rot. (See ''Pod and Stem Rot.")
Diaporthe phaseolorum is seedborne but most primary inoculum origi

Page 644
nates from mycelia, perithecia, and pycnidia that have overwintered in infested residue. Plants are infected at all growth stages. Ascospores produced in perithecia and
conidia in pycnidia during wet weather are disseminated by wind and splashed by rain to host plants. Two types of conidia—alpha and beta—are produced. Germ
tubes from conidia penetrate leaves and cotyledons through stomata but not directly through the leaf cuticle.
Disease development of pods and seeds is more severe at temperatures above 20°C during wet or humid weather in late summer and autumn when the plant growth
stage is between physiological maturity (R6R8) and harvest. Disease development may also be severe if plants remain unharvested during moist weather after
maturity. Seed infections are usually concentrated at the lower plant nodes but may occur throughout the plant under wet conditions or when harvest is delayed. Close
to 100% relative humidity for prolonged or cumulative periods is essential for seed infection to take place. A cumulative period involves periods of high relative
humidity interrupted by periods of low relative humidity. Secondary infection occurs from conidia produced in pycnidia within diseased tissue.
Disease tends to be more severe in earlysown or earlymaturing cultivars. Plants infected with bean pod mottle virus (BPMV) are more likely to have higher levels of
seed infection than plants not infected with BPMV. This probably is because BPMV delays the rate at which soybean plants lose moisture during the final stages of
seed maturation.
Distribution.
Symptoms.
Diseased seed may have white mycelium growing over it but often does not display any external sign of disease. Severely diseased soybean seeds are shriveled and
elongated, and their coats are cracked and whitish or "chalkyappearing."
Diseased seeds often fail to germinate in wet and cool soils at temperatures of 15° to 20°C. However, researchers do not agree on the exact temperature parameters.
Disease may also reduce emergence and stand establishment when seeds are incubated in dry soil at intermediate temperatures. Soil temperature and moisture
probably influence preemergence damping off by affecting the duration of time that damage occurs to the seed or seedling between sowing and germination or seedling
emergence. Some researchers think low water potential (15 bars) inhibits seedling growth more than the growth of the causal fungi does; however, growth of
Phomopsis spp. still continues at this soil water potential. If diseased seeds germinate, they often give rise to diseased seedlings, which serve as a source of inoculum.
Management.
Resistance to P. phaseoli has been reported to be due to physical characteristics, such as the presence or absence of pores and open or closed microphyles, of
impermeable seed coats.

Page 645
1. Harvest seed as promptly as possible after maturity.
2. Apply a foliar fungicide from mid flowering (R3R4) to late pod stage (R6R7).
Cause.
Phyllosticta sojicola (syn. P. glycinea). In the literature, the specific names "sojicola" and "glycinea" sometimes are spelled "sojaecola'' and "glycineum,"
respectively. Phyllosticta sojicola may be seedborne and also overwinters as pycnidia and mycelia in infested residue. During wet weather, conidia are produced in
pycnidia on residue and disseminated by wind to plant hosts. Phyllosticta leaf spot is favored by cool, wet weather.
Distribution.
Borneo, Bulgaria, Canada, China, Europe, Japan, the United States, and the former USSR.
Symptoms.
Symptoms of Phyllosticta leaf spot can occur on plants of all ages but are most common on the leaves of younger plants. Spots form on the leaf margins of young
plants and grow inward. Spots are dull green initially but later become gray to tan with a dark brown to purple border. The shapes of the spots can be round to oval
(2 cm in diameter), irregular, or Vshaped. Numerous pycnidia appear as small, black specks in the older lesions.
Small, narrow, gray lesions form on petioles and stems; these lesions and purple to redbrown bordered, circular lesions form on pods. Symptoms are often confused
with those of herbicide injury and drought stress.
Management
Phyllosticta Pod Rot
Cause.
Phyllosticta sojicola. The specific name "sojicola" sometimes is spelled "sojaecola" in the literature. Phyllosticta sojicola may be seedborne and also overwinters as
pycnidia and mycelia in infested residue. During wet weather, conidia are produced in pycnidia on residue and disseminated by wind to plant hosts. Phyllosticta pod
rot is favored by cool, wet weather.
Distribution.
Germany and the United States.
Symptoms.
Spots (8 mm in diameter) on pods have dark purplered borders that surround lighter, brownish centers on which numerous dark pycnidia

Page 646
are found. Infection is most severe on pods developing in the upper half of diseased plants.
Management
Cause.
Phymatotrichopsis omnivora (syn. Phymatotrichum omnivorum) survives for several years in soil as sclerotia and hyphal strands. Early in the growing season,
when soil temperatures have risen sufficiently, sclerotia germinate and form hyphal strands that make contact with the developing root systems of host plants. Root
contact is not necessary for planttoplant spread of P. omnivora because mycelial growth through soil occurs in advance of diseased roots. Planttoplant spread
within rows is more common than spread across rows. Phymatotrichum root rot is most prevalent in alkaline soils.
Distribution.
Northern Mexico and southwestern United States.
Symptoms.
Plants wilt rapidly and die. The root cortex is rotted and brown strands of fungal mycelium can be seen growing on the roots.
Management
1. Plowing under a green manure crop, such as sweet clover, lessens the disease severity in succeeding years.
2. Rotate soybean with plants in the grass family.
Phytophthora Root and Stem Rot
Phytophthora root and stem rot is also called Phytophthora root rot.
Cause.
Phytophthora megasperma f. sp. glycinea (syn. P. megasperma var. sojae and P. sojae). Phytophthora macrochlamydospora has been ascribed to be the
cause of a root and stem rot of soybeans in Australia.
Phytophthora megasperma f. sp. glycinea survives primarily as oospores and sometimes as mycelia in soil and infested residue. It is not known for certain how
oospores germinate in wet soils and form sporangia in which numerous zoospores form. The zoospores "swim" through soil water to roots, where they encyst and
germinate at an optimum soil temperature of 15°C. Leaf infection also occurs when infested soil particles are splashed or blown onto host plant leaves during a storm.
Oospores eventually form in diseased roots.

Page 647
Plants may be infected at any stage of growth, but the disease generally occurs early in the growing season. Phytophthora root rot is most common in "wet areas," such
as the low areas of a field; poorly drained soils; compacted soils; and soils with a high clay content. Disease may also occur on welldrained soils during a "wet"
growing season.
Other root rot fungi and northern rootknot nematodes may increase severity of root rot. Trifluralin herbicide and nitrogen added to soil have both been reported to
increase disease severity. On the basis of differing virulences On eight soybean genotypes, 26 physiologic races have been described. Presumably, more races will be
described in the future.
Distribution.
Asia, Australia, Canada, and the United States.
Symptoms.
Distinctive symptoms do not occur during seed rot and preemergence damping off. The most characteristic symptom is the stem rot phase, which is typified by a
brown discoloration of the lower stem and branches. The stem discoloration extends from below the soil line to 20 cm or more above the soil line and may involve
lateral branches near the soil. The taproot is dark brown and the entire root system may be rotted. In cases where the roots do not appear to be rotted the symptoms
can be confused with those of stem canker.
Leaves of diseased plants yellow and eventually become brown but remain attached to the plant. Sometimes there are no obvious symptoms except stunted plants that
are reduced in vigor. This latter symptom is often difficult to recognize without a sidebyside comparison with a resistant cultivar.
The disease pattern varies within a field but is often roughly circular, corresponding to the poorly drained areas, but can be linear from dead or dying individual or
groups of plants in a row. Diseased plants may often be found more easily at the end of rows than within a field.
Management
1. Grow resistant cultivars; however, several physiologic races of P. megasperma f. sp. glycinea exist and cultivars resistant to one race may be susceptible to others.
Soybean isolines with the Rpslk gene for resistance are also tolerant to the herbicide metribuzin. Several genes that confer resistance to specific races at the low
optimum temperature of 24°C are defeated by these races at the high optimum temperature of 32°C.
2. Apply systemic fungicide as a seed treatment and/or to the soil either as a band or an infurrow treatment. Greater amounts of fungicide are needed at the high
optimum temperature of 32°C to reduce disease severity than at lower temperatures (24° to 28°c).
3. Sow in welldrained soils that are warmer than 18°C.
4. Avoid growing susceptible cultivars in soils where disease has occurred.

Page 648
Pod and Stem Rot
Although the cause and general etiology of pod and stem rot are similar to Phomopsis seed rot, they are usually discussed as separate diseases. Pod and stem rot is
also called pod and stem blight.
Cause.
Diaporthe phaseolorum (syn. D. phaseolorum var. caulivora, D. phaseolorum var. sojae, and D. sojae), anamorph Phomopsis phaseoil (syn. P. batatae, P.
glycines, P. sojae, and Phoma subcircinata). Phomopsis longicolla is also a causal fungus and many researchers consider it to be the primary cause of seed decay.
Other reported names for causal fungi are P. phaseolorum f. sp. sojae and P. phaseoli f. sp. caulivora. The nomenclature of the causal fungi remains somewhat
unclear.
Diaporthe phaseolorum is seedborne but most primary inoculum originates from mycelia, perithecia, and pycnidia that have overwintered in infested residue. Plants
are infected at all growth stages. Ascospores produced in perithecia and conidia in pycnidia during wet weather are disseminated by wind and splashed by rain to
plant hosts. Two types of conidia—alpha and beta—are produced. Germ tubes from conidia penetrate leaves and cotyledons through stomata but not directly through
the cuticle. The fungus infects all parts of the soybean seed, including the seed coat, cotyledons, and embryo.
Diseased seeds often fail to germinate in wet soils at temperatures of 15° to 20°C. However, disease may also reduce emergence and establishment when seeds are
incubated in dry soil and intermediate temperatures (see "Phomopsis Seed Rot"). In the latter case, low water potential probably inhibits seedling growth more than
does the growth of the causal fungi, particularly Phomopsis spp. If infected seeds germinate, they often give rise to infected seedlings that serve as a source of
inoculum.
Disease development of pods and seeds is more severe if temperatures are above 20°C and wet weather occurs when plants are between physiological maturity (R6
R8) and harvest, or if plants remain unharvested after maturity. Phomopsis longicolla infects seeds during or after the yellow pod stage (R7). Seed infections are
usually concentrated at lower plant nodes but may occur throughout the plant when conditions are wet or harvest is delayed. Close to 100% relative humidity for
prolonged or cumulative periods is essential for seed infection to take place. A cumulative period involves periods of high relative humidity interrupted by periods of
low relative humidity. Secondary infection occurs from conidia produced in pycnidia.
Disease tends to be more severe in earlysown or earlymaturing cultivars. Plants infected with bean pod mottle virus (BPMV) are more likely to have high levels of
seed infection than plants uninfected with BPMV.
Distribution.
Symptoms.
Although soybeans are infected earlier in the growing season,

Page 649
symptoms of disease appear on pods and stems of diseased plants nearing maturity, especially if wet weather occurs at this time. The first symptom is the presence of
pycnidia on petioles that have fallen from the lower portions of plants to the soil surface. This is a good indication that pod and stem blight may be a potential problem
during the current growing season. The best symptom is the presence of numerous small, black pycnidia arranged in linear rows on stems but scattered randomly over
pods. During dry weather, pycnidia may be present only on lower stems or nodes.
Diseased seed may have white mycelium growing over the seed coat but often may not display any external signs of disease. Severely diseased seeds are shriveled,
elongated, have cracked seed coats, and are whitish and "chalkyappearing." Infected seeds germinate poorly and may damp off either before or after emergence,
resulting in a poor plant stand. The fungus may also become systemic but fail to induce symptoms in seedlings grown from infected seeds.
Management.
Resistance to P. phaseoli has been reported to be due to physical characteristics, such as the presence or absence of pores and open or closed microphyles, of
impermeable seed coats.
1. Harvest seed as promptly as possible after maturity.
2. Apply a foliar fungicide from midflowering (R3R4) to late pod stage (R6R7).
Pod Rot and Collar Rot
Cause.
Fusarium pallidoroseum (syn. F. semitectum) is seedborne.
Distribution.
India (from seed received from the United States).
Symptoms.
Plants having rotted pods do not show any other symptoms than less vigorous growth compared to healthy plants. All pods on diseased plants show drying symptoms
characterized by a black discoloration that starts from the distal end. Severely diseased pods produce no seeds, or if seeds are present, they are black, rotted, and
shriveled. Diseased pods are blackish on both inner sides, especially where the seed rests. Seed coats and cotyledons of diseased seeds also are black.
Seedlings initially have watersoaked, depressed, creamcolored lesions on cotyledons and hypocotyls. Lesions soon become dark brown to black and sometimes
coalesce and form enlarged spots on the diseased cotyledons. Spots enlarge longitudinally on the hypocotyl to the radicle. Seedlings eventually die.
Management.
Not reported.

Page 650
Powdery Mildew
Cause.
Microsphaera diffusa overwinters as cleistothecia on infested residue. Primary infection occurs from ascospores produced in cleistothecia and disseminated by wind
to host plants. Secondary infection occurs from conidia produced on diseased leaves and disseminated by wind to plant hosts. Development of powdery mildew
occurs later in the growing season during humid weather but without the presence of free water. Cooler than normal temperatures have been observed to favor
disease.
Distribution.
Brazil, Canada, China, Peru, South Africa, and the United States.
Symptoms.
Powdery mildew becomes evident about the middle of the growing season. Cotyledons, stems, pods, and leaf surfaces are diseased. Small colonies of thin, light gray
mycelia are seen on the upper surface of diseased leaves. In time, diseased areas enlarge, cover much of the diseased leaf surface, and have a white, powdery
appearance due to large numbers of conidia and conidiophores. Diseased plants may become chlorotic and display green islands and rusty patches on diseased
leaves. Luxuriant fungal growth may occur without the other symptoms.
Yield losses of up to 26% have been reported.
Management
1. Grow resistant cultivars. Some cultivars are susceptible as seedlings but not as adult plants. Reaction of soybeans is controlled by three alleles at the Rmd locus:
Rmdc confers resistance throughout the life of the soybean plant, Rind provides resistance at the adultplant stages, and rmd conditions susceptibility.
Purple Stain
Purple stain is also called Cercospora blight and leaf spot, lavender spot, purple blotch, purple speck, purple spot, and purple seed stain.
Cause.
Cercospora kikuchii (syn. Cercosporina kikuchii) overwinters as mycelium in seed coats and infested residue but rarely in embryos and cotyledons. Infected seed
gives rise to seedlings with infected cotyledons. Often seed coats slip off germinating seed before the cotyledons become infected. During warm, humid weather,
conidia are produced on diseased cotyledons and disseminated by wind and splashing rain to leaves, stems, and pods of host plants.
Seeds become infected when pods are inoculated with a conidial suspension. No infection of seeds occurs when flowers in full bloom or postbloom (desiccated
petals) are inoculated. In general, disease incidence increases with increasing pod wetness periods up to 30 hours. Some

Page 651
researchers have reported a minimum of 8 hours of dew is necessary for infection to occur, with 24 hours of dew being the optimum. However, other reports have
stated no disease occurs when pod wetness is less than 24 hours. Various optimum temperatures for infection have been reported in the 20° to 24°C range and at 25°
C. Schuh (1992) reported 25°C was the optimal temperature for infection.
Mycelium grows through pods and into seed coats through the funiculus. The fungus grows intercellularly in plant tissues, where nutrients are acquired through
membrane leakage caused by cercosporin.
Isolates from the weeds cocklebur, Xanthium strumarium; pitted morning glory, Ipomoea lacunosa; prickly sida, Sida spinosa; sicklepod, Cassia obtusifolia;
small flower morning glory, Jacquemontia tamnifolia; and spotted spurge, Euphorbia maculata caused lesions on the hypocotyls, cotyledons, stems, and leaves of
soybeans, and purple stain on seeds of soybeans. Conidia are dispersed by water from dead weeds to developing soybean seedlings. Weeds were colonized and
conidia produced on dead weed tissue, but no disease symptoms occurred on weeds.
Differences in pathogenicity apparently exist among isolates. Cercospora kikuchii isolates are divided into three groups based on colony coloration caused by
cercosporin, a red photoreactive polyketide, on potatodextrose agar. Cercospora kikuchii cp isolates produce a purple coloration, C. kikuchii cy isolates produce
a yellow background due to lipids, and C. kikuchii cc isolates produce a red coloration. Cercosporin may facilitate soybean seed coat tissue colonization by C.
kikuchii.
Distribution.
Symptoms.
Reduced seed size and yield losses result from purple stain. The best diagnostic symptom is a pale to dark purple discoloration, caused by cercosporin, that is thought
to be restricted only to seed coats. Some researchers have reported that C. kikuchii penetrates embryonic seed tissues and causes necrosis of cotyledonary cells and
vascular elements. However, this discoloration may be uncommon because others have stated that cotyledons are generally not infected or discolored.
Infected seeds can produce diseased seedlings with cotyledons that are shriveled and dark purple and defoliate prematurely. In the laboratory, germination is reduced
and stunted, low vigor seedlings result from soybean seeds when 50% or more of the seed coat is stained purple.
The fungus grows from cotyledons into stems, causing a necrotic area that may kill plants. Late in the season, thickened, and crustyappearing redbrown spots
develop on diseased leaves. There is no effect on maturity, lodging, and plant height. Yields are not reduced, but the value of the seed is lowered from a grading
standpoint. The purple discoloration does not affect seed used for processing since heating causes the discoloration to disappear.

Page 652
Certain isolates will reduce seed density and weight, increase free fatty acid content and protein, and reduce oil content when compared to inoculation with other
isolates.
Seedling emergence from purplestained seeds is lower than from healthy seeds. Prior infection with C. kikuchii reduces infection by other seedborne fungi,
particularly Diaporthe phaseolorum and Phomopsis spp. This may be explained, in part, by competition for nutrients or space. Another explanation is C. kikuchii
and other Cercospora spp. produce a nonspecific toxic compound, cercosporin, which is reported to be antagonistic to seedborne fungi of soybean.
There has been reported to be no difference in the incidence of purple stain on seed between plants arising from seeds with purple stain and from "healthyappearing"
seed free of purple stain.
Management
3. Grow latematuring cultivars, which in general are less susceptible than earliermaturing cultivars.
4. Some cultivars are moderately resistant.
Pyrenochaeta Leaf Spot
Pyrenochaeta leaf spot is also called Dactuliophora leaf spot, Pyrenochaeta leaf blotch, and red leaf blotch.
Cause.
Pyrenochaeta glycines (syn. Dactuliochaeta glycines and Dactuliophora glycines) overseasons as pycnidia and sclerotia. Optimum pycnidiospore germination is
at temperatures from 20° to 25°C.
Sclerotia are disseminated in contaminated soil during farming operations and may be splashed onto leaf surfaces by rainfall, where they germinate by forming infective
mycelium. Incidental dissemination may occur through seed lots contaminated with infested residue and soil peds carrying sclerotia. The disease cycle is not fully
understood, but pycnidia may develop from mycelium or directly on sclerotia. Both pycnidia and sclerotia apparently develop in lesions and are returned to soil upon
the defoliation and decomposition of diseased leaves. Red leaf blotch occurs during abundant rainfall and high humidity.
Distribution.
Cameroon, Ethiopia, Malawi, Nigeria, Rwanda, Uganda, Zaire, Zambia, and Zimbabwe.
Symptoms.
Lesions occur on diseased leaves, petioles, pods, and stems throughout the growing season and are often associated with primary leaf veins. Initially, dark red to
brown, circular to angular lesions (13 mm in diameter) appear on unifoliate leaves. Later, dark red spots develop on the upper surfaces and redbrown spots with
dark borders develop on the

Page 653
lower surfaces of diseased trifoliate leaves. A diffuse mycelial growth may surround lesions during high humidity. Lesions enlarge, coalesce, and form irregularshaped
blotches (310 mm in diameter) with buffcolored centers and dark margins. Older blotches merge and form large necrotic blotches (up to 2 cm in diameter) that are
surrounded by chlorotic halos. Necrotic tissue frequently falls out and gives a shothole appearance to diseased leaves. Diseased plants defoliate prematurely.
Lesions occur on stem petioles and pods below the uppermost leaf with symptoms. Petiole and pod lesions are ovoid (15 mm long) and mauve to redpurple.
Sclerotia develop primarily on the diseased lower leaf surfaces, and pycnidia develop in blotches on the upper leaf surfaces. Yield loss resuits from reduced seed size.
Management.
No measures are recommended.
Pythium Damping Off and Rot
Cause.
Pythium aphanidermatum, P. debaryanum, P. irregulare, P. myriotylum, P. torulosum, and P. ultimum. Pythium aphanidermatum, P. debaryanum, and P.
ultimum survive as oospores in soil and infested residue and saprophytically as mycelia in infested residue. At low temperatures (10° to 15°C) and wet soil, oospores
of P. debaryanum and P. ultimum germinate and form sporangia. Zoospores form in sporangia and "swim" through soil water to seed or to the roots of seedlings. At
higher temperatures, oospores may germinate directly and form germ tubes. Although soybean seed sown in cool and wet soil is most subject to infection by Pythium
spp., P. aphanidermatum is reported to cause disease at temperatures of 25° to 36°C.
Seedlings are most susceptible to infection. Soybeans become progressively more resistant as they grow older.
Distribution.
Wherever soybean is grown. Disease is most prevalent under wet soil conditions.
Symptoms.
Pythium damping off and rot may occur from the time seed is sown to the end of plant flowering. However, the disease is usually associated with seed rotting in the soil
or young seedlings being killed. Diseased plants occur singly, in small circular groups in the low, wet spots within the field, or uniformly over an entire field if there has
been a period of rain.
Diseased seeds may not germinate and become soft and overgrown with other fungi and bacteria, which give them a "fuzzy" appearance. Seedling rot or blight results
from infection after seed has germinated but before or just after the seedling has emerged through the soil. Roots infected by P. ultimum are brown and have a "wet"
or watersoaked appearance. Other symptoms attributed to P. ultimum include swollen hypocotyls and lesions at the junction of the hypocotyl and primary root.
Diseased seedlings may also have a curling growth habit and reddish to brown lesions on

Page 654
hypocotyls and cotyledons. Plants infected after emergence, wilt, and leaves are graygreen initially but become brown after one or two days. Such diseased plants are
easily pulled from the soil. As soil dries up, a diseased root resembles a "shoestring" attached to the cotyledon.
Pythium debaryanum causes the growing point to be retarded, which resuits in a "baldhead" symptom.
Pythium torulosum causes a seed rot or death of germinated seeds. On 2weekold or younger soybean seedlings, root tip discoloration and yellow lesions occurred
on the roots and hypocotyl base.
Management
2. Do not sow carryover seed or seed that has a high percentage of broken seed coats.
3. Sow highquality, highgerminating seed.
4. Grow soybean cultivars that are more resistant than others.
Red Crown Rot
Red crown rot is also called black root rot, Calonectria root rot, and Cylindrocladium root rot.
Cause.
Calonectria crotalariae, anamorph Cylindrocladium crotalariae. Cylindrocladium clavatum, Cylindrocladium floridanum, and Cylindrocladium scoparium,
and Calonectria ilicicola are also reported to be causal fungi on soybean.
Calonectria crotalariae overwinters as small (35425 m in diameter), irregularshaped microsclerotia that serve as primary inoculum. Microsclerotia germinate and
form hyphae that infect roots. The role of ascospores and conidia in the life cycle of red crown rot is not known. Colonization of lateral and taproots is optimum at a
temperature of 25°C.
Nematodes have been reported to increase injury by the causal fungus.
Distribution.
Possibly Brazil, Cameroon, Japan, Korea, and the southern United States.
Symptoms.
In Brazil, Cylindrocladium clavatum causes disease symptoms on soybeans identical to those caused by Cylindrocladium crotalariae. Individual plants or groups
of plants may show symptoms. The first symptom at early pod set (R3R4) is a yellowing of the top leaves of diseased plants. Later, interveinal tissue becomes brown
and defoliation occurs without wilting of the leaves. The insides of stems are graybrown and entire root systems become rotted. After stem tissue is killed, redorange
perithecia develop from 2.5 to 7.5 cm above the soil line.
Management
2. Delayed sowing will reduce initial inoculum.

Page 655
3. Experimentally, the application of glyphosate has been shown to reduce the incidence of disease.
Rhizoctonia Aerial Blight
Rhizoctonia aerial blight is also called aerial blight, foliage blight, Rhizoctonia foliage blight, and web blight.
Cause.
Rhizoctonia solani AG1 is a common soil fungus and an excellent saprophyte. Rhizoctonia solani survives as sclerotia and as saprophytic mycelium in soil and
infested residue for several years. In greenhouse inoculation studies, Rhizoctonia solani AG1 also infected several weed hosts and grew from the diseased weed to a
nearby soybean plant, demonstrating a potential overwintering site for the fungus.
Rhizoctonia solani AG1 IA produces sasakiitype sclerotia on diseased tissue (aerial blight) and R. solani AG1 IB and IC produce abundant microsclerotia on
diseased tissue (web blight) that function as airborne propagules and cause secondary infection. During prolonged warm, humid weather, soil or plant parts that
contain propagules of R. solani are splashed onto the lower plant leaves. Uninterrupted free moisture is most conducive to disease development. High humidity and
warm temperatures also favor disease development but encourage mycelial growth and sclerotial formation within lesions on diseased leaves.
Withinrow plant populations have no significant effect on disease or yield. Row spacings of 50 cm or more results in decreased disease but yields may be less than in
narrower rows because higher plant populations compensate for the increase in disease.
Rhizoctonia solani AG1 also causes seed and seedling rot. Infected seedlings serve as an inoculum source for the formation of disease foci. Isolates that cause
foliage blight on soybeans may not necessarily cause root and stem rot. (For further information, see ''Rhizoctonia Damping Off, Root, and Stem Rot.")
Distribution.
Brazil, China, India, Japan, Malaysia, Mexico, the Philippines, and the United States (including Puerto Rico).
Symptoms.
Aerial blight is characterized by the production of sasakiitype sclerotia on diseased tissue. Aerial blight first appears on diseased lower leaves, pods, and stems and
gradually progresses up the plant. Mycelia of the pathogen spread in the canopy by means of mycelial bridges between leaves, pods, and stems.
Lesions on diseased leaves vary from small spots to entire leaves being affected. Symptoms usually start at the bases of leaflet petioles with subsequent spread in a
fanshaped pattern to the rest of the leaflet. Lesions initially are watersoaked and graygreen, and the mycelium advances on the leaf surface ahead of the lesion
margin. Lesions become necrotic and dark brown to tan with a redbrown margin. Diseased areas that generally fall

Page 656
out during dry weather give leaves a ragged appearance. Diseased leaves droop down and severely diseased plants may be defoliated.
Web blight is characterized by the production of abundant microsclerotia on diseased tissues during the growing season. The microsclerotia function as the airborne
propagules that cause secondary infection. Microsclerotia infections serve as numerous foci for small circular lesions on diseased leaves.
Most stem infections occur at or below the soil line before the stems turn green. Lesions on stems and petioles initially appear as reddish, oval to linear, watersoaked
areas that become light brown, greenbrown, or redbrown. Later, lesions change color to tan, brown, or black, sometimes have redbrown margins, and dry up.
Sasakiitype sclerotia form when hypocotyls or stem lesions cease expanding.
Pods have small brown spots on them or the entire pod may be diseased. Symptoms of seed and seedling rot are circular lesions on the hypocotyls or the growing
points. Infection of the growing point stops further growth of the seedlings.
Management
1. Adjust time of sowing to avoid periods of high moisture.
2. Do not sow plants too thickly.
3. Apply foliar fungicide during reproductive phases.
Rhizoctonia Damping Off, Root, and Stem Rot
Cause.
Rhizoctonia solani AG4, AG5, and AG22, teleomorph Thanatephorus cucumeris, are common soil fungi and excellent saprophytes. Rhizoctonia solani
survives as sclerotia or saprophytic mycelia in soil and infested residue for several years. During wet soil conditions, sclerotia germinate and form mycelia, or mycelia
grow from precolonized residue and infect seeds, roots, and hypocotyls. Following wet soil conditions, root rot is favored by low temperatures that are followed by
warm temperatures (25°29°C optimum). Disease development is most severe on young plants.
Rhizoctonia solani AG1, the cause of Rhizoctonia foliar blight (aerial blight or web blight), also infects soybean seedlings. Diseased seedlings then become sources
of inoculum by producing mycelia that infect neighboring host plants. Seedling infection at an early stage thus has a significant effect on subsequent disease
development.
Distribution.
Symptoms.
Rhizoctonia root rot is first noticed as plants wilt and die during warm weather early in the growing season. The disease pattern within a field will vary from a single
plant or groups of dead plants in a row or in circular areas where the soil moisture is higher than in other areas of the field.

Page 657
Typical symptoms are decay of lateral roots and localized brown to redbrown lesions on diseased hypocotyls and lower stems that do not extend above the soil line.
The redbrown color is a good symptom to diagnose the disease, but it is best observed immediately after removing plants from soil because the color fades upon
exposure to air. The discoloration is usually limited to the cortical layer of main roots and hypocotyls and does not extend into the roots or stems. Diseased stems
remain firm and dry. Although Rhizoctonia root rot is associated with young plants, older plants may die if there is moisture stress and the diseased hypocotyls and
roots are sufficiently decomposed to limit uptake of water.
Management
1. Ridge soil around the bases of plants during cultivation to promote root growth above the diseased portions on the plant stem.
2. Apply seedprotectant fungicide.
3. Use good soil drainage.
Rust
Cause.
Phakopsora pachyrhizi is the causal agent of rust in Asia and Australia, and P. meibomiae is the causal agent of rust in the Americas. The pycnidiospore and
aeciospore stages are unknown. Teliospores form but have not been observed to germinate. Urediniospores are the overseasoning structures and are found on other
leguminous host plants the entire year in warm climates. Urediniospores are disseminated by splashing rain and wind. Upon germination, the resulting germ tube
penetrates directly through the cuticle or through stomates.
Infection occurs with a minimum of 6 hours of free moisture (8 hours is optimum) and optimal temperatures of 18° to 26.5°C. Urediniospores on dry foliage lose
infectivity in 1 to 2 days during sunny conditions but maintain infectivity under cloudy conditions. Phakopsora pachyrhizi has a wide host range that includes several
leguminous plants. Races of P. pachyrhizi exist.
Distribution.
Australia, Brazil, China, Colombia, Costa Rica, Japan, Korea, Taiwan, and the United States (Puerto Rico).
Symptoms.
The most commonly observed symptom is the sporulating uredinia on diseased lower leaf surfaces. Two infection types, tan (TAN) and reddish brown (RB), are
recognized. The RB lesion type signifies at least partial resistance. At the onset of disease, chlorotic or graybrown spots appear on diseased leaves and less frequently
on petioles and young stem tissues. On leaves, spots enlarge to about 1 mm square and become redbrown or tan lesions that are delineated by secondary or tertiary
leaf veins. Type RB has 02 uredinia on the abaxial surface, while TAN has 25 uredinia on the abaxial surface.

Page 658
Young lesions of soybean rust are identical to those of bacterial pustule except for the chlorotic ring around the bacterial pustule lesion. As bacterial pustules mature, a
crack or split occurs down the middle of the pustule. In contrast, rust uredinia have a distinct pore that has whitish urediniospores, which have been forced through the
pore opening, clumped around it. The lesion area and number of uredinia per lesion is greater on younger than on older leaves. Severely diseased plants are defoliated
and have reduced pod formation, seed numbers, and seed weights.
Management
1. Apply a foliar fungicide during the growing season.
2. Some accessions of soybean have resistance. Resistance has also been identified in accessions of the perennial Glycine spp., G. argyrea, G. canescens, G.
clandestina, G. latifolia, G. microphylla, and G. tomentella.
Scab
Cause.
Sphaceloma glycines.
Distribution.
Japan.
Symptoms.
Somewhat circular (4 mm in diameter), buffcolored fading to gray, and slightly raised lesions center on the veins of both leaf surfaces. Stem lesions are tiny, elliptical
spots that eventually coalesce and form large buffcolored areas (up to 2 cm long) that sometimes have redbrown margins. Pod lesions are initially red to brown but
become black with pale centers and redbrown margins at maturity. Seeds do not develop in diseased pods.
Management.
Soybean accessions with resistance are known.
Sclerotinia stem rot is also called Whetzelinia stem rot and white mold.
Cause.
Sclerotinia sclerotiorum (syn. Whetzelinia sclerotiorum). Sclerotinia minor has been associated with a Sclerotinia stem rot in Virginia. Sclerotinia sclerotiorum
survives as sclerotia for at least 18 months at soil depths of 5 to 30 cm and for about 12 months on the soil surface. Sclerotinia sclerotiorum is also seedborne after a
wet autumn.
During periods of high moisture, sclerotia germinate and either form several apothecia or mycelium. An apothecium forms at the end of a stipe and asci, each
containing eight ascospores, form in a layer on the apothecial surface. Ascospores disseminated by wind to host plants, germinate under moist conditions and
moderate air temperatures (20° to 28°c), and infect host plants of all ages. However, infection increases when the plant canopy closes, causing moderate temperatures
and higher humidity within the canopy.

Page 659
Spores initially colonize senescing flowers to obtain energy to parasitize living tissue on the same plant. When plants are crowded or become lodged, the fungal mat
may spread to other host plants and infect them.
Eventually, sclerotia form in piths, on stems, and, rarely, in pods. Since sclerotia are roughly the same size as soybean seed, they are "harvested" along with seed and
are "sown" with seed the following spring. The incidence of Sclerotinia stem rot in a field is determined primarily by the quantity of sclerotia in the field. Disease
development is favored by wet weather.
Several plant species are hosts.
Distribution.
Brazil, Canada, Hungary, India, Nepal, Nigeria, South Africa, and the United States.
Symptoms.
Seedlings damp off and some cultivars have brown lesions. Infection of older plants originates at stem nodes 10 to 50 cm above the soil line. Watersoaked lesions
progress acropetally and basipetally from the infected node along the stem and side branches. A white, cottonlike growth of mycelium occurs over the stem surface.
Mycelia and numerous round to oblong, dark brown to black sclerotia are produced in diseased stems and on plant surfaces. Many sclerotia are approximately the
same size and shape as seed.
Plants are killed when S. sclerotiorum girdles stems. On older plants (R2R3 growth stage), leaves wilt and remain attached to the plant for a long time. Diseased
seed is discolored, flattened, and smaller than healthy seed. Pods are rarely formed on the lower portions of diseased stems.
Management
1. Practice any cultural method that promotes drying out of the canopy, including growing soybean cultivars that do not readily lodge and sowing in rows wider than
50 cm apart. Sclerotia buried less than 2.5 cm in the soil often do not remain viable for more than 1 year. Deeply buried sclerotia may remain viable for 8 to 10 years.
Deep plowing may remove sclerotia from providing inoculum the next year, but in future years, they may be returned to the surface, where they could germinate.
2. Do not rotate soybean with other susceptible plants.
3. Reduce irrigation before the R1 growth stage.
Southern Blight
Southern blight is also called sclerotial blight and southern stem blight.
Cause.
Sclerotium rolfsii overwinters as sclerotia in soil and as mycelia in infested residue and seeds. Mycelia from sclerotia, residue, or seeds serve as primary inoculum.
High soil temperatures, relatively dry soil, and a low soil pH of 3 to 6 favor disease development. High relative humidity stimu

Page 660
lates aerial growth of mycelia on stems, branches, and leaves. Cool temperatures in the winter kill sclerotia and mycelia.
Distribution.
Wherever soybean is grown in tropical and subtropical areas, but southern blight has also been reported from temperate soybeangrowing areas.
Symptoms.
Disease is most severe in sandy soils during high soil and air temperatures. Preemergence damping off may occur. The best symptom is a white cottonlike mycelial
growth on diseased stems near the soil surface. Abundant tan to dark brown sclerotia the size of mustard seeds form on the surfaces of the mycelia. Disease on leaves
is infrequent but occurs when infested soil particles are disseminated to leaves. Leaf spots, which are circular (612 mm in diameter) and brown with concentric
markings, may have a clump of white mycelium with a sclerotium in the middle.
Management
1. Grow soybean cultivars that have resistance or tolerance.
3. Plow infected soybean residue 12 cm deep or deeper.
4. Apply lime to acid soils to obtain a pH of 6.5 to 7.0.
Stem Canker
Stem canker is also called soybean stem canker and southern stem canker when caused by southern isolates of Diaporthe phaseolorum.
Cause.
Diaporthe phaseolorum (syn. D. phaseolorum vat. caulivora), anamorph Phomopsis phaseoli. However, many researchers prefer to distinguish between the
northern and southern isolates of D. phaseolorum. Some refer to Diaporthe phaseolorum var. meridionalis as the southern or southeastern pathogen and retain the
name D. phaseolorum var. caulivora for the midwestern pathogen. Others refer to the southern or northern biotypes of D. phaseolorum var. caulivora.
Since the two pathogens are in genetically distinct vegetative compatibility groups, they exhibit different behavior. Isolates of D. phaseolorum from Iowa differ in
morphology and pathogenicity compared to isolates from the southern United States. At temperatures from 10° to 35°C, mycelial growth of southern isolates equals
or exceeds that of northern isolates. Mycelial growth of northern isolates is inhibited at 30°C, while southern isolates maintain maximum growth rates. Pathogenicity of
a southern isolate on soybean seedlings is not affected at temperatures of 21° to 30°C, but northern isolates are almost completely nonpathogenic at 30°C. The two
pathogens differ in their sensitivity to benomyl and triadimefon. At least two physiologic races are reported to exist.
The causal fungi are seedborne and overwinter as perithecia in infested residue and seeds. Seed infection is reported to be primarily internal. In

Page 661
fected seed gives rise to seedlings with diseased cotyledons, which serve as sources of further infection. However, because of the low levels of infected seed, poor
emergence of infected seed, and no effective secondary dissemination, there is little chance of an epiphytotic resulting directly from the sowing of infected seed. Also,
several weeds are hosts and may serve as potential sources of inoculum.
In the spring, ascospores are produced in perithecia during wet weather and disseminated by wind to host plants. Both perithecia and pycnidia of D. phaseolorum
var. caulivora are reported to develop on stems incubated at temperatures of 15°, 20°, 25°, and 30°C. Once spore deposition has taken place, either a prolonged
continuous wetting event or several discontinuous wetting periods will facilitate infection and subsequent disease development. It is reported that more than 24 hours
(120 to 144 hours maximum) of free moisture preceding a dry period are required for disease development.
Optimum temperatures for infection vary somewhat. Infection by both ascospores and conidia occurs at temperatures from 10° to 34°C (the optimum is 21°C). In
greenhouse trials in Arkansas, optimum infection occurred at temperatures from 22° to 30°C accompanied by 40 hours of leaf wetness. Because D. phaseolorum is a
splashdispersed pathogen, infection is likely to occur after a rain that is followed by dew periods of at least 24 hours and temperatures from 22° to 30°C.
Younger plant parts are more susceptible to infection by D. phaseolorum f. sp. meridionalis than older plants. Specifically, plants exposed to inoculum from
emergence to V3 stage become more diseased than plants exposed from the V3 through V10 stage. Most infections occur on lower leaf blades and petioles and not
directly through leaf scars or stem wounds.
Earlysown soybeans are more susceptible to D. phaseolorum var. caulivora than latersown soybeans. Seed infection occurs at 20°C and warmer and high relative
humidities up to 100% for prolonged periods at growth stages R6 to R8.
Stem canker is most severe under notill conditions because infested residue is in close proximity to aboveground plant parts. Disease incidence and severity were
reported to be significantly greater in soybean/wheat doublecropping than in soybean monocultures in the southern United States. Diaporthe and Phomopsis isolates
from cotton leaves and seedlings may also incite stem cankers on soybeans. Thus, cotton may serve as an alternate source of inoculum in warmer climates. However,
cropping system effects may relate to symptom expression rather than plant infection.
In greenhouse tests, a 50% defoliation by the soybean looper, Pseudoplusia includens, reduced canker length and mortality. Canker lengths were also reduced on
soybean cyst nematodeinfected plants.
When introduced into soybean plants, Diaporthe phaseolorum is reported to have produced a phytotoxin that caused symptoms characteristic of stem canker.

Page 662
Distribution.
Canada and the United States.
Symptoms.
Stem canker appears about midseason and continues until plant maturity. Plants infected during vegetative growth remain asymptomatic until they enter the
reproductive phase of growth 6070 days after sowing. Patches of scattered dead plants that still have their leaves attached occur in fields.
At first, small brown lesions occur on cotyledons, then extend into stems and kill diseased plants. On the lower part of diseased stems, small redbrown lesions occur
on leaf scars (after the petioles have fallen) and on nodes. Lesions progress acropetally, becoming sunken necrotic cankers that eventually girdle stems and cause the
upper part of a diseased plant to die. Cankers are usually unilateral and delimited by healthy tissue.
The lesions near the soil line can be confused with symptoms of Phytophthora root rot, but stem canker lesions can occur higher on the stem than those of
Phytophthora root rot. After plant death, perithecia may be seen as tiny black dots aligned in rows on stems and scattered randomly over pods.
Yield loss occurs when plants are killed before complete pod fill.
Management
2. Plow infested residue in the autumn, if possible, to hasten the decay of residue and reduce the level of inoculum.
Stemphylium Leaf Blight
Cause.
Stemphylium botryosum.
Distribution.
India.
Symptoms.
Initially, small, circular, necrotic spots with dark brown margins and gray centers appear on diseased leaves of all ages. Later, spots enlarge and coalesce, especially
along the leaf margins. A dark green fungal growth occurs on the surfaces of spots. Eventually, leaves dry up and defoliation occurs.
Management.
Not reported.
Sudden Death Syndrome
Cause.
Fusarium solani f. sp. glycines is a bluepurple to bluish, slowgrowing isolate of F. solani, which formerly was called strain A or form A (FSA or FSA). The
teleomorph is Nectria haematococca.

Page 663
Fusarium solani f. sp. phaseoli, which formerly was called strain B or form B (FSB or FSB), also is found associated with soybean roots but is now considered to
be the cause of seedling disease and root rot only. However, some researchers have considered sudden death syndromeinciting isolates of F. solani to be F. solani
f. sp. phaseoli, a subgroup within F. solani f. sp. phaseoli, or possibly a separate forma specialis.
Production of macroconidia by F. solani f. sp. glycines occurs on lower stems and roots of symptomatic plants. Sporulation occurs on taproots 10 cm or more
below the soil line. It is presumed that such sporulation contributes to the inoculum density of F. solani f. sp. glycines in soils. It is likely conidia produced on plants
are washed into soil and convert to chlamydospores. The fungus then resides in soil and in root debris mainly as chlamydospores, which constitute the primary
inoculum. Fusarium solani f. sp. glycines likely penetrates roots directly. Colonization appears to be limited primarily to cortical tissue of the root and lower stem.
Hyphae grow mainly intracellularly.
Fusarium solani f. sp. glycines infects roots in highyield environments. Cool temperatures during early soybean reproduction favor disease development. Symptom
development is greater when inoculated plants are incubated at 25°C than at 35°C. However, some researchers determined foliar symptoms were most severe from
22° to 24°C and root symptoms were most severe at 15°C. Disease is more severe on most soybean cultivars when they are sown early; however, the reverse was
true for some cultivars in Kentucky, but other cultivars were unaffected. High soil moisture favors disease development. Sudden death syndrome is prevalent in
irrigated fields or in fields with high soil moisture following rain.
Disease development may increase during the change from vegetative growth to reproductive growth because of the change in host physiology. As plants enter
reproductive development, net root growth is dramatically reduced and photosynthates are transported to the developing pods and seeds instead of to the vegetative
parts of the plants, which may reduce plant defenses.
Sudden death syndrome leaf symptoms can be incited independently of root symptoms, which suggests a phytotoxin(s) is translocated from the roots and is
responsible for foliar symptoms. A phytotoxic polypeptide and the phytotoxin monordin from culture filtrates of sudden death syndromeinciting isolates reproduced
foliar symptoms, but noninciting isolates did not.
High populations of the soybean cyst nematode (SCN), Heterodera glycines, have been thought to be associated with sudden death syndrome. However, in some
areas, this relationship does not always occur. Heterodera glycines possibly hastens the onset and increases the severity of foliar symptoms. The fungus is capable of
surviving in nematode cysts in vitro at a temperature of 10°C for a long enough time to overwinter in the field.

Page 664
This may influence its inoculum potential and dispersal. Typically, the fungus grows within individual cysts, where the probability of its survival until spring may be
greater than being free in soil or in infested soybean residue where competition with other microorganisms could be a factor. It is also possible that cysts provide a
food base for germination of chlamydospores and growth. Fusarium solani f. sp. glycines has infrequently been isolated from SCN eggs, but the effect of this
interaction has not been determined.
Fusarium solani isolates associated with sudden death syndrome are not hostspecific and readily infect other bean hosts. Sudden death syndrome incidence is
greater in notill than in conventional tillage systems.
Distribution.
The United States (Arkansas, Illinois, Indiana, Iowa, Kansas, Kentucky, Mississippi, Missouri, and Tennessee).
Symptoms.
Sudden death syndrome is a mid to lateseason disease favored by highyield environments. Symptoms are first noticed after flowering (R3R4) and continue through
maturity. If symptoms develop before the R6 stage, it is likely that complete defoliation and pod abortion will occur in 3 to 6 weeks.
The interveinal chlorosis of foliage is followed in 5 to 10 days by necrosis of the tissue. Necrosis continues to develop until only tissue near the major leaf veins remains
green. These symptoms appear throughout the plant but are most severe on the top leaves of a diseased plant. Leaves abscise at the apex of the petiole, leaving
leafless stems with attached petioles; later, the petioles may also abscise, causing premature plant defoliation.
Flower and pod abortion occurs. The abscission of pods is most pronounced at the top of the plant. Plants that develop symptoms at a later maturity produce smaller,
lighter seed than healthy plants.
Stem and root vascular tissues of diseased plants become reddish brown, but the pith remains a "normal" white color. The discoloration progresses outward from
vascular tissue. Roots of diseased plants appear normal at first, but plants with advanced symptoms have a discoloration of roots and lower stems that occurs together
with a lateral root rot. After considerable root degradation, chlamydospores may be observed in degraded, sloughed cortical tissue, and blue to bluegreen masses of
macroconidia may be visible on diseased roots near the soil line. Sporulation on root surfaces is always associated with root rot and is more frequent during or
immediately following periods of high soil moisture.
A seed and seedling rot is also reported to occur.
Management.
Significant differences in disease development between cultivars occurs at the R3 growth stage and are more distinct at the R6 growth stage. A single dominant gene,
Rfs, in the cultivar 'Ripley' controls resistance.

Page 665
Research has shown that differences appear to be associated with response of some cultivars to race 6 of the SCN. Cultivars susceptible to race 6 were susceptible
to SDS, and those that are moderately resistant or resistant to race 6 had low levels of resistance to SDS. With other cultivars, susceptibility to soybean cyst
nematode was not related to susceptibility to SDS.
Target Spot
Cause.
Corynespora cassiicola (syn. Cercospora melonis, Cercospora vignicola, Helminthosporium vignae, and H. vignicola) survives for 2 or more years as mycelia
and chlamydospores in infested residue and soil, and grows saprophytically on different kinds of plant residue in soil. Infection of roots and stems occurs early in the
growing season in moist soils at temperatures of 15° to 18°C. Later in the growing season, conidia splashed and blown to leaves cause infection when free moisture is
present or the relative humidity is 80% or more. A different race of C. cassiicola is thought to infect hypocotyls, roots, and stems than the race that infects leaves,
pods, and seeds.
Distribution.
Eastern Asia, Canada, Central America, and the United States.
Symptoms.
No symptoms develop at temperatures above 20°C. Target spot is most noticeable on diseased leaves later in the growing season. Lesions on leaves are redbrown
and vary from small specks to spots 12 mm or larger in diameter. The larger spots are generally zonate, suggesting a targetlike appearance. Spots are generally
surrounded by a light green to yellowgreen halo. Narrow, elongated spots may develop along veins of the upper leaf surface.
Spots on petioles and stems are dark brown and vary in shape from a small speck to an elongated, spindleshaped lesion. Spots on pods are generally round (1 mm in
diameter) with a slightly depressed, purpleblack center and brown margins. Sometimes small dark brown spots are formed on seeds.
Taproots, hypocotyls, and larger lateral roots have oval redbrown lesions that later become purple due to C. cassiicola sporulating. Lesions will grow larger and
coalesce as the plant matures.
Management
Thielaviopsis Root Rot
Thielaviopsis root rot is also called black root rot.

Page 666
Cause.
Thielaviopsis basicola survives as chlamydospores in infested residue. Chlamydospores germinate during moist soil conditions and temperatures from 16° to 20°C
and infect hypocotyls and roots early in the growing season. Chlamydospores are formed in diseased tissues and returned to soil at harvest time as diseased tissues
disintegrate. Seedborne infection is uncommon.
Distribution.
Canada, Germany, and the midwestern United States, particularly Michigan.
Symptoms.
The cortex of the hypocotyl below the soil line and taproots and fibrous roots become dark brown and necrotic. Frequently a severe root rot develops, causing
subsequent wilting of foliage or plant death.
Management
2. The herbicide chloramben has been reported to increase injury.
Top Dieback
Cause.
Diaporthe phaseolorum (syn. D. phaseolorum var. caulivora), anamorph Phomopsis phaseoli.
The causal fungi are seedborne and overwinter as perithecia in infested residue and seeds. Seed infection is reported to be primarily internal. Infected seed give rise to
seedlings with diseased cotyledons that serve as sources for the further infection of host plants.
Distribution.
Presumed to be similar to stem canker; however, distribution of top dieback may differ from stem canker.
Symptoms.
Disease develops late in the growing season and is distinct from the disease stem canker. The five or six uppermost internodes of diseased plants die prematurely.
Management
2. Plow infested residue in the fall, if possible, to hasten decay of residue and reduce the level of inoculum.
Twin Stem Abnormality Disease
Cause.
Sclerotium sp. and Macrophomina phaseolina.
Distribution.
Symptoms.
Symptoms, which appear after cotyledons have opened, have three distinct severity forms. The most severe form is type I. Elongation of

Page 667
the first internode that bears the primary leaves is completely inhibited. The apical meristem resembles a convex knob between the cotyledons. The cotyledons are
large and spongy and have a thickened hypocotyl. In 7 to 10 days, two pairs of primary leaves with rudimentary petioles and internodes form. At maturity, the plant is
stunted and bushy and may have two main stems originating from the cotyledonary node.
In type II, the moderately severe form, the first internode with underdeveloped primary leaves elongates to a limited extent. The original primary leaf primordials are
necrotic. Two secondary pairs of primary leaves develop from the cotyledonary node and continue to grow. Adult plants are stunted and bushy and may have two
main stems originating from the cotyledonary node.
In type III, the less severe form, the first internode with underdeveloped primary leaves elongates normally or excessively. Leaves remain wrapped around each other
and are bleached at the apex. When leaves open, the bleaching extends to the margin and inward, the apex is curved inward, and the entire leaf is wrinkled. The first
trifoliate leaf is formed with little or no elongation of the second internode. One or two pairs of leaves may form at the cotyledonary node but generally remain
rudimentary.
Management.
Not reported.
Verticillium Pod Loss
Cause.
Verticillium nigrescens. High soil moisture levels are related to increased infection. Increasing incidence is related to a long history of cotton production in the same
field in which soybeans are grown.
Distribution.
Symptoms.
Verticillium nigrescens normally grows from one end of a pedicel and rarely from other parts of the pod. The fungus can be isolated from flowers and pods at all
stages of development. The numbers of pods per plant and seed weight are reduced but there is no vascular discoloration or wilting.
Management.
Not reported.
Verticillium Wilt
Cause.
Verticillium dahliae is possibly seedborne.
Distribution.
Not known for certain, but V. dahliae has been isolated from soybeans growing in fields in the United States (Iowa).
Symptoms.
Vascular tissue in the lower portion of the diseased stem is discolored. Leaves die but remain attached to diseased plants that are scattered randomly throughout a
field.

Page 668
Inoculated plants display sudden wilt symptoms 7 to 10 days after inoculation. Early wilt symptoms occur as apical, marginal, or unilateral wilting of primary leaves.
Young tissues remain green and dry without initially becoming chlorotic. No pith discoloration occurs but a redbrown to black discoloration is restricted to the
vascular tissue.
Management.
Some cultivars are evidently resistant. Verticillium wilt is not considered an important disease, but possibly other diseases have been mistaken for it.
Yeast Spot
Yeast spot is also called Nematospora spot.
Cause.
Nematospora coryli is a yeast fungus that survives in and is transmitted primarily by the adult green stinkbug, Acrosternum hilare. Other species of stinkbugs known
to transmit N. coryli are the southern green stinkbug, Nezara viridula, and several Euschistus spp., including the brown stinkbug, E. servus. The stinkbug pierces
the pod wall and feeds on seed contents liquefied by salivary enzymes. During feeding, only yeast cells located in the region of the mouthparts are forced into the
developing seed.
Distribution.
Africa, Brazil, and the United States.
Symptoms.
Yeast spot is primarily a disease of seeds. Seeds infected early may not mature or remain small and shriveled. Where infection occurs during pod formation, seeds fail
to develop and pods drop prematurely. On developing green seeds, diseased tissue is slightly depressed and varies from a light cream or yellow to brown. There may
be varying amounts of dead tissue extending into diseased embryos. On the surfaces of the seed coats, lesions appear as very small, discolored punctures. Seed
shriveling caused by other diseases may be differentiated from that caused by yeast spot by observing these punctures. The outside of the pods display small, pinpoint,
discolored areas.
Management
2. Control stinkbugs by insecticides when nymphs average one per 30 cm of row.
Columbia Lance
Cause.
Hoplolaimus columbus can survive in dry soil for a long time and has a life cycle similar to the Meloidogyne spp. that cause root knot. Hoplolaimus columbus is an
ectoparasite that prefers to feed in the cortex area.

Page 669
Distribution.
The southeastern United States, particularly on sandy soils.
Symptoms.
Diseased plants are stunted and chlorotic. Roots are rotted and sparse. In areas of high nematode populations, root systems may be almost completely destroyed as
plants near maturity.
Management
3. Clean soil from equipment moved between fields.
5. Subsoil or chisel plow to a 36cm depth where hardpan conditions exist.
Lance
Cause.
Hoplolaimus galeatus.
Distribution.
Symptoms.
Diseased plants are stunted and chlorotic. The taproot becomes necrotic and large numbers of secondary and tertiary roots are produced.
Management
1. Grow tolerant varieties.
2. Sow early.
3. Use nematicides where practical.
4. Subsoil plow where hardpan conditions exist.
Lesion
Cause.
Pratylenchus spp. are endoparasitic nematodes that enter roots as larvae and attack the root cortex.
Distribution.
Symptoms.
Diseased plants may be yellowed and stunted. Initially, roots have small dark lesions. Other soilborne microorganisms then may enter the root through wounds made
by Pratylenchus spp. and cause root rot and a browning of the root system.
Management.
Reniform
Cause.
Rotylenchulus reniformis is a nematode species in which only females invade roots after feeding on the epidermal tissues. Rotylenchulus reniformis is semi
endoparasitic because the posterior portion of the female remains outside the root and swells to a kidney shape. Eggs are laid outside the root. Optimum root invasion
and nematode development occurs at a temperature of 29°C.

Page 670
Distribution.
Africa and the southeastern United States.
Symptoms.
Diseased plants are stunted and chlorotic. Small galls or root swellings sometimes occur on damaged roots.
Management
2. Apply nematicides where feasible.
Ring
Cause.
Criconemella ornata is an ectoparasitic nematode.
Distribution.
The United States, probably when soybean is grown in rotation with peanut.
Symptoms.
Diseased plants are chlorotic and have necrotic lesions on roots. The number of lateral roots is reduced.
Management.
Nematicides are reported to be effective on other crops.
Root Knot
Cause.
Meloidogyne species, including M. arenaria, M. hapla, M. incognita, and M. javanica. Meloidogyne arenaria, M. incognita, and M. javanica do not survive if
the soil temperature averages below 3°C during the coldest month. Infested soil contains eggs that hatch and produce larvae that move through soil and penetrate root
tips. Larvae migrate inside the infected root to the vascular tissues, where they become sedentary and commence feeding. Excretions of the larvae stimulate cell
proliferation, resulting in the development of syncytia, from which larvae derive their food. Females lay eggs that may be pushed out of the root into the soil.
Distribution.
Wherever soybean is grown in sandy, lighttextured soils in warm climates.
Symptoms.
Diseased plants will be stunted. Leaves turn yellow and wilt during hot, dry weather. Roots have knots or galls of different sizes that disrupt the flow of water and
nutrients to the tops of plants.
Management
1. Rotate with an alternate crop for 3 years if the species of nematode is known. Maize can be rotated with soybean to manage M. hapla. Cotton can be rotated to
manage all species except M. incognita.
2. Grow resistant cultivars; however, different races of M. incognita are known to occur.

Page 671
Sheath
Cause.
Hemicycliophora spp. are ectoparasitic nematodes that feed primarily on the root tips.
Distribution.
Widespread in sandy soils.
Symptoms.
Root tips are galled. Diseased plants are generally unthrifty.
Management.
Nematicides are reported to be effective.
Soybean Cyst
Cause.
Heterodera glycines survives in soil as eggs contained in cysts formed by female bodies. Spread of H. glycines in a field or over long distances is by any agent
capable of moving infested soil and residue. Larvae hatch from eggs, move through soil, and enter plants near the root tips. Nematodes migrate inside the root to
undifferentiated cortical and stelar tissues. Syncytia are formed by salivary excretions. As the female matures, it swells and breaks through the epidermis but its neck
remains in the root. Females are then inseminated by males and produce up to 500 eggs that are released into the soil or retained in the female's body until a cyst is
formed. Eggs have been reported to survive in cysts for up to 11 years. Eggs are deposited externally and larvae hatch to begin a new life cycle. Nematode
development is most rapid at 30°C. Different races exist.
Distribution.
Asia, Brazil, and the southeastern and midwestern United States.
Symptoms.
Injury to host plants is most serious in dry, sandy soils that are deficient in nutrients and organic matter. Not all plants display aboveground symptoms. Diseased plants
are stunted and chlorotic and may lose their leaves prematurely. Affected leaves are distributed over the plant. A yellowing starts at the leaflet margin and gradually
includes all of the blade.
Light to moderate infection will stimulate overproduction of lateral roots, but severely diseased plants have a small, necrotic root system with few or no Rhizobium
nodules. White to yellow females and brown cysts that developed from female bodies are attached to diseased roots and appear somewhat smaller than the head of a
pin.
Management
1. Grow resistant cultivars. Resistance to race 3 is conditioned by one dominant and two recessive genes in each parent.
2. Rotate soybean with other crops for 2 to 3 years.
3. Practice sanitation; clean soil from equipment moved between fields.
4. Apply nematicides to soil if feasible.
5. Irrigate to reduce water stress to plants; however, nematode damage is not reduced.

Page 672
6. Delay in sowing associated with doublecropping wheat in Missouri allowed for a significant decline in numbers of nematodes between early May and late June.
7. Tillage systems. A report from Missouri said populations of H. glycines were lower the first year in soybeans grown under notill tillage than in soybeans grown
under conventional tillage practices. No differences in populations were noted the second year.
8. In greenhouse tests, numbers of cysts and juveniles were reduced on plants cankered by Diaporthe phaseolorum var. caulivora.
Spiral
Cause.
Distribution.
Widespread.
Symptoms.
Symptoms on soybeans are relatively unknown. Under low to midlevel populations, a few root cells are destroyed, but roots are thought to be severely affected
when infected by high populations of nematodes.
Management.
Nematicides are effective.
Stem
Cause.
Ditylenchus dipsaci is an endoparasite. High humidity and rainy weather favor injury by D. dipsaci.
Distribution.
The United States.
Symptoms.
Diseased stems are stunted, swollen, and distorted. Young leaves are also infected and have a chlorotic spotting.
Management.
Stem nematode is not considered a serious problem on soybean.
Sting
Cause.
Belonolaimus gracilis and B. longicaudatus are nematodes that overseason in soil as eggs and larvae. Feeding by nematodes occurs only on root surfaces (not
internally). Disease occurs on sandy soils.
Distribution.
Symptoms.
Damage is confined to plants growing on sandy soils. Seedlings may be killed, which results in a stand loss. Diseased plants other than seedlings usually are not killed
but display stunted, chlorotic, or discolored symptoms similar to those of moisture stress.
Diseased roots initially have small, dark, sunken lesions that later enlarge and girdle root tips. Meristematic tissues are destroyed and root proliferation above the area
of discoloration results in a stubby and dark root system. Eventually, roots become severely rotted.

Page 673
Management
1. Use nematicides.
4. Clean soil from equipment moved between fields.
Machismo
Machismo is also called amachamiento and proliferacion de yemas.
Cause.
A phytoplasma. The causal agent, which is transmitted by the leafhopper Scaphytopius fuliginosus, is not known to be mechanically transmitted or seedborne.
Several weeds also serve as hosts.
Distribution.
Colombia and Mexico.
Symptoms.
Symptoms are most severe on plants infected while young. Symptoms first occur at the time of flowering or when pod formation begins. Frequently a branch that is
close to the ground will show symptoms but the rest of the plant will appear normal.
Pods may be in an upright position, rigid, curved, flat, and thin with no seed produced, or they may be transformed into corrugated, leaflike structures resembling
phyllody. Once floral parts have been transformed into leaflike structures, buds proliferate from leaf axils anywhere on the plant, causing a witches' broom.
Sepals may be larger and duller than normal and have the appearance of small leaves. Flowers are small and remain closed. In these cases, the pods or leaflike
structures grow through the tips of the unopened flowers.
Pods formed on diseased plants are slightly corrugated and thicker and softer than those on healthy plants. The roots of immature green seeds that germinate in the
pod rupture through the pod wall.
Diseased plants have a darker green color and remain green longer than healthy plants, which causes difficulty in harvesting.
Management
1. Control weed hosts.
2. Rogue infected plants.
3. Apply tetracycline.
Soybean Bud Proliferation
Cause.
A phytoplasma transmitted by seed and the leafhopper Scaphytopius acutus. It is not mechanically transmitted.
Distribution.
The United States (Arkansas and Louisiana).
Symptoms.
Symptoms occur at the onset of flowering. Diseased plants have

Page 674
delayed senescence and remain green after healthy plants have matured. There is a proliferation of adventitious buds. Pods are small, underdeveloped, and few in
number, and many contain only one large bean.
Management.
Not reported.
Witches' Broom
Cause.
A phytoplasmalike organism transmitted by the leafhoppers Orosius orientalis and O. argentatus.
Distribution.
Brazil, India, Indonesia, Japan, Mozambique, Nigeria, and Tanzania.
Symptoms.
Symptoms resemble those of machismo. Symptoms include a phylloid disorder of floral organs, shoot proliferation, and reduced leaflets.
Management.
Not reported.
Alfalfa Mosaic
Cause.
Alfalfa mosaic virus is seedborne and is transmitted by several aphid species.
Distribution.
Argentina, Brazil, Japan, Romania, South Africa, and the United States.
Symptoms.
Early infections result in the mottling or chlorotic spotting of diseased leaves. Later infections result in a yellow mottle, starshaped flecks, or slight crinkling.
Management.
Not reported.
Bean Pod Mottle
Cause.
Bean pod mottle virus (BPMV) is in the comovirus group. BPMV is transmitted by several insects, particularly the bean leaf beetle, Cerotoma trifurcata. BPMV is
commonly associated with soybean mosaic virus in diseased plants.
Distribution.
Ecuador and the United States.
Symptoms.
Young diseased leaves have a green to yellow mottling, particularly during rapid growth and cool weather, that disappears as leaves mature. Diseased plants under
moisture stress are less turgid than healthy plants and may have a yield loss if stress occurs during the reproductive phase.

Page 675
Management
1. Grow at least four rows of maize or sorghum between soybean and other legume fields and noncultivated areas.
2. Rogue out diseased plants from seed fields.
3. Control weeds, particularly in noncrop areas next to soybean fields.
Brazilian Bud Blight
Brazilian bud blight is also called tobacco streak.
Cause.
Tobacco streak virus (TSV) is in the ilarvirus group. TSV is seedborne and saptransmissible but is not known to be transmitted by insects. Symptoms appear sooner
on inoculated plants grown at 30°C than at lower temperatures, and under continuous light for 24 hours than under 12 hours of dark followed by 12 hours of light.
Distribution.
Brazil and the United States (Iowa and Oklahoma).
Symptoms.
Symptoms resemble those of bud blight caused by tobacco ringspot virus and are normally not seen on young infected plants. Some plants remain green after maturity
and have unexpanded and unfilled pods. Initially, irregular yellow spots develop on diseased leaves. Diseased plants then develop numerous stunted axillary branches
that produce dwarfed leaves. Mosaic symptoms and necrotic streaks develop in the stem pith, especially at the stem nodes. Necrotic blotches appear on pods.
Infection of the plant at any age delays seed maturation, but early infection prevents seed formation altogether. Diseased plants are stunted and stem tips curve and die.
Management
1. Grow at least four rows of maize or sorghum between soybean and other legume fields and noncultivated areas.
3. Control weeds, particularly in noncrop areas next to soybean fields.
Bud Blight
Cause.
Tobacco ringspot virus (TRSV) is in the nepovirus group. TRSV is seedborne and overwinters or is reservoired in a large number of legumes. TRSV is sap
transmitted by nematodes, particularly the dagger nematode, Xiphinema americanum; nymphs of Thrips tabaci; grasshoppers, Melanoplus differentialis; and
possibly other insects. TRSV is also transmitted by root grafts.
Distribution.
Australia, Canada, China, and the United States.
Symptoms.
Bud blight occurs sporadically, appearing only in certain years, and is frequently more severe in fields adjacent to legumegrass pastures or

Page 676
fencerows, where insects transmit the virus from perennial plants to soybeans. Symptoms of bud blight vary with the stage of growth at which the plants became
infected. When plants are infected before flowering, apical buds and shoots turn brown, curve downward and form a crook, and become dry and brittle; hence, the
name bud blight. Young diseased leaves develop a rusty flecking and the plants are stunted and produce little seed below 25°C. Several strains of TRSV cause
severely dwarfed and barren plants.
Plants infected while less than 5 weeks old are severely stunted because of shortened internodes or fewer nodes. Sometimes the stem below the blighted terminal bud
is internally discolored at the nodes. Brown streaks occasionally occur on petioles and large leaf veins. Petioles of the youngest trifoliate leaves are often thickened,
shortened, and occasionally curved, distorting shoot tips. Diseased leaf blades are rugose, bronzed, dwarfed, and cupped.
When plants are infected during flowering, small underdeveloped pods are produced. Infection after flowering results in conspicuous dark blotches on poorly filled
pods that eventually fall to the ground.
A good diagnostic symptom is the presence of diseased plants that remain green after normal plants have matured. These plants are easily found in a field in the
autumn. Losses of 100% have been reported.
Management
1. Do not grow soybean adjacent to legume fields. If this is not feasible, grow a buffer strip of a few rows of maize or forage sorghum between legumes and the
soybean field.
2. Control broadleaf weeds in noncrop areas adjacent to soybean fields before soybeans emerge.
3. Rogue infected plants from seed production fields.
Cowpea Chlorotic Mottle
Cause.
Cowpea chlorotic mottle virus, soybeaninfecting strain (CCMVS) is in the bromovirus group. CCMVS is transmitted by sap, the bean leaf beetle (Cerotoma
trifurcata), and the spotted cucumber beetle (Diabrotica undecimpunctata).
Distribution.
The United States.
Symptoms.
Diseased leaves are mottled, slightly crinkled, and tend to stand upright. Mottling is most intense on the diseased younger leaves. Plants are stunted and produce fewer
seeds, which are small in size and reduced in quality. Local necrotic lesions may be produced on resistant cultivars and veinal necrosis may occur on cultivars with
intermediate resistance.
Management.

Page 677
Cowpea Mild Mottle
Cause.
Cowpea mild mottle virus (CPMMV) is in the carlavirus group. CPMMV is transmitted mechanically and by the whitefly Bemisia tabaci but has been demonstrated
not to be seedborne.
Distribution.
Ivory Coast and Thailand.
Symptoms.
Diseased plants are stunted and show a light green mosaic. Inoculated seedlings display vein clearing that evolves into a yellow mosaic and occasional crinkling of
leaves. Leaves may also be curled downward or cupped upward. Some cultivars display a vein and top necrosis. Vein enations have also been reported as a
symptom.
Management.
Not reported.
Cowpea Mosaic
Cause.
Cowpea mosaic virus (CPMV) is in the comovirus group. CPMV is transmitted by sap and the bean leaf beetle, Cerotorna ruficornis.
Distribution.
Central America and the United States (including Puerto Rico).
Symptoms.
Inoculated primary leaves have chlorotic and necrotic lesions. A systemic light green mosaic occurs on diseased trifoliate leaves together with very severe leaf
malformation and bud blight.
Management.
Not reported.
Cowpea Severe Mosaic
Cause.
Cowpea severe mosaic virus (CPSMV) is in the comovirus group. CPSMV is transmitted by the beetle Cerotoma arcuata.
Distribution.
Brazil.
Symptoms.
Symptoms are identical to those of bud blight. Significant reductions occur in plant height, yield, number of pods per plant, and seed germination.
Management.
Not reported.
Delayed Maturity
Cause.
Possibly a viruslike agent that is seedborne and also spread by insects.
Distribution.
Symptoms.
Diseased plants remain green and have pronounced longitudinal ribs after healthy plants have matured. Diseased seeds often germinate inside the pod and rot. Pods
often are rough textured and have pronounced wrinkles and veins.
Management.
Not reported.

Page 678
Indonesian Soybean Dwarf
Cause.
Indonesian soybean dwarf virus is transmitted in a persistent manner by the aphid Aphis glycines.
Distribution.
Indonesia.
Symptoms.
Diseased plants are dwarfed and dark green with shortened leaf petioles and internodes. Upper leaves are small and curl upward. Lower leaves are rugose and brittle
and have shortened veins and interveinal white necrosis. Occasionally diseased leaves have numerous holes caused by their brittleness. Diseased plants produce few
pods.
Management.
Not reported.
Mung Bean Yellow Mosaic
Cause.
Mung bean yellow mosaic virus is transmitted by the whiteflies Bemisia tabaci and B. gossypipderda.
Distribution.
Asia.
Symptoms.
A yellowing on the veins of diseased leaflets later develops into a severe yellow mosaic.
Management.
Peanut Mottle
Cause.
Peanut mottle virus (PeMoV) is in the potyvirus group. PeMoV is transmitted by sap and in a nonpersistent manner by several species of aphids, but PeMoV is not
seedborne in soybeans. PeMoV can be spread from nearby peanut fields to soybean fields.
Distribution.
Symptoms.
A general mosaic that is similar to symptoms of diseased plants caused by other viruses occurs. Small chlorotic areas that enlarge but do not become continuous leave
striking, dark green islands on diseased leaves. Later, chlorotic patches, line patterns, or ring patterns occur on the third and fourth leaves after infection. Leaves that
develop even later display a general mosaic without distinct characteristics. Diseased leaves may pucker and curl down at the edges.
Management
2. Do not grow soybean following peanut.
3. Separate soybeans from peanut fields by 50 m or more.
4. Rogue volunteer peanut plants from soybean fields.

Page 679
Peanut Stripe
Cause.
Peanut stripe virus (PStV) is in the potyvirus group. PStV is transmitted mechanically and by aphids, but it is not seedtransmitted in soybeans. Infective virus particles
can be recovered from seed coats of immature soybean seeds, but as the seeds mature, the virus loses its infective properties. A possible source of inoculum for
soybeans may be diseased peanut seed sown in adjacent fields. PStV is then spread from the diseased peanuts to soybeans.
Distribution.
China and the southeastern United States.
Symptoms.
Symptoms vary according to cultivar and virus isolate. Diseased leaves develop necrotic local lesions that eventually develop into systemic necrosis. Some cultivars
develop only a mild mottle.
Management
1. Resistant lines have been identified.
2. Do not grow soybean adjacent to peanut.
Peanut Stunt
Cause.
Peanut stunt virus (PSV) is in the cucumovirus group. PSV overwinters in several legumes, such as lespedeza, crown vetch, and peanut, and is disseminated by
aphids.
Distribution.
The southeastern and central United States.
Symptoms.
Symptoms range from diffuse chlorotic lesions to necrotic local lesions on inoculated primary leaves. Vein clearing occurs, followed by a general mosaic of diseased
trifoliate leaves. Some diseased plants may be symptomless.
Management.
Not reported.
Soybean Chlorotic Mottle
Cause.
Soybean chlorotic mottle virus (SbCMV) is in the caulimovirus group. SbCMV is transmitted by sap but not by aphids or seed.
Distribution.
Japan.
Symptoms.
Diseased plants have mosaic symptoms and are stunted due to shortened internodes. Mechanically inoculated plants initially display vein clearing, chlorosis, and leaf
curling of diseased young leaves, which are also smaller than healthy leaves. Eventually, diseased leaves have mottled symptoms.
Management.
Not reported.

Page 680
Soybean Crinkle Leaf
Cause.
Possibly a virus that is transmitted by the whitefly Bemisia tabaci.
Distribution.
Thailand.
Symptoms.
Diseased leaves are twisted or curled, and the undersides have veinal enations on them. Plant foliage of diseased plants is darker green than that of healthy plants. In
the greenhouse, diseased plants have a yellow netting of veins 10 to 14 days after inoculation.
Management.
Not reported.
Soybean Dwarf
Cause.
Soybean dwarf virus (SDV) is in the luteovirus group. Another luteovirus, subterranean clover red leaf virus (SCRLV), is considered a strain of SDV. SDV is
transmitted by grafting and in a persistent manner by the aphids Aulacorthum solani and Acyrthosiphon pisum. SDV is not seed or saptransmitted. The
temperature for optimum transmission is 20°C.
Based on the symptomatology of SDVinfected plants, two strains exist: dwarfing (SDVD), and yellowing (SDVY). The two strains have small differences in host
range and physiochemical properties. SDVD is transmitted more efficiently than SDVY by the foxglove aphid, Aulacorthum solani.
Distribution.
Japan. If SCRLV is a strain, SDV also occurs in Australia and New Zealand.
Symptoms.
Diseased plants are severely stunted. Leaves are rugose, curl down, and may have interveinal yellowing.
Management.
Not reported.
Soybean Mosaic
Soybean mosaic is also called soybean crinkle.
Cause.
Soybean mosaic virus (SMV) is in the potyvirus group. SMV is seedborne and most primary inoculum consists of diseased seedlings derived from SMV infected
seed. SMV also overwinters in perennial weeds. Dissemination within a field, or secondary spread, occurs by the activities of several aphids that transmit SMV in a
nonpersistent manner. SMV is also readily saptransmissible.
Infection before the onset of flowering results in higher levels of seed transmission than in later infections. The percentage of SMVinfected seed will gradually
decrease when secondary spread is minimal and if SMV spread occurs after the onset of flowering.
Several strains of SMV have been reported to exist.

Page 681
Distribution.
Symptoms.
Symptoms vary from normalappearing leaves, in which veins are deep in the lamina, to rugose leaves, in which portions of the diseased upper leaf surface has
become invaginated into vesicles. The best diagnostic symptom is rugose leaves that appear on the third leaf formed after infection. If diseased plants are grown under
cool conditions, the rugose symptoms increase in severity on successive leaves, and the characteristic mosaic pattern of alternate light and dark green patches of leaf
tissue may appear. The mosaic symptom is more obvious on some cultivars than others. Leaves become leathery to the touch, coarse, and brittle as diseased plants
near maturity. Severely diseased leaves are narrow and have a willowleaf appearance. If diseased plants are grown under warm conditions at temperatures of 31°C
or more, symptoms are masked and leaves develop normally. When very susceptible cultivars are diseased, a yellowish vein clearing develops in the small branching
veins of developing leaves 6 to 14 days after infection.
Infected seed may not germinate. Seedlings from infected seed are spindly and have crinkled unifoliate leaves that curl downward and become chlorotic. Subsequent
trifoliate leaves are severely stunted and mottled and are more crinkled than the unifoliate leaves.
On pods, SMV has been reported to cause irregularshaped, depressed black lesions that are similar to those caused by Cercospora sojina and Colletotrichum
truncatum. Diseased seed is discolored; however, mottling of seed is not always indicative of the presence of SMV.
Yields have been reported to be significantly reduced only when 60% or more of the plants are diseased. The largest decreases in yield occurred in plants inoculated
with SMV 20 days after emergence. Decreased oil content and nodulation also occur.
Symptoms are enhanced when plants are dually infected with SMV and either cowpea mosaic virus or bean pod mottle virus.
Management
3. Practice good weed control in and around soybean fields.
Soybean Severe Stunt
This disease has some similarities, including symptoms, to Essex disease. The two diseases may be portions of the same disease syndrome.
Cause.
Soybean severe stunt virus (SSSV). SSSV is transmitted via soil, and the dagger nematode, Xiphinema americanum, is strongly associated with the occurrence of
the disease within a field. Soybean severe stunt has been associated with continuous cropping of the cultivar 'Essex.'

Page 682
Distribution.
The United States (Delaware and Virginia). The cultivar 'Essex' is severely diseased but other cultivars are also affected.
Symptoms.
Initial symptoms in the field occur on the first true leaves at the V1 stage of development. Diseased plants typically have thickened, dark green leaves; shortened
internodes, which cause a bunching of leaves and severe stunting; pith discoloration; and superficial stem lesions, as well as fewer flowers and fewer mature pods. A
reduction in seedling emergence and stand may also be attributable to infection with SSSV. Yields may be reduced within an affected area by as much as 90%.
Management
2. Rotate 2 years with a nonhost crop.
Soybean Yellow Shoot
Cause.
Soybean yellow shoot virus (VABS) is in the potyvirus group. VABS is mechanically transmitted.
Distribution.
Brazil.
Symptoms.
A golden mosaic and veinal and stem necrosis occurs on diseased young leaves and upper stems.
Management.
Not reported.
Tobacco Mosaic
Cause.
Tobacco mosaic virus soybean strain (TMVS). The host range of TMVS differs from that of TMV.
Distribution.
Yugoslavia.
Symptoms.
Diseased leaves exhibit vein clearing and a mild chlorotic mosaic.
Management.
Not Reported.
Tobacco Necrosis
Cause.
Tobacco necrosis virus is in the necrovirus group.
Distribution.
The United States.
Symptoms.
Small necrotic spots surrounded by a chlorotic halo, which occur on diseased secondary leaves, enlarge toward smaller leaf veins. Spots spread from small veins to
larger veins, midribs, and petioles and cause a systemic infection of diseased plants. Petioles and stems have a necrosis of phloem tissues and adjacent parenchyma.
Management.
Not reported.

Page 683
Yellow Mosaic
Cause.
Soybean yellow mosaic virus (SYMV) is in the potyvirus group. SYMV is disseminated by the aphids Aphis fabae, Macrosiphum gei, M. pisi, M. solanifolii, and
Myzus persicae. SYMV is not thought to be spread by infected seed, but it is easily saptransmissible. SYMV has a large host range.
Distribution.
Symptoms.
The symptoms caused by SYMV resemble those caused by soybean mosaic virus. Young diseased leaves develop a yellow mottling that is scattered in random spots
over leaves or is in indefinite bands along the major leaf veins. Rusty, necrotic spots develop in the yellowed areas as diseased leaves mature. Some strains of SYMV
produce severe mottling and crinkling of diseased leaves.
Management
2. Rogue diseased plants from seed fields.
3. Practice good weed control.
4. Grow cultivars that have some resistance.
Pod Necrosis
Cause.
Unknown. Alternaria alternata is isolated consistently from necrotic areas on diseased pods, but there was no significant correlation between incidence and reduced
seed weight among the 10 soybean cultivars that were tested. Species of Phomopsis and Diaporthe were isolated from seed in the upper and middle pods of
affected plants, but there was no correlation between incidence of these organisms and reduced seed weight.
Distribution.
Canada (southeastern Ontario).
Symptoms.
Affected areas of diseased plants within fields are circular to oblong and up to 0.5 ha in size. Symptoms appear on soybeans growing in sandy loam soils following
dry, warm weather. Diseased leaves are chlorotic and stunted. Internodes are shortened and necrotic spots appear on pods at the tops of diseased plants. Seed
weight is reduced.
Management.
Not reported.
Selected References
Abney, T. S., and Ploper, L. D. 1994. Effects of bean pod mottle virus on soybean seed maturation and seedborne Phomopsis spp. Plant Dis. 78:3337.

Page 684
Abney, T. S., Richards, T. L., and Roy, K. W. 1993. Fusarium solani from ascospores of Nectria haematococca causes sudden death syndrome of soybean.
Mycologia 85: 801806.
Adee, E. A., Grau, C. R., and Oplinger, E. S. 1997. Population dynamics of Phialophora gretata in soybean residue. Plant Dis. 81:199203
Almeidia, A. M. R., and Kihl, R. 1981. Necrose das vagens um novo sintoma causada pelo virus do mosaico da soja. Fitopathologia Brasileria 6:281283 (in
Portuguese).
Almeidia, A. M. R., and Silveira, J. M. 1983. Efeito da idade de inoculacao de plants de soja corn o virus do mosaico comum da soja e da percentagem de plantas
infecladas sobre o rendimento e algumas caracteristicas economicas. Fitopathologia Brasileira 8:229236 (in Portuguese).
Anaele, A. O., Bishnoi, U. R., and Pacumbaba, R. P. 1987. Bacterial blight of soybean incidence at three row spacings in notill and conventional planting systems.
Anahosur, K. H., and Fazalnoor, K. 1972. Studies on foliicolar fungi of soybean crop. Indian Phytopathol. 25:504508.
Anderson, T. R. 1987. Pod necrosis: A new disease affecting soybean on droughty soils in southwestern Ontario. (Abstr.) Can. J. Plant Pathol. 9:272.
Anjos, J. R., and Ghabrial, S. A. 1991. Studies on the synergistic interactions between soybean mosaic virus (SMV) and two comoviruses in mixed infections in
soybeans. Phytopathology 81:1167.
Anjos, J. R., and Lin, M. T. 1984. Bud blight of soybeans caused by cowpea severe mosaic virus in central Brazil. Plant Dis. 68:405407.
Backman, P. A., Williams, J. C., and Crawford, M. A. 1982. Yield losses in soybeans from anthracnose caused by Colletotrichum truncatum. Plant Dis. 66:1032
1034.
Balducchi, A. J., and McGee, D. C. 1987. Environmental factors influencing infection of soybean seeds by Phomopsis and Diaporthe species during seed
maturation. Plant Dis. 71:209212.
Black, B. D., Padgett, G. B., Russin, J. S., Griffin, J. L., Snow, J. P., and Berggren, G. T., Jr. 1996. Potential weed hosts for Diaporthe phaseolorum var.
caulivora, causal agent for soybean stem canker. Plant Dis. 80:763765.
Blackmon, C. W., and Musen, H. L. 1974. Control of the Columbia (lance) nematode Hoplolaimus columbus on soybeans. Plant Dis. Rptr. 58:641645.
Bonde, M. R., Peterson, G. L., and Dowler, W. M. 1988. A comparison of isozymes of Phakopsora pachyrhizi from the Eastern Hemisphere and the New World.
Bonde, M. R., Peterson, G. L., Nester, S. E., and Hartwig, E. E. 1996. Virulence of isolates of Phakopsora pachyrhizi and P. meibomiae on soybean genotypes.
(Abstr.). Phytopathology 86:S92.
Boosalis, M. G., and Hamilton, R. I. 1957. Root and stem rot of soybean caused by Corynespora cassicola (Berk. & Curt.) Wei. Plant Dis. Rptr. 41:696698.
Bradbury, J. F. 1986. Guide to plant pathogenic bacteria. C.A.B. International, Farnham Royal, United Kingdom. 332 pp.
Bristow, P. R., and Wyllie, T. D. 1986. Macrophomina phaseolina, another cause of the twinstem abnormality disease of soybean. Plant Dis. 70:11521153.
Bromfield, K. R., Melching, J. S., and Kingsolver, C. H. 1980. Virulence and aggressiveness of Phakopsora pachyrhizi isolates causing soybean rust.
Canady, C. H., and Schmitthenner, A. F. 1979. The effect of nitrogen on Phytophthora.

Page 685
root rot of soybeans. (Abstr.) Phytopathology 69:539.
Carson, M. L., Arnold, W. E., and Todt, P. E. 1991. Predisposition of soybean seedlings to Fusarium root rot with trifluralin. Plant Dis. 75:342347.
Chambers, A. Y. 1991. Effects of date of planting on severity of soybean stem canker. (Abstr.) Phytopathology 81:1135.
Cheng, Y. H., and Schenck, N. C. 1978. Effect of soil temperature and moisture on survival of the soybean root rot fungi Neocosmospora vasinfectum and
Fusarium solani in soil. Plant Dis. Rptr. 62:945949.
Daft, G. C., and Leben, C. 1972. Bacterial blight of soybeans: Epidemiology of blight outbreaks. Phytopathology 62:5762.
Daft, G. C., and Leben, C. 1973. Bacterial blight of soybeans: Fieldoverwintered Pseudomonas glycinea as possible primary inoculum. Plant Dis. Rptr. 57:156
157.
Dale, J. L., and Walters, H. J. 1985. Soybean bud proliferation of unknown etiology in Arkansas. Plant Dis. 69:811.
Damicone, J. P., Berggren, G. T., and Snow, J. P. 1987. Effect of free moisture on soybean stem canker development. Phytopathology 77:15681572.
Damsteegt, V. D. 1985. Vector relationships of two strains of soybean dwarf virus. (Abstr.) Phytopathology 75:1349.
Datnoff, L. E., Naik, D. M., and Sinclair, J. B. 1987. Effect of red leaf blotch on soybean yields in Zambia. Plant Dis. 71:132135.
Derrick, K. S., and Newsom, L. D. 1984. Occurrence of a leafhoppertransmitted disease of soybeans in Louisiana. Plant Dis. 68:343344.
Derrick, K. S., Newsom, L. D., and Briansky, R. H. 1984. Delayed maturity of soybeans. (Abstr.) Phytopathology 74:627.
Dhingra, O. D., and Muchovej, J. J. 1980. Twinstem abnormality disease of soybean seedlings caused by Cylindrocladium clavatum in central Brazil. Plant Dis.
70:977980.
Donald, P. A., Niblack, T. L., and Wrather, J. A. 1993. First report of Fusarium solani blue isolate, a causal agent of sudden death syndrome of soybeans, recovered
from soybean cyst nematode eggs. Plant Dis. 77:647.
Duncan, D. R., and Paxton, J. D. 1981. Trifluralin enhancement of Phytophthora root rot of soybean. Plant Dis. 65:435436.
Dunleavy, J. M. 1963. A vascular disease of soybeans caused by Corynebacterium sp. Plant Dis. Rptr. 47:612613.
Dunleavy, J. M. 1966. Factors influencing spread of brown stem rot of soybeans. Phytopathology 56:298300.
Dunleavy, J. M. 1980. Yield losses in soybeans induced by powdery mildew. Plant Dis. 64:291292.
Dunleavy, J. M. 1985. Transmission of Corynebacterium flaccumfaciens by soybean seed. (Abstr.) Phytopathology 75:1295.
Ellis, M. A., Ilyas, M. B., and Sinclair, J. B. 1974. Effect of cultivar and growing region on internally seedborne fungi and Aspergillus melleus pathogenicity in
soybeans. Plant Dis. Rptr. 58:332334.
Fagbenle, H. H., and Ford, R. E. 1970. Tobacco streak virus isolated from soybeans, Glycine max. Phytopathology 60:814820.
Farias, G. M., and Griffin, G.J. 1989. Roles of Fusarium oxysporum and F. solani in Essex disease of soybean in Virginia. Plant Dis. 73:3842.
Farr, D. F., Bills, G. R., Chamuris, G. P., and Rossman, A. Y. 1989. Fungi on Plants and Plant

Page 686
Products in the United States. American Phytopathological Society, St. Paul, MN. 1252 pp.
Fetzer, J., Kennedy, B., and Denny, R. 1988. Temperature and light regime effects on incubation time and leaf movements of soybean seedlings inoculated with
tobacco streak virus (TSV). (Abstr.) Phytopathology 78:1524.
Fletcher, J., Irwin, M. E., Bradfute, O. E., and Granada, G. A. 1984. A Machismolike disease of soybeans in Mexico. (Abstr.) Phytopathology 74:857.
Fletcher, J., Irwin, M. E., Bradfute, O. E., and Granada, G. A. 1984. Discovery of a mycoplasmalike organism associated with diseased soybeans in Mexico. Plant
Dis. 68:994996.
Fortnum, B. A., and Lewis, S. A. 1983. Effects of growth regulators and nematodes on Cylindrocladium black root rot of soybean. Plant Dis. 67:282284.
Gangopadhyay, S., Wyllie, T. D., and Luedders, V. D. 1970. Charcoal rot disease of soybean transmitted by seeds. Plant Dis. Rptr. 54:10881091.
GarciaJiminez, J., and Alfaro, A. 1985. Colletotrichum gloeosporioides: A new anthracnose pathogen of soybean in Spain. Phytopathology 69:1007.
Garzonio, D. M., and McGee, D. C. 1981. Pod and stem blight of soybean: The relative importance of seedborne and soilborne inoculum. (Abstr.) Phytopathology
71:218.
Garzonio, D. M., and McGee, D. C. 1983. Comparison of seeds and crop residues as sources of inoculum for pod and stem blight of soybeans. Plant Dis. 67:1374
1376.
Gillaspie, A. G., Jr., and Hopkins, M. S. 1991. Spread of peanut stripe virus from peanut to soybean and yield effects on soybean. Plant Dis. 75:11571159.
Gleason, M. L., and Ferriss, R. S. 1985. Irifluence of soil water potential on performance of soybean seeds infected by Phomopsis sp. Phytopathology 75:1236
1241.
Gleason, M. L., and Ferriss, R. S. 1987. Effects of soil moisture and temperature on Phomopsis seed decay of soybean in relation to host and pathogen growth rates.
Granada, G. A. 1979. Machismo disease of soybeans. I. Symptomatology and transmission. Plant Dis. Rptr. 63:4750.
Granada, G. A. 1979. Machismo disease of soybeans. II. Suppressive effects of tetracycline on symptom development. Plant Dis. Rptr. 63:309312.
Grau, C. R., Radke, V. L., and Gillespie, F. L. 1982. Resistance of soybean cultivars to Sclerotinia sclerotiorum. Plant Dis. 66:506508.
Gray, F. A., RodriguezKabana, R., and Adams, J. R. 1980. Neocosmospora stem rot of soybeans in Alabama. Plant Dis. 64:321322.
Gray, L. E. 1971. Variation in pathogenicity of Cephalosporium gregatum isolates. Phytopathology 61:14101411.
Gray, L. E. 1972. Recovery of Cephalosporium gregatum from soybean straw. Phytopathology 62:13621364.
Gray, L. E. 1991. Alternate hosts of soybean SDS strains of Fusarium solani. (Abstr.) Phytopathology 81:1135.
Groth, D. E., and Braun, E. J. 1989. Survival, seed transmission, and epiphytic development of Xanthomonas campestris pv. glycines in the northcentral United
Grybauskas, A. P. 1986. First report of soybean naturally infected with Leptosphaerulina briosiana. Plant Dis. 70:1159.
Guy, S. O., Grau, C. R., and Oplinger, E. S. 1989. Effect of temperature and soybean cultivar on metalaxyl efficacy against Phytophthora megasperma f. sp.
glycinea. Plant Dis. 73:236239.

Page 687
Hartman, G. L., and Sinclair, J. B. 1988. Dactuliochaeta, a new genus for the fungus causing red leaf blotch of soybeans. Mycologia 80:696706.
Hartman, G. L., Manandhar, J. B., and Sinclair, J. B. 1986. Incidence of Colletotrichum spp. on soybeans and weeds in Illinois and pathogenicity of
Colletotrichum truncatum. Plant Dis. 70:780782.
Hartman, G. L., Datnoff, L. E., Levy, C., Sinclair, J. B., Cole, D. L., and Javaheri, F. 1987. Red leaf blotch of soybeans. Plant Dis. 71:113118.
Heinrichs, E. A., Lehman, P. S., and Corss, I. C. 1976. Nematospora coryli yeastspot disease of soybeans in Brazil. Plant Dis. Rptr. 60:508509.
Helbig, J. B., and Carroll, R. B. 1982. Weeds as a source of Fusarium oxysporum pathogenic on soybean. (Abstr.) Phytopathology 72:707.
Helbig, J. B., and Carroll, R. B. 1984. Dicotyledonous weeds as a source of Fusarium oxysporum pathogenic on soybean. Plant Dis. 68:694696.
Hershman, D. E., Hendrix, J. W., Stuckey, R. E. Bachi, P. R., and Henson, G. 1990. Influence of planting date and cultivar on soybean sudden death syndrome in
Kentucky. Plant Dis. 74:761766.
Higley, P. M., and Tachibana, H. 1987. Physiologic specialization of Diaporthe phaseolorum var. caulivora in soybean. Plant Dis. 71:815817.
Hill, J. H., Bailey, T. B., Benner, H. I., Tachibana, H., and Durand, D. P. 1987. Soybean mosaic virus: Effects of primary disease incidence on yield and seed quality.
Plant Dis. 71:237239.
Hill, J. H., Lucas, B. S., Benner, H. I., Tachibana, H., Hammond, R. B., and Pedigo, L. P. 1980. Factors associated with the epidemiology of soybean mosaic virus
in Iowa. Phytopathology 70:536540.
Hirrel, M. C. 1983. Sudden death syndrome of soybean: A disease of unknown etiology. (Abstr.) Phytopathology 73:501.
Hirrel, M. C. 1984. Influence of overhead irrigation and row width on foliar and stem diseases of soybeans. (Abstr.) Phytopathology 74:628.
Hobbs, T. W., Schmitthenner, A. F., and Ellett, C. W. 1981. Diaporthe dieback of soybean caused by Diaporthe phaseolorum var. caulivora. (Abstr.)
Hobbs, T. W., Schmitthenner, A. F., Ellett, C. W., and Hire, R. E. 1981. Top dieback of soybean caused by Diaporthe phaseolorum var. caulivora. Plant Dis.
65:618620.
Irwin, J. A. G. 1991. Phytophthora macrochlamydospora, a new species from Australia. Mycologia 83:517519.
Iwaki, M., Roechan, M., Hibino, H., Tochihara, H., and Tantera, D. M. 1980. A persistent aphidborne virus of soybean, Indonesian soybean dwarf virus. Plant Dis.
64:10271030.
Iwaki, M., Thongmeearkom, P., Prommin, M., Honda, Y., and Hibi, T. 1982. Whitefly transmission and some properties of cowpea mild mottle virus on soybean in
Thailand. Plant Dis. 66:365368.
Iwaki, M., Thongmeearkom, P., Honda, Y., and Deena, N. 1983. Soybean crinkle leaf: A new whiteflyborne disease of soybean. Plant Dis. 67:546548.
Iwaki, M., Isogawa, Y., Tsuzuki, H., and Honda, Y. 1984. Soybean chlorotic mottle, a new caulimovirus on soybean. Plant Dis. 68:10091011.
Jain, R. K., McKern, N. M., Tolin, S. A., Hill, J. H., Barnett, O. W., Tosic, M., Ford, R. E., Beachy, R. N., Yu, M. H., Ward, C. W., and Shula, D. D. 1992.
Confirmation that fourteen potyvirus isolates from soybean are strains of one virus by comparing coat protein peptide profiles. Phytopathology 82:294299.
Jeger, M. J., Kenerly, C. M., Gerik, T. J., and Kock, D. O. 1987. Spatial dynamics of Phyma

Page 688
totrichum root rot in row crops in the Blackland region of north central Texas. Phytopathology 77:16471656.
Jin, H., Hartman, G. L., Nickell, C. D., and Widholm, J. M. 1996. Phytoxicity of culture filtrate from Fusarium solani, the causal agent of sudden death syndrome of
soybean. Plant Dis. 80:922927.
Joye, G. F., Berggren, G. T., and Berner, D. K. 1990. Effects of row spacing and withinrow plant population on Rhizoctonia aerial blight of soybean and soybean
yield. Plant Dis. 74:158160.
Keeling, B. L. 1987. Pathogenicity of two Diaporthe spp. isolates from soybean plants with ''sudden death syndrome" disease symptoms. (Abstr.) Phytopathology
77:1738.
Keeling, B. L. 1988. Influence of temperature on growth and pathogenicity of geographic isolates of Diaporthe phaseolorum var. caulivora. Plant Dis. 72:220222.
Kennedy, B. W., and Tachibana, H. 1973. Bacterial diseases, pp. 491504. In B. E. Caldwell (ed.), Soybeans: Improvement, Production and Uses. American
Society of Agronomy, Madison, WI.
Khan, M., and Sinclair, J. B. 1992. Pathogenicity of sclerotia and nonsclerotiaforming isolates of Colletotrichum truncatum on soybean plants and roots.
Killebrew, J. F., Roy, K. W., Lawrence, G. W., McLean, K. S., and Hodges, H. H. 1988. Greenhouse and field evaluation of Fusarium solani pathogenicity to
soybean seedlings. Plant Dis. 72:10671070.
Kuhn, C. W., Demski, J. W., and Harris, H. B. 1972. Peanut mottle virus in soybeans. Plant Dis. Rptr. 56:146147.
Kulik, M. M. 1988. Observations by scanning electron and brightfield microscopy on the mode of penetration of soybean seedlings by Phomopsis phaseoli. Plant
Dis. 72:115118.
Kunwar, I. K., Manandhar, J. B., and Sinclair, J. B. 1986. Histopathology of soybean seeds infected with Alternaria alternata. Phytopathology 76:543546.
Kunwar, I. K., Singh, T., Machado, C. C., and Sinclair, J. B. 1986. Histopathology of soybean seed and seedling infection by Macrophomina phaseolina.
Kuruppu, P. U., and Russin, J. S. 1997. Soil temperature effects on survival and infectivity of soybean red crown rot fungus, Calonectria ilicicola. (Abstr.).
Phytopathology 87: S55.
Lakshminarayana, C. S., and Joshi, L. K. 1978. Myrothecium disease of soybean in India. Plant Dis. Rptr. 62:231234.
Lalitha, B., Snow, J. P., and Berggren, G. T. 1989. Phytotoxin production by Diaporthe phaseolorum var. caulivora, the causal organism of stem canker of
soybean. Phytopathology 79:499504.
Laviolette, F. A., and Athow, K. L. 1971. Relationship of age of soybean seedlings and inoculum to infection by Pythium ultimum. Phytopathology 61:439440.
Leath, S., and Carroll, R. B. 1982. Screening for resistance to Fusarium oxysporum in soybean. Plant Dis. 66:11401143.
Lin, M. T., and Hill, J. H. 1983. Bean pod mottle virus: Occurrence in Nebraska and seed transmission in soybeans. Plant Dis. 67:230233.
Lockwood, J. L., Yoder, D. L., and Smith, N. A. 1970. Thielaviopsis basicola root rot of soybeans in Michigan. Plant Dis. Rptr. 54:849850.
Lohnes, D. G., and Nickell, C. D. 1994. Effects of powdery mildew alleles Rmdc, Rmd, and

Page 689
rmd on yield and other characteristics in soybean. Plant Dis. 78:299301.
Manandhar, J. B., Hartman, G. L., and Sinclair, J. B. 1986. Colletotrichum destructivum, the anamorph of Glomerella glycines. Phytopathology 76:282285.
Manandhar, J. B., Hartman, G. L., and Sinclair, J. B. 1988. Soybean germplasm evaluation for resistance to Colletotrichum truncatum. Plant Dis. 72:5659.
Marchett, M. A., Vecker, F. A., and Bromfield, K. R. 1975. Uredial development of Phakopsis pachyrhizi in soybeans. Phytopathology 65:822823.
Martin, K. F., and Walters, H. J. 1982. Infection of soybean by Cercospora kikuchii as affected by dew, temperature and duration of dew periods. (Abstr.)
McDaniel, L. L., Maratos, M. L., Goodman, J. E., and Tolin, S. A. 1995. Partial characterization of a soybean strain of tobacco mosaic virus. Plant Dis. 79:206211.
McGawley, E. C., Winchell, K. L., and Berggren, G. T. 1984. Possible involvement of Hoplolaimus galeatus in a disease complex of 'Centennial' soybean. (Abstr.)
McGee, D. C. 1992. Soybean Diseases: A Reference Source for Seed Technologists. American Phytopathological Society, St. Paul, MN. 151 pp.
McGee, D. C., and Biddle, J. 1985. A comparison between isolates of Diaporthe phaseolorum var. caulivora from soybean seeds in Iowa and stemcankered
soybeans in southern states. (Abstr.) Phytopathology 75:1332.
McGee, D. C., and Biddle, J. 1987. Seedborne Diaporthe phaseolorum var. caulivora in Iowa and its relationship to soybean stem canker in the southern United
McLaughlin, M. R., Thongmeearkom, P., Goodman, R. M., Milbrath, G. M., Ries, S. M., and Royse, D. J. 1978. Isolation and beetle transmission of cowpea
mosaic virus (severe subgroup) from Desmodium canescens and soybeans in Illinois. Plant Dis. Rptr. 62:10691073.
McLean, K. S., and Roy, K. W. 1988. Purple seed stain of soybeans caused by isolates of Cercospora kikuchii from weeds. Can. J. Plant Pathol. 10:166171.
Melching, J. S., Dowler, W. M., Koogle, D. L., and Royer, M. H. 1988. Effect of plant and leaf age on susceptibility of soybeans to soybean rust. Can. J. Plant
Pathol. 10:3035.
Melching, J. S., Dowler, W. M., Koogle, D. L., and Royer, M. H. 1989. Effects of duration, frequency, and temperature of leaf wetness periods on soybean rust.
Plant Dis. 73:117122.
Mengistu, A., and Grau, C. R. 1986. Variation in morphological, cultural, and pathological characteristics of Phialophora gregata and Acremonium sp. recovered
from soybean in Wisconsin. Plant Dis. 70:10051009.
Mengistu, A., and Grau, C. R. 1987. Seasonal progress of brown stem rot and its impact on soybean productivity. Phytopathology 77:15211529.
Meyer, W. A., and Sinclair, J. B. 1972. Root reduction and stem lesion development on soybeans by Phytophthora megasperma var. sojae. Phytopathology
62:14141416.
Meyer, W. A., Sinclair, J. B., and Khare, M. N. 1974. Factors affecting charcoal rot of soybean seedlings. Phytopathology 64:845849.
Milbrath, G. M., and Tolin, S. E. 1977. Identification host range and serology of peanut stunt virus isolated from soybean. Plant Dis. Rptr. 61:637640.
Mishra, B., and Prakash, O. 1975. Alternaria leaf spot of soybean from India. Indian J. Mycol. Plant Pathol. 5:95.
Moots, C. K., Nickell, C. D., and Gray, L. E. 1988. Effects of soil compaction on the inci

Page 690
dence of Phytophthora megasperma f. sp. glycinea in soybean. Plant Dis. 72:896900.
Muchovej, J. J., and Kimura, S. 1988. Cotyledon spot of soybean caused by seedborne Curvularia lunata var. aerea in Brazil. Plant Dis. 72:268.
Narayanasamy, P., and Durairaj, P. 1971. A new blight disease of soybeans. Madras Agric. J. 58:711712.
Nelson, B., Helms, T., Christianson, T., and Kural, I. 1996. Characterization and pathogenicity of Rhizoctonia from soybean. Plant Dis. 80:7480.
Nicholson, J. F., Dhingra, O. D., and Sinclair, J. B. 1972. Internal seedborne nature of Sclerotinia sclerotiorum and Phomopsis sp. and their effects on soybean
seed quality. Phytopathology 62:12611263.
O'Neill, N. R., Rush, M. C., Horn, N. L., and Carver, R. B. 1977. Aerial blight of soybeans caused by Rhizoctonia solani. Plant Dis. Rptr. 61:713717.
Otazu, V., Epstein, A. H., and Tachibana, H. 1981. Water stress effect on the development of brown stem rot of soybeans. (Abstr.) Phytopathology 71:247.
Pacumbaba, R. P. 1995. Seed transmission of soybean mosaic virus in mottled and nonmottled soybean seeds. Plant Dis. 79:193195.
Padgett, G. B., Snow, J.P., and Berggren, G. T. 1991. Effects of temperature on production of perithecia and pycnidia by Diaporthe phaseolorum vat. caulivora.
Park, E. W., and Lim, S. M. 1985. Overwintering of Pseudomonas syringae pv. glycinea in the field. Phytopathology 75:520524.
Pataky, J. K., and Lim, S. M. 1981. Effects of Septoria brown spot on yield components of soybean. (Abstr.) Phytopathology 71:248.
Pathan, M. A., Sinclair, J. B., and McClary, R. D. 1989. Effects of Cercospora kikuchii on soybean seed germination and quality. Plant Dis. 73:720723.
Pearson, C. A. S., Todd, T. C., and Schwenk, F. W. 1987. Influence of soybean cyst nematode (SCN) on root colonization by Macrophomina phaseolina.
Peterson, D. J., and Edwards, H. H. 1982. Effects of temperature and leaf wetness period on brown spot disease of soybeans. Plant Dis. 66:995998.
Phillips, D. V. 1971. Influence of air temperature on brown stem of soybean. Phytopathology 61:12051208.
Phillips, D. V. 1972. A soybean disease caused by Neocosmospora vasinfecta. Phytopathology 62:612615.
Phillips, D. V., Vesper, S. J., and Turner, J. T., Jr. 1983. Verticillium nigrescens associated with soybeans. (Abstr.) Phytopathology 73:504.
Ploetz, R. C., and Shokes, F. M. 1989. Variability among isolates of Diaporthe phaseolorum f. sp. meridionalis in different vegetative compatibility groups. Can. J.
Bot. 67:27512755.
Reis, C. H., Alves, A. M. C., and Kitajima, E. 1991. Studies with soybean yellow shoot virus: New potyvirus detected in Brazil. (Abstr.) Phytopathology 81:693.
Roane, C. W., and Roane, M. K. 1976. Erysiphe and Microsphaera as dual causes of powdery mildew of soybeans. Plant Dis. Rptr. 60:611612.
Roongruangsree, UTai, Olson, L. W., and Lange, L. 1988. The seedborne inoculum of Peronospora manshurica, causal agent of soybean downy mildew. J.
Rosenbrock, S. M., and Wyllie, T. D. 1987. Leptosphaerulina leaf spot of soybeans in Missouri. (Abstr.) Phytopathology 77:1689.

Page 691
Rothrock, C. S., Phillips, D. V., and Hobbs, T. W. 1988. Effects of cultivar, tillage, and cropping system on infection of soybean by Diaporthe phaseolorum var.
caulivora and southern stem canker symptom development. Phytopathology 78:266270.
Roy, K. W. 1982. Seedling diseases caused in soybean by species of Colletotrichum and Glomerella. Phytopathology 72:10931096.
Roy, K. W. 1997. Fusarium solani on soybean roots: Nomenclature of the causal agent of sudden death syndrome and identity and relevance of F. solani form B.
Plant Dis. 81:259266.
Roy, K. W. 1997. Sporulation of Fusarium solani f. sp. glycines, causal agent of sudden death syndrome, on soybeans in the midwestern and southern United
Roy, K. W., and Abney, T. S. 1977. Antagonism between Cercospora kikuchii and other seedborne fungi of soybeans. Phytopathology 67:10621066.
Roy, K. W., and McLean, K. 1984. Epidemiology of soybean stem canker in Mississippi. (Abstr.) Phytopathology 74:632.
Roy, K. W., and Miller, W. A. 1983. Soybean stem canker incited by isolates of Diaporthe and Phomopsis spp. from cotton in Mississippi. Plant Dis. 67:135137.
Roy, K. W., and Ratnayake, S. 1997. Frequency of occurrence of Fusarium pallidoroseum, effects on seeds and seedlings, and associations with other fungi in
soybean seeds and pods. Can. J. Plant Pathol. 19:188192.
Roy, K. W., Rupe, J. C., Hershman, D. E., and Abney, S. T. 1997. Sudden death syndrome of soybean. Plant Dis. 81:11001111.
Rupe, J. C., and Ferriss, R. S. 1984. The effect of moisture on infection of soybean seed by Phomopsis sp. (Abstr.) Phytopathology 74:632.
Rupe, J. C., Gbur, E. E., and Marx, D. M. 1991. Cultivar responses to sudden death syndrome of soybean. Plant Dis. 75:4750.
Rupe, J. C., Sutton, E. A., Becton, C. M., and Gbur, E. E. Jr., 1996. Effect of temperature and wetness period on recovery of the southern biotype of Diaporthe
phaseolorum var. caulivora from soybean. Plant Dis. 80:255257.
Russin, J. S., Layton, M. B., McGawley, E. C., Boethel, D. J., Berggren, G. T., and Snow, J. P. 1987. Interactions between soybean looper, stem canker fungus,
and soybean cyst nematode on soybean. (Abstr.) Phytopathology 77:1690.
Russin, J. S., Orr, D. B., Layton, M. B., and Boethel, D. J. 1988. Incidence of microorganisms in soybean seeds damaged by stink bug feeding. Phytopathology
78:306310.
Saharan, G. S., and Gupta, V. K. 1972. Pod rot and collar rot of soybean caused by Fusarium semitectum. Plant Dis. Rptr. 56:693694.
Schiller, C. T., Ellis, M. A., Tenne, F. D., and Sinclair, J. B. 1977. Effect of Bacillus subtilis on soybean seed decay, germination, and stand inhibition. Plant Dis.
Rptr. 61:213217.
Schiller, C. T., Hepperly, P. R., and Sinclair, J. B. 1978. Pathogenicity of Myrothecium roridum from Illinois soybeans. Plant Dis. Rptr. 62:882885.
Schlub, R. L., and Lockwood, J. L. 1981. Etiology and epidemiology of seedling rot of soybean by Pythium ultimum. Phytopathology 71:134138.
Schlub, R. L., Lockwood, J. L., and Komada, H. 1981. Colonization of soybean seeds and plant tissue by Fusarium species in soil. Phytopathology 71:693696.
Schneider, R. W., Dhingra, O. D., Nicholson, J. F., and Sinclair, J. B. 1974. Colletotrichum truncatum borne within the seed coat of soybean. Phytopathology
64:154155.
Schuh, W. 1991. Influence of temperature and leaf wetness period on conidial germina

Page 692
tion in vitro and infection of Cercospora kikuchii on soybean. Phytopathology 81:13151318.
Schuh, W. 1991. Relationship between pod development stage, temperature, pod wetness duration and incidence of purple seed stain of soybeans. (Abstr.)
Schuh, W. 1992. Effect of pod development stage, temperature, and pod wetness duration on the incidence of purple seed stain of soybeans. Phytopathology
82:446451.
Schwenk, F. W., and Nickell, C. D. 1980. Soybean green stem caused by bean pod mottle virus. Plant Dis. 64:863865.
Schwenk, F. W., and Paxton, J. D. 1981. Trifluralin enhancement of Phytophthora root rot of soybean. Plant Dis. 65:435436.
Seaman, W. L., Shoemaker, R. A., and Peterson, E. A. 1965. Pathogenicity of Corynespora cassiicola on soybeans. Can. J. Bot. 43:14611469.
Sherwood, J. L., and Jackson, K. E. 1985. Tobacco streak virus in soybean in Oklahoma. Plant Dis. 69:727.
Short, G. E., Wyllie, T. D., and Bristow, P. R. 1980. Survival of Macrophomina phaseolina in soil and in residue of soybean. Phytopathology 70:1317.
Shortt, B. J., Sinclair, J. B., and Kogan, M. 1981. Soybean seed quality losses associated with bean leaf beetles and Alternaria tenuissima. (Abstr.) Phytopathology
71:1117.
Sinclair, J. B. (ed.) 1982. Compendium of Soybean Diseases, Second Edition. American Phytopathological Society, St. Paul, MN. 104 pp.
Sinclair, J. B. 1993. Phomopsis seed decay of soybean—A prototype for studying seed disease. Plant Dis. 77:329334.
Sinclair, J. B., and Backman, P. A. 1989. Compendium of Soybean Diseases, Third Edition. American Phytopathological Society, St. Paul, MN. 106 pp.
Smith, E. F., and Backman, P. A. 1989. Epidemiology of soybean stem canker in the southeastern United States: Relationship between time of exposure to inoculum
and disease severity. Plant Dis. 73:464468.
Song, H. S., Lira, S. M., and Clark, J. M., Jr. 1993. Purification and partial characterization of a hostspecific pathotoxin from culture filtrates of Septoria glycines.
Sortland, M. E., and MacDonald, D. H. 1986. Development of a population of Heterodera glycines race 5 at four soil temperatures in Minnesota. Plant Dis.
70:932935.
Spilker, D. A., Schmitthenner, A. F., and Ellett, C. W. 1981. Effects of humidity, temperature, fertility and cultivar on the reduction of soybean seed quality by
Phomopsis sp. Phytopathology 71:10271029.
Stall, R. E., and Kucharek, T. A. 1982. A new bacterial disease of soybean in Florida. (Abstr.) Phytopathology 72:990.
Stewart, R. D. 1957. An undescribed species of Pyrenochaeta on soybean. Mycologia 49:115117.
Stuckey, R. E., Ghabrial, S. A., and Reicosky, D. A. 1982. Increased incidence of Phomopsis sp. in seeds from soybeans infected with bean pod mottle virus. Plant
Dis. 66:826829.
Subba Rao, K. V., Padgett, G. B., Berner, D. K., Berggren, G. T., and Snow, J. P. 1990. Choanephora leaf blight of soybeans in Louisiana. Plant Dis. 74:614.
Tachibana, H. 1971. Virulence of Cephalosporium gregatum and Verticillium dahliae in soybeans. Phytopathology 61:565568.

Page 693
Tachibana, H., and Shih, S. 1965. A leafcrinkling bacterium of soybean. Plant Dis. Rptr. 49:396397.
Tachibana, H., Jowett, D. D., and Fehr, W. R. 1971. Determination of losses in soybeans caused by Rhizoctonia solani. Phytopathology 61:14441446.
Thompson, T. B., Athow, K. L., and Laviolette, F. A. 1971. The effect of temperature on the pathogenicity of Pythium aphanidermatum, P. debaryanum, and P.
ultimum on soybean. Phytopathology 61:933935.
Thouvenel, J. C., Monsarrat, A., and Fauquet, C. 1982. Isolation of cowpea mild mottle virus from diseased soybeans in the Ivory Coast. Plant Dis. 66:336337.
Vakili, N. G., and Bromfield, K. R. 1976. Phakopsora rust on soybean and other legumes in Puerto Rico. Plant Dis. Rptr. 60:995999.
Velicheti, R. K., and Sinclair, J. B. 1989. Detection of Fusarium oxysporum in symptomatic soybean seeds. (Abstr.) Phytopathology 79: 1006.
Velicheti, R. K., and Sinclair, J. B. 1994. Production of cercosporin and colonization of soybean seed coats by Cercospora kikuchii. Plant Dis. 78:342346.
Velicheti, R. K., Kollipara, K. P., Sinclair, J. B., and Hymowitz, T. 1992. Selective degradation of proteins by Cercospora kikuchii and Phomopsis longicolla in
soybean seed coats and cotyledons. Plant Dis. 76:779782.
Vesper, S. J., Turner, J. T., Jr., and Phillips, D. V. 1983. Incidence of Verticillium nigrescens in soybeans. Phytopathology 73:13381341.
Walters, H. J. 1980. Soybean leaf blight caused by Cercospora kikuchii. Plant Dis. 64:961962.
Walters, H. J., and Martin, K. F. 1981. Phyllosticta sojaecola on pods of soybeans in Arkansas. Plant Dis. 65:161162.
Warwick, D., and Demski, J. W. 1988. Susceptibility and resistance of soybean to peanut stripe virus. Plant Dis. 72:1921.
Weldekidan, T., Carroll, R. B., and Evans, T. A. 1988. Association of Fusarium oxysporum with a new viruslike disease affecting Delaware soybeans. (Abstr.)
Welderkidan, T., Evans, T. A., Carroll, R. B., and Mulrooney, R. P. 1992. Etiology of soybean severe stunt and some properties of the causal virus. Plant Dis.
76:747750.
Wicklow, D. T., Bennett, G. A., and Shotwell, O. L. 1987. Secondary invasion of soybeans by Fusarium graminearum and resulting mycotoxin contamination.
Plant Dis. 71:1146.
Wilcox, J. R., and Abney, T. S. 1973. Effects of Cercospora kikuchii on soybeans. Phytopathology 63:796797.
Wilmot, D. B., Nickell, C. D., and Gray, L. E. 1989. Physiologic specialization of Phialophora gregata on soybean. Plant Dis. 73:290294.
Wrather, J. A., Anderson, S. H., and Wollenhaupt, N. C. 1991. Effects of tillage and row spacing on soybean foliar diseases, and Heterodera glycines population
dynamics. (Abstr.) Phytopathology 81:1185.
Wrather, J. A., Kendig, S. R., and Tyler, D. D. 1998. Tillage effects on Macrophomina phaseolina population density and soybean yield. Plant Dis. 82:247250.
Wyllie, T. D., and Rosenbroek, S. M. 1985. Crop rotation as a means of controlling populations of Macrophomina phaseolina in Missouri soils. (Abstr.)
Yang, X. B., Berggren, G. T., and Snow, J. P. 1988. Effect of free moisture and plant growth

Page 694
stage on disease focus development in Rhizoctonia aerial blight of soybean. (Abstr.) Phytopathology 78:1538.
Yang, X. B., Berggren, G. T., and Snow, J. P. 1988. Seedling infection of soybean by Rhizoctonia solani AG1, causal agent of aerial blight. Plant Dis. 72:644.
Yang, X. B., Berggren, G. T., and Snow, J. P. 1990. Seedling infection of soybean by isolates of Rhizoctonia solani AG1, causal agent of aerial blight and web
blight of soybean. Plant Dis. 74:485488.
Yang, X. B., Berggren, G. T., and Snow, J. P. 1990. Types of Rhizoctonia foliar blight on soybean in Louisiana. Plant Dis. 74:501504.

Page 695
19.
Diseases of Sugar Beet (Beta vulgaris)
Bacterial Leaf Spot
Cause.
Pseudomonas syringae (syn. P. apatata) survives on living plants, seed, and infested organic matter in the soil. Dissemination is by seed, but wounds are necessary
for infection to occur. Some research suggests that bacteria penetrate roots through wounds and move upward in the infected plant. Bacterial growth is optimum at
temperatures of 25° to 30°C.
Distribution.
Europe, Japan, and the United States.
Symptoms.
A seedling blight may occur. Dark brown to black streaks and spots occur on diseased leaves and infrequently on petioles and seed stalks.
Management
2. Apply seedtreatment fungicides.
Bacterial Pocket
Bacterial pocket is also called bacterial canker.
Cause.
Xanthomonas beticola survives in soil for long periods of time and is disseminated by any means that moves soil, such as irrigation water and machinery.
Xanthomonas beticola enters roots through wounds at or near the crown level. Normally only scattered plants are affected but occasionally an entire field of plants
shows symptoms if a hailstorm has occurred. The hail stones injure crowns and provide entrance wounds for bacteria to infect the injured plants.
Distribution.
The United States (Colorado, Maryland, Michigan, New Mexico, Utah, Virginia, Wisconsin, and Wyoming).

Page 696
Symptoms.
Galls develop on diseased crowns at the soil surface and also on the petioles and roots. The central portion of galls are watersoaked and discolored yellow due to the
presence of bacteria. Galls become rough and fissured as they enlarge, and the top of the diseased root becomes larger. The root surface below the galls also
becomes rough, ridged, and fissured. In the later stages of bacterial pocket, an abnormal number of leaves may develop.
Management
1. Grow sugar beet every 4 to 5 years in the same soil.
2. Provide proper soil fertility.
3. Avoid mechanical injury to plants.
Bacterial Vascular Necrosis and Soft Rot
Bacterial vascular necrosis and soft rot is also called Erwinia soft rot.
Cause.
Erwinia carotovora pv. betavasculorum survives in unharvested sugar beet and, for a short time, in soil and on weeds. Betavasculorum is sometimes referred to as
a subspecies. Bacteria are disseminated with soil and deposited in crowns, where infection begins as bacteria enter the plant, primarily through wounds. The vascular
tissue (xylem) of petioles and roots is invaded. Bacteria then multiply in the xylem tissue and progress toward the root tips. Optimum disease development occurs at
temperatures of 25° to 30°C. Young plants are the most susceptible to infection.
Disease occurs in low, poorly drained areas of fields and in furrowirrigated fields. Other factors that aid in the predisposition of sugar beet to disease are surplus or
adequate nitrogen applied to soils; a wide plant spacing, which results in rapid and succulent plant growth; and the use of sprinkler irrigation, which keeps wounds
moist for a long time and disseminates the causal bacteria.
Differences in aggressiveness exist among strains.
Distribution.
The United States (Arizona, California, Idaho, Texas, and Washington).
Symptoms.
Diseased beets are not easily recognized in the field until they are severely rotted. Symptoms include a gray to black, watery, internal rot of diseased taproots. The
vascular bundles in diseased roots are necrotic or discolored. Black longitudinal lesions run up the petioles. A black or foamy white exudate may occur on split crowns
of roots and on petiole lesions. Root tissue surrounding diseased vascular bundles turns pink to redbrown when it is exposed to air. Severely diseased roots become
hollow but the plant normally remains alive.
Management
1. Avoid practices that deposit soil in crowns or cause injury to crowns and petioles.

Page 697
2. Provide adequate drainage.
4. Sow early in the growing season and maintain optimum stands.
5. Use judicious amounts of nitrogen fertilizer.
Corynebacterium Infection
Cause.
Corynebacterium sepedonicum (syn. Clavibacter michiganense subsp. sepedonicum) is seedborne. Corynebacterium sepedonicum may be systemic and move
from roots into seeds. Strains of C. sepedonicum isolated from sugar beet seed were identical to strains causing potato bacterial ring rot.
Distribution.
The United States (Oregon).
Symptoms.
Sugar beet roots are symptomless. However, diseased sugar beets may be a source of inoculum for infecting potatoes grown in the field following sugar beet, thus
preventing the successful and permanent eradication of the potato bacterial ring rot disease.
Management.
Not reported.
Crown Gall
Cause.
Agrobacterium tumefaciens is a soil inhabitant and pathogen of several plant hosts. Bacteria enter roots through wounds caused by several agents. The production of
indoleacetic acid by A. tumefaciens is associated with gall formation and hypertrophy of diseased sugar beet tissues.
Distribution.
Wherever sugar beet is grown.
Symptoms.
Initially, small, wartlike growths form on diseased roots and soon develop into galls of various sizes. Diseased sugar beet plants are rarely killed but growth may be
stunted and the sugar content lowered. Galls are harvested along with roots; consequently, there is little loss in total weight.
Management.
Not necessary, since crown gall is seldom serious.
Scab
Cause.
Streptomyces scabies (syn. Actinomycetes scabies) is an actinomycete that survives in soil and infested plant residue as mycelia and spores. Infection occurs most
frequently in dry, light, sandy soils that have a neutral or slightly alkaline pH by hyphae growing into minute wounds or lenticels.
Distribution.
Wherever sugar beet is grown, but Fusarium head blight is a minor problem.

Page 698
Symptoms.
Small round spots that occur on diseased roots enlarge, turn brown, and rupture the epidermis. Eventually, raised corky areas occur that vary in size and shape to
resemble ''miniature raised terraces." The color of the scabby area varies from graywhite to dark tan. Sometimes the scabby area may be pitted or pocked, but the
injury is usually superficial and no decomposition occurs. Occasionally, taproots have brown, corky lesions that can restrict growth and cause roots to be "turnip
shaped."
Management.
Not necessary, since the appearance rather than the actual value of diseased beets is affected.
Cause.
Alternaria alternata (syn. A. tenuis) overwinters in infested plant residue as conidia and saprophytic mycelial growth. In the spring or during favorable growth
conditions for A. alternata, conidia, which are produced on residue and diseased plant tissue and disseminated by wind, primarily infect host plants that are deficient
in magnesium, manganese, phosphorous, or potassium. Alternaria brassicae infects yellowed tissue and is a foliar pathogen of some hybrids. Plants infected with
western yellows virus (WYV) are more likely to become infected than sugar beets without WYV. Infection occurs at temperatures of 7° to 10°C and high humidity.
Distribution.
Wherever sugar beet is grown. Alternaria leaf spot is most common in Europe.
Symptoms.
Symptoms occur late in the growing season. Initially, lesions are dark brown, zonate, circular to irregularshaped areas (210 mm in diameter). The dark brown
necrotic spots coalesce and form irregularshaped areas on diseased leaves.
Management.
Vigorous healthy plants do not ordinarily become diseased.
Aspergillus fumigatus Storage Rot
Cause.
Aspergillus fumigatus invades roots at temperatures of 30°C or more. The slimeproducing bacterium Leuconostoc mesenterioides, a secondary invader, is often
found in association with A. fumigatus.
Distribution.
Widespread. Aspergillus fumigatus was previously known to be a common saprophyte on beets in storage.
Symptoms.
A generic rot has been described.
Management
1. Reduce temperature of stored beets to below 30°C.

Page 699
2. Hybrids and breeding lines with resistance to Rhizoctonia solani are also resistant to A. fumigatus at temperatures of 30°C or less.
Beet Rust
Cause.
Uromyces betae is an autoecious rust that produces pycnia, aecia, uredinia, and telia only on sugar beet and other varieties of Beta vulgaris. Uromyces betae
overwinters as uredinia and telia on volunteer host plants and infested residue, and may be seedborne. Uredinia and telia are produced during damp, cool weather in
the summer. Aecia may be produced in the autumn or in the spring on sugar beet plants, usually the secondyear beets grown for seed production. Optimum disease
development occurs during moist weather at temperatures of 15° to 22°C.
Distribution.
Asia, Europe, and the United States (Arizona, California, New Mexico, and Oregon). Beet rust is of minor economic importance.
Symptoms.
Initially, pustules, which appear as slight raised areas surrounded by a chlorotic halo, are randomly dispersed or aggregated in rings on the green tissue of leaves, seed
stalks, and petioles. The epidermis ruptures and exposes urediniospores and teliospores in redbrown pustules that average 2 mm in diameter. Pustules become dark
brown toward the end of the growing season.
Management.
Beet Tumor
Beet tumor is also called crown wart.
Cause.
Physoderma leproides (syn. Urophylyctis leproides) survives as resting sporangia in infested residue in soil. Sporangia are disseminated primarily by splashing
water. Only older leaves become diseased. In Europe, beet tumor is associated with wet soils in irrigated areas.
Distribution.
Argentina, Europe, North Africa, and the United States (California). Beet tumor is not an economically important disease.
Symptoms.
Galls occur on diseased leaf blades, petioles, and crowns of beets. Galls on leaf blades and petioles are greenbrown, roughtextured, and less than 1 cm in diameter.
Eventually the small galls coalesce and form larger galls that extend over the entire diseased leaf blade. Diseased leaves are stunted and malformed.
Galls on diseased crowns are attached by a narrow base and are sometimes 8 to 10 cm in diameter on mature sugar beet. These galls vary from red to greenbrown.
When galls are cut open, small cavities filled with brown spores can be seen. No galls form on taproots.
Management.
Not reported.

Page 700
Black Root
The damping off phase is also called Aphanomyces seedling disease. A Pythium sp. and a Rhizoctonia sp., two fungi implicated in the black root complex, cause a
damping off of seedlings. However, since Aphanomyces cochlioides infects plants throughout the growing season, it will be the causal agent discussed here.
Cause.
Aphanomyces cochlioides survives as oospores in infested soil residue. Some weeds may aid in the survival and the increase of inoculum in soil. Oospores germinate
in wet soil at an optimum temperature that varies from 22° to 28°C and form sporangia in which sporangiospores are produced. After 3 to 4 hours, each
sporangiospore produces a papilla through which a zoospore is released. The zoospore "swims" to roots and germinates, forming a germ tube that penetrates the host
root. Oospores eventually form in diseased tissue.
In Spain, Aphanomyces cochlioides was associated with latesown sugar beet.
Distribution.
Canada, Europe, Japan, Spain, and the United States. Black root is most severe in the Great Lakes region of the United States.
Symptoms.
In some areas, Aphanomyces seedling disease is considered one of the most common seedling diseases of sugar beet. Seedlings commonly are killed, but disease is
also considered to be severe at times on older plants.
Initially, diseased leaves are yellowed and mottled, and plants remain stunted. Most lateral roots are dead and blackened. New roots are killed shortly after they are
produced, which causes the main roots to have a "tasseled" appearance due to the groups of dead, black, lateral roots. The ends of main roots may also have dark
lesions.
Symptoms from Spain were described as a postemergence damping off. A brown discoloration of the hypocotyl began at the soil surface and frequently extended to
the base of the cotyledons.
Management
1. Do not rotate sugar beet with legumes.
2. Control weeds.
4. Maintain welldrained soil. Limit irrigation during the seedling stage. In greenhouse studies, seedling disease incidence was reduced when soils were irrigated prior
to sowing.
Botrytis Storage Rot
Botrytis storage rot is also called clamp rot.
Cause.
Botrytis cinerea survives as sclerotia in soil or in infested residue that is incorporated into soil or is lying on the soil surface. Sclerotia germinate and produce mycelia
on which conidiophores and conidia are borne.

Page 701
Conidia disseminated by wind infect sugar beet roots through wounds. Conidia are abundantly produced on diseased tissue. Eventually, sclerotia develop in mycelium
on the outside of diseased roots and either dislodge and fall into the soil or remain attached to diseased plant tissue.
Distribution.
Symptoms.
Rotted tissue is normally dark brown or black. In the latter case, Phoma betae may also be present. Dark gray fungal growth consisting of mycelium, conidia, and
conidiophores are present on rotted tissue. Eventually, dark brown to black round sclerotia (25 mm in diameter) form in mycelia on the outsides of diseased roots.
Management.
Resistance is present in some germplasms.
Cause.
Cercospora beticola overwinters as spores and stromata on infested residue in the soil, and, following severe disease, on seed. Cercospora beticola also infects
several weed hosts, including redroot pigweed, Amaranthus retroflexus; lambsquarters, Chenopodium album; prickly lettuce, Lactua scariola; common mallow,
Malva neglecta; sweet clover, Melilotus spp.; common plantain, Plantago major; curly dock, Rumex crispus; and dandelion, Taraxacum spp. Cercospora
beticola also overwinters on infested weed residue.
In the spring or early summer, conidia are produced from mycelium and disseminated by wind, splashing rain, and insects to the leaves of host plants. Conidia
germinate optimally in the presence of free water and temperatures of 25° to 35°C and produce germ tubes that penetrate through the stomata on leaf surfaces.
Secondary infection occurs from conidia produced through the stomata within leaf spots in 7 to 21 days.
Distribution.
Wherever sugar beet is grown; however, Cercospora leaf spot is important only in areas of high relative humidity or abundant moisture.
Symptoms.
Spots occur mostly on leaves and occasionally on petioles. Initially, small, light brown spots appear on diseased older outer leaves. The circular spots rapidly increase
in size to 3 to 5 mm in diameter and become a brownish or purplish color. Numerous spots coalesce and form large necrotic areas on the diseased leaves. As the
spots mature, their centers become ash gray to black with brown to bright purple borders. Similar lesions appear on petioles; however, these lesions are normally
longer and more elliptical than the lesions on leaves. Conidia and conidiophores appear as black, dotlike structures on the centers of spots on the upper surfaces of
diseased leaves and sometimes in spots on the lower surfaces. During periods of several hours of leaf wetness and high humidity, necrotic spots become gray due to
the production of conidiophores and conidia. At this time, the "silver" conidia may be seen in the spots by using magnifi

Page 702
cation. Numerous spots cause leaves to become yellow and die. Severe disease causes the destruction of the older, outer leaves and the production of new leaves,
which results in elongated and coneshaped crowns. Blighted leaves collapse and fall to the ground but remain attached to the crowns.
The upper portion of root, which is not covered by soil, may also have spots. Such spots are slightly sunken, circular to oval (25 mm in diameter), and initially brown
purple but later become gray in the center. Tissue beneath the lesions is brown to a depth of about 1.5 mm.
Cercospora leaf spot will reduce tonnage and recoverable sugar.
Management
2. Apply foliar fungicides during the growing season before disease becomes severe. Economic losses occur when Cercospora leaf spot exceeds 3% severity by
harvest.
3. Rotate to nonhost crops for 2 to 3 years.
5. Locate new fields at least 100 m from old fields.
Charcoal Rot
Cause.
Macrophomina phaseolina (syn. M. phaseoli and Sclerotium bataticola) survives as sclerotia in soil and infested residue. Sclerotia of M. phaseolina are most
commonly disseminated by any means that moves soil. Sclerotia germinate and form germ tubes that penetrate stressed, weakened, or injured host plants. Sclerotia
are eventually formed in diseased tissue. Pycnidia infrequently may be produced on diseased plant tissue and the subsequent conidia disseminated by wind to host
plants. Charcoal rot is most severe during high soil and air temperatures (31°C is the optimum air temperature).
Distribution.
India, Russia, Ukraine, and the United States (the hot interior valleys of California).
Symptoms.
Symptoms initially occur on halfgrown and mature plants. Leaves rapidly wilt, then gradually turn brown and die but remain attached to crowns. Brownblack,
irregularshaped, necrotic areas develop only on crowns or the upper portions of roots. Diseased areas have a silvery sheen, and the outer portion of the oldest
diseased area is thin and loosely attached to the underlying tissue. Under this outer layer, the numerous black sclerotia resemble a sprinkling of charcoal. An entire
diseased root becomes discolored brownblack and has masses of sclerotia in cavities beneath the outer layer. Diseased roots may shrink and become mummified.
Management.
Not reported.

Page 703
Downy Mildew
Cause.
Peronospora farinosa (syn. P. farinosa f. sp. betae and P. schachtii) overwinters as oospores and mycelia in infested plant residue, wild and volunteer Beta spp.,
and infested seed. Sporangia are borne two ways: (1) under cool, moist conditions, oospores germinate and produce mycelia on which sporangia are borne and (2) at
temperatures of 4° to 10°C, sporangia are produced from overwintered mycelia. Sporangia are disseminated by wind to sugar beet foliage, where they germinate at
temperatures of 4° to 10°C. Infection occurs at temperatures of 7° to 15°C in the presence of relative humidities of 80% and above. Secondary inoculum is provided
by the production of sporangia that are disseminated by wind to leaves and germinate during high relative humidity. Oospores are eventually produced in diseased
leaves.
Distribution.
Europe and the United States, primarily California, Oregon, and Washington.
Symptoms.
Seedlings may be killed. The primary bud is usually destroyed in older diseased plants and plant growth stops. Symptoms occur on cotyledons, primary leaves, and
growing points. Primary leaves in the centers of crowns become infected, which results in small, distorted, thickened, light green, and puckered leaves with downward
curled margins. Both leaf surfaces are covered with a gray downy growth consisting of mycelium, conidia, and conidiophores. Diseased leaves may appear lighter
green than normal or have a distinct purple cast. In either case, the leaves eventually wilt and die. If conditions become unfavorable for the development of downy
mildew, a secondary heart rot may occur together with a chlorosis of older diseased leaves that resembles virus yellows infection.
When older leaves become infected, light green, irregularshaped spots (1225 mm in diameter) appear on the diseased upper leaf surfaces. Opposite the spots on the
upper leaf surface, the lower leaf surface is covered with a gray growth consisting of mycelium, conidia, and conidiophores. Diseased seed beets have stunted and
distorted young lateral branches. Mycelium and oospores may develop within seed clusters.
Management
1. In the United States, grow resistant cultivars.
2. In Europe, separate seed crops from root crops by 1.0 to 1.5 km.
Dry Rot Canker
Dry rot canker and Rhizoctonia crown rot are both caused by Rhizoctonia solani. However, symptoms are distinct and the two diseases are discussed separately.

Page 704
Cause.
Rhizoctonia solani survives as bulbils, or thickened hyphae, in infested residue. The fungus resumes growth and forms mycelium that penetrates the host plant. "Dry
rot" is caused by a weak strain of R. solani that infects under "dry" conditions and temperatures of 30° to 35°C. The strain of R. solani causing "dry rot" is apparently
different from those causing crown rot and root rot.
Distribution.
The United States.
Symptoms.
Initially, leaves of diseased plants wilt during the warmest part of the day but regain their turgidity at night. Eventually, leaves permanently wilt and turn brown. Root
surfaces have circular brown lesions with alternate dark and light concentric rings that develop into cavities filled with the brown pithy remains of the diseased root
tissue. There is a sharp brown line between diseased and healthy tissue. In the latter stages of disease, all the vascular tissues become brown and darker than normal.
Management
1. Follow recommended tillage and fertility practices.
2. Rotate sugar beet with small grains and maize.
3. Avoid billing soil up around plants.
Fusarium Root Rot
Fusarium root rot is known locally as tip rot in some sugar beetgrowing areas.
Cause.
The causal organism is temporarily referred to as F. oxysporum f. sp. betae, Texas strain (syn. F. oxysporum f. sp. spinaciae). However, isozyme analyses show
the Texas isolates to be distinct from other isolates of F. oxysporum f. sp. betae; therefore, the Texas sugar beet isolates may be a new forma specialis or a new race
of F. oxysporum f. sp. betae. A suggested but not yet proposed name for the causal organism is F. oxysporum f. sp. radicisbetae. The causal fungus is presumed
to survive as chlamydospores in soil and infested residue.
Distribution.
Symptoms.
Fusarium root rot is similar, symptomatically, to Fusarium yellows; however, it is distinct in that a severe root rot also occurs that is not associated with Fusarium
yellows. The disease is first observed as a single rustcolored streak in the central stele of diseased young plants. No external root symptoms are apparent at this time.
However, during the hottest period of the day, diseased plants may wilt slightly, but no other foliar symptoms are evident and disease would not be detected by a
casual observer.
Obvious foliar symptoms of wilting and leaf chlorosis become apparent about 60 days after emergence and coincide with ambient daytime tem

Page 705
peratures above 27°C. At this time, diseased roots show vascular necrosis and discoloration typical of Fusarium yellows, but the external portion of the root frequently
is also rotted at the distal end and has black streaks traveling upward. At first, only the tip of the diseased sugar beet is discolored. Eventually, half of the main taproot
may become black and rotted. In extreme instances, the diseased portion of the root completely rots, leaving only remnants of vascular bundles. The root rot is
distinguished from bacterial vascular necrosis and soft rot in that the bacterial disease causes a watery rot throughout the root and crown.
Management.
Not reported.
Fusarium Tip Rot
Cause.
Fusarium javanicum (syn. F. radicicola) survives as chlamydospores in soil or as mycelia in infested plant residue.
Distribution.
The United States.
Symptoms.
The first symptoms appear about midseason, when leaves start to wilt. Root tips are rotted with a white fungus mycelium growing on the diseased root surfaces.
Eventually, the interior of roots has a brown rot but the exterior does not show any symptoms.
Management.
Not reported.
Fusarium Yellows
Cause.
Fusarium oxysporum f. sp. betae (syn. F. oxysporum f. sp. spinaciae) survives in soil and infested residue as chlamydospores, mycelia, and spores. In the spring or
summer, chlamydospores germinate in the presence of host roots and form mycelia that penetrate the roots and grow into the vascular (xylem) system.
Fusarium oxysporum f. sp. betae forms tyloses and produces toxic substances that affect xylem tissue, preventing water from reaching the tops of diseased plants.
After death or maturity of the diseased plant, the fungus grows out of the vascular tissue and sporulates on the plant surface. Chlamydospores are formed either from
conidia or mycelium and survive in soil for several years.
Distribution.
Europe, India, and the United States.
Symptoms.
About midseason, yellowing occurs between the veins of the largest leaves; occasionally only half of the diseased leaf is affected. The large veins and a narrow border
surrounding the veins usually remain green. As the disease progresses, diseased leaves wilt during warm weather, droop down, and touch the soil surface. Eventually,
parts of these leaves will turn brown and dry out. As diseased leaves die, leaf blades pull upward along the midribs, margins dry up and become discolored brown,
and leaf

Page 706
tips bend to one side. Leaves ultimately become "heaped" around the crown.
The yellowing and progression of disease symptoms will eventually occur on younger heart leaves. Roots may not show any external symptoms, but in cross section,
vascular tissue has a graybrown discoloration. The seed stalks of seed beets will wilt and die prematurely.
Management.
Grow sugar beet in the same field once every 4 years or longer.
Fusarium, Miscellaneous Species
Several Fusarium spp. reported isolated from sugar beet piles produce the following mycotoxins: acetylneosolaniol, deoxynivalenol, HT2, T2, zearalenone, and 15
acetyldeoxynivalenol.
Penicillium Storage Rot
Cause.
Penicillium claviforme. Conidia are disseminated by wind to plant hosts and enter roots through wounds and tissue rotted by Phoma betae. Penicillium
aurantiogriseum (syn. P. cyclopium), P. brevicompactum (syn. P. stoloniferum), P. bordzilowskii, P. duclauxii, P. expansum, P. funiculosum, P.
purpurogenum (syn. P. rubrum), and P. variabile have also been reported as storage rot pathogens.
Distribution.
Symptoms.
A white mycelial growth that resembles "tufts" and consists of conidiophores, conidia, and sparse mycelia grows on brown, rotted tissue.
Management.
Research is being conducted on breeding for resistance and on the use of fungicides in storage piles.
Phoma Leaf Spot
Cause.
Phoma betae infects sugar beet during all stages of growth. The teleomorph, Pleospora betae (syn. P. bjoerlingii), is found in Europe but apparently is not common
in the United States and Canada.
Phoma betae overwinters as mycelium and conidia on and in infected seed, and for up to 26 months as mycelia and pycnidia in soil and infested residue in the soil. In
Europe, Pleospora betae overwinters as perithecia in infested residue. Conidia produced in pycnidia during moist weather are exuded in a gelatinous matrix, then are
disseminated primarily by splashing rain to plant hosts. Ascospores of Pleospora betae are produced in perithecia and disseminated by wind to plant hosts. Only
older, outer leaves are infected by both types of spores. Pycnidia eventually develop in spots and produce conidia that function as secondary inoculum. Phoma leaf
spot is most severe during periods of high humidity and temperatures of 15° to 32°C.

Page 707
Distribution.
Wherever sugar beet is grown. Damage is usually slight on sugar beet grown for sugar.
Symptoms.
Initially, small lightcolored spots that soon become light brown develop on diseased leaves. As spots enlarge, alternate light and dark brown concentric rings develop
with at least one dark brown ring being prominent. Black pycnidia develop in the dark rings. Spots, which are round to oval (12 cm in diameter), may coalesce and
form large necrotic areas.
Management
2. Control common lambsquarters, Chenopodium album, because this weed is also a host for P. betae.
3. Grow sugar beet in infested soil once every 4 years.
Phoma Root Rot and Storage Rot
Phoma root rot and storage rot is also called blackleg.
Cause.
Phoma betae overwinters as mycelia and conidia on and in seed, and for up to 26 months as mycelia and pycnidia in soil and infested residue in the soil. Conidia are
produced in pycnidia during moist weather, exuded in a gelatinous matrix, and disseminated by splashing rain to the upper root near the crown. Infection also occurs
by soilborne inoculum, presumably mycelia growing from infested residue.
Weather and soil conditions unfavorable to normal growth of sugar beet favor infection of host plants by P. betae. Beets that do not die in the field and are delivered
into storage piles act as centers of infection within the pile. Temperatures for optimum root rot and storage rot are 5° to 20°C. Sugar beet is infected during all growth
stages.
Distribution.
Symptoms.
Sugar beets affected by Phoma root rot occur randomly over a field. Occasionally, several plants in a limited area will be diseased. The first visible symptom is a
wilting of leaves, which was preceded by small brown spots on the upper root near the crown. Spots are soft and watery and spread to cover a large area. Often, the
centers of diseased areas are dark brown and "pithy," but margins of diseased areas are soft and watery. The outer surface of diseased roots remains unbroken while
rot develops just beneath it. Black vertical growth fissures that may occur on the hypocotyl are, likely, the result of soilborne inoculum.
The centers of crowns are very susceptible to rot and removal of portions of crowns during harvest exposes this tissue to further infection by P. betae. About 80 days
after roots have been harvested and stored, rot begins. The first indication of rot is in the center of the crown. From there, it spreads in a conelike pattern into the
adjacent crown and down into the

Page 708
main taproot. Rotted tissue is black or dark brown and has occasional pockets lined with the white mycelium of the fungus.
Management
1. Treat seed with a seedprotectant fungicide to prevent seedborne infection.
2. Practice cultural methods that promote vigorous growth of sugar beet.
3. Grow sugar beet in infested soil once every 4 years.
4. Resistance to storage rot occurs in some germplasms.
Phymatotrichum root rot is also called Texas root rot.
Cause.
Phymatotrichopsis omnivora (syn. Phymatotrichum omnivorum. Phymatotrichum omnivora is considered a synonym in some literature.). Phymatotrichopsis
omnivora survives as sclerotia in soil. Infection occurs when soil temperatures exceed 28°C.
Distribution.
Symptoms.
Initially, diseased leaves become yellowed or bronzed, which is followed by a sudden wilting of the entire plant. Eventually, roots develop a yellow to tan rot. A thin,
feltlike layer of yellowish mycelium develops on root systems and, occasionally, crustlike spore mats develop on soil surfaces.
Management.
Do not grow sugar beet in infested soil.
Phytophthora Root Rot
Cause.
Phytophthora drechsleri overwinters as oospores in soil or infested residue. Oospores germinate in the presence of moisture to form sporangia in which zoospores
are borne. Zoospores ''swim" to roots, where they germinate and form a germ tube that penetrates the host's roots. Phytophthora root rot occurs in wet or poorly
drained soils; temperatures of 28° to 31°C are optimum.
Phytophthora megasperma has been reported to cause a similar root rot in England, and P. cryptogea has been reported as a cause of Phytophthora root rot in
Wyoming.
Distribution.
England, Iran, and the United States.
Symptoms.
The first noticeable symptom is a wilting of diseased leaves during the warmest part of the day. Leaves may recover their turgidity at night. Necrotic spots appear on
roots either some distance below the crown or only on the tips of roots. Later, the entire lower portions of diseased roots become rotted and adventitious lateral roots
often grow above the diseased areas. Frequently, the rotted portion breaks down completely

Page 709
so that the lower portions of roots are a mass of discolored vascular strands that resemble the ends of a frayed rope. The advancing edge of the necrosis is a narrow
band of blackbrown discolored tissue that sometimes is separated from healthy tissue by a narrow, light buffcolored band. Small empty cavities frequently occur in
necrotic tissue.
Phytophthora cryptogea was reported to cause a firm brown decay on the distal 3 to 5 cm of taproots and a sharp demarcation between healthy and diseased
tissues.
Management.
Grow sugar beet in welldrained soils. The cultivar R2 may be susceptible to infection by P. cryptogea.
Powdery Mildew
Cause.
Erysiphe polygoni (E. betae is a synonym in some literature) overwinters as mycelia or haustoria in the crowns of Beta spp. in sugar beetgrowing areas of the
southwestern United States. In the northwestern states of the United States, E. polygoni survives in axillary bud tissue of seed beets. During the growing season,
leaves of sugar beet initially become infected by conidia disseminated by wind north and east from the southwestern sugar beetgrowing areas. Secondary inoculum is
provided by conidia produced on diseased leaves.
Powdery mildew is favored by warm temperatures (25°C optimum) and relatively dry weather. Conidia will germinate at a high relative humidity but production and
viability of conidia are optimum at 30% to 40% relative humidities.
Powdery mildew is more severe on older plants, probably due to reduced air circulation, light, and temperature and increased humidity under the denser canopy of
older sugar beets. Susceptibility to E. polygoni is increased in plants previously infected by one of the beetyellowing viruses. Different races of E. polygoni exist on
sugar beet.
Distribution.
Symptoms.
Symptoms of powdery mildew on sugar beet in the United States appear 2 to 6 months after sowing. The most distinguishing symptom is a white powderyappearing
material consisting of mycelium, conidiophores, and conidia on diseased leaf surfaces. This fungus growth is superficial and does not penetrate far into leaf cells.
Prematurely killed leaves become brown but retain the white fungal growth. Cleistothecia, which appear as tiny dark specks, are found in mycelia in Europe, but they
have been found only once in the United States.
Management
1. Apply foliar fungicides during the period of rapid root growth.
2. Grow cultivars that are less susceptible to infection. Beta maritima provides a source of resistance.

Page 710
Pythium Damping Off
Cause.
Pythium spp., including P. aphanidermatum, P. intermedium, P. purpurogenum (syn. P. rubrum) and P. ultimum. The life cycles of most Pythium spp. are as
follows: Survival is as oospores in soil. Oospores germinate in the presence of water by releasing zoospores that "swim" to roots. Zoospores germinate and form germ
tubes that penetrate the host. Eventually, conidia, sporangia, and oospores are formed in rotted tissue. Secondary infection is by further production of zoospores that
are spread to adjacent plants by water. Infrequently, sporangia and conidia germinate directly and form germ tubes that penetrate the host.
Pythium damping off is most severe at temperatures of 12° to 20°C and wet soil conditions. The exception is infection by Pythium aphanidermatum, which infects
host plants in warmer, wet soils. Thickly sown seeds are more susceptible to infection than seeds sown at the recommended plant population.
Distribution.
Symptoms.
Diseased seeds are soft, light brown, and often overgrown with the white mycelia of Pythium or secondary fungi. Seedlings killed before emergence have a light
brown, soft, watersoaked rot. Seedlings may also be killed after emergence. Plants that survive will recover when secondary thickening starts in the hypocotyls.
Management
2. In experimental tests, osmopriming seed in NaCl or polyethylene glycol reduced damping off.
Pythium Root Rot
Cause.
Pythium aphanidermatum and P. deliense. Pythium irregulare and P. sylvaticum also have been reported pathogenic to sugar beet. The life cycles of most
Pythium spp. are as follows: Survival is as oospores in soil. Oospores germinate in the presence of water by releasing zoospores that "swim" to roots. Zoospores
germinate and form germ tubes that penetrate the host. Eventually, conidia, sporangia, and oospores are formed in rotted tissue. Secondary infection is by further
production of zoospores that are spread to adjacent plants by water. Infrequently, sporangia and conidia germinate directly and form germ tubes that penetrate the
host.
Root rot caused by P. aphanidermatum is most severe at soil temperatures greater than 27°C at a soil depth of 10 cm for at least 12 hours a day. Excessive soil
moisture and poorly drained soils with a high pH are also favorable for disease development.
Distribution.
Iran and the United States (Arizona, California, Colorado, and Texas).

Page 711
Symptoms.
Pythium root rot symptoms become evident later in the growing season. Initially, older leaves become yellow, wilt, and die as the disease progresses to the younger
leaves. Leaf petioles have brown, sunken necrotic areas that extend from the petiole base to the leaf blade. Eventually, all diseased leaves die and the crowns and
roots become diseased. The diseased portion of roots extends internally from the crown down toward the root tip, and from secondary infections along the roots.
Diseased root tissue is somewhat firm.
Management
1. Avoid growing in infested fields where the inoculum threshold is known to be above the desirable level.
2. Increase the frequency and decrease the duration of irrigation.
Ramularia Leaf Spot
Cause.
Ramularia beticola overwinters in milder climates as mycelia or conidia in infested residue in the soil and, possibly, on seed. Conidia are produced during humid
weather conditions at temperatures of 17° to 20°C and disseminated by wind to infect the older leaves of host plants.
Distribution.
Canada (British Columbia), Europe, and the United States (primarily northern California, Colorado, Oregon, and Washington).
Symptoms.
Spots resemble those caused by Cercospora beticola but are larger and more angular. Spots are circular (47 mm in diameter) and white to light tan, are surrounded
by a brown or purplish border, and have tufts of white mycelium growing in the center. Diseased leaves become yellow, then necrotic, and die.
Management
1. Grow cultivars resistant to Cercospora leaf spot. These cultivars are also resistant to Ramularia leaf spot.
2. Apply copper foliage fungicides before disease becomes severe.
Rhizoctonia Crown and Root Rot
Rhizoctonia crown and root rot is also called brown rot. Dry rot canker and Rhizoctonia crown rot and root rot are both caused by Rhizoctonia solani. However, the
symptoms are distinct and the two diseases are discussed separately.
Cause.
Rhizoctonia solani. The teleomorph Thanatephorus cucumeris, anamorph R. solani AG3 and AG5, is reported from Minnesota. In the Red River Valley of the
North, AG1 through AG5 were isolated along with multinucleate isolates that did not anastomose with any tester isolates. Anastomosis groups AG4 and AG5
predominated on seedlings and AG22 on older plants. AG22 is considered to cause crown and root rot, and AG1, AG22, AG4, and AG5 cause damping
off.
In Ohio, most multinucleate isolates are in either anastomosis group

Page 712
AG2 or AG4. AG2 isolates predominate in finetextured soils, whereas AG2 and AG4 isolates are either equal in number or AG4 predominates in coarser
textured soils. AG4 isolates are more virulent to sugar beet seedlings, and AG2 isolates are more virulent to 6 to 8weekold plants.
In Texas, the predominate isolates from mature sugar beet were AG22, but most isolates obtained from seedlings were AG4 and AG5.
Rhizoctonia solani survives as bulbils, or thickened hyphae, and sclerotia in soil and in infested residue in the soil. Sclerotia survive for less than 2 years in soil in the
Red River Valley of the North. When R. solani resumes growth, mycelium is formed that penetrates host plants through the crowns or the bases of leaf petioles.
Rhizoctonia solani moves from plant to plant within a row by mycelial growth. Propagules are disseminated by water and tillage equipment.
Disease is most severe in poorly drained soils at temperatures from 25° to 33°C. Depositing soil in and around sugar beet crowns (hilling) increases the incidence and
severity of root rot. In Texas, disease is mainly a problem on sugar beet that either is sown late in the growing season or is resown.
Distribution.
Symptoms.
The first symptom is a darkening of the petiole base on halfgrown to nearly mature sugar beet roots. The petiole is weakened at the point of infection and leaves fall to
the soil and form a rosette of dead leaves around the crown. Foliage wilts as crowns become rotted. Eventually, roots become diseased below the diseased crowns
and have a dark brown to black discoloration on the surfaces and a light to dark brown dry rot of internal tissue. Deep cracks often occur at or near diseased crowns.
Infrequently, just the root tip may be rotted off 15 to 20 cm below the soil surface.
Symptoms of T. cucumeris are a superficial white to gray, dusty hymenial growth on sugar beet petioles.
Management
1. Follow recommended tillage and fertility practices.
2. Rotate with small grains and maize as a general practice. However, research in Texas demonstrated that sugar beet following alfalfa has a high incidence of disease`
sugar beet following sorghum and winter wheat has the next highest disease incidence, and sugar beet following cotton, fallow, and sunflower had the least incidence of
disease. Therefore, it is recommended that sugar beet not follow wheat in a rotation in Texas because AG4 is highly virulent to each species. In Minnesota, AG22
was pathogenic to sugar beet and common bean; therefore, avoid rotating sugar beet with common bean.
3. Avoid hilling up soil around plants.

Page 713
4. Some breeding lines display levels of resistance. Disease on moderately resistant sugar beet cultivars decreases as plant age increases.
Rhizoctonia Foliage Blight
Cause.
Rhizoctonia solani, teleomorph Thanatephorus cucumeris. AG3 and AG5 were found on petioles of sugar beet in sugar beet fields in the Red River Valley of the
North. Potato debris (discarded potato culls or soilborne root residue of the previous crop) served as a source of inoculum of AG3 for infection of the subsequent
sugar beet crop. AG5 was reported on other crops grown in the region, including soybean and wheat. AG3 formed sclerotia on roots, but isolates of AG5 did not.
Windels et al. (1997) reported that the occurrence of hymenia of T. cucumeris on sugar beet was not an indicator of disease on these plants, at least in the Red River
Valley of the North. The presence of hymenia on sugar beet in the field was significant in that genetic recombination and inoculum production of R. solani occurred on
a nonhost crop. In the Windels (1994) study, infection of sugar beet by T. cucumeris was related to AGs of R. solani associated with the previous crop, i.e., AG3
for potato and AG5 for wheat.
Rhizoctonia solani survives as resting mycelia and sclerotia in infested residue and soil. Optimum formation of the teleomorph in the field requires high relative
humidity and temperatures of 20° to 30°C. During moist weather in the early part of the growing season, fungal propagules are splashed by rain and infect the leaves
of young plants. Halfgrown and mature plants are resistant to infection. Disease occurs at temperatures of 21° to 25°C and 100% relative humidity. About 3 weeks
after infection, basidia and basidiospores of T. cucumeris are produced on leaves. The basidiospores function as secondary inoculum and are disseminated by wind
and splashed by rain to surrounding host plants. Dry weather in midseason prevents further disease development.
Distribution.
The United States (Colorado, Maryland, Michigan, Nebraska, Ohio, and Virginia).
Symptoms.
Black spots (612 mm in diameter) form on diseased leaves. Spots become necrotic, dry up, and break away from healthy tissue, giving diseased leaves a ragged
appearance. A circular zone of secondary spots surrounds the original spot or the place where the spot had been. About 3 weeks after infection, a filmy graywhite
growth consisting of mycelium, basidia, and basidiospores of T. cucumeris can be observed on leaf surfaces. The spread of secondary inoculum causes plants to
become diseased in a circular pattern (5 to 10 m in diameter), with the original diseased plant serving as the disease focus in the center of the circle.
Management.
Grow sugar beet in the same soil once every 4 to 5 years.

Page 714
Rhizopus Root Rot
Cause.
Rhizopus arrhizus (syn. R. oryzae) and R. stolonifer survive in soil and infested residue as spores and mycelia. The fungi are generally considered to be weak
parasites that infect through crown wounds of host plants that have been predisposed by excess soil moisture. Larvae of insects, such as Eumerus sp., wound healthy
tissue, thereby providing infection courts for Rhizopus spp. to enter the plant. Rhizopus stolonifer infects at temperatures of 14° to 16°C, and R. arrhizus infects at
temperatures of 30° to 40°C. Sugar beet plants are especially vulnerable to infection after thinning.
Distribution.
Canada, Italy, Russia, Ukraine, and the United States.
Symptoms.
Leaves wilt during the warmest part of the day but normally recover their turgidity at night. As disease progresses, leaves permanently wilt and are transformed into a
dry, brittle rosette. Superficial graybrown necrotic areas appear on the bases of diseased roots and gradually spread upward toward the crowns. Root tissues
become dark and spongy and, eventually, entire roots become discolored black. White mycelium, which later turns dark, appears on diseased root surfaces.
Eventually, the causal fungi grow deeper into roots, causing internal cavities that become filled with a clear liquid that is rich in aceticlike acid.
Symptoms of root rot caused by R. arrhizus, have been described as a foamy white exudate that often exudes from the crowns of dead and dying plants. Diseased
root tissue has a soft to spongy texture and varies from tan to black.
Management
1. Maintain proper soil drainage.
2. Avoid injuring plants.
Sclerotium Root Rot
Sclerotium root rot is also called southern Sclerotium root rot and southern root rot.
Cause.
Sclerotium rolfsii survives as sclerotia in soil and is disseminated by anything that moves sclerotiainfested soil, such as water and machinery. Sclerotia germinate by
producing germ tubes that penetrate a host. Later in the growing season, sclerotia are formed in mycelia growing over diseased plant surfaces. Disease development is
favored by temperatures of 25° to 35°C and moist soil.
Distribution.
Czechoslovakia, Japan, Korea, Mediterranean countries, Middle East, and the southwestern United States.
Symptoms.
Initially, the tops of diseased plants have an unthrifty appearance; eventually, the leaves wilt. Root surfaces are covered with a white, cottony, mycelial growth that
extends into the soil surrounding the dis

Page 715
eased roots. Scattered throughout the mycelial growth are small, round sclerotia that resemble white, tan, or brown mustard seeds.
Management
1. Do not grow sugar beet in soils with high numbers of sclerotia.
2. Do not put dump dirt on fields to be cropped to sugar beet.
3. Apply heavy amounts of nitrogen to soil.
Seedling Rust
Cause.
Puccinia subnitens is a dioecious rust. The pycnial and aecial stages occur on sugar beet; the uredinial and telial stages occur on saltgrass, Distichlis stricta.
Distribution.
Russia, Ukraine, and the United States (Rocky Mountain states).
Symptoms.
Symptoms generally occur only on the diseased lower surfaces of cotyledons, but infrequently can be found on the first true leaves. Bright yelloworange aecial
pustules are aggregated into rings on the lower leaf surfaces. Pycnia may be present on the upper leaf surfaces.
Management.
Not necessary, since seedling rust is of no economic importance.
Verticillium Wilt
Cause.
Verticillium alboatrum survives as dark resting mycelia in infested residue and soil. Verticillium alboatrum enters through lateral roots and grows into the vascular
system. Conidia are formed on dead plant tissue but are not considered to be significant in the spread of V. alboatrum.
Distribution.
Europe and the United States (Colorado, Idaho, Nebraska, and Washington).
Symptoms.
Diseased leaves initially are yellow. Eventually, the outer leaves wilt and dry up, while inner leaves become twisted and deformed. In cross section, the vascular system
may show a slight to dark brown discoloration. Although lateral roots through which the fungus entered into the host plant are usually black and watersoaked, little or
no root rot occurs.
Management.
Rotate sugar beet with other crops for several years.
Violet Root Rot
Cause.
Rhizoctonia crocorum, teleomorph Helicobasidium brebissonii (syn. H. purpureum). Rhizoctonia crocorum is referred to as the mycelial stage and overwinters as
sclerotia in soil and on the roots of weed hosts. Sclerotia germinate late in the growing season and form mycelia that grow over and through soil to sugar beet roots.
Rhizoctonia crocorum spreads from plant to plant by mycelial growth through soil. During this time, basidia form on

Page 716
the mycelial mat. Rhizoctonia crocorum contacts a root and forms an infection cushion from which mycelium penetrates into the host root and eventually grows over
it. Eventually, sclerotia form in the mycelium.
Reports of the effects of soil moisture and pH are conflicting. Some researchers state disease is more prevalent under wet soil conditions and high soil pH. Others
maintain these conditions are not a factor in disease development. Fungal growth is optimum at a temperature of 13°C.
Distribution.
Symptoms.
Violet root rot is a late season disease in the United States. Usually all beets within an area will be diseased. Initially, plants wilt and leaves become light green. Purplish
spots occur on root surfaces, and a purple fungal growth develops near the root tip and eventually covers the entire root. The area on the root covered by the fungus
is somewhat depressed. In cross section, the root shows a sharp line between healthy tissue and the surrounding brown diseased tissue. Diseased roots carry
excessive amounts of soil because fungus mycelium binds the soil to the roots.
Management.
Most measures are relatively ineffectual; however, the following may partially aid in managing violet root rot:
1. Rotate sugar beet with other crops.
2. Control weeds in fields.
Clover Cyst
Cause.
Heterodera trifolii. Females reproduce parthenogenetically. The life cycle is similar to that of H. schachtii. (See "Sugar Beet" in this section.)
Distribution.
Europe.
Symptoms.
Sugar beet stands may be lost or have uneven growth. Outer leaves of diseased plants become chlorotic, then wilt. Storage roots are not well formed and have
branched root systems and excessive growth of fibrous roots.
Management
1. Rotate sugar beet every 4 to 5 years with crops such as small grains. It has been reported that rotation with resistant crops is warranted economically when the
infestation is about 1000 eggs or larvae per 100 g of airdried soil.
2. Equipment should be cleaned between fields.
3. Tare dirt should be returned to nonagricultural soil.
4. Sow as early as feasible.
5. Apply nematicides where feasible. However, nematicide effectiveness may be affected by soil temperature and soil type.

Page 717
False Root Knot
Cause.
Nacobbus aberrans and N. dorsalis.
Distribution.
The United States. Nacobbus aberrans is found in Colorado, Kansas, Montana, Nebraska, South Dakota, and Wyoming; N. dorsalis is found in California.
Symptoms.
Necrosis and galllike swellings occur on diseased roots.
Management.
No specific management has been developed. Presumably, measures used to manage other nematodes will be of some value.
Nebraska Root Gall
Cause.
Nacobbus batatiformis overwinters as eggs in soil and as adults in galls. Nematodes are disseminated by any mode that transports soil, such as irrigation water and
tillage equipment. Eggs are deposited in a gelatinous matrix outside galls and hatch into larvae that "swim" in moisture to penetrate surrounding roots and rootlets. Galls
form at the point of penetration and contain from one to several eggproducing females. Growth and reproduction of nematodes is optimum at soil temperatures of 24°
to 35°C.
Distribution.
The United States (western Nebraska).
Symptoms.
Severely diseased sugar beets are stunted and wilt during warm weather. Numerous galls up to 1 cm in diameter are formed, predominantly on lateral roots. Many
small rootlets are produced on each gall, creating a hairlike or "whiskery" appearance.
Management
1. Rotate sugar beet at least every 4 years.
2. Sow sugar beet early in growing season because of nematode inactivity in cool soils.
3. Control weeds, especially lambsquarters and kocia, in sugar beet fields since they may harbor N. batatiformis.
4. Apply nematicides in the form of fumigants to soil.
Needle
Cause.
Longidorus attenuatus, L. caespiticola, L. elongatis, and L. leptocephalus.
Distribution.
England and the United States. However, needle nematodes are not a problem in the United States.
Symptoms.
Tips of seedling taproots may be killed. Lateral roots have stubby ends that later become brown and die.
Management.
Follow general management practices used to manage nematodes.

Page 718
Root Knot
Cause.
Meloidogyne arenaria, M. incognita, M. javanica, M. hapla, and M. naasi. Meloidogyne incognita and M. javanica cause the greatest damage in the United
States. Nematodes overwinter as eggs or secondstage juveniles in soil, galls, and root tissue. Meloidogyne arenaria, M. incognita, and M. javanica do not survive
if the temperature averages below 3°C during the coldest month. Meloidogyne hapla is limited by temperatures of 27°C or greater.
Larvae move through soil and penetrate root tips of host plants. The nematodes then migrate through infected roots into the vascular tissues, where they become
sedentary and commence feeding. Larval excretions stimulate cell proliferation, resulting in development of syncythia from which larvae derive their food. Females lay
eggs that may be pushed out of roots into the soil.
Distribution.
Symptoms.
Initially, small, light tan galls form on fibrous roots and taproots. Later, galls are a darker brown and may be of different shapes: Rounded galls are caused by M.
hapla; elongated or spiralshaped galls are caused by M. naasi; irregularshaped, clublike swellings are caused by M. incognita. The galls or swellings along the fine
roots resemble a string of beads. Root rot may occur.
Plants may be severely diseased without obvious aboveground symptoms. The common aboveground symptom is the presence of small, yellow, stunted plants. Plants
under moisture stress may wilt and collapse.
Management
1. Rotate sugar beet for 4 to 5 years with other crops, such as small grains. However, this is not considered effective.
2. Control weeds.
3. Apply nematicides in the form of fumigants to soil.
Stem and Bulb
Cause.
Ditylenchus dipsaci.
Distribution.
Europe.
Symptoms.
Diseased seedlings have a swelling of the epicotyl, hypocotyl, midribs, and main veins of leaves and the occasional formation of galls. Severely diseased plants are
stunted and have multiple crowns. Crown cankering and girdling may occur at the scars of diseased petioles. Root rot occurs later in the growing season.
Management
1. Rotate sugar beet with nonhost plants.
2. Control weeds.
3. Remove infested residue from fields.

Page 719
Stubby Root
Cause.
Paratrichodorus anemones, P. pachydermus, P. teres, Trichodorus cylindricus, T. primitivus, and T. viruliferus.
Distribution.
Europe and the United States. However, stubby root nematodes are not considered economically important in the United States.
Symptoms.
Tips of the taproots of diseased seedlings may be killed. Lateral roots have stubby ends that later turn brown and die.
Management.
Use general practices recommended for managing nematodes.
Sugar Beet
Sugar beet nematode is sometimes called the sugar beet cyst nematode.
Cause.
Heterodera schachtii survives in soil as cysts filled with eggs. Eggs hatch over an extended period of time, sometimes up to several years. The resulting larvae
penetrate roots and take up positions in the cortex. The female bodies break through the epidermis, leaving only the head embedded in the root. Eventually, eggs
develop in the female and largely displace other organs. Upon reaching maturity, female bodies are transferred into a brown cyst. Optimum growth and multiplication
of Heterodera schachtii occur at temperatures of 13° to 28°C. Heterodera schachtii can mature, increase in number, and continue egg production on respiring,
excised roots.
Distribution.
Symptoms.
The initial disease symptoms is stunted or killed plants in small, distinct areas within a field. Young plants wilt and die shortly after thinning. Small white cysts, about the
size of a pinhead, are attached to the diseased feeder roots. Later, these cysts turn dark orangebrown and are difficult to see and to differentiate from the host root.
The taproot may be small and extremely ''hairy" due to the proliferation of fibrous roots.
An aboveground symptom is the presence of small, yellow, stunted plants with sprawling, wilted leaf petioles. In nematodeinfested fields, sugar beet is more
susceptible to leaf spot and other diseases.
Management
1. Rotate sugar beet for 4 to 5 years with crops such as small grains. It has been reported that rotation with resistant crops is warranted economically when the
infestation is about 1000 eggs or larvae per 100 g of airdried soil.
2. Equipment should be cleaned between fields.
3. Tare dirt should be returned to nonagricultural soil.
4. Sow as early as feasible.
5. Apply nematicides where feasible. However, nematicide effectiveness may be affected by soil temperature and soil type. Nematode populations increase in soils
treated with carbamate herbicides.

Page 720
6. Grow a "catch" crop. Radishes have been demonstrated to be successful.
Rosette Disease
Rosette disease is also called witches' broom.
Cause.
A phytoplasmalike organism.
Distribution.
Italy.
Symptoms.
A typical rosettetype growth of diseased foliage has been reported. A prolific growth of small leaves and stems occurs together with an epinasty, which gives foliage a
"bushy" appearance.
Management.
Not reported.
Diseases Caused by Rickettsia
Beet Latent Rosette
Cause.
A rickettsialike organism transmitted by nymphs and adults of the beet lace bug, Piesma quadratum, and by dodder, Cuscuta campestris. The organism is
persistent in vectors and remains infectious for 10 to 30 days.
Distribution.
Germany and the United States.
Symptoms.
Initially, there is a leaf twisting, downward turning of leaf tips and chlorosis of diseased young leaves. Later in the rosette stage, a cluster of terminal and axillary shoots
with straplike leaves is formed that resembles a witches' broom. The rosette remains after the death of mature, healthy leaves.
Management.
No management measures have been developed because it is not considered a serious disease.
Yellow Wilt
Cause.
A rickettsialike organism transmitted by the leafhopper, Paratamus exitiosus, and by dodder, Cuscuta californica and C. campestris, and by grafting.
Distribution.
Argentina and Chile.
Symptoms.
Leaves yellow or diseased plants wilt and collapse. New leaves may be dwarfed and often turn downward at the tips. Frequently only portions of leaves or the veins
of some diseased leaves become yellow. Leaves of plants that have been diseased for a long time may be necrotic or be

Page 721
come straplike. Root tips may become necrotic and form tufts on roots, which cause plants to wilt during periods of high temperatures and low soil moisture, often
resulting in plant death.
Management
1. Avoid growing sugar beet in soils where disease has caused losses.
2. Grow resistant varieties when they become available.
Beet Crinkle
Beet crinkle is known as leaf curl in England and as kopfsalat in parts of Germany.
Cause.
A suspected virus. The virus is transmitted by adult lacebugs (Piesma quadratum), but the nymphs also can pick up the virus. The insect hibernates in grass and
under trees and hedges around sugar beet fields. The virus multiplies in both larval and adult stages of the insect. Mechanical transmission has been done by grafting
from diseased beet to beet.
Three forms of the disease have been recognized: a severe and progressive form that starts early in the year; a similarly severe form interrupted by periods of normal
growth; and a slight form that starts much later. It is not known whether these disease forms are due to different virus strains.
Distribution.
Central Europe. The disease is now confined to Germany and Poland.
Symptoms.
Diseased leaf and petiole veins become crooked, translucent, glassy, and swollen. Veins do not grow as fast as the rest of the leaf, causing both veins and leaves to
have a markedly "crinkly" appearance. New leaves formed from crowns remain small and curved inward, forming a compact bunch that gives the diseased plant the
appearance of a cabbage. Older diseased leaves die.
Management
1. Control insects with insecticides.
2. Grow an early trap crop of beet around field edges and plow it under before the main sugar beet crop has germinated.
Beet Curly Top
Beet curly top is also called curly top, sugar beet curly top, sugar beet curly leaf, western yellow blight virus, and tomato yellows.
Cause.
Beet curly top virus (BCTV) is in the geminivirus group. BCTV overwinters in a large number of perennial plants and is transmitted hundreds of kilometers by the
beet leafhopper, Circulifer tenellus, in a persistent man

Page 722
ner. The beet leafhopper can feed for a minute on a diseased plant and acquire BCTV, then carry BCTV for a month or more. However, BCTV does not multiply in
the leafhopper body, and if an insect has fed only once on a diseased plant, its ability to transmit the virus diminishes during successive feedings. BCTV is not
transmitted through the egg.
Distribution.
Canada, the Mediterranean basin, and the United States.
Symptoms.
Plants infected prior to or immediately after thinning will not continue to grow. The most common field symptoms are dwarfing of diseased leaves, with the leaf edges
rolling and curling inward, together with vein clearing, swelling, and spinelike growths. Eventually, swollen veins give rise to small nipplelike swellings along veins and
veinlets. Sometimes a sticky brown fluid may be exuded and collect in droplets along petioles and the edges of diseased leaves. In cross section, roots have concentric
black rings together with phloem tissue that becomes necrotic and cracks. There may be an increase in the number of rootlets.
Infection late in the growing season produces few symptoms except for a slight vein clearing and swelling of leaves.
Management
2. Control vectors.
Beet Distortion Mosaic
Cause.
Beet distortion mosaic virus (BDMV) is soilborne and mechanically transmitted. There is some evidence that the vector is the fungus Polymyxa betae. BDMV
particles are long flexuous rods (12 × 2002400 nm) that are similar in size to those of wheat spindle streak mosaic virus.
Distribution.
Symptoms.
A distortion and mosaic of diseased leaves occurs.
Management.
Not reported.
Beet Leaf Curl
Cause.
Beet leaf curl virus (BLCV) is in the geminivirus group. BLCV overwinters in its vector, the beet lace bug (Piesma quadratum), which hibernates in protected areas.
In the spring, vectors move into sugar beet fields and transmit BLCV to young plants. BLCV is transmitted in a persistent manner by the beet lace bug, which remains
infective for the rest of its life.
Distribution.
Europe.
Symptoms.
Initially, vein clearing occurs in the youngest leaves, which crinkle and curl inward, forming a structure similar to a lettuce head. Diseased leaves and roots are badly
stunted.

Page 723
Management
1. Do not grow sugar beet in areas where disease occurs.
2. Apply insecticides to sugar beet near overwintering areas of the vector.
Beet Marble Leaf
The causal virus may be a strain of beet mosaic virus.
Cause.
Marble leaf virus is transmitted by the aphids Myzus persicae, M. fabae, and M. eurphorbiae. The virus is also transmitted by rubbing juice from diseased plants
onto healthy plants.
Distribution.
The United States (Oregon).
Symptoms.
Local lesions on diseased plants appear 9 days after inoculation as chlorotic spots (1 mm in diameter). Lesions slowly increase in size to a diameter of 2 to 3 mm. A
small necrotic spot that sometimes is surrounded by one or more rings ranging in color from yellow to green may develop in the center of the lesion. If lesions are
numerous, inoculated leaves die prematurely.
Systemic symptoms appear 10 to 30 days after inoculation. Initially, symptoms consist of a vein chlorosis or mottling on diseased young leaves and various patterns of
chlorosis on halfgrown leaves. Chlorotic areas are wider than veins, may be continuous or broken, and in some cases are accompanied by indefinite mottle. As leaves
mature, vein chlorosis becomes less conspicuous and the leaves become mottled and the chlorotic areas are not conspicuous or well defined. As leaves age further,
mottling becomes indefinite and the tissue between the main veins turns yellow. Leaves appear dry and papery.
Management.
Not reported.
Beet Mild Yellowing
Cause.
Beet mild yellowing virus (BMYV) is in the luteovirus group. BMYV survives in perennial weeds and overwintered sugar beets. BMYV is transmitted by the peach
aphid, Myzus persicae, which remains infective throughout its life after once acquiring the virus. Isolates of BMYV are serologically indistinct from beet western
yellows virus.
Distribution.
The British Isles, Russia, and possibly the western United States.
Symptoms.
Diseased leaves have an orangeyellow discoloration.
Management.
Insecticides are used to control the vector in Great Britain.
Beet Mosaic
Cause.
Beet mosaic virus (BtMV) is in the potyvirus group. BtMV survives in perennial plants and overwintered sugar beets and is transmitted in a non

Page 724
persistent manner by several species of aphids. All stages and forms of the aphids can carry BtMV. Aphids feed a few seconds to acquire BtMV but rapidly lose it in
a few hours during subsequent feeding. Consequently, an aphid must frequently feed on diseased plants in order to reacquire the virus. BtMV is not transferred to
young aphids by the female aphid. Disease is most severe where crops of two growing seasons overlap or where diseased plants have overwintered.
Distribution.
Wherever sugar beet is grown. Incidence of the disease depends on the buildup of the aphid population.
Symptoms.
Initially, circular chlorotic spots with sharply defined margins occur on young diseased leaves. Spots often occur as chlorotic rings with green centers. Usually the
mosaic pattern consists of irregularshaped patches that are various shades of green.
Management
1. Do not overlap crops of two growing seasons.
2. Destroy wild and escaped beets in the vicinity of newly sown fields.
Beet PseudoYellows
Cause.
Beet pseudoyellows virus (BPYV) is in the closterovirus group. BPYV is transmitted by the common greenhouse white fly Trialeurodes vaporariorum. BPYV is
acquired in 1 hour of feeding and is transmitted in a 1 hour feeding period. The latent period in T. vaporariorum is less than 6 hours. BPYV is retained in the vector
for 6 days. Several other plants are also hosts.
Distribution.
The United States (the Salinas Valley in California).
Symptoms.
Chlorotic spotting or splotching occurs uniformly on older and intermediateaged leaves. Eventually, the yellowing becomes more intense and general, with older
diseased leaves almost entirely chlorotic except for small scattered islands of green tissue. Irregularshaped, bright yellow areas (1015 mm in diameter) may also form
on older leaves. Leaves become thickened and brittle.
Management.
Not reported.
Beet Ring Mottle
Beet ring mottle virus may be a strain of cucumber mosaic virus.
Cause.
Beet ring mottle virus is transmitted mechanically and by a number of aphid species.
Distribution.
The United States (the Salinas Valley in California). The disease is not of any economic importance.

Page 725
Symptoms.
Inoculated plants initially display chlorotic rings (23 mm in diameter) on diseased lower leaves. The rings enlarge to 4 to 5 mm in diameter and tend to coalesce. A
systemic symptom is a distortion of the young diseased leaves, which are stunted and markedly narrowed to a lanceolate form. Leaf margins are wavy, and in some
cases, leaves have more blade tissue on one side of the midrib than on the other, which tends to twist and distort the diseased leaves. The distribution of chlorotic
pinpoint spots gives leaves a distinct mottle. Diseased plants become stunted.
Management.
Not reported.
Beet Soilborne
Cause.
Beet soilborne virus (BSBV) is in the furovirus group. BSBV is a rigid, rodshaped, bipartite virus. Two serogroups of BSBV, Ahlum and Wierthe, have been
identified in Europe.
BSBV is transmitted by the soilborne fungus Polymyxa betae. Polymyxa betae survives in field soil as cystosori, each of which is a mass of resting spores. Cystosori
give rise to zoospores (one zoospore per resting spore), which "swim" through free soil water until they contact a host root and encyst. Encysted zoospores produce a
structure called a stachel through which zoosporic cytoplasm enters the host cell and becomes a plasmodium. Only primary root tissue of young roots is infected;
optimum infection occurs at a temperature of 25°C. The host cell then becomes infected with BSBV if P. betae is viruliferous. After a time, the plasmodium develops
into a zoosporangium, which releases additional zoospores that repeat the infection cycle. However, some plasmodia develop into cysts, and often nearly every cell in
the small feeder roots will contain a cyst. As root cells senesce, cysts are eventually released into the soil, where they can remain viable for years without loss of
virulence.
Sugar beet is the only host.
Distribution.
Western Europe and the United States.
Symptoms.
Sugar beet frequently is a symptomless host. The actual affect of BSBV on sugar beet is unknown, but in greenhouse studies, yield losses have been reported in
mechanically inoculated sugar beet.
Management.
Not reported.
Beet Soilborne Mosaic
Cause.
Beet soilborne mosaic virus (BSBMV) is a furolike virus. BSBMV is morphologically similar to beet necrotic yellow vein virus (BNYVV) but is seriologically distinct
and was originally designated as TX7 and TX8. Particles are 19 nm wide and from 50 to 400 nm long.
BSBMV is a rigid, rodshaped virus transmitted by the soil fungus

Page 726
Polymyxa betae. Polymyxa betae survives in field soil as cystosori, each of which is a mass of resting spores. Cystosori give rise to zoospores, one zoospore per
resting spore, which "swim" through free soil water until they contact a host root and encyst. Encysted zoospores produce a structure called a stachel through which
zoosporic cytoplasm enters the host cell and becomes a plasmodium. Only primary root tissue of young roots is infected; optimum infection occurs at a temperature of
25°C. The host cell then becomes infected with BSBMV if P. betae is viruliferous. After a time, the plasmodium develops into a zoosporangium, which releases
additional zoospores that repeat the infection cycle. However, some plasmodia develop into cysts, and often nearly every cell in the small feeder roots will contain a
cyst. As root cells senesce, cysts are eventually released into the soil, where they can remain viable for years without loss of virulence.
Distribution.
The United States (California, Colorado, Idaho, Minnesota, Nebraska, Texas, and Wyoming).
Symptoms.
Foliar symptoms include slight leaf distortion, subtle overall mottling, and light green or yellow blotches and bands that follow primary leaf veins. As diseased leaves
age, the bands can progress to broad chlorotic areas that usually remain associated with the veins. The bands may become bright yellow but typically are broader than
the yellowvein symptom caused by BNYVV.
Occasionally, systemically infected leaves exhibit a mottled or mosaic pattern or symptoms that are very similar to the veinbanding symptom of BNYVV. Some
BSBMV isolates cause bright yellow veinal chlorosis more typically associated with infection by BNYVV. Systemic foliar symptoms caused by BSBMV appear in
fieldgrown sugar beet more frequently than do those caused by BNYVV.
Roots are often asymptomatic, but some beets systemically infected with BSBMV exhibit root symptoms more typically associated with rhizomania, including stunting,
proliferation of lateral roots, and constriction of the main taproot.
In greenhouse studies, some isolates of BSBMV have significantly reduced growth of sugar beet seedlings.
Management.
Not reported.
Beet Western Yellows
Cause.
Beet western yellows virus (BWYV) is in the luteovirus group. BWYV overwinters in several weed hosts or overwintered sugar beet plants and is transmitted mainly
by the green peach aphid, Myzus persicae, and infrequently by other aphid species. Known hosts are Brassica napus var. napobrassica, Capsella bursapastoris,
Cardamine oligosperma, Cardaria draba, Erodium cicutarium, Lactuca scariola, Matricaria maritima, Polygonum lap

Page 727
athifolium, Raphanus raphanistrum, Senecio vulgaris, Sisymbrium officinale, and Stellaria media.
Myzus persicae can acquire BWYV after a 5minute feeding on a diseased plant and transmit it after a 10minute feeding on a healthy plant. An aphid can remain
infective for several days. Different strains of BWYV exist.
An ST9associated RNA is a newly discovered type of plant infectious agent that depends on BWYV for encapsidation but not for replication. The agent is not a
satellite virus.
Distribution.
Canada, Israel, and the United States (California, Illinois, and Oregon).
Symptoms.
It is difficult to differentiate between the symptoms of beet western yellows and beet yellows on sugar beet. At first, the light chlorotic spotting that occurs on diseased
older and middleaged leaves gradually becomes more intense in color. Chlorotic areas may be sharply delimited by veins. Eventually, diseased older leaves become
thick, brittle, and yellow except for green areas adjacent to the veins. Such leaves are frequently attacked by Alternaria spp.
Management
2. Eliminate weeds near and adjacent to sugar beet fields.
Beet Yellow Net
Beet yellow net is sometimes identified as yellow net and the causal virus as yellow net virus (YNV).
Cause.
Beet yellow net is thought to be caused by the beet yellow net virus (BYNV) and tentatively is placed in the luteovirus group. BYNV overwinters in sugar beet and
possibly in weed hosts. BYNV is transmitted mainly by the green peach aphid, Myzus persicae. Once an aphid has acquired BYNV, it often remains infective for life.
It is possible that BYNV cannot be transmitted without beet mild yellowing virus as a carrier virus.
Distribution.
England and the United States (California).
Symptoms.
An intense yellow chlorosis of veins and veinlets of diseased leaves looks like a yellow network against a background of green interveinal tissue. The vein bands may
coalesce until nearly all of the leaf is chlorotic. Diseased plants are conspicuous in the field and contrast with the surrounding healthy green plants. Leaf texture is
smooth and soft, not brittle as with beet yellows virus. Usually, the first symptoms are expressed on the youngest plant leaf. As the diseased leaf expands and matures,
chlorosis involves more of the veinlet network. It has been reported, in some circumstances, that early symptoms fade as new leaves appear normal and that infected
plants are difficult to locate.

Page 728
Occasionally a severely diseased plant will have a complete chlorosis of older leaves. No stunting or malformation occurs.
Management.
Not necessary.
Beet Yellow Stunt
Cause.
Beet yellow stunt virus (BYSV) is in the closterovirus group. BYSV is primarily reservoired in annual sowthistle, Sonchus oleraceus, and is most efficiently
transmitted by the sowthistle aphid, Nasonovia lactucae. However, N. lactucae apparently does not reproduce on sugar beet. The green peach aphid, Myzus
persicae, is abundant on sugar beet but is a relatively inefficient vector. The potato aphid, Macrosiphum euphorbiae, also is an inefficient vector. For this reason
spread of BYSV in a field is marginal. Disease incidence is high in rows adjacent to areas where sowthistle is present but becomes progressively less with increased
distance from the virus source.
Distribution.
he United States (California).
Symptoms.
Initially, there is a severe twisting, cupping, and epinasty of one or two diseased intermediateaged leaves. Petioles are shortened, and leaves become mottled and
yellow. Young diseased leaves are dwarfed, malformed, twisted, and slightly mottled. As leaves age, mottling becomes more intense, and at times, leaves become
completely chlorotic. Diseased plants are severely stunted and sometimes collapse and die.
Management.
Control sowthistle adjacent to sugar beet fields.
Beet Yellow Vein
Cause.
There is no evidence that the causal agent of beet yellow vein is a virus. The causal organism, however, can be transmitted by grafting, juice inoculation, and the
leafhopper Aceratagallia calcaris.
Distribution.
The United States.
Symptoms.
Very young diseased leaves are dwarfed and the main veins are yellow. The main veins of all affected leaves are either a continuous or broken yellow, with chlorosis
that extends 1 mm or more into surrounding tissue and is visible on both sides of leaves. Commonly, half of a diseased plant may be severely stunted, while the other
half grows normally.
Management.
Not reported.
Beet Yellows
In some literature the "s" is left off of "yellows" and the causal organism is described as beet yellow virus.
Cause.
Beet yellows virus (BYV) is in the closterovirus group. BYV likely survives in overwintered sugar beets and is transmitted by the green peach aphid, Myzus persicae;
the black bean aphid, Aphid fabae; and infrequently

Page 729
by other aphids in a semipersistent manner. BYV has a retention time in A. fabae of 24 to 48 hours. The maximum acquisition time is reached in 6 hours, and
inoculation periods occur within 1 hour but maximum transmission efficiency is reached after a 6hour inoculation access. BYV is not passed on to the progeny of
vectors nor is it retained after molting.
Date of sowing apparently does not influence the pattern or distribution of BYV in a field.
Distribution.
Symptoms.
Younger diseased leaves have a vein clearing or vein yellowing that may appear bright yellow or necrotic. Secondary and intermediate veins frequently appear sunken
and develop an etch symptom. Older leaves become thickened and brittle, followed by a chlorosis that begins at the leaf margins and tips and spreads downward
between veins. Chlorosis may vary from pale green to orange or red, depending on the variety. Small reddish or brown spots develop on many of the older yellowed
leaves. Chlorotic areas feel waxy or, in severely diseased plants, dry, causing plants to rustle when shaken or brushed. Such leaves do not wilt easily during dry
weather and will splinter when crushed. Early infected leaves eventually become necrotic starting from where they first became chlorotic. The necrotic spots and
yellow color often give leaves a bronze cast.
Management
1. Based on a forecasting system, insecticides are used to control vectors in England.
2. Eliminate escaped and overwintered beets.
3. Separate new beet fields from known sources of infection by 2 to 3 km.
Cucumber Mosaic
Cause.
Cucumber mosaic virus (CMV) is in the cucumovirus group. CMV overwinters in several perennials, has a large host range, and is disseminated by more than 60
species of aphids. Aphids only have to feed a few seconds to acquire the virus, but they rapidly lose it during subsequent feedings. Consequently, an aphid must
frequently feed on diseased plants in order to reacquire the virus. CMV is not transferred to young aphids by the female aphid. CMV is transmitted by seeds of some
plants but not by sugar beet seed.
Distribution.
Because of the large host range, CMV is generally distributed wherever sugar beet is grown. However, it is not considered a serious disease.
Symptoms.
Large, irregularshaped patches of bright yellow tissue contrast with the dark green of the leaf. Symptoms are of a mosaic type but the pattern is coarser and more
contrasting than that found in beet mosaic. Leaves commonly are dwarfed and distorted and have blisterlike areas of green tissue. Necrosis often occurs in large
areas of the diseased older leaves.

Page 730
Management.
Control weeds around sugar beet fields.
Lettuce Chlorosis
Cause.
Lettuce chlorosis virus (LCV) is in the closterovirus group. LCV is transmitted by the sweet potato white fly, Bemisia tabaci ''B" biotype.
Distribution.
Symptoms.
Interveinal yellowing and thickened leaves occur in plants that are naturally infected. Interveinal reddening occurs in the leaves of inoculated plants.
Management.
Not reported.
Lettuce Infectious Yellows
Cause.
Lettuce infectious yellows virus (LIYV) is in the closterovirus group. LIYV survives in a wide range of weeds and commercial crops and is transmitted in a semi
persistent manner by the sweet potato white fly, Bemisia tabaci. Cotton is a major source of high populations of this whitefly.
Distribution.
Symptoms.
A very mild mottling develops into an interveinal yellowing of diseased leaves. A necrosis eventually develops in the chlorotic areas of the diseased leaves.
Management
1. Alter the sowing of cucurbits to provide a 1 to 3week period in July or August when cucurbits are not present.
2. Do not grow sugar beet near areas of diseased plants.
3. Destroy infested residue of cucurbits and lettuce after harvesting.
4. Control weeds in the field being sown and in nearby fields.
Rhizomania Disease
Rhizomania disease is also called beet necrotic yellow vein.
Cause.
Beet necrotic yellow vein virus (BNYVV) is in the furovirus group. Wild type isolates typically contain four singlestranded RNA species unlike most furoviruses,
which possess bipartite, singlestranded RNA genomes.
BNYVV is transmitted by the soilborne fungus Polymyxa betae and by inoculation of sap. However, BNYVV is not present in all fungal populations. Movement of
P. betae and BNYVV is primarily by the physical movement of soil during tillage and harvest operations. A lesser means of spread is through furrow irrigation.
Polymyxa betae is an obligate parasite that survives in field soil as cys

Page 731
tosori, each of which is a mass of resting spores that can survive up to 10 years in the soil. Cystosori give rise to zoospores (each resting spore produces a single
zoospore), which "swim" through free soil water until they contact a host root and encyst. Encysted zoospores produce a structure called a stachel through which
zoosporic cytoplasm enters the host cell and becomes a plasmodium. Only primary root tissue of young roots is infected; optimum infection occurs at a temperature of
25°C. The host cell then becomes infected with BSBMV if P. betae is viruliferous. After a time, the plasmodium develops into a zoosporangium, which releases
additional zoospores that repeat the infection cycle. However, some plasmodia develop into cysts, and often nearly every cell in the small feeder roots will contain a
cyst. As root cells senesce, cysts are eventually released into the soil, where they can remain viable for years without loss of virulence.
Polymyxa betae infects latesown plants sooner than earlysown plants. Temperatures at early sowing favor plant growth over fungus growth, but the numerous
fibrous roots in older plants favor late infection. Disease is most severe at a soil temperature of 20°C for an extended time and wet soils that are neutral to slightly
alkaline. Polymyxa betae is unable to infect sugar beet roots in soil when the matric potential is 0.4 bar or less.
Greater levels of infection by P. betae occur with viruliferous isolates than with nonviruliferous isolates. BNYVV causes roots to proliferate, resuiting in more
susceptible tissue for P. betae to infect. The increase in susceptible tissue does not result in increased infection per unit of root length but may maintain adequate
inoculum for subsequent infection by P. betae. Most of the damage caused by the fungusvirus complex is due to the virus, but the aggressiveness of the vector is also
important. BNYVV infrequently moves systemically in diseased plants and depends on the fungus vector for most celltocell movement.
Different isolates of BNYVV have been found in California. Three other virus entities also have been found, but their relationship to Rhizomania disease is not known.
Differences in vectoring ability occur among isolates of P. betae.
Distribution.
Rhizomania has been found in France, Italy, Japan, and the United States.
Symptoms.
Diseased roots are stunted and have a proliferation of lateral rootlets on the main taproot, which gives it a "bearded" look. Roots are frequently rotted and constricted
below the soil level. Both viruliferous and nonviruliferous isolates of P. betae reduce total dry root mass of sugar beets. Much of the direct damage to roots by
BNYVV only is root tip death, which results in a loss of apical dominance and an increased amount of root branching and lower accumulation of root mass.
The vascular system is discolored, and diseased leaves are upright and slightly chlorotic. Leaves proliferate, resulting in excessive crown tissue.

Page 732
Leaves may also lose turgidity and wilt without becoming discolored. Rarely, distinct veinal yellowing of diseased leaves with necrotic lesions is evident.
Nonviruliferous isolates of P. betae have been shown to significantly reduce the top mass of sugar beets, but viruliferous isolates did not significantly reduce the top
mass.
Management.
No economically effective control measure is known. Resistance to the virus has been identified in a wild beet species, Beta maritima, and in several sugar beet
breeding lines.
Savoy
Savoy is also called beet savoy.
Cause.
Beet savoy virus (BSV) overwinters in its vector, the pigweed bug (Piesma cinerea), in grassy or woody areas. Infection occurs mainly at the edges of sugar beet
fields. BSV is not mechanically transmitted nor is it seedborne. There is a possibility that the causal agent may be a phytoplasma.
Distribution.
The United States, primarily east of the Continental Divide.
Symptoms.
The more pronounced effects are found on the innermost diseased leaves, which are dwarfed, curled downward, and savoyed. This gives the lower leaf surface a
netted appearance due to veinlets first clearing, then thickening. Later, roots will be generally discolored and phloem will appear necrotic. Both leaves and roots are
markedly stunted.
Management
1. Sugar beet fields should be located several hundred meters from woods or uncultivated land that could serve as an insect source.
2. Grow a barrier crop between the sugar beet field and a potential insect source.
Yellows
Cause.
Soybean dwarf virus (SDV). The subterranean clover red leaf virus is considered a strain of SDV.
Distribution.
Australia (Tasmania).
Symptoms.
An interveinal chlorosis initially occurs on diseased older leaves, then develops into a bright yellow color that is occasionally accompanied by a veinal necrosis. Yellow
leaves sometimes develop orange tints. Symptoms rarely extend to the younger leaves except those on severely diseased plants that have a mottled appearance.
Diseased leaves generally are thickened and brittle.
Management.
Not reported.

Page 733
Selected References
Altman, J. 1981. Increase in cyst nematode populations in soil treated with cycloate and diallate. (Abstr.) Phytopathology 71:199.
Boxch, U., Abbas, H. K., and Mirocha, C. J. 1988. Production of mycotoxins by Fusarium cultures on sugar beet substrate. (Abstr.) Phytopathology 78:1552.
Bugbee, W. M. 1975. Dispersal of Phoma betae in sugar beet storage yards. Plant Dis. Rptr. 59:396397.
Bugbee, W. M. 1975. Penicillium claviforme and Penicillium variabile: Pathogens of stored sugar beets. Phytopathology 65:926927.
Bugbee, W. M. 1979. Resistance to sugar beet storage rot pathogens. Phytopathology 69:12501252.
Bugbee, W. M. 1983. Infection and movement of endophytic bacteria in sugar beet plants. (Abstr.) Phytopathology 73:806.
Bugbee, W. M., and Campbell, L. G. 1990. Combined resistance in sugar beet to Rhizoctonia solani, Phoma betae, and Botrytis cinerea. Plant Dis. 74:353355.
Bugbee, W. M., and ElNashaar, H. M. 1983. A newly recognized symptom of sugar beet root infection caused by Phoma betae. Plant Dis. 67:101102.
Bugbee, W. M., and Gudmestad, N. C. 1988. The recovery of Corynebacterium sepedonicum from sugar beet seed. Phytopathology 78:205208.
Bugbee, W. M., and Nielsen, G. E. 1978. Penicillium cyclopium and Penicillium funiculosum as sugar beet storage rot pathogens. Plant Dis. Rptr. 62:953954.
Bugbee, W. M., and Soine, O. C. 1974. Survival of Phoma betae in soil. Phytopathology 64:12581260.
Bugbee, W. M., Gudemestad, N. C., Secor, G. A., and Nolte, P. 1985. Sugar beet: A natural host for Corynebacterium sepedonicum. (Abstr.) Phytopathology
75:1379.
Bugbee, W. M., Gudmestad, N. C., Secor, G. A., and Nolte, P. 1987. Sugar beet as a symptomless host for Corynebacterium sepedonicum. Phytopathology
77:765770.
Duffus, J. E. 1965. Beet pseudoyellows virus, transmitted by the greenhouse whitefly (Trialeurodes vaporariorum). Phytopathology 55:450453.
Duffus, J. E. 1972. Beet yellow stunt, a potentially destructive virus disease of sugar beet and lettuce. Phytopathology 62:161165.
Duffus, J. E., and Liu, H. Y. 1987. First report of Rhizomania of sugar beet from Texas. Plant Dis. 71:557.
Duffus, J. E., Larsen, R. C., and Liu, H. Y. 1986. Lettuce infectious yellows virus—A new type of whiteflytransmitted virus. Phytopathology 76:97100.
Ellis, P. J. 1992. Weed hosts of beet western yellows virus and potato leafroll virus in British Columbia. Plant Dis. 76:11371139.
Engelkes, C. A., and Windels, C. E. 1992. Formation and survival of sclerotia of AG22 of Rhizoctonia solani on sugar beet roots. (Abstr.) Phytopathology
81:1186.
Engelkes, C. A., and Windels, C. E. 1996. Susceptibility of sugar beet and beans to Rhizoctonia solani AG22 IIIB and AG22 IV. Plant Dis. 80:14131417.
Gerik, J. S., and Duffus, J. E. 1988. Differences in vectoring ability and aggressiveness of isolates of Polymyxa betae. Phytopathology 78:13401343.
Gerik, J. S., and Hubbard, J. C. 1989. Effect of soil water matric potential on infection by Polymyxa betae and beet necrotic yellow vein virus. (Abstr.).

Page 734
Giannopolitis, C. N. 1978. Lesions on sugar beet roots caused by Cercospora beticola. Plant Dis. Rptr. 62:424427.
Giunchedi, L., and Langenberg, W. G. 1982. Beet necrotic yellow vein virus transmission by Polymyxa betae Keskin zoospores. Phytopathol. Medit. 21:57.
Griffin, G. D. 1988. Comparative nematicidal control of Heterodera schachtii on sugar beet as affected by soil temperature and soil type. Plant Dis. 72:617621.
Halloin, J. M., and Roberts, D. L. 1991. A parasitic storage rot of sugar beets caused by Aspergillus flavus. Plant Dis. 75:751.
Harveson, R. M., Rush, C. M., and Wheeler, T. A. 1996. The spread of beet necrotic yellow vein virus from point source inoculations as influenced by irrigation and
tillage. Phytopathology 86:12421247.
Heidel, G. B., Rush, C. M., Kendall, T. L., Lommel, S. A., and French, R. C. 1997. Characteristics of beet soilborne mosaic virus, a furolike virus infecting sugar
beet. Plant Dis. 81:10701076.
Herr, L. J., and Roberts, D. L. 1980. Characterization of Rhizoctonia populations obtained from sugar beet fields with differing soil textures. Phytopathology 70:476
480.
Hills, F. J., and Worker, G. F., Jr. 1983. Disease thresholds and increases in fall sucrose yield related to powdery mildew of sugar beet in California. Plant Dis.
67:654656.
Hine, R. B., and Ruppel, E. G. 1969. Relationship of soil temperature and moisture to sugar beet root rot caused by Pythium aphanidermatum in Arizona. Plant
Dis. Rptr. 53:989991.
Kontaxis, D. G., Meister, H., and Sharma, R. K. 1974. Powdery mildew epiphytotic on sugar beets. Plant Dis. Rptr. 58:904905.
Langenberg, W. G., and Kerr, E. D. 1982. Polymyxa betae in Nebraska. Plant Dis. 66:862.
Limburg, D. D., Mauk, P. A., and Godfrey, L. D. 1997. Characteristics of beet yellows closterovirus transmission to sugar beets by Aphis fabae. Phytopathology
87:766771.
Lindsten, K., and Rush, C. M. 1994. First report of beet soilborne virus in the United States. Plant Dis. 78:316.
Liu, H. Y., and Duffus, J. E. 1985. The viruses involved in Rhizomania disease of sugar beet in California. (Abstr.) Phytopathology 75:1312.
Liu, H. Y., Duffus, J. E., and Gerik, J. S. 1987. Beet distortion mosaic virus—A new soilborne virus of sugar beet. (Abstr.) Phytopathology 77:1732.
Maas, P. W. T., and Heijbroek, W. 1982. Biology and pathogenicity of the yellow beet cyst nematode, a host race of Heterodera trifolii on sugar beet in the
Netherlands. Nematologica 28:7793.
MacDonald, J. D., Leach, L. D., and McFarlane, J. S. 1976. Susceptibility of sugar beet lines to the stalk blight pathogen Fusarium oxysporum f. sp. betae. Plant
Dis. Rptr. 60:192196.
Marco, S. 1984. Beet western yellows virus in Israel. Plant Dis. 68:162163.
Martyn, R. D., Rush, C. M., Biles, C. L., and Baker, E. H. 1989. Etiology of a root rot disease of sugar beet in Texas. Plant Dis. 73:879884.
Mukhopadhyay, A. N. 1987. CRC Handbook on Diseases of Sugar Beet. Volume II. CRC Press, Inc., Boca Raton, FL. 177 pp.
Ramirez, M. C., Raposo, R., and MateoSagasta, E. 1994. Occurrence of Aphanomyces cochlioides dampingoff of sugar beet in Spain. Plant Dis. 78:102.
Ruppel, E. G., and Tomasovic, B. J. 1977. Epidemiological factors of sugar beet powdery mildew. Phytopathology 67:619621.

Page 735
Ruppel, E. G., Harrison, M. D., and Nielson, A. K. 1975. Occurrence and cause of bacterial vascular necrosis and soft rot of sugar beet in Washington. Plant Dis.
Rptr. 59:837840.
Ruppel, E. G., Hills, F. J., and Mumford, D. L. 1975. Epidemiological observations on the sugar beet powdery mildew epiphytotic in western USA in 1974. Plant
Dis. Rptr. 59:283286.
Ruppel, E. G., Jenkins, A. D., and Burtch, L. M. 1980. Persistence of benomyltolerant strains of Cercospora beticola in the absence of benomyl. Phytopathology
70:2526.
Rush, C. M. 1987. Root rot of sugar beet caused by Pythium deliense in the Texas panhandle. Plant Dis. 71:469.
Rush, C. M., and Heidel, G. B. 1995. Furovirus diseases of sugar beets in the United States. Plant Dis. 79:868875.
Rush, C. M., and Winter, S. R. 1990. Influence of previous crops on Rhizoctonia root and crown rot of sugar beet. Plant Dis. 74:421425.
Rush, C. M., Carling, D. E., Harveson, R. M., and Mathieson, J. T. 1994. Prevalence and pathogenicity of anastomosis groups of Rhizoctonia solani from wheat
and sugar beet in Texas. Plant Dis. 78:349352.
Schneider, C. L., and Robertson, L. S. 1975. Occurrence of diseases on sugar beet in a crop rotation experiment in Saginaw County, Michigan in 19691971. Plant
Dis. Rptr. 59:194197.
Schneider, C. L., Ruppel, E. G., Hecker, R. J., and Hogaboam, G. J. 1982. Effect of soil deposition in crowns on development of Rhizoctonia root rot in sugar beet.
Plant Dis. 66:408410.
Stanghellini, M. E., and Kronland, W. C. 1977. Root rot of mature sugar beets by Rhizopus arrhizus. Plant Dis. Rptr. 61:255256.
Stanghellini, M. E., Von Bretzel, P., and Kronland, W. C. 1981. Epidemiology of Pythium aphanidermatum root rot in sugar beets. (Abstr.) Phytopathology
71:905.
Stanghellini, M. E., Von Bretzel, P., Olsen, M. W., and Kronland, W. C. 1982. Root rot of sugar beet caused by Pythium deliense. Plant Dis. 66:857858.
Staples, R., Jansen, W. P., and Anderson, L. W. 1970. Biology and relationship of the leafhopper Aceratagallia calcaris to yellow vein disease of sugar beets. J.
Econ. Entomol. 63:460463.
Tamada, T. 1975. Beet Necrotic Yellow Vein Virus. Commonwealth Mycological Institute. Descriptions Plant Viruses. Set. 9, No. 144.
Thompson, S. V., Hills, F. J., Whitney, E. D., and Schroth, M. N. 1981. Sugar and root yield of sugar beets as affected by bacterial vascular necrosis and rot,
nitrogen fertilization, and plant spacing. Phytopathology 71:605608.
Timmerman, E. L., D'Arcy, C. J., and Splittstoesser, W. E. 1984. Beet western yellows virus in Illinois. (Abstr.) Phytopathology 74:1271.
Vaughn, K. M., and Rush, C. M. 1991. Reducing Aphanomyces seedling disease of sugar beets by limited irrigation. (Abstr.) Phytopathology 81:1164.
Vincelli, P. C., Wilcox, W. F., and Beaupr'e, C. MS. 1990. First report of Phytophthora cryptogea causing root rot of sugar beet in Wyoming. Plant Dis. 74:614.
von Bretzel, P., Stanghellini, M. E., and Kronland, W. C. 1988. Epidemiology of Pythium root rot of mature sugar beets. Plant Dis. 72:707709.
Whitney, E. D. 1971. The first confirmable occurrence of Urophlyctis seproides on sugar beet in North America. Plant Dis. Rptr. 55:3032.

Page 736
Whitney, E. D. 1987. Identification and aggressiveness of Erwinia carotovora subsp. betavasculorum on sugar beet from Texas. Plant Dis. 71:602603.
Whitney, E. D., and Duffus, J. E. (Ed.). 1986. Compendium of Beet Diseases and Insects. American Phytopathological Society, St. Paul, MN. 76 pp.
Windels, C. E., and Nabben, D. J. 1987. Rhizoctonia solani and Rhizoctonialike binucleates associated with sugar beet plants in the Red River Valley. (Abstr.)
Windels, C. E., Kuznia, R. A., and Call, J. 1994. First report of Thanatephorus cucumeris (Rhizoctonia solani AG3 and AG5) on sugar beet. (Abstr.).
Windels, C. E., Kuznia, R. A., and Call, J. 1997. Characterization and pathogenicity of Thanatephorus cucumeris from sugar beet in Minnesota. Plant Dis. 81:245
249.
Wisler, G. C., and Duffus, J. C. 1997. First report of lettuce chlorosis virus naturally infecting sugar beets in California. Plant Dis. 81:550.

Page 737
20.
Diseases of Sugarcane (Saccharum officinarum)
Bacterial Mottle
Bacterial mottle is also called leaf stripping and chlorotic mottle.
Cause.
Pectobacterium carotovorum var. graminarium persists in diseased standing cane, cane residue, and grasses, specifically elephant grass, Pennisetum purpureum;
para grass, Brachiaria mutica; and guinea grass, Panicum maximum. Bacteria are disseminated by flooding water, primarily during the hot, wet season. Bacteria
are exuded through stomata of diseased cane or grasses and carried by water to other hosts, where they enter through wounds in the stem or the buds of growing
points. Bacteria are not efficiently disseminated by wind or rain. Seed cane that is infected ordinarily fails to germinate.
Distribution.
Australia. The disease is most common in lowlying areas that are subject to flooding.
Symptoms.
Initially, one to many creamywhite stripes (12 mm wide) extend from or near the bases of leaf blades upward and parallel to leaf veins. As diseased leaves age,
stripes enlarge and the orange to brownred discolored areas developing within them often involve most of the stripe.
Systemic infection causes diseased leaves to have a chlorotic mottling, often without any distinct striping. Sometimes shoots become almost completely chlorotic. As
the diseased chlorotic leaves become older, the abundant small brownred flecks and short, narrow stripes that appear cause the chlorotic leaves to look pink.
Diseased shoots are stunted, and leaf margins wither, causing diseased leaves to curl inward. Eventually the entire shoot may die. Diseased stalks may tiller excessively
due to the production of several side shoots at their

Page 738
bases. A witches' broom effect may occur several centimeters above the soil level when older cane has been infected and characteristic leaf symptoms are present.
During warm, humid weather, small whitish drops of bacterial exudate may occur on the undersides of diseased leaves.
Management
2. Plant only healthy seed cane.
3. Destroy diseased plants in a field.
4. Control infested grasses in waterways adjacent to cane fields.
Gumming Disease
Gumming disease is also called gummosis, Cobb's disease of sugarcane, and gum disease.
Cause.
Xanthomonas campestris pv. vasculorum. A second bacterium, X. officinarum sp. nov., has been implicated in gumming disease. Xanthomonas campestris pv.
vasculorum survives from one planting to the next in cuttings and may infect healthy sets through contaminated knifes or tools. Dissemination over a large distance is
ordinarily through the movement of infected cuttings. Dissemination also occurs by machinery, the brushing of diseased plants against healthy ones, and insects.
Bacteria enter sugarcane leaves through small wounds caused by machinery, insects, or leaves brushing against each other. Secondary infections are primarily by
bacteria or gum oozing from wounds of diseased plants during wet weather and being disseminated from diseased to healthy plants by windblown rain.
Distribution.
Africa, Australia, South America, the United States (Puerto Rico), and the West Indies.
Symptoms.
Symptoms start 2 to 3 weeks after wet weather has occurred. Longitudinal streaks (36 mm wide) follow the course of the vascular bundles on mature leaves that
have not started to discolor. Most streaks start at the diseased leaf apex or margin and vary in length from a few millimeters to the full length of the leaf, but streaks do
not extend into the leaf sheath. Young lesions have welldefined margins, but margins of older streaks become diffuse. The streaks are yellow to orange flecked with
patches of red. Tissue starts to die at the point of infection and progresses along the length of the streak, which becomes grayish. Symptoms on leaves may seem to
disappear during dry weather, particularly if diseased leaves are shed as they age.
On the youngest diseased leaf blades and the undersides of midribs, systemic infection causes short, narrow, welldefined dark red streaks that extend into leaf
sheaths. Sometimes creamywhite streaks almost half the width of the leaf start from the leaf base. Red blotches are lacking at first

Page 739
but may develop as systemic diseased leaves mature. Chlorotic areas speckled with red dots may occur on portions of one or many diseased leaves. This symptom
may involve the entire top of the diseased plant and usually causes the growing point to die. Although some diseased shoots may recover, a large percentage of
diseased stalks wilt and die.
A yellow to orange gummy mass exudes from cut ends of severely diseased stalks. Gum pockets that frequently form in the growing point region can be observed
when diseased stalks are cut longitudinally.
Management
2. Plow out diseased crop; however, ratoons usually suffer less loss than plant crops.
Leaf Scald
Cause.
Xanthomonas albilineans is a gramnegative bacterium that colonizes the vascular system of leaves, stalks, and roots. Bacteria enter through the wounded buds of
cuttings and are transmitted primarily by planting the infected stalks into noninfested fields but also are transmitted mechanically on contaminated cutting implements,
particularly cane knives. Spread may also occur by aerial means, leaftoleaf contact, roottoroot contact, and soil infestation. Tolerant cultivars may disseminate
bacteria over considerable distances since symptoms of leaf scald do not occur or go unnoticed on tolerant cultivars.
Distribution.
Worldwide.
Symptoms.
Two types of symptoms have been described: acute and chronic. The chronic, or characteristic, symptom is the presence of one or more straight, welldefined,
narrow (3 mm wide), white or chlorotic stripes that extend over and around the vascular bundles the full length of diseased leaf blades and sheaths. The narrow stripes
may become necrotic and the resulting necrosis can expand to encompass the entire diseased leaf. Young shoots and stalks may die, and shoots exhibiting symptoms
similar to diseased leaves may develop from axillary buds on mature stalks.
Acute symptoms are the sudden wilting and death of diseased stalks. Frequently the progressive withering of diseased leaves gives the plant a scalded appearance.
Entire leaves become chlorotic on severely diseased plants, and young shoots may also be chlorotic as they emerge from the soil. Internodes of stalks are shortened,
weak, and produce side shoots from the germination of lateral buds.
Diseased vascular bundles have a light red discoloration at the nodes, the juncture of the lateral side shoots, and throughout the stalk. Some vessels are plugged with a
reddish gumlike substance, but there is no bacterial ooze.

Page 740
Some diseased plants may be symptomless. Symptoms may also disappear as diseased plants continue to grow but, conversely, may become more severe as cane
approaches maturity if plant growth is retarded for any reason.
Large reductions in yield and sugar content occur, and juice purity is affected.
Management
1. Quarantine seed cane into areas where leaf scald does not occur.
2. Grow resistant cultivars. Two mechanisms may play an important role in resistance: resistance to colonization of the apex, which is characterized by the absence of
symptoms, and resistance to colonization of the upper and lower parts of the stalk.
3. Maintain diseasefree seed cane nursery programs. These rely on heat therapy, sanitation, and a rigid monitoring system to ensure diseasefree seed cane.
Mottled Stripe
Cause.
Pseudomonas rubrisubalbicans survives in standing cane and infested residue. Dissemination is by wind and rain.
Distribution.
Africa, Australia, the Caribbean region, South America, and the United States. Most cane cultivars are susceptible but mottled stripe is not considered a serious
disease.
Symptoms.
Disease symptoms occur only on leaves. Creamywhite stripes (14 mm wide and a maximum of 1 m in length) with distinct edges occur parallel to leaf veins. Stripes
frequently develop within reddish discolored areas on a diseased leaf to give a red and white mottled effect to the leaf. If the red areas are large, stripes have a general
reddish appearance.
Management.
Not reported.
Ratoon Stunting Disease
Ratoon stunting disease is also called Q. 28 disease.
Cause.
Clavibacter xyli subsp. xyli is a small, xylemlimiting coryneform bacterium. Clavibacter xyli subsp. xyli infects a wide variety of graminaceous plants, including
johnsongrass, sorghum, maize, sweet sudangrass, and bermudagrass.
Clavibacter xyli subsp. xyli is disseminated only mechanically by cutting knives, mechanical harvesters, tools, and cuttings taken from diseased plants. The bacteria
are easily spread in susceptible cultivars but not in resistant cultivars. Disease spread within rows of susceptible plants will follow the direction of harvest from a
diseased plant source. The incidence of

Page 741
ratoon stunting disease in test plots increased with the number of ratoon crops harvested.
Distribution.
Wherever sugarcane is grown. Ratoon stunting disease is widely regarded as the most important disease affecting commercial sugarcane production in the world.
Symptoms.
The only external symptoms are stunting and unthriftiness of diseased plants. Ratoons display more pronounced disease symptoms than does older cane. Ratoons are
slow to start, particularly in dry weather, and continue to be retarded in growth. Disease is usually not lethal but yield is reduced due to the production of thinner,
shorter stalks. Stunting is not uniform from stool to stool and a stand of plants within a field may display uneven growth. Diseased cane wilts sooner than healthy cane.
Internal symptoms may include a salmonpink discoloration below the growing point of young cane. In mature cane, a yellow, orange, pinkred, or redbrown
discoloration of vascular bundles occurs in the nodes below the region of leaf sheath attachment. However, this is not considered a reliable symptom to diagnose the
disease.
Management
1. Grow resistant cultivars. No cultivars are immune, but resistance may be conferred by physical features of the vascular structure at the stalk nodes. These features
include a more profuse branching of the metaxylem and fewer xylem vessels that pass directly through stalk nodes without terminating.
2. Plant only cuttings from healthy plants.
3. Treat infected cuttings with hot water or hot air. Treated cuttings should have a protectant fungicide applied.
4. Destroy all volunteer cane.
5. Sterilize cutting tools.
Red Stripe and Top Rot
Cause.
Pseudomonas avenae (syn. P. rubrilineans) persists in older, withered leaves and in soil for at least 32 days. Bacterial exudate seeps to the diseased leaf surface
during warm, wet weather and forms droplets of bacterial ooze. Bacteria, which are disseminated primarily by wind and rain and rarely by cuttings or any other
mechanical means, enter plants through wounds or stomates. All portions of the plant may become diseased, including leaves, stalks, and roots. Bacterial exudate
forms galls on the lower portion of the plants or runs down the leaf and causes stem infection.
Distribution.
Wherever sugarcane is grown.
Symptoms.
Initially, watersoaked stripes surrounded by a chlorotic zone develop on diseased leaves. Stripes are 14 mm × 1540 cm but become wider

Page 742
when they extend down into the leaf sheaths. Stripes later become discolored dark red to maroon and eventually coalesce, forming bands of alternating maroon stripes
and chlorotic areas.
The vascular bundles near the growing point of the stalk become slightly red. This discoloration extends down the stalk as a red ring onefourth to onehalf the
distance from the rind to the center. The center of the ring is watersoaked and rapidly decomposes, but the outside portion does not change. Eventually, rot extends
down to the base of a stalk, leaving a hollow central cylinder. The terminal bud and spindle leaves die, which often results in the growth of lateral buds that also display
a red discoloration. Diseased stalks in an advanced stage of decomposition emit an unpleasant odor that can be detected for a considerable distance.
Management
2. Rogue diseased stools from seedling nurseries.
Cause.
Alternaria alternata (syn. A. tenuis) is a common saprophyte.
Distribution.
Cuba, India, and Taiwan.
Symptoms.
Spots on diseased leaves that initially appear as minute, watersoaked areas eventually elongate and become elliptical to irregularshaped and have redbrown to dark
brown margins. The leaf area between the spots becomes necrotic and sometimes the entire diseased leaf dies.
Management.
Not reported.
Banded Sclerotial Leaf Disease
Cause.
Thanatephorus cucumeris (syn. Pellicularia sasakii), anamorph Rhizoctonia solani, survives as sclerotia in soil. Other grasses, particularly bermudagrass,
Cynodon dactylon, are also diseased. Only older leaves of cane become infected by coming in contact with a diseased grass leaf or infested soil during periods of
high humidity.
Distribution.
Africa, Australia, Asia, Caribbean, Central America, and the United States. Banded sclerotial leaf disease is considered of minor importance.
Symptoms.
Older diseased leaves and, occasionally, diseased leaf sheaths have a series of broad bands across the leaf or sheath. The initial brown

Page 743
green irregularshaped areas that occur become discolored brown, then yellow to light tan and have definite redbrown borders. Dark brown to black, irregular to
sphericalshaped (25 mm in diameter) sclerotia are present in the diseased areas of the plant.
Management.
Not necessary.
Black Rot
Cause.
Ceratocystis adiposa (syn. C. major, Ceratostomella adiposa, Endoconidiophora adiposa, and Ophiostoma adiposa) persists as perithecia and mycelia in
infested residue. Conidia produced from mycelia are disseminated by wind, splashing water, insects, and by any means that moves soil. Black rot is more prevalent in
loose, cloddy soils that have large air pockets. In the United States, black rot is most common in seed cane bedded in the autumn, possibly because of air spaces that
form around the seed cane at this time. Infection occurs through the cut ends of seed cuttings.
Distribution.
Australia, Brazil, China, Dominican Republic, India, Indonesia, Panama, Peru, Taiwan, and the United States.
Symptoms.
Seed cuttings become soft and watery at the ends. The interior of diseased cuttings initially is dark purple, then becomes black and emits an odor that resembles
fermenting pineapples. Black mycelial growth of C. adiposa occurs on the cut ends of seed cane and is the obvious external symptom.
Management
2. Plant cuttings in the autumn rather than storing them in beds.
Black Stripe
Cause.
Cercospora atrofiliformis.
Distribution.
Taiwan.
Symptoms.
Initially, small, yellow, round or oval spots occur on diseased leaves. Eventually, the spots enlarge to 0.51.2 × 5.036.0 mm and become brownblack.
Management.
Not necessary.
Brown Rot
Cause.
Corticium sp. is a saprophyte and a minor pathogen of trees.
Distribution.
Australia. Brown rot has been found only in sugarcane planted in soil recently cleared of trees.

Page 744
Symptoms.
Diseased stools initially are unthrifty. Eventually, the leaves wilt and die and the death of the entire stool follows. A thick layer of brown mycelium extends a few
centimeters above the soil line on the diseased stalk and binds the leaf sheaths together. Mycelium also grows over the lower leaf sheaths and belowground plant parts,
binding soil to plants and causing dead roots and stems to appear several times thicker than they actually are. Stalks below the soil level are killed and turn brown.
Dead tissue dries out quickly and is separated from healthy tissue by a narrow dark brown band.
Management.
Not necessary, since brown rot is of minor importance.
Brown Spot
Cause.
Cercospora longipes persists in infested leaf residue and diseased leaves of standing cane. Conidia are produced on both diseased leaf surfaces but are more
abundant on the lower leaf surfaces. Dissemination of conidia is by wind, rain, and cuttings contaminated with conidia.
Distribution.
Presumed to be present wherever sugarcane is grown; however, it has not been reported from Australia or Taiwan. Brown spot is not considered an important
disease.
Symptoms.
Numerous spots first appear on both surfaces of diseased older leaves and progress up the plant. Spots are redbrown and surrounded by a narrow yellow halo, oval
to linear, and vary in size from specks to 13 mm in length. The centers of the older spots become tan and surrounded by a red zone and a yellow halo. Spots may
coalesce and form large, irregularshaped redbrown patches on diseased leaves. Severely diseased leaves may die prematurely, which gives diseased plants and
entire fields a ''fiery" appearance.
Management
2. Treat seed cane cuttings with a seedprotectant fungicide.
Brown Stripe
Cause.
Cochliobolus stenospilus, anamorph Bipolaris stenospila. It is unknown how C. stenospilus survives in the absence of cane in subtropical areas where cane is not
grown yearround. Presumably, C. stenospilus may either infect other members of the grass family or mycelia may survive in infested residue.
Conidia develop in lesions on older dead leaves and are disseminated by wind for a considerable distance. Conidia germinate on leaves in the presence of free
moisture and the resulting germ tubes infect leaves through the stomates. Cochliobolus stenospilus is a weak facultative parasite and is

Page 745
more likely to infect plants predisposed by other causes, such as dry weather.
Distribution.
Symptoms.
Symptoms of brown stripe are most severe in dry weather and when growing conditions for the host are suboptimal. Initially, young leaves have small (0.5 mm in
diameter) watery spots that soon become elongated, redbrown to brown, and sometimes are surrounded by a narrow chlorotic halo. Frequently, spots occur in a
row across a leaf, which is the result of conidia germinating in the moisture within the spindle. Eventually, the spots elongate and form definite stripes (210 mm in
length) with a narrow yellow margin. As lesions mature, they become longer, sometimes up to 75 mm in length, but are only 4 to 5 mm wide. When disease is severe,
stripes coalesce and prematurely kill the diseased leaves. Infrequently, top rot develops.
Management
2. Maintain plants in a vigorous growing condition with proper fertility and moisture.
Collar Rot
Cause.
Hendersonina sacchari.
Distribution.
Argentina, Bangladesh, India, Indochina, Mauritius, the Philippines, and Sri Lanka.
Symptoms.
The top leaves of a diseased plant become necrotic and dry from the diseased leaf margin inward, leaving only a green midrib. The interior of the upper nodes is dried
up, often with cavities of various sizes that eventually extend throughout the stalk. The tissue of the lower diseased internodes is watery and brown with patches of red,
which becomes the dominant color in the basal internodes. Roots growing from the diseased basal internodes are rotted and have a dark brown to blackish
discoloration. Diseased stalks are lighter in weight than the stalks of healthy plants.
Management.
Not necessary, because collar rot is of minor importance.
Common Rust
Common rust is also called sugarcane rust and sugarcane leaf rust.
Cause.
Puccinia melanocephala. Urediniospores and teliospores are produced on sugarcane. Other spore stages and alternate hosts are not known. Urediniospores are
disseminated by wind and water. Infection occurs under humid conditions at temperatures of 16° to 29°C. In Puerto Rico, the opti

Page 746
mum rainfall for infection is 13 to 16 cm/month and plants are most susceptible to infection when they are 2 months old.
Disease severity has been associated with edaphic conditions in Florida. Disease severity is negatively correlated with soil pH. High levels of soil phosphorus are
associated with high rust severity. At two locations, high levels of soil magnesium and potassium were associated with lower rust severity.
Distribution.
Symptoms.
Symptoms occur mostly on diseased leaves. The uredinia are tiny, brownish, elongated spots that occur on both leaf surfaces but are more common on the lower leaf
surfaces than the upper leaf surfaces. Spots increase in length to 2 to 10 mm, become orangebrown to brown, and are surrounded by a small yellowish halo. Orange
urediniospores initially are subepidermal but later rupture the leaf epidermis. The surrounding tissue is killed, which sometimes results in the death of young diseased
leaves. Uredinia eventually darken in color on the lower diseased leaf surfaces due to the formation of telia either in the uredinium or in separate telia.
Management.
Covered Smut
Covered smut is also called kernel smut.
Cause.
Sphacelotheca macrospora infects ovules in the spikelet, replacing seed with smut spores.
Distribution.
Taiwan.
Symptoms.
Diseased plants appear normal until flowering time, when ovaries are slightly swollen and elliptical or ovoid in shape. The graygreen membrane that initially covers the
ovaries later turns brown. When the membrane ruptures it exposes a blackish powdery mass of chlamydospores surrounded by a sticklike central column.
Management.
Not necessary.
Culmicolous Smut
Culmicolous smut is also called smut, sugarcane smut, and inflorescence smut.
Cause.
Ustilago scitaminea survives as chlamydospores in dry soil and infested residue, as mycelia in latent infections in planting materials, and as spores on cuttings. Spore
viability was lost after 7 to 9 weeks in five different soils at three moisture levels in Louisiana. Therefore, spores produced during one season will not persist in soil to
the next season under conditions in

Page 747
Louisiana. Chlamydospores and sporidia in soil may be disseminated by water and infect cuttings.
Each chlamydospore germinates under moist conditions to form a three or fourcelled promycelium. The promycelium produces a hypha that functions as an infection
thread, or sporidia bud from each of its cells. The sporidia, in turn, either germinate and form a hypha or bud off and form more sporidia.
Ustilago scitaminea, a parasite of meristematic tissues, enters only through the lower part of the bud below the scales. Wounding increases infection, and when an
infected bud begins to grow, the fungus grows just behind the growing tip. After a latent period of 4 to 7 months, the apical meristem is stimulated to produce a long,
unbranched, whiplike appendage in which chlamydospores are produced. The enveloping membrane is ruptured and the chlamydospores are exposed and passively
released to become windborne. A smut whip may release millions of spores per day during an infectious period that lasts up to 3 months.
Diseased buds on standing cane may either give rise to smutted whips the same season or mycelia may remain dormant within the buds. Severe winters in northern
sugarcanegrowing areas damage or kill sugarcane buds, causing a decrease in disease incidence. In tropical areas, more than one disease cycle can occur per
growing season. True seedlings may also become infected.
Sugarcane smut severity is greater during a dry season, when plants are predisposed to infection.
Distribution.
Symptoms.
The typical symptom, a long, whiplike structure varying in size from a few to several centimeters, is produced from the apex of the diseased stalk and doubles back.
Depending on the cultivar, diseased shoots either grow at a faster rate than healthy shoots, resulting in the emergence of typical smut whips above the crop canopy, or
produce short, curved whips in the canopy.
The narrow unbranched whip, or sorus, contains dark brown to blackish chlamydospores that are surrounded by a thin silvery membrane. Eventually, the membrane
ruptures and exposes a dark mass of chlamydospores that are blown away by the wind, leaving only a core parenchyma and fibrovascular elements. When infection
occurs early, diseased canes have small, narrow leaves and slender stalks with widely spaced nodes, which result either in clumps of spindly canes or small grassy
shoots that are followed by smutted whips. The whips are usually straight when short but become irregularly curved when they are 1.0 to 1.5 m long.
After the production of smutted tops, buds lower on the diseased stalks begin to grow and terminate in a black whip. Sometimes smutted side

Page 748
shoots occur on an apparently healthy stalk.
Some unusual symptoms have been described from Hawaii. Whips often remain confined under the leaf sheaths and have a characteristic serpentine form. Buds from
which lateral bud sori originated are flattened, elongated, and larger than the typical symptoms displayed by diseased buds.
Callous outgrowths, an atypical symptom, are most abundant at a position on stalks between normalappearing tissue and areas displaying "typical" smut symptoms.
Galls in this region are generally limited to nodal areas and are initiated either in the region of the root band and intercalary meristem, or from a leaf sheath scar.
Outgrowths sometimes appear randomly on internodes positioned near or adjacent to the bases of whips. Initially, the callus is smooth and lacks chlorophyll.
Eventually, buds, or leaflike structures, are differentiated. It is not uncommon to have 40 to 60 buds on a gall. Buds continue to grow and terminate by forming a
whip.
Symptoms on true seedlings are the presence of earlydeveloped, thin, grassy stems with short, slender internodes and no visible buds or root initials. In the uppermost
part of the diseased plant, the leaf sheaths are absent and leaf blades are subtended by long bristlelike hairs. Most seedlings die from severe lodging, but those that
live produce a short, whiplike structure containing chlamydospores.
Management
1. Rogue out diseased shoots or stools.
2. Select healthy planting material.
3. Treat planting stock with a protectant fungicide.
4. Avoid ratooning of affected cane fields.
5. Rotate sugarcane with a resistant crop.
Other Fungi Reported to Cause Smut
Sorosporium indicum
Sphacelotheca consimilis
S. cruenta (syn. S. chrysopogonis, S. holci, and Ustilago cruenta)
S. erianthi (syn. U. erianthi)
S. papuae
S. pulverulenta (syn. Cintractica pulverulenta, U. pulverulenta, and U. pulverulenta)
S. sacchari (syn. U. sacchari and U. sacchariciliaris)
S. schweinfurthiana (syn. U. schweinfurthiana)
S. schweinfurthiana var. minor
Ustilago consimilis
U. courtoisii

Page 749
Curvularia Leaf Spot and Seedling Blight
Cause.
Curvularia lunata.
Distribution.
Africa, Argentina, Asia, India, and the United States (Hawaii).
Symptoms.
Leaves have scattered circular to oval redbrown spots that enlarge into irregular, dark brown patches. Leaves become chlorotic, necrotic, and dry up. Seedlings also
become diseased and die.
Management.
Not reported.
Downy Mildew (Peronosclerospora sacchari)
Downy mildew is also called leaf stripe and Sclerospora leaf stripe.
Cause.
Peronosclerospora sacchari (syn. Sclerospora sacchari), which survives as oospores in leaf residue, is disseminated primarily by diseased seed pieces but also by
airborne and waterborne conidia. Conidia are produced on diseased plants at temperatures of 2° to 25°C and a relative humidity of 90% or more. Sporulation also
depends on actual sunlight or radiant energy beyond a certain level. Disseminated by splashing water for a short distance and by wind for up to 400 m from their
source, conidia germinate in the presence of free moisture. Infection takes place on very young leaf tissues while they are still in the spindle, or in young buds on stalks.
Oospores are produced in the mesophyll tissue of diseased leaves as sugarcane matures.
Peronosclerospora sacchari can infect other plants, particularly maize, Zea mays, and teosinte, Euchlaena mexicana. These plants may be important in the spread
of downy mildew but are of little importance in perpetuating the disease from one season to the next.
Distribution.
Downy mildew occurs only in the Eastern Hemisphere. It has been reported from Australia, Fiji, India, Japan, New Guinea, the Philippines, Taiwan, and Thailand.
Symptoms.
Welldefined chlorotic stripes on leaves as they emerge from the spindle become more prominent as the leaves elongate. Stripes are light green at first but become
yellow as the diseased leaves mature. Stripes are separated by green tissue and are confined between the larger leaf veins. Stripes are 125 mm wide and vary in
length from 2.5 to several centimeters, often extending the length of the blade. During high humidity and temperatures, a velvety, whitish growth consisting of mycelium,
conidia, and conidiophores occurs on stripes. As the diseased leaves become older, stripes become dark red.
Following secondary infection, a symptom called the "humpup" stage occurs. This symptom is manifest by diseased stalks that increase in height until some are almost
twice as tall as healthy plants. These stalks become light, brittle, and watery. The spindle leaves of the stalks are few in num

Page 750
ber, short, and discolored with yellow stripes. Spindle leaves fail to unfold, cling together at the top of the diseased plant, and eventually become twisted. These leaves
wither and shred.
In contrast, plants that grow from diseased seed pieces are severely stunted and have twisted and shredded leaves.
Management
2. Obtain planting material from a diseasefree source.
3. Harvest diseased plants early and plow the field.
4. Rogue out diseased stools in fields that have ratooned early.
Downy Mildew (Peronosclerospora spontanea)
Cause.
Peronosclerospora spontanea (syn. Sclerospora spontanea).
Distribution.
The Philippines and Taiwan.
Symptoms.
Chlorotic stripes on leaves as they emerge from the spindle become more prominent as the leaves elongate. Stripes are light green at first but become yellow as the
diseased leaves mature. The stripes are separated by green tissue and are confined between the larger leaf veins. During high humidity and temperatures, a velvety,
whitish growth consisting of mycelium, conidia, and conidiophores occurs on the stripes. As the diseased leaves age, the stripes change color from yellow to dark red.
Management
2. Obtain planting material from a diseasefree source.
3. Harvest diseased plants early and plow the field.
4. Rogue out diseased stools in fields that have ratooned early.
Downy Mildew LeafSplitting Form
Downy mildew leafsplitting form is also called leafsplitting disease.
Cause.
Peronosclerospora miscanthi (syn. Sclerospora miscanthi). Mycosphaerella striatiformans is also reported to be a causal fungus. Peronosclerospora miscanthi
persists in soil and in infested residue in soil as oospores and, probably, as mycelia from which conidia are produced. Infection is caused by both oospores and
conidia. Conidia are produced during periods of high humidity and are disseminated by wind to host plants. Oospores are abundantly produced within leaf tissue as
plants mature and are disseminated by any means that moves soil. Peronosclerospora miscanthi is also disseminated by planting diseased seed cane.
Distribution.
Fiji, Papua New Guinea, the Philippines, and Taiwan. Downy mildew leafsplitting form is considered to be of minor importance.

Page 751
Symptoms.
Initially, greenyellow stripes are produced that often extend the entire length of diseased leaves. The color of stripes progressively changes from yellow to redbrown
and, finally, to dark red. Eventually, the diseased leaf tissue disintegrates and splits along the lesion lines to change leaves into whiplike bundles of fibers. White
velvety masses of mycelia, conidia, and conidiophores are produced on the lower surfaces of leaf lesions.
Management
2. Place cuttings in water at 46°C for 20 minutes and then at 52°C for 20 minutes to eliminate the causal fungus.
Drechslera Seedling Blight and Leaf Spot
Cause.
Drechslera spicifera (syn. Bipolaris spicifera and Helminthosporium spicifera).
Distribution.
India.
Symptoms.
In the seedling blight phase, diseased plants are stunted and have poor root development. Leaf spot symptoms on leaves of diseased seedlings are small, elongated to
elliptical, reddish specks, with dark reddish margins, that enlarge and coalesce. Leaf tips die and dry up; eventually, the entire diseased plant wilts and dies.
Management.
Not necessary. Drechslera leaf spot and seedling blight is considered to be an unimportant disease.
Dry Top Rot
Cause.
Ligniera vascularum (syn. Sorosphaera vascularum) survives in infested residue and soil. Ligniera vascularum is an obligate parasite; therefore, a possible life
cycle based on closely related genera is as follows: Ligniera vascularum persists as resting spores in infested residue. Orangebrown spherical spores are 17 to 25
m in diameter and have walls that are 1.5 m thick. Ligniera vascularum is disseminated in diseased seed cane by any means that transports residue, and by water
that moves spores.
As residue decomposes, resting spores are liberated into the soil, where they germinate under favorable conditions and form zoospores. Zoospores "swim" to root
hairs, where they encyst and form infection hyphae that penetrate host plants. A plasmodium is formed within the infected plant cells and spreads from cell to cell in the
plant. In olderinfected cells, several cell walls may form within the plasmodium, transforming it into several zoosporangia. Zoospores form in zoosporangia that are
liberated into soil and rupture to release the zoospores. Zoospores infect roots directly or fuse with a compatible zoospore to form a zygote, which then infects host
roots. Dry top rot is most severe on sugarcane grown in wet soils.

Page 752
Distribution.
Barbados, Cuba, and the United States (Florida and Puerto Rico).
Symptoms.
Initially, spindle leaves wither and leaf tips dry. Leaves appear to lose their green color, then roll, and wilt. Growing points then die and the entire diseased stalk wilts.
Internodes at the tops of diseased plants or near the growing point are shortened or stunted, shrunken, flaccid, and thinner, giving the stalk a tapered appearance.
Later stages of the disease include a complete drying and necrosis of spindle and upper leaves, death of the shoot apex and stalk, and, possibly, death of the entire
stool. The spindle leaves become detached from stalks that die and expose the withered internodes. The most severely diseased plants die.
Longitudinal and cross sections of the vascular bundles in the lower diseased stalk internodes are orange, yellow, pink, or red due to orangebrown spherical spores
clogging the vascular system. Spore masses flow from excised vascular bundles placed in a drop of water. In some xylem vessels, usually above the region where
spores are found, a gray granular substance or plasmodium can be found.
Management
1. Plant diseasefree cane.
2. Take cuttings from the tops of young cane if only infected cane is available for seed.
3. Rotate sugarcane with legumes.
4. There is genetic variability among cultivars.
Ergot
Cause.
Claviceps purpurea and C. pusilla. Balansia sp. is also reported to cause ergot. Claviceps spp. survive or overseason as sclerotia that germinate in free moisture in
darkness at temperatures of 35° to 40°C. Subsequent ergot development occurs in humid weather.
Distribution.
Claviceps purpurea is the causal fungus of ergot in the "temperate" regions of Australia, India, and the Philippines. Claviceps pusilia is the causal fungus in the
warmer regions of the world.
Symptoms.
Initial symptoms are a stickiness and drooping of arrows when spikelet blooming is most active. Inflorescences rapidly turn black due to growth of saprophytic fungi.
Eventually, typical hard, black, sclerotial bodies replace kernels.
Management.
Not usually necessary. Elimination of susceptible material in sugarcane fields and adjacent fields is an aid to disease management.

Page 753
Eyespot
Cause.
Bipolaris sacchari (syn. Drechslera sacchari and Helminthosporium sacchari) persists within infested residue in geographical areas where sugarcane is not grown
during the winter. Conidia produced on lesions and infested residue are disseminated a considerable distance by wind. Bipolaris sacchari is also seedborne. Eyespot
is most severe during periods of high moisture and temperatures of 24° to 31°C. Eyespot is most severe during the winter months in the tropics.
Distribution.
Symptoms.
Seedling disease symptoms are redbrown spots on coleoptiles a few days after planting. Leaves then become chlorotic and seedlings die.
Initially, eyespot lesions on older plants are small, watery spots that are darker green than healthy tissue. In 3 to 4 days, spots become oval (610 mm in length) and
redbrown with a tan margin. Eventually, spots become gray and have a less noticeable halo. The redbrown areas lengthen and form streaks or "runners" from the
original spots to the tips of leaves. Occasionally a short redbrown streak develops in the opposite direction. Spots and runners may coalesce. As diseased leaves die,
leaf tips become redbrown, which gives a field of diseased plants a brownish cast. Infection of leaves in the spindle may allow the disease to move into the terminal
portions of stalks and cause top rot. Stalks of highly susceptible cultivars have elongated brown lesions.
Management
2. Do not apply large amounts of nitrogen fertilizer before eyespot is likely to occur.
3. A 2year cropping system has been suggested: Sugarcane is planted and harvested every 3 years, immediately following the eyespot season.
Foliage Blight of Seedlings
Cause.
Exserohilum rostratum (syn. Bipolaris rostrata, Drechslera rostrata, and Helminthosporium rostratum).
Distribution.
Widespread.
Symptoms.
Narrow, reddish stripes occur on diseased seedling leaves. The stripes eventually enlarge, coalesce, and become dark brown. Leaf sheaths become dark brown to
olivaceous due to the production of conidia and conidiophores. Diseased plants are usually stunted.
Management.
Not reported.

Page 754
Fusarium Sett and Stem Rot
Cause.
Gibberella fujikori, anamorph Fusarium moniliforme, and G. subglutinans persist in a wide range of infested residue and as perithecia in infected cane. Large
numbers of conidia are produced on infested residue. Dissemination is mainly by airborne conidia and ascospores. Infection is through the ends of cane cuttings, young
adventitious roots, and nodal leaf scars of the stalk portion planted into infested soil. The common sugarcane borer, Diatraea saccharalis, and its parasite, Bassus
stigmaterus, also disseminate spores and aid infection by wounding sugarcane stalks, which provides entrances for spores disseminated by insects and wind. Roots
may be infected without being wounded.
Distribution.
Symptoms.
Starting from the cut ends, vascular bundles become red. Young roots become purple, then decay. Buds may swell but not germinate or may germinate but slight
growth occurs. When such sets are split, vascular bundles are purplered and the surrounding parenchyma tissue is brown.
In standing cane, nodes and internodes may be infected at the point of infestation by the cane borer. Vascular bundles are dark red and the surrounding parenchyma
tissue is purplish or brownred. Diseased leaves turn yellow and dry up. Tops of diseased plants die, although the stalk tissue appears healthy. If harvest is delayed,
the entire stalk will decompose.
Management
2. Dip or spray cuttings with a fungicide.
3. Rotate sugarcane with nonsusceptible crops.
Iliau
Cause.
Clypeoporthe iliau (syn. Gnomonia iliau), anamorph Phaeocytostroma iliau. In the autumn, perithecia and pycnidialike structures in which conidia are produced
are commonly found submerged in the leaf sheath tissue of diseased mature plants. Ascospores are disseminated by wind and water. Conidia are exuded from
pycnidia during moist weather and disseminated by splashing water and, less commonly, by wind. Clypeoporthe iliau and P. iliau are also disseminated by infected
seed cane. Primarily young plants are infected during cool, moist weather. Seedlings produced from infected seed cane are infected early in the growth of the plant and
may die before stalk elongation. Clypeoporthe iliau spreads rapidly from stalk to stalk when seed cane is stored in covered mats or piles.
Distribution.
Australia, Brazil, Cuba, the Philippines, and the United States (Hawaii and Louisiana).

Page 755
Symptoms.
Diseased plants remain small and many break over and die. Overlapping leaf sheaths adhere together due to the growth of fungus mycelium that binds the sheaths.
Outer leaves die and white fungal mycelium can be seen after the leaf sheaths are stripped. When the fungus grows into stalks, there is a necrotic area inside the rind
that is reddish, while the rest of the stalk interior remains white. Diseased stalks shrivel, become weakened, and often break over. The surface of necrotic tissue
becomes rough due to the development of perithecia, whose sharp beaks project above the tissue surface.
Management.
Leaf Blast
Leaf blast is also called leaf blast of sugarcane and leaf spot of sugarcane.
Cause.
Didymosphaeria taiwanensis persists as perithecia in infested residue. Leaves injured by frost are most susceptible to infection.
Distribution.
Generally widespread, but leaf blast is not known to occur naturally in the United States. Leaf blast is considered to be of minor importance.
Symptoms.
Yellow spots (0.51.0 × 3.025.0 mm) occur on both surfaces of diseased leaves. Spots become purplered and coalesce, forming long, narrow streaks that turn
entire diseased leaves purplered. Leaves may wither and die, starting from the leaf tip back. Perithecia appear as small black objects in the dead areas of diseased
leaves.
Management.
Not necessary.
Leaf Blight
Cause.
Leptosphaeria taiwanensis, anamorph Stagonospora taiwanensis, causes leaf blight throughout the year in high rainfall areas.
Distribution.
Japan, Okinawa, the Philippines, and Taiwan.
Symptoms.
Small, narrow, elliptical or elongate, spindleshaped, yellowish spots are produced on both sides of diseased immature leaves that are in the spindle. Spots become
redbrown and elongate into streaks that often coalesce. Severely diseased leaves die and dry up, giving distant diseased plants a redbrown appearance.
Occasionally purplered lesions occur on leaf sheaths, especially in the latter stages of disease development. Perithecia appear as small black specks in the margins of
the oldest lesions.
Management.

Page 756
Leaf Scorh (Leptosphaeria bicolor)
Cause.
Leptosphaeria bicolor.
Distribution.
Kenya.
Symptoms.
Spindleshaped lesions enlarge and coalesce, giving leaves a scorched appearance.
Management.
Not reported.
Leaf Scorch (Stagonospora sacchari)
Cause.
Stagonospora sacchari persists in infested leaves as mycelia and pycnidia but does not survive well in soil. During moist weather, conidia are exuded out of pycnidia
in a gelatinous mass that sticks firmly to leaf surfaces when the gelatinous mass dries up. Subsequent moisture or rain loosens conidia from the dried gelatinous mass
and disseminates them to adjacent leaves or plants. Conidia are rarely airborne. Diseased leaves that adhere to the seed piece also provide a source of inoculum.
Disease severity is greatest during moist weather.
Stagonospora sacchari produces two toxins—toxin I(6ethylsalicylic acid) and toxin II (epoxydon)—that are capable of inducing leaf necrosis on susceptible
cultivars at 30 µg/ml and 25 µg/ml, respectively.
Distribution.
Asia, Africa, Central America, and South America.
Symptoms.
Very small red or redbrown spots that occur on diseased young leaves ultimately enlarge, become spindleshaped, and have a yellow margin. Eventually, spots
coalesce and extend along vascular bundles for 517 cm or more, becoming spindlelike streaks. At first, the streaks are redbrown but later become tan with a dark
red border. Numerous pycnidia appear as small, black, pimplelike objects in the older lesions. Occasionally lesions extend to the upper parts of diseased leaf
sheaths, but no pycnidia are ordinarily produced in them. During dry weather, severely diseased leaves will appear scorched. Spots on older diseased leaves remain
small and do not develop into streaks.
Management.
Marasmius Sheath and Shoot Blight
Cause.
Marasmiellus stenophyllus (syn. Marasmius stenophyllus) is saprophytic in infested residue and infects host plants predisposed by other means or through wounds.
Dissemination is by any means that moves mycelial strands and spores.
Distribution.
Wherever sugarcane is grown. Marasmius sheath and shoot blight is of minor importance.

Page 757
Symptoms.
White mycelium grows over the lower portions of diseased plants, causing leaf sheaths to adhere tightly to stalks. White mushrooms develop at the base of diseased
stalks. Mature leaves of diseased plants are covered with red spots that develop during dry weather periods. The underground portion of stems and young shoots may
also become infected.
Management.
Most cultivars are resistant.
Myriogenospora Leaf Binding
Myriogenospora leaf binding is also called leaf binding and tangle top.
Cause.
Myriogenospora aciculispora persists as perithecia in infested residue.
Distribution.
Argentina, Brazil, and the United States (Louisiana). Myriogenospora leaf binding is not common.
Symptoms.
Diseased plants are stunted, and the tips of unfolded leaves adhere to adjacent older leaves. As new leaves elongate, their tips are held firmly along the midrib of the
previously unfolded leaf by a black stroma of the causal fungus, giving diseased plants a ''whiplike" appearance. Although growing points and shoots may be killed,
new shoots commonly develop from the basal buds or buds formed later. A few healthy shoots may develop in diseased stools. Perithecia may occur in the tips of
diseased leaves in the spindle.
Management.
Not necessary.
Northern Poor Root Syndrome
Northern poor root syndrome is also known as poor root syndrome. Pachymetra root rot is considered a significant component but is described as a separate disease.
Cause.
A complex of organisms, including Pachymetra chaunorhiza, Pythium graminicola, Pythium myriotylum, and nematodes. Pachymetra chaunorhiza causes the
primary root rot symptom for the root rot component of the syndrome. Oospores of P. chaunorhiza survive in fallow soil for at least 5 years. Inoculum density
decreases when resistant cultivars are grown.
Distribution.
Australia (Queensland) in the widely grown cultivar 'Q90'. Pythium myriotylum has also been identified from sugarcane in Taiwan.
Symptoms.
Disease symptoms are premature wilting, unthrifty growth, and a tendency for stools to tip at the ground level, resulting in a reduction of subsequent ratoon stool
numbers.
A soft, flaccid rot develops in the root cortex. Both primary and secondary roots develop various lesions and a general discoloration, and development is restricted
and the fine root system is poorly developed. Dis

Page 758
eased roots contain high numbers of verrucose oogonia of Pachymetra chaunorhiza. The underground portions of stalks and the root system can be easily uprooted
if diseased sugarcane plants lodge.
Pythium myriotylum is reported to cause red to black elliptical lesions on roots and a rot of root tips. Root dry weight of some cultivars is reduced.
Management.
Cultivar resistance has been identified for Pachymetra root rot.
Orange Rust
Orange rust is also called sugarcane leaf rust.
Cause.
Puccinia kuehnii. Urediniospores and teliospores are produced on sugarcane. Other spore stages and alternate hosts are not known for certain; however,
spontaneums, wild sugarcane, and related genera have been suggested as collateral hosts. Urediniospores are disseminated by wind and water. Infection occurs during
humid conditions at temperatures of 16° to 29°C.
Distribution.
Asia, Australia, and Oceania.
Symptoms.
Symptoms are similar to those caused by P. melanocephala (common rust) except uredinia are cinnamon to yellowbrown.
Management.
Pachymetra Root Rot
Pachymetra root rot is considered to be an important component of northern poor root syndrome and the probable cause of the root rot component of the syndrome.
Cause.
Pachymetra chaunorhiza does not have a saprophytic growth stage. Oospores, the only known propagules, are produced in rotted roots. The disease occurs in the
high rainfall districts. It is suspected that P. chaunorhiza colonized sugarcane from a native Australian grass, but the alternative host is yet to be identified.
Pachymetra chaunorhiza can infect sorghum, but disease is generally restricted and oospore production is sparse. Pachymetra chaunorhiza can also infect clones
of Saccharum spontaneum and Erianthus spp.
Distribution.
Australia (high rainfall districts of Queensland).
Symptoms.
Aboveground symptoms include the loss of plant vigor, poor stooling, uneven stalk height, thin stalks, and a loss of stool anchorage. Lodged stools are often uprooted,
and many stools are pulled out of the ground during normal harvesting operations because of the loss of stool anchorage.
Initial root symptoms are a watersoaking of the diseased root section

Page 759
that develops into a soft, flaccid rot of primary and larger secondary roots; lesions and general discoloration of primary and secondary roots; and poor fine root
development. The rot occurs in the root tip region and, in susceptible cultivars, may extend the length of the entire root. In field soils that have a high population of P.
chaunorhiza propagules, root systems may be greatly restricted, with many short, flaccid roots extending from the stool. A red discoloration up to 2 mm long that
usually encircles the root accompanies the flaccid rot, indicating the limit of disease. In advanced stages of the disease, diseased roots are held intact only by the root
epidermis because all other root structures have disintegrated. Where high inoculum levels occur, 80% to 90% of primary shoot roots in susceptible cultivars may be
completely decomposed.
Diseased roots contain high numbers of oospores that have a verrucose oogonial wall.
Management.
Grow a resistant or tolerant cultivar.
Philippine Downy Mildew
Philippine downy mildew is also called sleepy disease.
Cause.
Peronosclerospora philippinesis (syn. Sclerospora indica and S. philippinesis).
Distribution.
India and the Philippines.
Symptoms.
Diseased seedling leaves have chlorotic streaks. Diseased mature leaves have necrotic streaks and are frequently deformed.
Management.
Not reported.
Cause.
Phyllosticta hawaiiensis.
Distribution.
Widespread.
Symptoms.
Symptoms on sugarcane are not well known. General leaf spots are reported to occur on diseased foliage.
Management.
Not reported.
Phytophthora Rot of Cuttings
Cause.
Phytophthora megasperma and P. erythroseptica persist in soil and infested residue as oospores. Sporangia normally germinate indirectly by producing zoospores
but occasionally germinate directly and produce germ tubes. Zoospores "swim" through soil water to plant host roots, where they encyst and germinate and form germ
tubes that penetrate the

Page 760
host plant. Infection occurs more frequently through the nodal areas than through cut ends. Oospores are eventually produced in diseased tissue. Phytophthora rot is
most severe when a long, cool spring follows a cold, wet winter.
Distribution.
Symptoms.
Seed pieces planted in infested soil do not produce roots and few buds germinate. Initially, interiors of diseased seed pieces are watersoaked, followed by the
occurrence of pink to orangered streaks. With yellowstalked cultivars, the discolored streaks appear through the stalk rind of the diseased plant. Streaks may also
be seen in the rind of darkstalked cultivars, but these streaks are not as distinct and are darker colored. Eventually, the entire seed piece becomes watersoaked and
the color darkens to redbrown and is accompanied by an etherlike odor.
Management
2. Improve soil drainage.
Pineapple Disease
Cause.
Ceratocystis paradoxa, anamorph Chalara paradoxa (syn. Thielaviopsis paradoxa), which persists as saprophytic mycelia in infested soil residue, infects seed
pieces by conidia growing into the cut ends. Sometimes seed pieces are infected prior to being planted. Standing cane may also become infected by airborne conidia
that enter stalks through injuries caused by rodents, insects, or machinery. Pineapple disease is often most severe in poorly drained areas within a field where soils
remain wet and relatively cool.
Distribution.
Symptoms.
Primarily the central core sugarcane cuttings are affected. Initially, the central core becomes reddened but stays firm. Later, the interiors of diseased stalks break down
and become hollow and discolored black, but vascular bundles remain intact. Cuttings may decay before buds germinate or diseased shoots die back after growing
only a few centimeters. In the early stages of decomposition, a pineapplelike odor may occur. Leaves on diseased stalks of standing cane wilt, then the stalks die.
Management
1. Make a cutting of at least three nodes to protect the center node.
2. Do not plant under conditions of low soil temperatures or excessive wetness or dryness.
3. Protect seed piece ends with a fungicide.
4. Do not plant too deep in the soil.

Page 761
Pokkah Boeng
Pokkah boeng is also called Fusarium sett and stem rot, knife cut, and pokkah boeng chlorosis.
Cause.
Gibberella fujikori, anamorph Fusarium moniliforme, and G. subglutinans persist as saprophytic mycelia in infested residue and as perithecia in diseased cane.
Large numbers of conidia are ultimately produced on infested residue. Conidia and ascospores are disseminated primarily by wind to host plants. Infection occurs
through the spindle, along the margins of partially unfolded leaves, where a small opening is formed during periods of dry weather. Conidia enter the spindle and are
carried down to the susceptible region, where they germinate during wet weather. Mycelium grows through the soft cuticle into the inner plant tissues.
Distribution.
Symptoms.
Pokkah boeng occurs when susceptible plants are in a rapid stage of growth, usually when they are 3 to 7 months old. A chlorotic area develops on the basal portion
of diseased lower leaves as they emerge from the spindle. Red spots or stripes often develop on the chlorotic areas. Affected areas usually are confined to only a few
leaves on one side of the spindle, but sometimes the young stem is penetrated by fungus mycelium. Diseased leaves are frequently deformed and do not unfold
normally but remain short. Often diseased areas are torn. Sometimes cavities develop in internodes and present a ladderlike appearance. Occasionally, during wet
weather, a soft rot develops in diseased areas. Usually diseased plants recover and new leaves develop normally.
Management.
Purple Spot of Sugarcane
Cause.
Pseudocercospora rubropurpurea (syn. Cercospora rubropurpurea).
Distribution.
Taiwan.
Symptoms.
Redpurple to dark purple and irregularshaped to circular (212 mm in diameter) leaf spots are most distinct on the upper surfaces of diseased leaves.
Management.
Not reported.
Pythium Root Rot
Cause.
Pythium aphanidermatum, P. arrhenomanes, R catenulatum, R dissotocum, P. graminicola, P. mamillatum, and P. splendens.
Root rot caused by P. arrhenomanes occurs during high temperatures in the early winter followed by alternate wet and dry periods in autumn but

Page 762
not in summer plantings. Shoots growing in loam soils are more susceptible than those growing in sand.
Weeds, particularly johnsongrass, can serve as hosts for P. arrhenomanes and may be involved in the etiology of Pythium root rot.
Distribution.
Widely distributed.
Symptoms.
Necrotic dark reddish lesions occur on diseased roots. Root tips are flaccid, watersoaked, and necrotic. The growth of fine feeder roots is reduced.
Diseased shoots exhibit stunting and wilting and eventually may be killed. Poor ratooning may also occur.
Management.
Plant sugarcane in welldrained soils.
Red Leaf Spot
Red leaf spot is also called purple spot.
Cause.
Dimeriella sacchari persists as perithecia in infested residue.
Distribution.
Australia, Bangladesh, Cuba, Fiji, Japan, Java, Nepal, New Guinea, Panama, the Philippines, Taiwan, Tanzania, Tobago, and Trinidad. Red leaf spot is of minor
importance.
Symptoms.
Leaf tips are more severely affected than the other parts of diseased leaves. Spots begin as red dots that later become round or elliptical (0.52.0 mm in diameter) and
have a yellow margin. Later, the color changes to purplered. Perithecia appear as small black specks in the older spots. When disease is severe, premature death of
leaves may occur.
Management.
Not necessary.
Red Rot
Cause.
Glomerella tucumanensis (syn. Physalospora tucumanensis), anamorph Colletotrichum falcatum, persists in diseased plants. Cuttings are a major source of
inoculum because of the conidia and mycelia present on, or in, seed pieces. Incipient infections may be present in bud scales, leaf scars, other nodal tissues, and stalk
borer tunnels. Conidia and ascospores are produced in diseased plant tissue and are primarily disseminated by water; therefore, it takes a relatively long time for
leaves higher on plants to become infected. Conidia are the principal source of stalk infections. Conidia are produced directly on mycelia or in acervuli in the lesions on
midribs, then are washed down behind the leaf sheaths, where they germinate and become established in the nodes and internodes. Seed pieces taken from this cane
are internally diseased or have dormant mycelia in bud scales, leaf scars, and other nodal tissues. Conidia are also present on the cutting surface.

Page 763
Disease development decreases with a decrease in temperature from 31.0° to 21.1°C. Disease development is optimum at temperatures from 29.4° to 31°0°C.
Injuries caused by insects and machinery predispose sugarcane to infection. Disease severity can be increased by the occurrence of drought conditions during the initial
growth processes of vegetatively propagated sugarcane stalks.
Distribution.
Symptoms.
All plant parts may be diseased, but red rot is most important on standing stalks, planted cuttings, and leaf midribs. In the early stages of disease, stalks display no
external symptoms. Tissues inside diseased stalks become a dull red and give a mottled appearance to stalk interiors. Red vascular bundles pass through reddened
areas and extend into healthy tissues. The reddish discoloration and cavities that contain either mycelium or a clear liquid may occur through the length of diseased
stalks. Eventually, diseased internal tissues become dark, shrink, and dry out. The stalk exteriors of severely diseased plants may become discolored redbrown and
have acervuli that appear as dark tufts or black hairlike objects under magnification.
Seed pieces may rot during periods adverse to sugarcane growth, such as too wet or too dry conditions. Diseased seed pieces are rotted and have various shades of
red, brown or gray discoloration. Gray mycelia develop in pith cavities and acervuli develop on the exteriors of seed pieces. Nodal tissue of susceptible cultivars
becomes red to almost black.
Initial symptoms on leaves are small red spots on the upper surfaces of midribs. Spots enlarge and produce elongated lesions which fuse together and form lesions that
extend the entire length of diseased leaves. Spots become tan, have dark red margins, and are covered with acervuli that look like numerous black tufts. Diseased
leaves may wilt, then dry up.
Management
2. Use only healthy cane for seed pieces.
3. Plant when conditions are proper for rapid germination. Maintain proper soil moisture.
4. Harvest susceptible cultivars before they have passed the peak of maturity.
Red Rot of Leaf Sheath and Sprout Rot
Cause.
Athelia rolfsii (syn. Pellicularia rolfsii), anamorph Sclerotium rolfsii, persists as sclerotia in soil and on infested host plant residue. Red rot of the leaf sheath occurs
during warm, wet weather.
Distribution.

Page 764
Symptoms.
Irregularshaped, orangered discolored areas with distinct margins develop on lower diseased leaf sheaths. White mycelium grows into the inner sheaths and binds
them loosely together. The underlying rind becomes discolored light brown and has a distinct margin. As diseased stalks mature, the affected area dies and dries up,
causing an extensive shallow canker. Small, round, brownish sclerotia develop between sheaths, along the edges or over the surface of diseased areas. In severe
cases, leaves gradually dry up and die. Most shoots of a diseased stool are thin and stunted and have many short internodes.
Management.
Not necessary.
Red Spot
Cause.
Distribution.
The United States (Mississippi). Red spot is thought to be of little economic importance.
Symptoms.
Bright red lesions (1525 × 2035 mm) occur on the midribs of diseased leaves.
Management.
Not reported.
Red Spot of Leaf Sheath
Red spot of leaf sheath is also called red leaf sheath rot of sugarcane.
Cause.
Mycovellosiella vaginae (syn. Cercospora vaginae). Red spot of leaf sheath is favored by warm, moist weather.
Distribution.
Wherever sugarcane is grown. Red spot of leaf sheath is of minor importance.
Symptoms.
Small, round, bright red spots with sharp margins occur on the diseased upper leaf sheaths. Spots coalesce and form bright red, irregularshaped patches that extend
through the diseased upper leaf sheaths into the inner sheaths. Later, dark brown to black conidia and conidiophores appear as a "sooty" coating on all diseased areas
but are the most abundant on the inside of diseased leaf sheaths.
Management.
Not necessary.
Rhizoctonia Sheath and Shoot Rot
Cause.
Rhizoctonia solani.
Distribution.

Page 765
Symptoms.
Similar to those of banded sclerotial leaf disease (see earlier discussion of this disease).
Management.
Not necessary.
Rind Disease
Rind disease is also called sour smell and sour rot.
Cause.
Phaeocytostroma sacchari (syn. Melanconium sacchari and Pleocyta sacchari) produces stromata inside diseased tissues. The stroma enlarges and develops
enough pressure to eventually split the plant epidermis and form a pustule. During moist conditions, conidia are produced inside stromata and exuded in a long,
gelatinous, threadlike structure through the top of pustules. Conidia are disseminated by wind and rain. Infection normally occurs through wounds in the plant host and
in plants not growing vigorously because of drought or overmaturity.
Distribution.
Australia, the United States (Hawaii), and the West Indies.
Symptoms.
Symptoms are most common on stalks but also occur on leaf blades and sheaths. Numerous black, coiled, hairlike fruiting structures exude from pustules that have
broken through the surfaces of diseased tissues. Internal diseased stalk tissues have a dark discoloration and a sour smell. Diseased leaves may yellow, dry up, and be
covered with the black, coiled structures. A symptom from Hawaii is that the nodes become redbrown and, later, the internodes become light brown.
Management.
Harvest mature sugarcane as soon as possible.
Ring Spot
Ring spot is also called ring spot of sugarcane leaf.
Cause.
Leptosphaeria sacchari, anamorph Phyllosticta sp., persists as saprophytic mycelia on dead leaves.
Distribution.
Wherever sugarcane is grown. Ring spot is usually of minor importance.
Symptoms.
Symptoms occur on diseased leaf blades and leaf sheaths. Spots initially are dark green to brownish, then become redbrown and oval or diamondshaped and are
surrounded by narrow chlorotic borders. Later, the centers of spots become tan and are surrounded by narrow red margins. Often an older spot may still be
surrounded by a yellow margin. Older spots have fruiting structures of various fungi that appear as blackish specks.

Page 766
Management.
Ring Spot of Sugarcane
Cause.
Pseudocercospora saccharicola (syn. Cercospora saccharicola).
Distribution.
Taiwan.
Symptoms.
Initially, leaf spots are circular to elliptical, dark green to brown, and generally surrounded by a narrow redbrown to maroon border. Eventually, spots become gray
and are surrounded by a purplebrown margin up to 7.5 mm wide.
Management.
Not reported.
Sclerophthora Disease
Sclerophthora disease is also called Sclerospora disease and downy mildew.
Cause.
Sclerophthora macrospora (syn. Sclerospora macrospora) persists in a large number of grass hosts and seed pieces. Transmission is primarily by planting infected
seed pieces, which give rise to a high percentage of diseased plants. Young sugarcane plants have been successfully infected by placing sporangia in the spindle.
Sporangia or conidia are abundantly produced on the undersides of diseased leaves during periods of heavy dew or fog. Sporangiophores grow through stomates and
produce one to five sporangia on their tips. The windborne sporangia germinate indirectly in the presence of free water and produce zoospores that "swim" to host
tissue, where they encyst and produce germ tubes that penetrate plant host tissue.
Sclerophthora disease is confined to low areas within fields that are subject to flooding. Oospores are abundantly produced in diseased leaf tissue, but their role in
survival and dissemination has not been determined, since they have not been observed to germinate.
Distribution.
Australia, Mauritius, Peru, South Africa, and the United States. Sclerophthora disease is usually of minor importance.
Symptoms.
Diseased stools are normally severely stunted, but tall plants or a cluster of small, dwarfed shoots frequently arise from a diseased stool. The cluster of small, dwarfed
shoots is a profuse tillering that gives diseased plants the appearance of clumps of coarse grass. When these stools produce cane, it is common to find stem galls of
various sizes and shapes on them.
Diseased leaves are small, coarse, and brittle and are yellowgreen because of the irregularshaped, yellowwhite streaks (onehalf to several centimeters long)
located between veins. Chlorotic blotches of varying sizes and shapes that also occur on diseased leaves give leaves a mosaic appearance. During rapid plant growth,
leaves droop and their edges become

Page 767
wavy. However, during poor growing conditions, diseased leaves become stiff and erect, and margins die and dry out, which cause shredding and give leaf edges a
ragged appearance. Leaf tips may curl into one or more loops.
Using magnification, oospores can be observed as numerous white specks along veins on diseased plants. No downy or external mycelial growth can be observed,
although sporangia are produced on diseased leaf surfaces. Infection of older cane causes plant tops to develop symptoms, while plant parts below the infection(s)
remain healthy. Buds on the diseased upper cane may proliferate and produce clusters of shoots at each node.
Management
1. Plant only seed pieces from healthy cane.
2. Do not plant in poorly drained areas in a field.
3. Rogue infected stools.
4. Destroy wild grasses adjacent to a cane field.
Sheath Rot
Cause.
Cytospora sacchari.
Distribution.
Widespread, but Cytospora sheath rot is considered of minor economic importance.
Symptoms.
Diseased leaves die from the leaf tips. Severely diseased shoots are killed.
Management.
Not reported.
Sooty Mold
Cause.
Capnodium sp. and Fumago sp. are fungi that grow in insect secretions.
Distribution.
Widespread.
Symptoms.
A dark brown to black film or crust consisting of fungal growth occurs on leaves and sheaths.
Management.
Not necessary.
Sugarcane Stubble Decline
Cause.
A complex of factors, including low winter temperatures and freezes, poor soil aeration and drainage, the physiological maturity of plants at time of harvest, the
condition of the stubble root system as affected by cultural practices and Pythium root rot, weed competition, a stalk rot caused by Glomerella tucumanensis, single
and combined effects of ratoon stunting disease caused by Clavibacter xyli subsp. xyli, and sugarcane mosaic virus.

Page 768
Distribution.
In the cooler sugarcane growing areas of the United States.
Symptoms.
Stubble gradually deteriorates, thereby preventing ratoon crops from developing. Yields of the ratoon or stubble crops progressively decline, and the crop cycle is
generally limited to the plant cane crop and two ratoon crops.
Management.
Pythium root rot is reduced by tolerant interspecific hybrid cultivars.
Tar Spot
Tar spot is also called black spot of leaves.
Cause.
Phyllachora sacchari. Ascospores in residue are a source of primary infection. Spores are disseminated by wind and rain.
Distribution.
Argentina and Asia.
Symptoms.
Black fungal stromata on diseased leaves resemble tar.
Management.
Not reported.
Target Blotch
Cause.
Helminthosporium sp.
Distribution.
Cuba, South Africa, and the United States (Florida). Target blotch is not economically important.
Symptoms.
Symptoms occur only in the winter on diseased leaf blades and midribs of mature cane. Spots are small and redbrown initially, then become tan to brownish necrotic
areas with irregular concentric rings that resemble a target. The spots develop first on the rolled leaves in leaf spindies, but the target symptom becomes more
pronounced as diseased leaves unroll. Spots cease to develop when leaves are unrolled from the spindle.
Management.
Not necessary.
Veneer Blotch
Cause.
Deightoniella papuana.
Distribution.
The British Solomon Islands, New Britain, and Papua New Guinea.
Symptoms.
Small, oval, light green to tan spots with a thin redbrown margin occur on diseased leaves. Next, two more similar spots occur, one on each side of the original spot.
Then two more spots occur, each flanking the second pair, and so on until up to 12 spots (1.2 × 61.0 cm), each larger than the preceding spot, have formed on each
side of the original spot. The center

Page 769
of each spot finally becomes brown, which gives each spot a beautiful pattern similar to figured veneer of wood. Conidiophores cause a thick, matlike appearance in
the older spots on the undersides of leaves and occasionally on upper leaf surfaces.
Management.
Not reported.
White Rash
White rash is also called anthracnose maculata, Elsinoe disease, spotted anthracnose, and white speck.
Cause.
Elsinoe sacchari, anamorph Sphaceloma sacchari.
Distribution.
Brazil, Japan, Malaysia, the Philippines, Taiwan, and the United States (Florida and Puerto Rico). White rash is considered to be of minor importance.
Symptoms.
Symptoms occur on diseased leaf blades, midribs of leaves, and occasionally leaf sheaths. Lesions are tiny; yellowish (but sometimes described as purplish); round,
elliptical, or fusiform spots (0.10.5 × 0.21.0 mm) that become yellow to tan and finally whitish, sometimes with redbrown margins. These slightly elevated spots
with distinct centers coalesce and form narrow, elongated streaks. A diseased area has the appearance of lacework.
Management.
Not necessary.
Wilt
Cause.
Fusarium sacchari (syn. Cephalosporium sacchari). Fusarium sacchari persists as saprophytic mycelia in infested residue. Abundant microconidia are produced
on mycelia and disseminated by wind to plant hosts. Fusarium sacchari is also disseminated by infected seed cane and by any means that transports residue.
Infection commonly occurs through insect wounds. Wilt development is more severe at a soil pH of 7.08.0 and an increase in the carbon:nitrogen ratio.
Distribution.
Symptoms.
Symptoms occur from when cane is halfgrown until harvest time. The first noticeable symptom is the wilting of a single cane or an entire clump. Initially, leaves
become yellow, then dry up. The diseased stem pith has light purple or reddish streaks and becomes light and hollow, making it worthless for milling. A foul odor
occurs after splitting a diseased stalk, and a cottony mycelial growth with abundant microconidia is present in pith cavities. A diseased seed piece usually does not
produce eyes and roots. Occasionally, an eye may swell or grow slightly before it dies. The interior of such a seed piece has a brown discoloration.

Page 770
Management
2. Plant only healthy seed pieces.
Yellow Spot
Cause.
Mycovellosiella koepkei (syn. Cercospora koepkei) persists in infested residue. Conidia, which are produced on the ends of conidiophores that emerge through
stomata in disease spots during wet, humid weather, are disseminated by splashing rain and by wind to new infection sites. Conidia are more numerous on the lower
surfaces than the upper surfaces of diseased leaves.
Distribution.
Africa, Asia, Australia, Brazil, Colombia, and Cuba.
Symptoms.
Yellowgreen spots (up to 12 mm in diameter) occur on the youngest diseased leaves. Small, reddened areas first appear on diseased lower leaf surfaces, then
increase on both leaf surfaces to give diseased plants and entire fields a general rusty yellow appearance at leaf maturity. A dirty, gray fungal growth develops
somewhat profusely on the lower surfaces but sparsely on the upper surfaces of diseased leaves. Spots coalesce and cover large areas of leaves until, at maturity,
most of the leaf surfaces may be affected. Consequently, leaves shrivel and die prematurely.
Management
2. Apply foliar fungicides during the growing season.
Zonate Leaf Spot
Cause.
Gloeocercospora sorghi. Presumably G. sorghi persists as sclerotia on infested residue.
Distribution.
Areas where sorghum and sugarcane are grown in the same culture.
Symptoms.
Initially small, redbrown, watersoaked spots that sometimes have a narrow chlorotic halo occur on diseased leaves near the soil surface. Spots enlarge, elongate in a
direction parallel with the veins, and become dark red or tan. Eventually, the spots occur as circular areas on diseased leaves or as semicircular patterns along the leaf
margins. Spots typically are circular redpurple bands that alternate with tan areas and give a concentric or zonate pattern with irregular borders. Spots vary in
diameter from a few millimeters to several centimeters and may cover the entire width of a diseased leaf.
During warm, wet weather, conidia are produced in lesions as a pinkish gelatinous spore mass that forms above a stomate. Sclerotia eventually appear as small, black,
raised bodies in lines parallel to the veins.

Page 771
Plants that were severely diseased in the seedling stage may become defoliated or die. Plants infected when older may have their foliage destroyed before maturity.
Management
1. Rotate sugarcane with a nonhost.
Lance
Cause.
Hoplolaimus columbus.
Distribution.
Unknown.
Symptoms.
Diseased root systems are coarse and depleted. Top and root weights are not significantly reduced.
Management.
Not reported.
Lesion
Cause.
Pratylenchus spp. feed only in root cortex.
Distribution.
Australia, Hawaii, Mauritius, and the United States (Louisiana).
Symptoms.
Diseased roots are thickened, have discolored lesions, and have fewer fine roots than healthy roots.
Management.
Fumigate soil with a volatile nematicide.
Root Knot
Cause.
Meloidogyne spp. Root knot nematodes multiply best in moderately dry, welldrained soils. Weeds in cane fields may also serve as hosts.
Distribution.
Symptoms.
Knots or galls on diseased roots form at or near the root tips and appear as nodules or elongated thickenings. Thickened roots are often curled. The apical meristem is
affected and growth is retarded or stopped; there is little or no proliferation of the lateral roots.
Management.
Spiral
Cause.
Helicotylenchus spp., Rotylenchulus spp., and Scutellanema spp.
Distribution.

Page 772
Symptoms.
In pot experiments, diseased roots were blunted and malformed and the number of branch rootlets was reduced.
Management.
Grassy Shoot
Cause.
A phytoplasmalike organism is transmitted by infected seed pieces, mechanically by cutting knives, and by the aphids Aphis idiosacchari, A. sacchari, and A.
maidis. Seed pieces can be infected by juice from chlorotic leaves. Jowar is another host.
Distribution.
India, Taiwan, and Thailand.
Symptoms.
Typically, a mass of stunted, crowded shoots grows from diseased seed pieces or ratoon stools. Some shoots are void of chlorophyll, and if enough shoots are
affected, the stools may die. Stalks produced in a diseased stool have long, delicate, scaly buds that develop into slender chlorotic shoots.
Symptoms of secondary infection occur in the leaves of numerous tillers at the base of stools. White to yellow welldefined stripes become diffuse or remain distinct on
thin and chlorotic leaves.
Management.
Plant only diseasefree cuttings.
White Leaf
Cause.
A phytoplasmalike organism that is transmitted by the leafhopper Matsumuratettix hiroglyphicus.
Distribution.
Asia.
Symptoms.
A diagnostic symptom of white leaf is leaves that are totally chlorotic in the spindle portion of tillers. Early foliar symptoms consist of a single white or cream line
parallel to the midrib of one leaf in the spindle. Later, symptoms may involve stripes, mottling, or total chlorosis of leaves. Stripes may extend the entire leaf length but
do not involve the leaf sheath. Stripes may vary in color and intensity and have welldefined or slightly diffuse margins. Mottling occurs as irregularshaped islands of
green that may appear as dots, streaks, or patches on a white background.
Symptoms become masked during times of relatively low temperatures. If low temperatures occur when diseased plants are mature, the newly developed leaves
become green again. In young plants or those inoculated by insect vectors, symptoms disappear shortly after their initial appearance. However, typical symptoms may
again develop on these diseased plants when the temperatures rise again.

Page 773
Management
1. Sugarcane planted during December through April is less diseased than sugarcane planted during July through October.
3. Plant diseasefree cuttings.
Banana Streak
Cause.
Banana streak virus (BSV) is transmitted from banana to sugarcane by the pink sugarcane mealybug, Saccharicoccus sacchari. BSV has vitallike bacilliform
particles measuring approximately 30 × 150 nm. It is serologically related to sugarcane bacilliform virus.
Distribution.
Colombia.
Symptoms.
Diseased leaves have chlorotic streaks.
Management.
Not reported.
Chlorotic Streak
Cause.
Sugarcane chlorotic streak virus (SCCSV) is disseminated when healthy and diseased plants are grown together in quartz sand and when healthy plants are grown in
soil obtained from diseased plants in fields. This mode of dissemination suggests a soilborne vector and infection through the roots. SCCSV is also disseminated by
running water, in stalk cuttings used for seed, and from plant to plant in the field in a manner that suggests an insect vector. The leafhopper Draeculacephala portola
has been implicated as a possible vector.
The disease is most prevalent in lowlying, poorly drained areas within a field and in plants growing in potassiumdeficient soil. Several grasses, including Arundo
donax, Brachiaria mutica, Panicum maximum, and Pennisetum purpureum, also are hosts.
Distribution.
Australia, Guyana, Java, and the United States (Puerto Rico).
Symptoms.
Symptoms are more common in ratoons than in plant cane and are most prevalent in early summer. One to many yellowish to whitish streaks with wavy, irregular
margins occur on both sides of diseased leaves, leaf midribs, and leaf sheaths. Streaks are short, narrow, and faint but later, particularly on older foliage, the streaks
are well marked (315 mm wide) and extend the entire lengths of diseased leaf blades. Centers of older streaks become necrotic in sections or along the entire streak
length. Leaf symptoms may disappear when streaked leaves senesce.

Page 774
Young diseased plants have stiff, erect leaves and wilt, even in the presence of abundant moisture. Young shoots die or become stunted, eventually causing an entire
field to have an uneven appearance. Vascular bundles are entirely discolored through the node.
Management
2. Treat cane in a hot water treatment at 52°C.
3. Obtain diseasefree planting material.
4. Rogue out infected plants in a seed field if disease incidence is less than 2%.
5. Improve soil drainage.
Dwarf
Cause.
Sugarcane dwarf virus (SCDV) is not known to be mechanically transmitted and the vectors are not known. Infection may occur from an alternate host plant or from
soil, but no evidence presently exists.
Distribution.
Australia.
Symptoms.
Diseased plants are stunted and have short, stiff, erect, distorted, fanlike tops. Numerous small (less than 1 mm wide and of variable length), white, longitudinal stripes
occur most abundantly on the younger diseased leaves. Wide, diffuse, chlorotic stripes that later become necrotic and have a papery texture occur primarily near leaf
margins. Transverse splitting of midribs occurs.
Stools of susceptible cultivars in the advanced stages of disease appear as groups of grassy shoots. Infected stools that ratoon usually produce diseased plants.
Management
1. Rogue out diseased plants.
3. Plant only diseasefree seed cane.
Fiji Disease
Cause.
Sugarcane Fiji disease virus (SFDV) is in the fijivirus group. SFDV is transmitted by at least two leafhoppers, Perkinsiella saccharicida and P. vastatrix. Both
species acquire SFDV as nymphs. Other leafhopper species, such as P. vitiensis, may also be vectors. SFDV is not mechanically transmitted. Sugarcane is the only
known host for SFDV.
Distribution.
Australia, Fiji, Java, the Philippines, and New Guinea.
Symptoms.
Elongated swellings or galls occur along the larger veins, the vascular bundles on the undersides of diseased leaves, and the vascular bun

Page 775
dles of diseased stalks. The last leaves to unfold from spindles are shortened or crumpled. Diseased shoots grow to a normal height and produce healthylooking
leaves of normal length and color until the leaves unfold from spindles, then short, deformed, twisted leaves are produced and plant growth ceases completely. The
upper half or twothirds of these leaves appear burned or scalded before expanding, leaving short, crumpled stumps. Galls are produced on both healthyappearing
and deformed leaves during the advanced stages of Fiji disease prior to plant death. Shoots either remain alive for several months or die in a short time.
Management
2. Plant only diseasefree cuttings.
3. Harvest diseased plants earlier than normal.
4. Plow under diseased plants.
5. Rogue out diseased stools if disease incidence is low.
Mosaic
Mosaic is also called sugarcane mosaic.
Cause.
Sugarcane mosaic virus (SCMV) is in the potyvirus group. SCMV now includes the former SCMV strains A, B, D, E, and MB in one group; the former SCMV
strains SC, BC, and Sabi from Australia and the former maize dwarf mosaic virus (MDMV) strain B in the United States are in another group. SCMV has a wide host
range and infects a large number of wild and cultivated grasses.
SCMV is transmitted by numerous aphid species, including Aphis gossypii, Carolinaia cyperi, Hysteroneura setariae, Rhopalosiphum maidis, R. padi, and
Schizaphis graminum. Sugarcane infected with SCMV in the first year are not foci for infections in succeeding years. SCMV is also mechanically transmitted with
difficulty, and it is rarely seedborne in maize.
Distribution.
Symptoms.
Symptoms are most obvious in diseased leaves that have just unrolled from spindles. Leaves have irregular, oval or oblong, pale green blotches of various sizes that
are not limited by veins. Blotches are various widths throughout their length and do not resemble stripes. Diseased leaves ordinarily are not distorted, but some
cultivars have stunted shoots that culminate in twisted and distorted leaves. Some cultivars have a stem mottling that causes tissue death and results in a cankered area.
Other cultivars have small and deformed sticks and some areas of discoloration in internal tissue. Mosaic symptoms sometimes disappear from leaves of growing
plants and healthyappearing plants grow from infected seed cane.

Page 776
Management
2. Rogue out diseased plants when disease incidence is low.
3. Do not plant sorghum next to sugarcane or rotate the two crops.
Sereh
Cause.
Sugarcane sereh disease virus (SCSDV) is transmitted through cuttings. SCSDV is not mechanically transmitted nor are vectors known.
Distribution.
Australia, India, Indonesia, Sri Lanka, Taiwan, the United States (Hawaii), and the West Indies.
Symptoms.
Normally, diseased shoots are of different heights and secondary shoots from basal buds are similarly affected. In some stools, taller stalks that develop have
shortened internodes near the top and leaves in a fanlike arrangement. Hairy adventitious roots may be produced on some nodes and abundant side shooting may
occur.
A severe symptom is that shoots from infected cuttings cease to grow after reaching a certain height, which causes diseased stools to be converted into a ''bunchlike"
tuft. A less severe symptom is reddishcolored vascular bundles in the nodes and sometimes in the internodes. Diseased vascular bundles sometimes are narrow, dull
red stripes on leaf blades.
Management
2. Plant certified diseasefree cane.
3. Do not grow ratoon crops.
Streak Disease
Cause.
Maize streak virus (MSV) sugarcane strain is transmitted by the leafhoppers Cicadulina bipunctella zeae, C. mibla, and other Cicadulina spp. Work done with
maize strains shows the leafhoppers can acquire the virus as nymphs or adults in a few minutes of feeding and remain infective throughout their lives. MSV is also
transmitted in cuttings from diseased plants but not mechanically. Several strains of MSV exist; each is virulent to one or a few hosts, mainly grasses, and avirulent or
weakly virulent to other hosts.
Distribution.
Africa.
Symptoms.
Symptoms are most obvious on the youngest diseased leaves. Diseased leaves have a pattern of straight, narrow, translucent stripes (0.5 × 0.51.0 mm long and of
uniform width) that follow leaf veins. Streaks may coalesce and be relatively wide on the leaves of young shoots developing from infected cuttings. Diseased leaves
may be crinkled and narrower than normal.

Page 777
Management.
Resistant cultivars are being developed.
Striate Mosaic
Cause.
Sugarcane striate mosaic virus (SCSMV). It is possible that more than one virus causes this disease, with one virus causing striations and another virus causing
stunting. The virus(es) are setttransmitted. SCSMV is associated with poor growing conditions in a field, such as areas with excessive sand or waterlogged soils.
Distribution.
Australia (northern Queensland).
Symptoms.
A few to numerous short (0.52.0 mm long), fine, light green striations develop initially on the youngest diseased leaves but become difficult to see as the leaves
mature. Striations are less numerous around larger vascular bundles, giving younger leaves a striping effect. Sometimes the entire tops of leaves are yellowed. Striations
occur on lower midribs but not on the top midribs. Stunting and poor stooling usually occur.
Management
2. Maintain plants in vigorous growing conditions.
Sugarcane Bacilliform
Cause.
Sugarcane bacilliform virus (SCBV) is closely related serologically to banana streak virus (BSV) and is in the badnavirus group. SCBV and BSV can be considered
as strains of the same virus. Virus particles are bacilliform in shape and contain a doublestranded DNA genome.
SCBV is transmitted mechanically, but the major vector is considered to be the pink sugarcane mealybug, Saccharicoccus sacchari.
Distribution.
Widely distributed where sugarcane is grown.
Symptoms.
Symptoms are variable but may include flecks or freckles on diseased leaves or diagnostic symptoms may be absent.
Management.
Not reported.
Sugarcane Mild Mosaic
Cause.
Sugarcane mild mosaic virus (SCMMV) is a closterolike virus that occurs in mixed infections with sugarcane bacilliform virus (SCBV). SCMMV is transmitted
mechanically and by the pink sugarcane mealybug, Saccharicoccus sacchari, in the absence of SCBV.
Distribution.
Malawi, Mauritius, and the United States (Florida).
Symptoms.
A very mild mosaic occurs on diseased leaves or no apparent foliar symptoms occur.

Page 778
Management.
Not reported.
Sugarcane Red Leaf Mottle
Cause.
Peanut clump virus (PCV) is a furovirus transmitted by the soil fungus, Polymyxa graminis. The fungus develops within the roots of several species of Gramineae but
not within roots of peanuts. The fungus can survive in soil for several years.
Distribution.
Burkina Faso, Senegal, and Sudan.
Symptoms.
Symptoms on diseased leaves are variable and include a reddish mottle surrounded by a mild mosaic together with diamondshaped chlorotic spots, discolored
stripes, and streaks of varying thickness.
Management.
Not reported.
Sugarcane Yellow Leaf Disease
Cause.
Sugarcane yellow leaf diseaseassociated virus (SCYLaV) may have some serological relationship to barley yellow dwarf virus. SCYLaV appears to be an isometric
virus with several characteristics of a luteovirus. SCYLaV particles are found only in phloem companion cells and in the cytoplasm, not in the nucleus.
Disease is likely related to a phloem dysfunction.
Distribution.
Brazil. Symptoms similar to sugarcane yellow leaf disease have been described for some cultivars in Australia, the United States (Hawaii), and other sugarcane
producing countries.
Symptoms.
Symptoms in diseased plants are not visible in the youngest two or three leaves and become evident only in mature leaves. The first symptom is the intense yellowing
on the abaxial surface of the midrib. Older leaves, usually the sixth or seventh from the growing tip, show a red discoloration on the adaxial surface of the midrib.
Discoloration subsequently spreads to the leaf blade, proceeding from the tip toward the base of the leaf, and is followed eventually by tissue necrosis. Roots and
stalks show impaired growth and production is significantly reduced.
Management
2. Maintain plants in vigorous growing conditions.
Yield Decline
Cause.
Unidentified soil microorganisms that do not infect roots and may be associated with the organic matter fraction of soil.

Page 779
Distribution.
Australia (Queensland).
Symptoms.
Yield is reduced 20% to 40%. Root browning occurs and there is reduced growth of fine roots.
Management.
Not reported.
Selected References
Abbott, E. V. 1964. Black rot. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier Publishing Company,
New York.
Abbott, E. V. 1964. Brown spot. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier Publishing
Company, New York.
Abbott, E. V. 1964. Collar rot, In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier Publishing Company,
New York.
Abbott, E. V. 1964. Dry top rot. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier Publishing
Company, New York.
Abbott, E. V. 1964. Myriogenospora leaf binding, In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier
Publishing Company, New York.
Abbott, E. V. 1964. Red leaf spot (purple spot). In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier
Abbott, E. V. 1964. Red spot of the leaf sheath. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier
Abbott, E. V., and Hughes, C. G. 1961. Red rot. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.). Elsevier
Abbott, E. V., and Matsumoto, T. 1964. Banded sclerotial disease. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer
(eds.). Elsevier Publishing Company, New York.
Abbott, E. V., and Tippett, R. L. 1941. Myriogenospora on sugarcane in Louisiana. Phytopathology 31:564566.
Abbott, E. V., Wismer, C. A., and Martin, J. P. 1964. Rind disease. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer
(eds.). Elsevier Publishing Company, New York.
Ammar, E. D., Kira, M. T., and AbulAta, A. E. 1980. Natural occurrence of streak and mosaic diseases on sugarcane cultivars at upper Egypt and transmission of
sugarcane streak by Cicadulina bipunctella zeae China. Egypt. J. Phytopathol. 12:2126.
Anderson, D. L., Raid, R. N., Irey, M. S., and Henderson, L. J. 1990. Association of sugarcane rust severity with soil factors in Florida. Plant Dis. 74:683686.
Astudillo, G. E., and Birchfield, W. 1980. Pathology of Hoplolaimus columbus on sugarcane. (Abstr.) Phytopathology 70:565.
Beniwal, M. A., and Satyavir. 1991. Effect of atmospheric temperature on the development of red rot of sugarcane. Indian Phytopathol. 44:333338.
Birch, R. G., and Patil, S. S. 1983. The relation of blocked chloroplast differentiation to

Page 780
sugarcane leaf scald disease. Phytopathology 73:13681374.
Bourne, B. A. 1961. Fusarium sett or stem rot. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.). Elsevier Publishing
Company, New York.
Braithwaite, K. S., Egeskov, N. M., and Smith, G. R. 1995. Detection of sugarcane bacilliform virus using the polymerase chain reaction. Plant Dis. 79:792796.
Byther, R. W., and Steiner, G. W. 1974. Unusual smut symptoms on sugarcane in Hawaii. Plant Dis. Rptr. 58:401405.
Cassalett, C., Victoria, J. I., Carrillo, P., and Ranjel, H. 1983. Resistance to sugarcane smut (Ustilago scitaminea Sydow). (Abstr.) Phytopathology 73:126.
Chatenet, M., and Saeed, I. 1995. First report of sugarcane red leaf mottle virus in Sudan. Plant Dis. 79:321.
Chu, H. T. 1964. Leafsplitting disease. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wisner (eds.). Elsevier Publishing
Company, New York.
Comstock, J. C., Ferreira, S. A., and Tew, T. L. 1983. Hawaii's approach to control of sugarcane smut. Plant Dis. 67:452457.
Comstock, J. C., Miller, J. D., and Farr, D. F. 1994. First report of dry top rot of sugarcane in Florida: Symptomatology, cultivar reactions, and effect on stalk water
flow rate. Plant Dis. 78:428431.
Comstock, J. C., Shine, J. M., Jr., Davis, M. J., and Dean, J. L. 1996. Relationship between resistance to Clavibacter xyli subsp. xyli colonization in sugarcane and
spread of ratoon stunting disease in the field. Plant Dis. 80:704708.
Croft, B. J. 1989. A technique for screening sugarcane cultivars for resistance to Pachymetra root rot. Plant Dis. 73:651654.
Damann, K. E. 1992. Effect of sugarcane cultivar susceptibility on spread of ratoon stunting disease by the mechanical harvester. Plant Dis. 76:11481149.
Damann, K. E. Jr., and Benda, G. T. A. 1983. Evaluation of commercial heattreatment methods for control of ratoon stunting disease of sugarcane. Plant Dis.
67:966967.
Davis, M. J., Dean, J. L., and Harrison, N. A. 1988. Distribution of Clavibacter xyli subsp. xyli in stalks of sugarcane cultivars differing in resistance to ratoon
stunting disease. Plant Dis. 72:443448.
Dean, J. L. 1981. Inoculation of wounded and unwounded sugarcane with Ustilago scitaminea. (Abstr.) Phytopathology 71:870.
Dissanayake, N., Hoy, J. W., and Griffin, J. L. 1997. Weed hosts of the sugarcane root rot pathogen, Pythium arrhenomanes. Plant Dis. 81:587591.
Eagan, B. T. 1964. Rust. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier Publishing Company, New
York.
Edgerton, C. W. 1958. Sugarcane and Its Diseases. Louisiana State University Press, Baton Rouge.
Grisham, M. P. 1994. Strains of sorghum mosaic virus causing sugarcane mosaic in Louisiana. Plant Dis. 78:729732.
Harrison, N. A., and Davis, M. J. 1988. Colonization of vascular tissues by Clavibacter xyli subsp. xyli in stalks of sugarcane cultivars differing in susceptibility to
ratoon stunting disease. Phytopathology 78:722727.
Hoy, J. W., and Grisham, M. P. 1988. Spread and increase of sugarcane smut in Louisiana.

Page 781
Hoy, J. W., and Jiaxie, Z. 1991. Longevity of teliospores of Ustilago scitaminea in soil. (Abstr.) Phytopathology 81:1204.
Hoy, J. W., and Schneider, R. W. 1988. Role of Pythium in sugarcane stubble decline: Effects on plant growth in field soil. Phytopathology 78:16921696.
Hoy, J. W., Zheng, J., Grelen, L. B., and Geaghan, J. P. 1993. Longevity of teliospores of Ustilago scitaminea in soil. Plant Dis. 77:393397
Hughes, C. G. 1961. Gumming disease. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.). Elsevier Publishing
Company, New York.
Hughes, C. G., and Ocfemia, G. O. 1961. Yellow spot disease. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.).
Elsevier Publishing Company, New York.
Humbert, R. P. 1968. Control of pests and diseases. In The Growing of Sugar Cane. Elsevier Publishing Company, New York.
Isakeit, T., Magarey, R. C., and Croft, B. J. 1992. Transmission of soilborne yield decline of sugarcane in northern Queensland, Australia. (Abstr.). Phytopathology
82:1089.
Kao, J., and Damann, D. E., Jr. 1978. Microcolonies of the bacterium associated with ratoon stunting disease found in sugarcane xylem matrix. Phytopathology
68:545551.
Lee, Y. S., and Hoy, J. W. 1992. Interactions among Pythium species affecting root rot of sugarcane. Plant Dis. 76: 735739.
Liao, C. H., and Chen, T. A. 1981. Isolation, culture and pathogenicity to Sudangrass of a corynebacterium associated with ratoon stunting of sugarcane and with
Bermudagrass. Phytopathology 71:13031306.
Liu, L. J. 1983. Sugarcane rust: The components of the epidemic and their usefulness in disease forecasting in Puerto Rico. (Abstr.) Phytopathology 73:796.
Lo, T. T. 1961. Leaf scorch. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.). Elsevier Publishing Company, New
York.
Lockhart, B. E. L., and Autrey, L. J. C. 1988. Occurrence in sugarcane of a bacilliform virus related serologically to banana streak virus. Plant Dis. 72:230233.
Lockhart, B. E. L., Autrey, L. J. C., and Comstock, J. C. 1992. Partial purification and serology of sugarcane mild mosaic virus, a mealybugtransmitted closterolike
virus. Phytopathology 82:691695.
Magarey, R. C. 1994. Effect of Pachymetra root rot on sugarcane yield. Plant Dis. 475477.
Magarey, R. C., and Mewing, C. M. 1994. Effect of sugarcane cultivars and location on inoculum density of Pachymetra chaunorhiza in Queensland. Plant Dis.
78:11931196.
Martin, J. P. 1961. Brown stripe. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.). Elsevier Publishing Company,
New York.
Martin, J. P. 1964. Iliau. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and E. A. Wismer (eds.). Elsevier Publishing Company, New
York.
Martin, J.P., and Robinson, P. E. 1961. Leaf scald. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.). Elsevier
Martin,J. P., and Wismer, C. A. 1961. Red stripe. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.). Elsevier
Matsumoto, T., and Abbott, E. V. 1964. Red rot of the leaf sheath. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer
(eds.). Elsevier

Page 782
Purdy, L. H., Liu, L. J., and Dean, J. L. 1983. Sugarcane rust, a newly important disease. Plant Dis. 67:12921296.
Qhobela, M., and Claflin, L. E. 1989. Xanthomonas officinarum sp. nov., a second organism involved in sugarcane gumming disease. (Abstr.). Phytopathology
79:1191.
Reichel, H., Belalcazar, S., Munera, G., Arevalo, E., and Narvaez, J. 1997. First report of banana streak virus infecting sugarcane and arrowroot in Colombia. Plant
Dis. 81:552.
Ricaud, C., Egan, B. T., Gillaspie Jr., A. G., and Hughes, C. G. 1989. Diseases of Sugarcane: Major Diseases. Elsevier Science Publishers. New York, NY. 399 pp.
Shaw, D. E. 1964. Veneer blotch. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier Publishing
Company, New York.
Sreeramulu, T., and Vittal, B. P. R. 1970. Incidence and spread of red rot lesions on midribs of sugarcane leaves. Plant Dis. Rptr. 54:226231.
Steib, R. J. 1961. Phytophthora seed piece rot. In Sugar Cane Diseases of the World, Vol. I. J. P. Martin, E. V. Abbott, and C. G. Hughes (eds.). Elsevier
Steindl, D. R. L. 1964. Bacterial mottle. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier Publishing
Company, New York.
Subramanium, L. S., and Chona, B. L. 1938. Notes on Cephalosporium sacchari Butler (causal organism of sugarcane wilt). Indian J. Agric. Sci. 8:189190.
Taballa, H. A. 1969. Smut on true seedlings of sugarcane. Plant Dis. Rptr. 53:992993.
Todd, E. H. 1960. Elsinoe disease of sugarcane in Florida. Plant Dis. Rptr. 44:153.
Todd, E. H. 1962. Target blotch of sugarcane in Florida. Plant Dis. Rptr. 46:486.
Van der Zwet, T., and Forbes, I. L. 1961. Phytophthora megasperma, the principal cause of seedpiece rot of sugarcane in Louisiana. Phytopathology 59:634
640.
Vega, J., Scagliusi, S. M. M., and Ulian, E. C. 1997. Sugarcane yellow leaf disease in Brazil: Evidence of association with a luteovirus. Plant Dis. 81:2126.
Venkatasubbaiah, P., Kohmoto, K., Otani, H., Hamasaki, T., Nakajima, H., and Hokama, K. 1987. Two phytotoxins from Stagonospora sacchari causing leaf
scorch of sugarcane. Ann. Phytopathol. Soc. Japan 53:335344.
Victoria, J. I., Carrillo, P., and Cassalett, C. 1983. Chemical control of sugarcane smut (Ustilago scitaminea Sydow) by seedcane treatment. (Abstr.)
Williams, J. R. 1969. Nematodes as pests of sugarcane. In Pests of Sugar Cane, Elsevier Publishing Company, New York.
Yen, W. Y. 1964. Leaf blight. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier Publishing Company,
New York.
Yen, W. Y., and Chi, C. C. 1964. Leaf blast. In Sugar Cane Diseases of the World, Vol. II. C. G. Hughes, E. V. Abbott, and C. A. Wismer (eds.). Elsevier
Yin, Z., and Hoy, J. W. 1997. Effect of stalk desiccation on sugarcane red rot. Plant Dis. 81:12471250.
Zummo, N. 1986. Red spot (Helminthosporium rostratum) of sweet sorghum and sugarcane, a new disease resembling anthracnose and red rot. Plant Dis. 70:800.

Page 783
21.
Diseases of Sunflower (Helianthus annuus)
Apical Chlorosis
Cause.
Pseudomonas syringae pv. tagetis is seedborne. Other Compositae also are hosts.
Distribution.
The United States (Kansas, Minnesota, North Dakota, and Wisconsin).
Symptoms.
Diseased plants are scattered throughout a field, occurring singly or in small groups within a row. A common symptom is a leaf chlorosis, but without lesions, that is
most frequent and severe on diseased seedlings but may occur on sunflower at all growth stages. Diseased leaves, including veins, are pale yellow to white. Often only
a portion of the initially affected leaf is chlorotic, but subsequently formed leaves, including veins, are uniformly chlorotic.
Diseased seedlings are frequently stunted and die; however, infection of older plants rarely results in stunting. Systemic chlorosis of seedlings lasts up to 8 weeks and
involves eight to 10 leaves, but chlorosis on older prebloom plants is frequently limited to a few leaves. Chlorotic leaves do not recover. Symptoms apparently do not
occur on subapical, fully expanded leaves on plants past the bud stage. Thus, subsequent leaves on diseased plants are normal in color.
Management.
Grow the most resistant cultivar. Differences in resistance exist among sunflower cultivars.
Bacterial Leaf Spot (Pseudomonas spp.)
Cause.
Pseudomonas cichorii, P. syringae pv. aptata, and P. syringae pv. mellea.
Distribution.
Brazil, Canada, Japan, Spain, and the former Yugoslavia.

Page 784
Symptoms.
Generally, diseased leaves have large necrotic lesions surrounded by narrow yellow halos. Light and dark brown lesions occur on diseased stems. The vascular system
is discolored and white exudate may be present on leaf axils.
Management.
Not reported.
Bacterial Leaf Spot (Pseudomonas syringae pv. helianthi)
Bacterial leaf spot is also called angular bacterial leaf spot.
Cause.
Pseudomonas syringae pv. helianthi. It is likely that disease is accentuated by frequent rainfall and humid conditions during the growing season.
Distribution.
South Africa and likely other sunflowergrowing areas.
Symptoms.
Initial lesions on diseased leaves, stems and petioles are watersoaked spots. Spots become dark brown, necrotic (12 mm in diameter), and angularshaped. Lesions
sometimes coalesce and make diseased leaves dry and brittle.
Management.
Not reported.
Bacterial Wilt
Cause.
Pseudomonas solanacearum.
Distribution.
Bulgaria, Mauritius, Tanzania, the United States (Puerto Rico), the former USSR, and Zimbabwe.
Symptoms.
The initial symptom is an overall wilting of the diseased plant. A black discoloration at the base of the stem spreads upward (90 to 120 cm) until the diseased plant
eventually fails over.
Management.
Some cultivars have a higher percentage of tolerant or resistant plants than other cultivars.
Crown Gall
Cause.
Agrobacterium tumefaciens. Bacteria enter the root system or stem through wounds near the soil line. Once inside the host plant, bacteria invade other plant tissue
intercellularly and stimulate the surrounding cells to divide.
Distribution.
Widely distributed. However, crown gall is rarely observed under natural conditions.
Symptoms.
Initially, small overgrowths occur on diseased stems or roots, particularly near the soil line. This overgrowth later turns into galls that are spherical and white. As the
galls enlarge and their surfaces become convo

Page 785
luted, the surfaces become dark brown to black. There is no definite size and shape of galls as they develop in an irregular and disorganized manner. Diseased plants
with galls at the crown or main root remain weak and grow poorly. In addition to the formation of galls, diseased plants may remain stunted and have small chlorotic
leaves and, in severe cases, a lengthwise splitting of the stem. The diseased plants may show epinasty, suppression of lateral buds, and production of adventitious
roots.
Management.
No practical disease management strategy is available. Most sunflower cultivars appear to have a high degree of resistance or tolerance.
Erwinia Stalk Rot and Head Rot
Cause.
Erwinia carotovora pv. carotovora and E. carotovora pv. atroseptica. Bacterial stalk rot occurs after extended wet periods late in the growing season, which
suggests that only stressed or senescing plants become infected. Infection occurs at the petiole axils, a site on the host plant that collects water and consequently serves
as a favorable environment for bacterial "residence" and insect activity. Infection is aided by wounds caused by insects, hail, or mechanical damage. The sunflower
budworm, Suleima helianthana, preferentially oviposits in this axil and larvae feed and exit from the same location. In South Africa, the bacteria enter sunflower
tissue through lesions caused by Alternaria helianthi at the bases of leaf petioles. In the former Yugoslavia, disease has been reported to occur following damage by
hailstones.
Distribution.
Europe, South Africa, and the United States.
Symptoms.
Diseased stems are black on the outside, with the blackening often centered around a petiole axil. An inkblack, watery breakdown of the pith results in a hollowing of
stems. This breakdown is odorless unless stems are in an advanced state of decomposition. Plants often lodge under the weight of maturing heads. In some instances,
heads will also develop soft rot symptoms.
Symptoms from the former Yugoslavia have been described as follows: Greenblack spots occur on stalks and eventually coalesce to cover most of the stalk surface,
causing stalks to soften and dry up. Flowers and seeds are also discolored.
Management.
Do not rotate sunflower with potatoes.
Achene Blemish Syndrome
Cause.
Alternaria alternata, Cladosporium sp., and Ulocladium atrum. Western flower thrips, Frankliniella occidentalis, are associated with infection of the

Page 786
achenes. Alternaria alternata induces a significantly higher disease incidence than the other two fungi, but mixtures of all three fungi result in a higher disease
incidence than each fungus alone.
Achenes were susceptible to infection only at the time of their development.
Distribution.
Israel.
Symptoms.
Symptoms become visible just before physiological maturity. Small, scattered lesions that vary in color, size, and shape occur on the surfaces of diseased achene
shells. The brown, black, or gray lesions sometimes are surrounded by a dark halo. Lesions range in size from 0.5 to 2.0 mm and are round, oval, elongated, or
irregularshaped. Diseased achenes do not differ in size or weight from healthy achenes, nor is seed taste altered. However, diseased crops are judged by the
sunflower industry to be of lower quality than healthy crops.
Management.
Not reported.
Alternaria Leaf Blight, Stem Spot, and Head Rot
Alternaria leaf blight, stem spot, and head rot is also called Alternaria leaf and stem spot, and black spot.
Cause.
Alternaria alternata (syn. A. tenuis), A. chrysanthemi, A. helianthi (syn. Helminthosporium helianthi), A. helianthicola, A. helianthinficiens, A. leuconthemi,
A. longissima, A. protenta, A. tenuissima, and A. zinniae. Most Alternaria spp. are seedborne as conidia on seed coats and mycelia within seed coats. Alternaria
spp. also overwinter as mycelia in infested stem residue on the soil surface and, to a lesser extent, within residue buried in soil. The inoculum from infested residue
decreases later in the growing season. Alternaria leaf blight, stem spot, and head rot occurs under warm (25°28°C), humid conditions that cause extended periods of
leaf wetness. Plants are most susceptible to infection at the anthesis or seedfilling stages of plant growth.
Distribution.
Generally, wherever sunflower is grown. Alternaria helianthi is recognized as the most prevalent and damaging species worldwide.
Symptoms.
Earlysown seedlings are more severely diseased than latersown seedlings. Dark brown, oval, necrotic spots occur on diseased heads, leaves, petals, petioles, and
stems. Often leaves of younger plants (in the vegetative or budding stage of plant growth) have dark brown necrotic spots surrounded by a chlorotic halo. Other leaf
symptoms are described as gray centers (several millimeters to 1.5 cm in diameter) with dark brown margins. Severely diseased plants are defoliated and frequently
lodge. Symptoms caused by A. alternata are described as brown zonate spots on basal

Page 787
leaves that progress to the upper leaves. Spots eventually coalesce and diseased leaves dry up and defoliate. Disease severity varies from premature declining of lower
leaves to extensive defoliation of the entire diseased plant.
Stem lesions begin as black flecks or streaks that later enlarge to cover large areas of the diseased stems. Stems are girdled and diseased plants are eventually killed.
Head diameter, number of seeds per head, and oil content are reduced.
Symptoms specifically ascribed to A. zinniae are not noticeable until after flowering; however, seedling blight occurred when seeds were inoculated. Such seedlings
either failed to emerge or had dark lesions on the hypocotyls and cotyledons that caused seedlings to damp off after emergence. Leaf spots, which are circular and
uniformly dark colored, have a targetlike appearance. Severe leaf disease results in defoliation. Brown superficial flecks or streaks occur on stems, petioles, and
backs of heads and, when numerous, form large necrotic areas. Severe stem infection causes lodging.
Management
3. Delay sowing.
4. Rotate for 1 year with a nonsusceptible crop.
5. Apply a seedtreatment fungicide.
Ascochyta Leaf Spot
Cause.
Ascochyta sp. and A. compositarum.
Distribution.
Japan and Kenya.
Symptoms.
Dark spots occur on diseased leaves.
Management.
Not reported.
Botrytis Head Rot
Botrytis head rot is also called gray mold and gray mold head rot.
Cause.
Botrytis cinerea is seedborne and infects host plants during periods of abundant moisture. Botrytis head rot is common during wet weather in the autumn when the
harvest is delayed.
Distribution.
Europe.
Symptoms.
Brown lesions on the backs of diseased sunflower heads later become a soft rot that is covered with gray fungal growth typical of B. cinerea. Eventually, only the
vascular bundles remain from the decomposed heads. Seedling blight may occur, thereby reducing stands.

Page 788
Management.
Not reported.
Cephalosporiurn Wilt
Cause.
Cephalosporium acremonium (syn. Acremonium strictum) is weakly pathogenic on young, healthy, growing sunflowers. Infection occurs through insect wounds
and mechanical injuries from wind, hail, and cultivation. Plants become more susceptible as they mature and heads form.
Distribution.
The United States (Indiana).
Symptoms.
The described symptoms were caused by a combination of C. acremonium and Erwinia carotovora pv. carotovora. Brown lesions are present on the outside of
diseased stalks. The inside of the stalks is hollow, causing them to bend and collapse under the weight of a maturing head. The head frequently cannot be harvested or
decomposes, which reduces the yield. Plants injected with spores at the onset of senescence developed black necrotic areas on stems that were covered with
mycelium.
Management.
Not reported.
Cause.
Cercospora bidentis, C. helianthi, and C. pachypus.
Distribution.
Cercospora bidentis is reported from India, C. helianthi from Venezuela, and C. pachypus from the Philippines and Uganda.
Symptoms.
Tan spots develop on diseased leaves.
Management.
Not reported.
Charcoal Rot
Cause.
Macrophomina phaseolina (syn. Sclerotium bataticola and Rhizoctonia bataticola) is seedborne as pycnidia and sclerotia. Sclerotia develop on the inner surfaces
of pericarps and seed coats. Charcoal rot is most severe at high soil temperatures (30°C and above) and low soil moisture. The sunflower stem weevil,
Cylindrocopturus adsperus, carries M. phaseolina as weevils emerge from overwintered roots and stalks and transmit the fungus while feeding and ovipositioning in
stalks. Other fungi also contribute to the discoloration of stalks infected by M. phaseolina and parasitized by larvae of the stem weevil.
Distribution.
Wherever sunflower is grown in warmer climates. Charcoal rot rarely occurs in northern sunflowergrowing areas.
Symptoms.
Symptoms usually occur after flowering. Premature ripening of diseased stems occurs together with prematurely ripened, poorly filled,

Page 789
small, and distorted heads that have a zone of aborted flowers.
Diseased stems have a brown to black discoloration with or without typical gray areas on their surfaces. Stalk bases are gray and only vascular bundies or fibers
remain, giving the insides of stems a shredded appearance. Portions of diseased lower stems are hollow and frequently there is a mixture of frass and fragments of pith
tissue both in the lower stems and the upper taproots. Vascular fibers become covered with small, black sclerotia that resemble pepper or flecks of charcoal.
When diseased seed is sown, the seeds either do not germinate, or if germination occurs, there is a discoloration of roots, hypocotyls, and cotyledons. Pycnidia and
sclerotia eventually develop on diseased parts.
Management
1. Rotate sunflower with a resistant crop, such as small grains.
3. Grow cultivars that have resistance.
4. Irrigate at flowering stage or at flowering and ripening stages.
Cladosporium Leaf Spot
Cause.
Cladosporium cladosporoides.
Distribution.
India.
Symptoms.
The initial chlorotic spots on diseased leaves later become gray to olive green and are surrounded by a chlorotic halo. The underside of the diseased leaf has a moldy
appearance due to the sporulation and growth of C. cladosporoides. Under high humidity conditions, the spots elongate along the veins, resulting in extensive chlorotic
patches. The upper half of the leaf is usually more severely diseased than the lower half.
Management.
Not reported.
Cause.
Curvularia lunata.
Distribution.
Egypt.
Symptoms.
Diseased leaves have tan lesions (up to 2 mm in diameter) with reddish or dark brown margins. Lesions may coalesce and form necrotic areas up to 1 cm long.
Management.
Not reported.
Downy Mildew
Cause.
Plasmopara halstedii and P. helianthi f. helianthi survive as oospores in the soil and as mycelium and zoosporangium in seed. Sowing infected seed

Page 790
rarely results in systemically infected seedlings, but infected seed is how P. halstedii is introduced into soil.
During wet soil conditions in the spring, oospores germinate and produce zoosporangia in which zoospores are formed and released, then ''swim" to roots, where they
encyst and germinate. Infection occurs primarily in the zone of radicle elongation or adjacent to it. The fungi then become systemic and grow upward inside the plant.
Sporulation on belowground and aboveground plant parts occurs in the form of zoosporangia that are disseminated by wind and rain to other host plants, where
secondary infection occurs through apical buds or leaves. Oospores are produced in diseased tissues and returned to the soil during harvest. Plants can be infected
from germination until the flowering stage of plant growth, but systemic infection usually occurs after plant emergence since host plants become increasingly resistant
with age.
At least eight different races of P. halstedii exist.
Distribution.
Wherever sunflower is grown, except Australia.
Symptoms.
Seedlings have light green or yellowish areas that spread out from the leaf midrib in the diseased leaf. During wet weather, a downy, whitish, fungal growth consisting
of zoosporangia and mycelium occurs on the undersides of diseased leaves opposite the yellowed areas. These plants are systemically infected and most of them die.
As diseased plants continue to grow, leaves become wrinkled and distorted, and the entire plant is stunted. Diseased plants usually produce normalsized heads that
remain upright and contain empty seeds.
Management
1. Sow only clean, healthy seed.
2. Grow sunflower in the same soil once every S years. Rotation should include small grains.
3. Control weeds in sunflower fields that may serve as alternate hosts.
4. Treat seed with a systemic fungicide.
Cause.
Drechslera hawaiiensis. Older leaves are more susceptible to infection than are younger ones.
Distribution.
India.
Symptoms.
The small, brown spots that initially occur on diseased leaves gradually increase in size (0.110.0 mm in diameter), are round to irregularshaped, have a pinkbrown
center that becomes gray, and are encircled by a chlorotic zone. Leaves become blighted during severe disease. Plant growth and yield are affected.

Page 791
Management.
Not reported.
Fusarium moniliforme Wilt
Cause.
Fusarium moniliforme likely survives as mycelia in infested residue and by growth on collateral hosts.
Distribution.
India.
Symptoms.
Diseased leaves are chlorotic and drooping, followed by wilting and death of the plant. Pronounced stunting occurs when diseased plants are infected in the
preflowering stage. Vascular elements of roots are brown.
Management.
Not reported.
Fusarium oxysporum Wilt
Cause.
Fusarium oxysporum survives as chlamydospores in infested residue and soil. Young plants up to the age of 6 weeks are highly susceptible to infection and die in a
short time. Plants 10 weeks and older are not susceptible.
Distribution.
Symptoms.
The lower leaves of diseased plants change from green to yellow, often with a distortion that affects only one side of the leaf. Diseased plants wilt, tend to fall over,
and become desiccated. Older diseased plants have a tendency to recover.
Management.
Not reported.
Fusarium Pith Canker
Fusarium pith canker is also called pith canker.
Cause.
Plectosphaerella cucumerina, anamorph Fusarium tabacinum (syn. Microdochium tabacinum). Plectosporium has been described as the new genus for F.
tabacinum. Optimum growth in culture is at temperatures of 25°26°C. Disease is only observed when high relative humidity and low temperatures occur in the
summer.
Distribution.
Italy. However, M. tabacinum is a common fungus both in arable soil and on decaying plant material. It has been reported in Australia, other parts of Europe, New
Zealand, and the United States.
Symptoms.
Symptoms have been reported only on stems, where external necrotic streaks and a pale pinkishred discoloration of the pith occur.

Page 792
Management.
Not reported.
Helminthosporium Leaf Blight
Cause.
Helminthosporium helianthi.
Distribution.
Argentina, India, Tanzania, Turkey, and Uganda.
Symptoms.
Diseased leaves have blackishbrown zonate spots (10 to 30 mm in diameter) that have ashy centers. Spots are irregularshaped.
Management.
Not reported.
Myrothecium Leaf and Stem Spot
Cause.
Myrothecium roridum and M. verrucaria. The fungi likely survive in infested residue and soil. Disease is favored by warm, moist weather.
Distribution.
India.
Symptoms.
Lesions on diseased leaves tend to be circular and light brown or tan. Lesions are sometimes surrounded by a dark brown halo.
Management.
Not reported.
Phialophora Yellows
Phialophora yellows is also called wilt.
Cause.
Phialophora asteris f. sp. helianthi is soilborne and overwinters as saprophytic mycelia in infested residue. The severity of Phialophora yellows increases during
periods of moist weather or excess soil moisture.
Distribution.
Canada (Manitoba) and Italy.
Symptoms.
Phialophora yellows is an inconspicuous disease. Symptoms may be confused with those caused by nitrogen deficiency, other mineral deficiencies, or injury from
excess water.
The first symptoms are obvious as diseased sunflowers approach flowering. First, the lower leaves turn a dull light green, then large areas of leaves become dull
yellow, starting at the apex and margins and extending inward. Leaf margins and the angularshaped patches (510 mm long) of yellowed leaf interveinal leaf tissues
become necrotic. Symptoms move progressively up diseased plants. The bottom leaves dry and wither, whereas upper leaves remain green. The vascular tissue inside
the stalk becomes brown. Diseased plants are stunted, and heads remain small and sterile.
Microscopic observations reveal hyaline hyphae in the vascular tissues of stems.
Management.
Grow cultivars that have some resistance.

Page 793
Phoma Black Stem
This disease is also called black stem, Phoma black stem, and Phoma girdling. In North Dakota, Phoma girdling is one aspect of premature death.
Cause.
Phoma macdonaldii, teleomorph Leptosphaeria lindquistii, overwinters as perithecia, pycnidia, and mycelia in infested stalk residue. Primary inoculum is
ascospores and conidia produced during moist weather. Conidia are disseminated by splashing rain and wind, and ascospores by wind to host plants. Disease occurs
under wet conditions during and after plant flowering.
Distribution.
Argentina, Canada, and the United States.
Symptoms.
Symptoms are most noticeable after flowering. Lesions start at the bases of leaf petioles and spread along stems. Numerous lesions coalesce and form large, black
patches on diseased stems, and dark, irregularshaped lesions occur on leaves and flowers. Leaves infected early are killed, and the stems weaken and lodge.
Pycnidia, which resemble tiny, black bumps, are produced in mature lesions. Diseased plants produce small heads with little seed.
Symptoms of premature death are difficult to distinguish from normal senescence, especially in earlymaturing cultivars. Premature death most often occurs in circular
areas within a field, although scattered individual plants also may die.
Management
1. Rotate sunflower with nonhost plants.
2. Differences in susceptibility exist among sunflower lines.
Phoma Leaf Blight
Cause.
Phoma exigua.
Distribution.
India.
Symptoms.
Initially, irregularshaped yellowish patches or spots develop on diseased leaves. Later, the spots become reddish brown to dark black and coalesce, forming
irregularshaped patches. Symptoms, such as a black crust that is rough to the touch due to the numerous submerged pycnidial bodies, are more pronounced on upper
leaf surfaces. Diseased leaves become leathery and brittle and have blighted margins.
Management.
Not reported.
Phomopsis Brown Stem Canker
Cause.
Phomopsis helianthi, teleomorph Diaporthe helianthi. Diaporthe helianthi overwinters as perithecia on infested stem residue on the soil sur

Page 794
face. Ascospores produced during wet, cool weather are the principal source of infection throughout the growing season. Hyphae from germinated ascospores infect
leaves, then become systemic and grow into the xylem tissue and, finally, through the stem cortex. There may be more than one species or biotype that attack
sunflower.
Distribution.
The United States and the former Yugoslavia.
Symptoms.
Leaf symptoms are necrotic areas surrounded by chlorotic tissue that starts at the apical ends or edges of diseased leaves. Leaf veins and petioles darken into brown
to black cankers that later become ashy gray around the diseased petiole bases. Leaf symptoms reported from Ohio were characterized by interveinal bronzing.
Spots on stalks are initially light brown and about 10 mm wide. Eventually, these spots become darker in color, have a wet appearance, and increase in length (1520
cm) and in width, girdling the diseased stalks. At the death of epidermal tissue, the spots again become light brown, and they have dark brown borders of different
widths. Several internodes may become discolored as disease progresses into the interiors of stalks and destroys pith tissue and causes hollow areas. Pycnidia, which
resemble tiny, black bumps, are abundant in diseased tissue. Diseased plants ripen prematurely and the percentage of oil in seeds decreases.
Management.
Not reported.
Cause.
Phymatotrichopsis omnivora (syn. Phymatotrichum omnivorum) survives for several years in soil as sclerotia and hyphal strands. Early in the growing season,
when soil temperatures have risen sufficiently, sclerotia germinate and form new hyphal strands that make contact with the developing root systems of host plants. Root
contact is not necessary for planttoplant spread of P. omnivora because mycelial growth through soil occurs in advance of diseased roots. Planttoplant spread
within rows is more common than spread across rows. Phymatotrichum root rot is most prevalent in alkaline soils.
Distribution.
Symptoms.
Diseased plants wilt rapidly and die. The root cortex is rotted and brown strands of fungus mycelium can be seen growing on the roots.
Management
1. Plowing under a green manure crop, such as sweet clover, lessens disease severity in succeeding years.
2. Rotate sunflower with plants in the grass family.

Page 795
Phytophthora Stem Rot
Cause.
Phytophthora drechsleri. Phytophthora cryptogea has also been identified as a causal fungus; however, some researchers have suggested P. drechsleri may be a
synonym of P. cryptogea. Phytophthora drechsleri has been identified as the cause of Phytophthora black stem rot of sunflower in Iran. However, Phytophthora
black stem rot is probably the same disease as Phytophthora stem rot.
The fungus overwinters as oospores in infested residue and probably in soil. Oospores germinate and form sporangia in which zoospores are produced. The
zoospores are liberated from the sporangia and "swim" to plant hosts, where they encyst and germinate. Secondary inoculum is by sporangia produced on diseased
tissue and disseminated by wind and splashing rain to other host plants. Eventually, oospores are formed in diseased tissue. Phytophthora stem rot is most severe
under wet soil conditions, when stems contact water or wet soil.
Distribution.
Iran and the United States (California).
Symptoms.
A dark brown to black discoloration occurs that partially or totally girdles diseased stems, primarily on the area of the stem that is relatively near the soil surface.
Decay spreads to internal stem tissues, which become weakened and cause plants to fall over.
Management.
No disease management strategy is effective at present. However, some sunflower hybrids in Iran are reported to be more resistant than others.
Powdery Mildew
Cause.
Erysiphe cichoracearum, anamorph Oidium asterispunicei; E. cichoracearum var. latispora, anamorph Oidium latisporum; Leveillula compositarum f.
helianthi; L. taurica; Oidiopsis sicula; and Sphaerotheca fuliginea. The fungi survive as cleistothecia on infested residue. During the summer, ascospores are
formed in cleistothecia and are disseminated by wind to leaves of host plants, where the lower leaves become more heavily infected than the upper leaves. Conidia are
produced on the surfaces of diseased leaves and serve as secondary inoculum by being disseminated by wind to healthy tissue. Cleistothecia are formed in mycelium
growing on the surfaces of diseased leaves.
Distribution.
Wherever sunflower is grown.
Symptoms.
Symptoms occur after full bloom and are more obvious on the lower leaves. Initially, white powdery areas consisting of mycelium and conidia appear primarily on
leaves, but all aboveground plant parts may be diseased. Later, the whitish fungal growth becomes gray, and cleistothecia

Page 796
appear as small black objects within the surface fungal growth. Severely diseased leaves become yellow and dry up.
Management.
Not necessary, since powdery mildew occurs too late in the growing season to affect yield.
Rhizopus Head Rot
Cause.
Rhizopus oryzae (syn. R. arrhizus and R. nodosus), R. microsporus, and R. stolonifer (syn. R. nigricans) are cosmopolitan in the soil as spores and occur as
saprophytic mycelia in decaying plant residue.
Sporangia, which require free water to germinate, are readily disseminated by wind and rain and may be transferred by insects and birds. Birds may disseminate the
fungi directly from a rotted to a healthy head by inoculum that adheres to their claws or beaks. Heads damaged by mechanical implements, such as irrigation
equipment, and by birds, hail, and insects (particularly larvae of the sunflower moth, Homoeosoma electellum) are most subject to infection because infective
mycelium can only penetrate plant hosts through wounds. In Texas, larvae of the sunflower moth are directly correlated to the incidence of Rhizopus head rot.
The rate of head rot is dependent primarily on the temperature. Diseased heads may become completely rotted within 3 to 7 days at temperatures of 20° to 30°C.
Susceptibility of sunflower to infection by R. oryzae is dependent upon the age of the susceptible host plant at infection. At the bud stage, sunflower heads are
basically resistant. However, sunflower becomes susceptible at initiation of anthesis, after which the heads become highly susceptible to infection as they age. Wet
weather following flowering favors disease development.
Distribution.
Wherever sunflower is grown. However, Rhizopus head rot is predominant in countries where flowering and seed maturation occur at high temperatures.
Symptoms.
Initial symptoms of Rhizopus head rot in sunflower are small, watersoaked spots on the back of the diseased head. The spots gradually enlarge, and as mycelium
invades more of the parenchyma tissue, the receptacle becomes brown, soft, and pulpy. During wet weather, coarse, threadlike strands or woolly masses of whitish
fungus mycelium may be seen in the hollow part of the flower receptacle. Later, the woolly masses of whitish mycelium are interspersed with numerous black spore
producing sporangia the size of pinheads. The mycelium and sporangia are evident externally and are especially conspicuous in the vicinity of diseased achenes. At
death, sunflower heads shred.
Management.
Cultivars with upright heads are more susceptible to infection than cultivars with nodding heads.

Page 797
Rust
Cause.
Puccinia helianthi, P. xanthi, and Uromyces junci. Puccinia helianthi is an autoecious, longcycled rust that produces pycnia, aecia, uredinia, and telia on
sunflower. Survival in northern areas is by teliospores that overwinter on infested residue. In the spring and early summer, teliospores germinate and produce
basidiospores at temperatures of 6° to 28°C. Basidiospores are disseminated by wind to host plants, where they germinate and infect leaves. In 10 to 12 days, pycnia
develop at the point of basidiospore infection. Each pycnium produces pycniospores and receptive hyphae. Pycniospores are carried to compatible receptive hyphae
of other pycnia by insects or splashing water. The nuclei of pycniospores fuse with nuclei of receptive hyphae, migrate down the hyphae, and form aeciospores in aecia
on the opposite side of the leaf from the pycnia. Aeciospores are disseminated by wind to leaves, where they germinate. Uredinia, in which urediniospores are
produced, are formed in the aeciospore infections. Urediniospores are windborne and serve as secondary inoculum, or the repeating stage, and produce new uredinia
at each point of infection. Toward host plant maturity or during conditions unfavorable for disease, telia develop in uredinia lesions.
Urediniospore germination occurs at temperatures of 4° to 20°C and requires 6 to 10 hours of leaf wetness. The temperatures for minimum, optimum, and maximum
infection are 4°, 10° to 24°, and 30°C, respectively. Temperatures for optimum secondary sporulation are 20° to 35°C.
Generally, warm, humid weather favors disease development. Different physiologic races of P. helianthi exist in nature.
Distribution.
Symptoms.
Pycnia occur on diseased upper surfaces of leaves as small clusters of pale yellow or orange spots. Aecia appear on the lower surfaces of leaves, opposite the pycnia,
as yellow or orange spots. Uredinia first occur in midsummer as dark brown, powdery spots on both surfaces of the lower leaves and sometimes on stems. Severely
diseased leaves die and dry up. Telia occur as diseased plants mature and appear as dark brown to black spots.
Management
2. Rotate sunflower, and locate fields as far as possible from fields where sunflower was grown the previous year.
3. Sow sunflower early in the season.
4. Destroy volunteer and wild sunflowers in the vicinity of commercial fields.
5. Apply labeled foliar fungicides. The suggested time to apply fungicides is when rust reaches 5% severity on the lower leaves during the R1 stage, when the flower
buds are just visible, to the R6 stage, the end of flowering when the ray flowers are wilting.

Page 798
Sclerotinia Basal Stalk Rot and Wilt
Cause.
Sclerotinia minor survives in soil and seed lots as sclerotia. During moist soil conditions, sclerotia germinate to produce hyphae that infect the lower stems of plant
hosts. Sclerotia are eventually produced on and in the diseased areas of the stem.
Distribution.
Australia.
Symptoms.
A brownish canker forms on diseased stems at the soil line. Eventually, white mycelium covers the diseased areas and black to dark brown sclerotia form within the
mycelium. Diseased plants suddenly wilt.
Management
1. Sow clean, healthy seed that is free of sclerotia.
2. Control weeds in sunflower fields.
3. Plow infested residue deep into the soil.
Sclerotinia Basal Stalk Rot and Wilt, and Midstalk Rot
This disease is also called Sclerotinia white mold.
Cause.
Sclerotinia sclerotiorum (syn. S. libertiana and Whetzelinia sclerotiorum) overwinters primarily as sclerotia in soil and intermixed with seeds in storage. The
sclerotia are then sown, along with the seeds, the following spring. Survival is also as mycelia in infested stalk residue and rotted or healthyappearing seed. However,
survival of mycelia in infested stems is too low to be a significant source of pathogenic inoculum. Sclerotia are disseminated by any means that moves soil.
Sclerotia on or near the soil surface germinate two ways: (1) Myceliogenically, or directly, by producing mycelia that infect stalks and roots. The taproothypocotyl
axis is the primary site of infection; therefore, disease incidence is increased when seed is planted adjacent to sclerotia. (2) Carpogenically, or indirectly, by producing
apothecia on which ascospores are borne in a layer of asci. The ascospores are disseminated by wind to host plants and are the major cause of midstalk infections.
The initial infected plants serve as primary infection foci from which S. sclerotiorum spreads through root contact between adjacent plants when mycelia grow from
diseased to healthy plants.
Although infection may happen at any stage of plant growth, there are two times during plant growth when most infections occur. The first time is during seed
germination and seedling establishment; it is attributed to myceliogenic germination of incompletely melanized or injured sclerotia. The second cycle, from plant bud
formation through seed development, is possibly attributable to carpogenic germination of black sclerotia induced by exogenous nutrients. Disease is most severe when
frequent rains and high humidity occur after flowering.

Page 799
The hyperparasites Coniothyrium minitans and Talaromyces flavus, anamorph Penicillium vermiculatum, parasitize mycelia and sclerotia on root surfaces, thus
reducing inoculum in soil.
Distribution.
Symptoms.
Wilt symptoms on single diseased plants or groups of diseased plants appear at flowering time after a period of warm weather. Upper leaves droop and, in 2 to 3
days, all diseased leaves dry out and plants die. Young dead plants turn black, but older plants remain tan.
Wilted plants have soft, watersoaked, gray to brown cankers that encircle stems 7 to 25 cm above the soil line. Large, black, irregularshaped sclerotia are produced
in dense white mycelium on canker surfaces or in diseased stalks. Stems of diseased plants become shredded and break over at the soil line.
A similar symptom called middle stalk occurs when cankers extend a maximum of 125 cm above the soil line. This happens when the surface soil is wet for 10 to 14
days, causing sclerotia to germinate.
Management
1. Rotate sunflower with cereals, but avoid rotations with canola, common bean, mustard, and safflower since these plants are also hosts for S. sclerotiorum.
Susceptible crops should not be sown for 4 to 6 years after a severe outbreak of disease.
2. Sow healthy seed that is free of sclerotia.
3. Control weeds in sunflower fields that serve as alternate hosts.
4. Deepplow infested residue. Sclerotia buried deeply in soil cannot germinate. However, sclerotia in surrounding fields must also be buried for this to be effective
since airborne inoculum may initiate infections.
5. Plant spacings of 36 cm or greater at 26,00049,000 plants/ha will maximize yield under disease conditions; however, some researchers reported that plant spacing
did not make a difference.
6. Leaving stalks undisturbed through the winter in northern areas reduces the survival of sclerotia in stalks, possibly because of mycoparasites. It is suggested that
tillage be done in spring.
7. Apply a fungicide seed treatment. Treatment of sunflower seed with benomyl, iprodione, procymidone, or vinclozolin virtually eliminated seedborne S.
sclerotiorum.
8. Levels of resistance occur in genotypes.
Sclerotinia Head Rot
This disease is also called Sclerotinia white mold.
Cause.
Sclerotinia sclerotiorum (syn. S. libertiana and Whetzelinia sclerotiorum) overwinters primarily as sclerotia in soil or among seeds. Survival is also as mycelia in
infested stalk residue and rotted or healthyappearing seed.

Page 800
However, survival of mycelia in infested stems is too low to be a significant source of pathogenic inoculum. Sclerotia are disseminated by any means that moves soil.
Sclerotia on or near the soil surface germinate two ways: (1) Myceliogenically, or directly, by producing mycelia that infect stalks and roots. The taproothypocotyl
axis is the primary site of infection; therefore, disease incidence is increased when seed is sown adjacent to sclerotia. (2) Carpogenically, or indirectly, by producing
apothecia on which ascospores are borne in a layer of asci. The ascospores are disseminated by wind to host plants and are the major cause of head infections.
Circumstantial evidence suggests that senescent florets provide a food base for ascospore infections.
Distribution.
Generally distributed wherever sunflower is grown.
Symptoms.
The soft, watersoaked spots that initially occur on diseased heads later dry out and give diseased plant tissues a pinkish color. A white, cottonlike mold grows over
diseased areas during humid conditions. Diseased heads eventually become partially or entirely rotted, leaving only vascular bundles and fibers, which cause heads to
have a shredded or brushlike appearance. Seed hulls are discolored and scurfy. Large black sclerotia develop below the seed layer in the head or around seeds. The
presence of sclerotia in seed lots gives high acidity values and is the main reason for poor oil quality.
Management
1. Rotate sunflower with cereals, but avoid rotations with canola, common bean, mustard, and safflower since these plants are also hosts for S. sclerotiorum.
Susceptible crops should not be sown for 4 to 6 years after a severe outbreak of disease.
2. Sow healthy seed that is free of sclerotia.
3. Control weeds in sunflower fields that serve as alternate hosts.
4. Deepplow infested residue. Sclerotia buried deeply in soil cannot germinate. However, sclerotia in surrounding fields must also be buried for this to be effective
since airborne inoculum may initiate infections.
5. Plant spacings of 36 cm or greater at 26,00049,000 plants/ha maximize yield under disease conditions; however, some researchers found plant spacing did not
make a difference.
6. Leaving stalks undisturbed through winter in northern areas reduces the survival of sclerotia in stalks, possibly because of mycoparasites. It is suggested that tillage
be done in spring.
7. Apply a fungicide seed treatment. Treatment of sunflower seed with benomyl, iprodione, procymidone, or vinclozolin virtually eliminated seedborne S.
sclerotiorum.
8. Levels of resistance occur in genotypes.

Page 801
Sclerotium Basal Stalk and Root Rot
Sclerotium basal stalk and root rot is also called southern blight.
Cause.
Sclerotium rolfsii, teleomorph Athelia rolfsii, overwinters as sclerotia in soil and grows as saprophytic mycelia in soil residue. Sclerotia germinate in dry soil during
periods of high soil temperatures and form mycelia that infect seed and host plants of all ages. Cool soil temperatures kill sclerotia and mycelia. Sclerotium rolfsii
occurs most commonly in neutral to acidic sandy soils. Delayed sowing due to wet weather may favor disease development.
Distribution.
In the warm sunflowergrowing areas throughout the world.
Symptoms.
Discolored areas on diseased crowns and stems are sometimes accompanied by whitish, fanshaped mycelia. Diseased plants normally wilt, die, and eventually dry
out. Sclerotia are frequently produced at the bases of diseased plants.
Management.
Do not rotate sunflower with other susceptible crops.
Septoria Leaf Spot
Cause.
Septoria helianthi. Little is known of the survival and dissemination of S. helianthi, but it is presumed that S. helianthi overwinters as pycnidia on infested residue.
Conidia are produced in pycnidia and are disseminated by wind and splashing rain to host tissue, which is similar to the survival and dissemination of other Septoria
species. Humid weather is conducive for disease development, which normally does not occur during dry weather.
Distribution.
Canada, China, the United States, and possibly other sunflowergrowing areas in the world.
Symptoms.
Septoria leaf spot occurs on plants of any age, but symptoms usually begin on the lower leaves after flowering. The watersoaked, circular (612 mm in diameter)
spots become gray with a dark margin. Other descriptions depict spots as brown with a narrow yellow border that gradually fuses with the surrounding green tissues.
Spots coalesce and produce irregularshaped dead areas on leaves. Tiny, indistinct, dark brown pycnidia form in lesions.
When temperatures are moderately high and moisture is abundant, leaves are dropped progressively from the bottom of the plant upward until only a few leaves are
left on a diseased plant. Diseased plants are normally not seriously damaged.
Management.
Not reported.

Page 802
Verticillium Wilt
Verticillium wilt is also called leaf mottle.
Cause.
Verticillium alboatrum and V. dahliae. Although the causal fungus was originally identified as V. alboatrum, some researchers think Verticillium dahliae is the
only causal organism. Verticillium dahliae survives as microsclerotia in soil, on external and internal pericarp tissue, on testas, and as mycelia in seed. Most infection
presumably occurs from microsclerotia that germinate and infect host plant roots. Mycelium grows into the xylem tissue and produces microconidia that spread
upward in the waterconducting cells. Eventually, the fungus grows through xylem tissue to all parts of the plant and into the seed. At plant death, microsclerotia are
produced from mycelia and returned to the soil at harvest.
Distribution.
Canada, China, Russia, South America, Ukraine, and the United States.
Symptoms.
Symptoms on single plants or groups of diseased plants first occur on the lower leaves and gradually progress up the plant at flowering time. Tissue between leaf veins
becomes chlorotic, then brown, which gives diseased leaves a mottled appearance. Black areas occur on diseased stems, particularly near the soil line. In cross
section, the vascular system of diseased stems is brown to black. Severely diseased plants are stunted and either mature prematurely or die before flowering.
Management
2. Grow sunflower in the same field once every 5 years.
3. Sow diseasefree seed treated with a fungicide seed protectant.
White Rust
White rust is also called gray stem spot and white blister.
Cause.
Albugo tragopogonis (syn. Cystopus tragopogonis) overwinters as oospores in infested soil residue and, in milder climates, as mycelia or sporangia on weeds and
volunteer sunflowers. Little is known of the source and dissemination of primary inoculum, but presumably oospores are disseminated to leaves, germinate, and form
zoospores. Sporangia may also be produced on overwintered diseased plants and disseminated by wind to host plants, where they germinate and yield zoospores.
Zoospores penetrate stomata, encyst, and eventually germinate and form mycelia.
Secondary inoculum is by sporangia that are formed on diseased lower leaf surfaces and are windborne to host plants, where they form zoospores that germinate and
infect the plant. Oospores eventually form in diseased tissue. Disease development is favored by temperatures of 10° to 20°C and high rainfall.

Page 803
Distribution.
Argentina, Australia, Russia, Ukraine, and Uruguay. White rust likely occurs in other countries also, but it is not considered a serious disease.
Symptoms.
Creamywhite blisterlike pustules appear most commonly on the undersides of leaves located near the bottom of diseased plants. Tissue on the upper leaf surfaces,
opposite pustules, is raised and yellowgreen. No scorching or shriveling of diseased leaves occurs.
Gray localized lesions on diseased stems are caused by oospores that have formed intracellularly in the stem epidermis. Stem lodging occurs following the collapse of
tissues of the cambial region and vascular rays.
Management.
Not necessary.
Yellow Rust
Yellow rust is also called Coleosporium rust.
Cause.
Coleosporium helianthi and C. pacificum (syn. C. madiae). Coleosporium pacificum is a heteroecious, longcycled rust fungus that has Monterey pine, Pinus
radiata, as an alternate host. The uredinial and telial stages occur on sunflower; the pycnial and aecial stages occur on Monterey pine.
Distribution.
The West Coast of the United States.
Symptoms.
Uredinia occur as golden yellow pustules on diseased sunflower leaves.
Management.
Not reported.
Dagger
Cause.
Distribution.
Not known for certain, but probably widespread.
Symptoms.
An aboveground symptom is a slight to moderate stunting. Belowground symptoms are a reduction in the feeder roots accompanied by necrosis of a portion of the
root system.
Management.
Not reported.
Lesion
Cause.
Pratylenchus hexincisus is endoparasitic; its larvae enter roots and attack the root cortex.
Distribution.
Wherever sunflower is grown. However, sunflower normally is not severely affected.

Page 804
Symptoms.
Diseased plants may be yellowed and stunted. Initially, roots have small dark lesions. Other soilborne microorganisms may enter the root through wounds caused by
Pratylenchus spp., which results in root rot and a browning of the root system.
Management.
Not necessary.
Pin
Cause.
Paratylenchus projectus has been reported to be a mild parasite on sunflower; therefore, large populations appear necessary for substantial plant growth reduction.
Populations of pin nematodes in greenhouse tests developed best at temperatures of 20° to 25°C.
Distribution.
Korea and the United States.
Symptoms.
Seed yields were reduced in greenhouse tests.
Management.
Early sowing may reduce damage.
Reniform
Cause.
Rotylenchulus reniformis is a nematode in which only females invade roots after feeding on epidermal tissues. Rotylenchulus reniformis is semiendoparasitic
because the posterior portion of the female remains outside the root and swells to a kidney shape. Eggs are laid outside the root. Optimum temperature for root
invasion and nematode development is 29°C.
Distribution.
Africa and the southeastern United States; however, sunflower normally is not severely affected.
Symptoms.
Diseased plants are stunted and chlorotic. Small galls or root swellings may sometimes occur on damaged roots.
Management.
Not necessary.
Root Knot
Cause.
Meloidogyne arenaria, M. incognita, and M. javanica. These nematodes do not survive if the temperature averages below 3°C during the coldest month.
Distribution.
Not known but probably widespread.
Symptoms.
Diseased plants are reduced in stand and vigor, and wilt during the day but often recover their turgidity at night. Diseased plants are easily pulled from the soil due to
the destruction of the root system. Numerous galls are present on diseased roots.

Page 805
Management.
Not reported.
Spiral
Cause.
Helicotylenchus sp. is an ectoparasite.
Distribution.
Widespread.
Symptoms.
Symptoms on sunflower are relatively unknown. Under low to midlevel populations, a few root cells are destroyed, but roots are severely affected when infected by
high populations of nematodes.
Management.
Not reported.
Stunt
Cause.
Tylenchorhynchus nudus and Quinisulcius acutus are ectoparasites.
Distribution.
Not known, but presumably these nematodes are widespread on sunflower.
Symptoms.
Aboveground symptoms are a moderate plant stunting and chlorosis. The belowground symptom is a reduction in root growth.
Management.
Not reported.
Aster Yellows
Cause.
Aster yellows phytoplasma survives in several dicotyledonous plants and in leafhoppers. Transmission is primarily by the aster leafhopper, Macrosteles fascifrons.
Distribution.
Symptoms.
Either the entire head or a pieshaped sector of the diseased head displays symptoms. Flowers remain green instead of normally turning yellow. Structures resembling
small leaves, but larger than normal flowers, replace the floral parts in diseased flower heads. Eventually, diseased portions turn brown and die; the brown
discoloration extends downward as a narrow stripe along the stem. Sometimes head symptoms are not evident, but a black slimy rot occurs on stalks below the
diseased heads.
Diseased plants may be stunted or break over. Other diseased plants may set seed only on the normal portion of their heads.
Management.
Not reported.

Page 806
Sunflower Mosaic
Cause.
Sunflower mosaic is caused by three different viruses. Cucumber mosaic virus (CMV) is in the cucumovirus group. CMV is mechanically transmitted and has a wide
host range. Sunflower virus and tobacco mosaic virus are the other two causal viruses.
Distribution.
The United States (Maryland).
Symptoms.
Symptoms of mosaic and chlorotic rings are most severe on diseased leaves that are younger than 2 months. Diseased plants are stunted and sometimes have discrete,
narrow, light brown streaks on petioles and stems. Malformed heads that have shriveled seed are produced.
Management.
Not reported.
Yellow Leaf Spot Mosaic
Cause.
A virus that resembles tomato spotted wilt virus.
Distribution.
Ukraine.
Symptoms.
A yellow spotted mosaic is produced on diseased leaves.
Management.
Not reported.
Disease Caused by Nonparasitic Factors
Bract Necrosis
Cause.
Nonparasitic. Disease is caused by temperatures of 40°C or higher.
Distribution.
Symptoms.
Disk flowers and bracts have a brown discoloration that becomes black after a rain. When bract necrosis occurs during the bud stage, buds remain unopened. Some
injured buds may open but produce few or no disk flowers and little pollen.
Management.
Not reported.
Selected References
Allen, S. J., Brown, J. F., and Kochman, J. K. 1983. Effects of temperatures, dew period and light on the growth and development of Alternaria helianthi.

Page 807
Allen, S. J., Brown, J. F., and Kochman, J. K. 1983. The effects of leaf age, host growth stage, leaf injury and pollen on infection of sunflowers by Alternaria
helianthi. Phytopathology 73:896898.
Arsenijevic, J. 1970. A bacterial soft rot of sunflower (Helianthus annuus L.). Acta Phytopathol. Acad. Sci. Hungary 5:317326.
Banihashemi, Z. 1975. Phytophthora black stem rot of sunflower. Plant Dis. Rptr. 59:721724.
Bernard, E. C., and Keyserling, M. L. 1985. Reproduction of rootknot, lesion, spiral, and soybean cyst nematodes on sunflowers. Plant Dis. 69:103105.
BlancoLopez, M. A., and JimenezDiaz, R. M. 1983. Effect of irrigation on susceptibility of sunflower to Macrophomina phaseoli. Plant Dis. 67:12141217.
Campos, V. P., Huang, S. P., Tanaka, M. A. S., and Rezende, A.M. 1982. Ocorrencia de Meloidogyne incognita em cultural de girassol no Est. Minas Gerais,
Brasil. Fitopathologia Brasileira, pp. 309310 (in Portuguese).
Carson, M. L. 1985. Epidemiology and yield losses associated with Alternaria blight of sunflowers. Phytopathology 75:11511156.
Carson, M. L. 1987. Effects of two foliar pathogens on seed yield of sunflower. Plant Dis. 71:549551.
De Waele, D., and Bolton, C. 1988. Trophurus pakendorfi n. sp. from sunflower in South Africa (Nemata: Telotylenchinae). Phytophylactica 20:153156.
Donald, P. A., Bugbee, W. M., and Venette, J. R. 1986. First report of Leptosphaeria lindquistii (sexual stage of Phoma macdonaldii) on sunflower in North
Dakota and Minnesota. Plant Dis. 70:352.
Donald, P. A., Miller, J. F., and Venette, J. R. 1986. Reaction of sunflower lines to Phoma macdonaldii. (Abstr.). Phytopathology 76:956.
Donald, P. A., Venette, J. R., and Gulya, T. J. 1987. Relationship between Phoma macdonaldii and premature death of sunflower in North Dakota. Plant Dis.
71:466468.
Dwan, J. M., and Sobrino, E. 1987. First report of Pseudomonas syringae pv. helianthi on sunflower in Spain. Plant Dis. 71:101.
Fakir, G. A., Rao, M. H., and Thirumalachar, J. J. 1976. Seed transmission of Macrophomina phaseolina in sunflower. Plant Dis. Rptr. 60:736737.
Fourie, D., and Viljoen, A. 1996. Bacterial leaf spot of sunflower in South Africa. Plant Dis. 80:1430.
Gudmestad, N. C., Secor, G. A., Nolte, P., and Straley, M. L. 1984. Erwinia carotovora as a stalk rot pathogen of sunflower in North Dakota. Plant Dis. 68:189
192.
Gulya, T. J., Urs, R. R., and Banttari, E. E. 1981. Apical chlorosis of sunflower incited by Pseudomonas tagetis. (Abstr.) Phytopathology 71:221.
Gulya, T. J., Urs, R. R., and Banttari, E. E. 1982. Apical chlorosis of sunflower caused by Pseudomonas syringae pv. tagetis. Plant Dis. 66:598600.
Gulya, T. J., Ooka, J. J., and Mancl, M. K. 1985. Diseases of cultivated sunflower in Hawaii. Plant Dis. 69:542.
Herd, G. W., and Phillips, A. J. L. 1988. Control of seedborne Sclerotinia sclerotiorum by fungicidal treatment of sunflower seed. Plant Pathol. 37:202205.
Hoes, J. A. 1972. Sunflower yellows, a new disease caused by Phialophora sp. Phytopathology 62:10881092.
Hoes, J. A. 1975. Sunflower diseases in western Canada. In Oilseed and Pulse Crops in Western Canada. Modern Press, Saskatoon, Saskatchewan.

Page 808
Hoes, J. A., and Huang, H. C. 1985. Effect of betweenrow and withinrow spacings on development of Sclerotinia wilt and yield of sunflower. Can. J. Plant Pathol.
7:98102.
Holley, R. C., and Nelson, B. D. 1986. Effect of plant population and inoculum density on incidence of Sclerotinia wilt of sunflower. Phytopathology 76:7174.
Huang, H. C. 1976. Importance of Coniothyrium minitans in survival of Sclerotinia sclerotiorum in wilted sunflower. Can. J. Bot. 55:289295.
Huang, H. C., and Dueck, J. 1980. Wilt of sunflower from infection by mycelialgerminating sclerotia of Sclerotinia sclerotiorum. Can. J. Plant Pathol. 2:4752.
Huang, H. C., and Hoes, J. A. 1980. Importance of plant spacing and sclerotial position to development of Sclerotinia wilt of sunflower. Plant Dis. 64:8184.
Huang, H. C., and Kozub, G. C. 1990. Cyclic occurrence of Sclerotinia wilt of sunflower in western Canada. Plant Dis. 74:766770.
Infantino, A., and Di Giambattista, G. 1997. First report of Sclerotium rolfsii on sunflower in Italy. Plant Dis. 81:960.
Jeffrey, K. K., Lipps, P. E., and Herr, L. J. 1984. Effects of isolate virulence, plant age, and crop residues on seedling blight of sunflower caused by Alternaria
helianthi. Phytopathology 74:11071110.
Jeffrey, K. K., Lipps, P. E., and Herr, L. J. 1985. Seedtreatment fungicides for control of seedborne Alternaria helianthi on sunflower. Plant Dis. 69:124126.
JimenezDiaz, R. M., BlancoLopez, M. A., and Sackston, W. E. 1983. Incidence and distribution of charcoal rot of sunflower caused by Macrophomina
phaseolina in Spain. Plant Dis. 67:10331036.
Jones, B. L., and Van Der Walt, L. 1987. Bacterial stalk rot of sunflower in South Africa. (Abstr.). Phytophylactica 19:121.
Jones, B. L., and Van Der Wait, L. 1988. Occurrence of sunflower stalk rot incited by Erwinia carotovora in South Africa. Plant Dis. 72:994.
Kajornchaiyakul, P., and Brown, J. F. 1976. The infection process and factors affecting infection of sunflower by Albugo tragopogi. Brit. Mycol. Soc. Trans. 66:91
95.
Klisiewicz, J. M., and Beard, B. H. 1976. Diseases of sunflower in California. Plant Dis. Rptr. 60:298301.
Kolte, S. J. 1985. Diseases of Annual Edible Oil Seed Crops, Volume III: Sunflower, Safflower, and Nigerseed Diseases. CRC Press, Inc., Boca Raton, FL. 154
pp.
Lagopodi, A. L., and Thanassoulopoulos, C. C. 1998. Effect of a leaf spot disease caused by Alternaria alternata on yield of sunflower in Greece. Plant Dis.
82:4144.
Ljubich, A., Gulya, T. J., and J. F. Miller. 1988. A new race of sunflower downy mildew in North America. (Abstr.). Phytopathology 78:1580.
McDonald, W. C. 1964. Phoma black stem of sunflowers. Phytopathology 54:492493.
McDonald, W. C., and Martens, J. W. 1963. Leaf and stem spot of sunflowers caused by Alternaria zinniae. Phytopathology 53:9396.
McLaren, D. L., Huang, H. C., Kozub, G. C., and Rimmer, S. R. 1994. Biological control of Sclerotinia wilt of sunflower with Talaromyces flavus and
Coniothyrium minitans. Plant Dis. 78:231235.
Middleton, K. J. 1971. Sunflower diseases in South Queensland. Queensland Agric. J. 97:597600.
Mihaljcevic, M., MuntanolaCvetkovic, M., Vukojevic, J., and Petrov, M. 1985. Source of infection of sunflower plants by Diaporthe helianthi in Yugoslavia.
Phytopathol. Zeitschr. 113:334342.
Morris, J. B., Yang, S. M., and Wilson, L. 1983. Reaction of Helianthus species to Alternaria helianthi. Plant Dis. 67:539540.

Page 809
MuntanolaCvetkovic, M., Mihaljcevic, M., and Petrov, M. 1981. On the identity of the causative agent of a serious PhomopsisDiaporthe disease in sunflower
plants. Nova Hedwigia 34:417435.
MuntanolaCvetkovic, M., Mihaljcevic, M., Vukojevic, J., and Petrov, M. 1985. Comparison of Phomopsis isolates obtained from sunflower plants and debris in
Yugoslavia. Brit. Mycol. Soc. Trans. 85:477483.
Orellana, R. G. 1971. Fusarium wilt of sunflower, Helianthus annuus: First report. Plant Dis. Rptr. 55:11241125.
Orellana, R. G., and Quacquarelli, A. 1968. Sunflower mosaic caused by a strain of cucumber mosaic virus. Phytopathology 58:14391440.
Palm, M. E., Gams, W., and Nirenberg, H. I. 1995. Plectosporium, a new genus for Fusarium tabacinum, the anamorph of Plectosphaerella cucumerina.
Mycologia 87:397406.
Parmelee, J. A. 1972. Additions to the autoecious species of Puccinia on Heliantheae in North America. Can. J. Bot. 50:14571459.
Piening, L. J. 1976. A new bacterial leaf spot of sunflowers in Canada. Can. J. Plant Sci. 56:419422.
Putt, E. D. 1964. Breeding behavior of resistance to leaf mottle or Verticillium wilt in sunflowers. Crop Sci. 4:177179.
Rashid, K. Y. 1993. Incidence and virulence of Plasmopara halstedii on sunflower in western Canada during 19881991. Can. J. Plant Pathol. 15:206210.
Reddy, P. C., and Siradhana, B. S. 1978. A new leaf spot disease of sunflower in India. Plant Dis. Rptr. 62:508.
Rich, J. R., and Dunn, R. A. 1982. Pathogenicity and control of nematodes affecting sunflower in north central Florida. Plant Dis. 66:297298.
Richeson, M. L. 1981. Etiology of a late season wilt in Helianthus annuus. Plant Dis. 65:10191021.
Rogers, E. C., Thompson, T. E., and Zimmer, D. E. 1978. Rhizopus head rot of sunflower: Etiology and severity in the southern plains. Plant Dis. Rptr. 62:769771.
Sackston, W. E. 1960. Botrytis cinerea and Sclerotinia sclerotiorum in seed of safflower and sunflower. Plant Dis. Rptr. 44:664668.
Sackston, W. E. 1981. The sunflower crop and disease: Progress, problems, and prospects. Plant Dis. 65:643648.
Sackston, W. E., McDonald, W. C., and Martens, J. W. 1957. Leaf mottle or Verticillium wilt of sunflower. Plant Dis. Rptr. 41:337343.
Shtienberg, D. 1994. Achene blemish syndrome: A new disease of sunflower in Israel. Plant Dis. 78:11121116.
Shtienberg, D. 1997. Rhizopus head rot of confectionery sunflower: Effects on yield quantity and quality and implications for disease management. Phytopathology
87:12261232.
Shtienberg, D., and Vinta, H. 1995. Environmental influences on the development of Puccinia helianthi on sunflower. Phytopathology 85:13881393.
Smolik, J. D. 1987. Effects of Paratylenchus projectus on growth of sunflower. Plant Disease 71:975976.
Stovold, G. E., and Moore, K. J. 1972. Diseases of sunflower. Agric. Gazette of New South Wales 83:262264.
Styer, D. J., and Durbin, R. D. 1982. Isolation of Pseudomonas syringae pv. tagetis from sunflower in Wisconsin. Plant Dis. 66:601.
Tosi, L., and Zazzerini, A. 1995. Phialophora asteris f. sp. helianthi, a new pathogen of sunflower in Italy. Plant Dis. 79:534537.

Page 810
Viljoen, A., Kruger, H., and van Wyk, P. S. 1997. Histopathology of sunflower stems infected by Albugo tragopogonis. (Abstr.). Phytopathology 87:S100.
Watters, B. L., Herr, L. J., and Lipps, P. E. 1983. A new stem canker disease of sunflower. (Abstr.). Phytopathology 73:798.
Wehtje, G., and Zimmer, D. E. 1978. Downy mildew of sunflower: Biology of systemic infection and the nature of resistance. Phytopathology 68:15681571.
Yang, S. M. 1983. Bract necrosis, a nonparasitic disease of sunflower. (Abstr.). Phytopathology 73:844.
Yang, S. M. 1984. Etiology of atypical symptoms of charcoal rot in sunflower plants parasitized by larvae of Cylendrocopturus adsperus. Phytopathology 74:479
481.
Yang, S. M. 1988. Diseases of cultivated sunflower in Liaoning Province, People's Republic of China. Plant Dis. 72:546.
Yang, S. M., and Gulya, T. 1986. Prevalent races of Puccinia helianthi in cultivated sunflower on the Texas high plains. Plant Dis. 70:603.
Yang, S. M., and Owen, D. F. 1982. Symptomatology and detection of Macrophomina phaseolina in sunflower plants parasitized by Cylindrocopturus adspersus
larvae. Phytopathology 72:819821.
Yang, S. M., Morris, J. B., Unger, P. W., and Thompson, T. E. 1979. Rhizopus head rot of cultivated sunflower in Texas. Plant Dis. Rptr. 63:833835.
Yang, S. M., Rogers, C. E., and Luciani, N. D. 1983. Transmission of Macrophomina phaseolina in sunflower by Cylindrocopturus adspersus. Phytopathology
73:14671469.
Yang, S. M., Berry, R. W., Lutterell, E. S., and Vongkaysone, T. 1984. A new sunflower disease in Texas caused by Diaporthe helianthi. Plant Dis. 68:254255.
Yarwood, C. E. 1969. Sunflower, a new host of Coleosporium madia. Plant Dis. Rptr. 53:648.
Zazzerini, A., and Tosi, L. 1987. New sunflower disease caused by Fusarium tabacinum. Plant Dis. 71:10431044.
Zimmer, D. E. 1975. Some biotic and climatic factors influencing sporadic occurrence of sunflower downy mildew. Phytopathology 65:751754.

Page 811
22.
Diseases of Tobacco (Nicotiana tabacum)
Angular Leaf Spot
Angular leaf spot is also called blackfire.
Cause.
Pseudomonas syringae pv. angulata (syn. Pseudomonas angulata) survives in soil and infested residue, and persists as a parasite on the roots of weeds and winter
grains. Dissemination of P. syringae pv. tabaci over a long distance is by contaminated transplants. Water blown by wind is the most important means of
dissemination from plant to plant in the field and over short distances. Bacteria are splashed onto leaves, where they are forced into leaf stomates or wounds, and
move into flooded intercellular spaces. Leaf tissues must be watersoaked before infection can occur. Optimum conditions for infection occur during rainstorms
accompanied by high winds.
The major difference between P. syringae pv. tabaci and P. syringae pv. angulata is that P. syringae pv. tabaci produces toxin and Pseudomonas syringae pv.
angulata does not.
Distribution.
Wherever tobacco is grown.
Symptoms.
Symptoms suddenly appear a few days after rainy periods as angular to irregularshaped (113 mm in diameter) black to brownish watersoaked spots that rapidly
kill tissue and form dark brown angularshaped spots. As the spots age, their centers become light tan with dark borders and fall out during rainy weather. A thin
yellow band often occurs around spots. Spots eventually coalesce and cover large areas of a diseased leaf. On rapidly growing plants, diseased leaves become
''puckered" and torn. Symptoms in plant beds are similar to those in fields.

Page 812
Management
1. Plow planting beds in the autumn.
2. Steam or fumigate planting beds plowed in the spring.
3. Sow only seed from healthy plants.
4. Treat seed with bactericides.
5. Apply bactericide sprays to plants in the seedbed and field.
6. Use only diseasefree transplants.
8. Provide proper drainage for plant beds.
9. Do not grow tobacco in a field for 2 or more consecutive years.
10. Avoid working in a field when leaves are wet.
Barn Rot
Cause.
Erwinia carotovora subsp. carotovora (syn. Bacillus polymyxa, E. aroideae, E. carotovora, and E. chrysanthemi). The fungi Alternaria alternata, Botrytis
cinerea, Pythium spp., Rhizopus arrhizus, and Sclerotinia sclerotiorum also are associated with barn rot.
Overwintering occurs on infested or infected seed. Infected seed is an important source of inoculum and, presumably, is the primary source of infection. Dissemination
is by conveyors that move tobacco plants.
Barn rot occurs when wet, mechanically primed leaves are packed tightly into bulkcuring barns that have poor air circulation. Barn rot also occurs in stick barns with
poor circulation when they are overfilled with wet tobacco leaves. Mechanical leaf harvesters injure leaves, creating wounds for bacteria to enter.
Distribution.
Symptoms.
A watery, soft rot occurs during the yellowing stage of tobacco curing. A watersoaked brownish discoloration begins in the petioles or laminae, darkens to a dark
brown or black discoloration, and spreads throughout the leaves, causing them to decompose. Often leaves break away from strings and fall to the barn floor. There is
an odor of decaying vegetation within a barn. The damage may vary from a few leaves to the entire contents of a barn.
Management
1. Avoid placing wet tobacco in the barn.
2. Do not crowd leaves on a stick.
3. Do not crowd sticks together in the barn.
4. Use heat and ventilation to dry out excess moisture rapidly if wet tobacco is placed in a barn.
5. Do not injure tobacco.

Page 813
Black Rust
Cause.
Bacterium pseudozoogloae. This may be the same bacterium as Pseudomonas syringae pv. tabaci. Bacterium pseudozoogloae survives within infested residue
and is disseminated by splashing rain.
Distribution.
Indonesia and possibly Japan and Italy.
Symptoms.
Symptoms occur on diseased lower leaves as plants approach maturity. The dark green spots that appear initially become necrotic and dark brown in the center and
have zonate concentric rings. A dark green margin that surrounds each spot eventually reaches 1 to 2 cm in diameter. The margins remain dark green after diseased
leaves have dried.
Management.
No management other than to remove and burn the lower diseased leaves.
Blackleg
Blackleg is the seedling form of hollow stalk.
Cause.
Erwinia carotovora subsp. carotovora (syn. E. aroidea and E. carotovora subsp. atroseptica) survives in soil and infested residue. Cool and "heavy" clay soils
with a neutral pH favor survival of causal bacteria. Erwinia carotovora subsp. carotovora is disseminated to fields on infected transplants and by any means that
moves soil. Bacteria may also be spread within a planting bed by maggot flies of Hylemyia spp. Host plants become infected by leaves touching infested soil. Bacteria
then spread through the petioles and into the stems. Blackleg is most severe during damp, cloudy weather over a wide range of temperatures.
Distribution.
Wherever tobacco is grown. However, blackleg is rarely a severe problem.
Symptoms.
Blackleg occurs in irregular circular areas approximately 1 m in diameter within plant beds. Rotted petioles and stems become black and eventually split open or rot
off.
Some plants may be slightly affected and display no disease symptoms. When these plants are set in the field, they may grow normally. However, if symptomless
plants are removed from beds and kept overnight for planting the next day, all plants may become rotted and slimy.
Management.
As soon as blackleg is noticed, the covering should be removed from the plant bed to reduce humidity.
Crown Gall
Cause.
Agrobacterium tumefaciens (syn. Rhizobium radiobacter var. tumefaciens) is a soil inhabitant that is disseminated by anything that moves soil and

Page 814
enters plants through wounds caused by any means. Bacteria then stimulate cells to divide and eventually form a tumor. The following steps are thought to occur in
tumor development: (1) Bacteria enter a wound cell and bind to a specific intracellular wound site. (2) Bacterial DNA is transferred to the plant cell and causes it to
divide. (3) Bacterial DNA increases and is transferred to plant cells that are free of bacterial cells. These plant cells also divide and contribute to the tumor
development.
Tumor development is optimum at a temperature of 25°C but is inhibited at higher temperatures.
Distribution.
Crown gall is distributed worldwide, but it rarely occurs on tobacco.
Symptoms.
Round tumors or overgrowths that occur on diseased roots of shoots are several times larger than the stem or root. The round tumors have large indentations that
make them appear convoluted.
Management.
Not necessary.
Frenching
Cause.
Bacillus cereus is a nonpathogenic bacterium common in soil and dust, and on plant surfaces. Bacillus cereus does not enter or infect plants. A diffusate is produced
in soil by B. cereus that acts as a toxin to tobacco. The toxin disturbs the nitrogen metabolism of plants, which increases different amino acids, particularly isoleucine.
The excess of free amino acids then causes the tobacco abnormalities. Frenching is more prevalent on wet soils that sometimes lack available nitrogen or other
materials. Frenching does not occur at soil temperature of 21°C or less.
Distribution.
Wherever tobacco is grown. Frenching rarely causes much damage.
Symptoms.
Frenching begins to occur on 2 to 3weekold plants and continues until flowering. Chlorosis occurs initially along margins of young leaves and eventually covers all
interveinal areas but the leaf veins remain green. "Diseased" plants are stunted and have a large number of small, narrow, distorted, brittle leaves. Axillary buds of
severely diseased plants are stimulated, which causes a rosette of small, narrow, light green leaves that gives a witches' broom effect.
Management
1. Ensure that soils are properly drained and fertilized.
2. Do not plant into alkaline soils and avoid heavy applications of lime.
3. Apply fall applications of elemental sulfur.

Page 815
Granville Wilt
Granville wilt is also called bacterial wilt and several other names in countries where the disease occurs.
Cause.
Pseudomonas solanacearum is a bacterium that survives in soil and infects plants through root wounds caused by several factors. Bacteria are disseminated by
infected seedlings. During periods of high soil moisture, bacteria that are released from diseased roots spread to the roots of adjacent plant hosts, particularly where
the roots intermingle. Disease severity is greatest during high soil temperatures (30° to 35°C) and excess moisture.
Distribution.
Wherever tobacco is grown in warm temperate and semitropical areas of the world. Pseudomonas solanacearum is rarely found in areas where the mean
temperature in the winter is below 10°C.
Symptoms.
Initially, one or two leaves on young, succulent plants droop during the day but recover their turgidity at night. Often only half a leaf wilts. If the disease progresses
slowly, diseased leaves become light green and gradually turn yellow. In severe disease conditions, the whole plant wilts and dies within a few days.
Light tan to yellowbrown streaks occur in the vascular tissue. Eventually, the streaks darken, and in advanced stages, blackened areas occur on the surface of
diseased stalks. A dirty white to brownish slimy ooze in the form of glistening beads occurs on a cut stem. When the two cut edges of a stem are pulled apart slightly, a
bacterial strand stretches between the two pieces.
Eventually, roots become dark brown to black and rotted. In moist soils, roots become soft and slimy.
Management
2. Do not transplant plants showing wilting or other disease symptoms.
3. Do not grow tobacco in soil containing P. solanacearum for at least 5 years. Crops to include in a rotation are grasses, legumes, small grains, cotton, maize,
soybean, and sorghum.
4. Practice good nematode control.
Hollow Stalk
Blackleg is the seedling form of hollow stalk.
Cause.
Erwinia carotovora subsp. carotovora (syn. E. aroidea and E. carotovora subsp. atroseptica) survives in soil and in infested soil residue that is composed
primarily of decayed root crowns. Soils high in clay content and of neutral pH favor survival of the bacterium. Disease development is most rapid during wet weather
over a wide range of temperatures. Bacteria enter

Page 816
plants through wounds made during topping, suckering, and harvesting. Bacteria are disseminated in contaminated soil on workers' hands during topping and
suckering. Mineral oil, which is used to control suckering, apparently favors the reproduction of E. carotovora subsp. carotovora in and on plants.
Distribution.
Wherever tobacco is grown. However, hollow stalk is rarely an important disease.
Symptoms.
The first disease symptom appears at topping and suckering time and commonly is a discoloration in the pith at the break made at topping and at any stem wound.
Disease may occasionally begin at the bottom of plants. The pith rapidly becomes brown, followed by a "soft" rotting and disintegration. The pith eventually becomes a
foulsmelling slimy pulp that dries up to form a hollow stem. The top leaves wilt first, and as disease progresses down the stem, successive leaves wilt, hang down next
to the stalk, or fall off and cause the entire diseased stalk to be bare. Black or brown sunken lesions form in leaf axils.
Diseased leaves may rot in the curing barn and smell like decaying vegetation. The leaf petiole rots at the point where the string is attached and the leaf falls to the
floor.
Management
1. Do not top and sucker during damp or cloudy weather.
2. Reduce humidity in curing barns when wet, succulent tobacco leaves are hung.
3. Avoid manual topping.
4. Use sucker control agents other than mineral oils.
Leaf Gall
Leaf gall is also called fascination.
Cause.
Rhodococcus fascians (syn. Corynebacterium fascians) is commonly found in soil and does not need a wound to infect a plant. Disease occurs due to an imbalance
of growth hormones in diseased plants caused by the bacteria. Optimum growth occurs at temperatures of 25° to 28°C.
Distribution.
Not known for certain, but leafy gall rarely occurs on tobacco.
Symptoms.
Numerous short, fleshy, thick stems or multiple buds with misshapen leaves develop at or below the soil line; however, the main stem of the diseased plant appears
normal but may be somewhat stunted. The proliferated growth may reach a diameter of 2 to 8 cm and resemble a leafy gall.
Management.
Not necessary.

Page 817
Philippine Bacterial Leaf Spot
Cause.
Pseudomonas aeruginosa is a common soil saprophyte and is seedborne. Bacteria enter the plant through wounds and stomates of watersoaked leaves.
Dissemination is by splashing rain.
Distribution.
The Philippines.
Symptoms.
Bleached white spots that vary in size from a pinpoint to several millimeters in diameter occur on seedling leaves. Diseased areas develop a wet rot that becomes
necrotic and disintegrates. Petioles and stems also become diseased during wet weather, causing death of diseased plants.
Diseased plants in the field have whitish or opaque lesions that eventually become brown and zonate and are bordered by a chlorotic zone that disappears as leaves
mature. Lesions, which are most numerous on the bottom leaves, coalesce and form large, irregularshaped, dead areas. After curing, brown spots disappear but the
white spots are still evident.
Management
4. Treat seed with a bactericide.
5. Apply bactericide to foliage of plants in seedbeds and in fields.
6. Use only transplants that are free of disease.
9. Do not grow tobacco in infested soil for 2 consecutive years.
10. Avoid working in a field when the tobacco leaves are wet.
Wildfire
Cause.
Pseudomonas syringae pv. tabaci (syn. P. tabaci) survives in soil, infested residue, infested dry leaves, and some types of manufactured tobacco, and as a parasite
on the roots of weeds, grasses, and winter grains. Bacteria are commonly disseminated by windblown water from plant to plant in the field and over long distances.
Dissemination is less common on contaminated transplants. Bacteria are splashed onto leaves, where they infect through stomates or wounds. Watersoaked areas of
leaf tissue, which develop as a result of flooding intercellular spaces, must be present before infection occurs. Bacteria are forced into leaf openings and then move into
flooded intercellular spaces.
Optimal infection conditions occur during rainstorms accompanied by high winds. Optimum growth in culture is at temperatures of 24° to 28°C. The major difference
between P. syringae pv. tabaci and P. syringae pv. angu

Page 818
lata is that P. syringae pv. tabaci produces toxin and Pseudomonas syringae pv. angulata does not.
Distribution.
Symptoms.
Wildfire may suddenly appear in areas approximately 1 to 2 m in diameter in the wettest part of plant beds on tender, rapidly growing plants after a cool, rainy period.
During high humidity, small, circular, yellowgreen, watersoaked spots develop on diseased leaves. Spots rapidly turn brown and are surrounded by yellowgreen
halos, which give plants a scorched appearance. Severely diseased seedlings, which eventually die, are normally in the middle of an area of diseased plants.
Older diseased plants have spots that are circular, and have a brown and dead center (1225 mm in diameter) that is surrounded by a yellowgreen, watersoaked
border or halo. Spots coalesce and form large dead areas on diseased leaves. Leaves that are diseased only on one side become twisted and distorted.
Management
5. Apply bactericide to foliage of plants in seedbeds and in fields.
6. Use only transplants free of disease.
10. Avoid working in a field when leaves are wet.
Wisconsin Bacterial Leaf Spot
Cause.
Bacterium melleum. However, this is probably a strain of Pseudomonas syringae pv. tabaci. Some researchers suggest B. melleum is an intermediate between P.
syringae pv. tabaci and P. syringae pv. angulata. Therefore, Wisconsin bacterial leaf spot may have been confused with wildfire.
Distribution.
Europe and the United States (Wisconsin). There has been no report of the disease from Wisconsin since 1937.
Symptoms.
Initially, circular pinpointsized specks surrounded by distinct chlorotic zones appear on diseased leaves and enlarge rapidly during periods of high temperatures and
humidity to form spots that are approximately 1 cm in diameter. Necrotic tissue in spots becomes brown and lesions on veins are brown and sunken. Irregularshaped
spots form when the smaller spots coalesce.

Page 819
Diseased seedlings have inconspicuous angular spots that are surrounded by chlorotic margins. The necrotic tissue becomes brown as the spots age. When spots are
numerous, foliage appears blighted.
Management
5. Apply bactericide to the foliage of plants in seedbeds and in fields.
6. Plant only disease.free transplants.
10. Avoid working in a field when tobacco leaves are wet.
Anthracnose
Cause.
Colletotrichum destructivum overwinters as mycelia and acervuli in infested residue and soil, and is seedborne. Conidia are produced in acervuli and disseminated
by wind and splashing rain to host plant leaves. Anthracnose develops over a wide temperature range (18° to 32°C) and a high relative humidity.
Distribution.
Asia, Africa, Australia, Brazil, and the United States.
Symptoms.
Young leaves have small, depressed, light green, watersoaked spots that enlarge to 3 mm in diameter and give the undersides of diseased leaves a "greasy"
appearance. As spots age, they dry out, become a graywhite color that resembles paper, and are surrounded by raised watersoaked borders that become brown.
Large spots are zonate and have dark brown centers. Diseased leaves become wrinkled and distorted, and die. Small diseased plants are stunted or killed. Large
diseased plants have watersoaked areas that later form redbrown cankers up to 12 mm long on leaf midribs and petioles.
Management
1. Apply foliar fungicides to plants in plant beds and in fields.
2. Fumigate infested soils.
4. Destroy all weeds in the vicinity of plant beds.
5. Do not grow peppers and tomatoes in seedbeds.

Page 820
Ascochyta Leaf Spot
Ascochyta leaf spot is also called ragged leaf spot.
Cause.
Ascochyta phaseolorum. Survival is presumably as pycnidia in infested residue in the soil. Ascochyta leaf spot is more severe at cool temperatures (around 22°C)
during wet weather.
Distribution.
Asia, Europe, and the United States.
Symptoms.
Symptoms occur on diseased plants of all ages. Spots are circular (2.5 cm in diameter) with gray to brown centers that fall out and give a ragged appearance to the
diseased leaf. Spots coalesce and form large dead areas. Scattered black pycnidia are found in the centers of older lesions and on the stems of young diseased
seedlings.
Management.
Apply foliar fungicides.
Barn Spot
Barn spot is the curing phase of frogeye.
Cause.
Cercospora nicotianae.
Distribution.
Africa, Central America, Southeast Asia, and the United States.
Symptoms.
Black spots (16 mm in diameter) occur on flucured tobacco leaves in the barn.
Management
1. Sow only diseasefree seed.
2. Remove residue from plant beds.
3. Apply foliar fungicides before transplanting.
4. Do not overfertilize with nitrogen.
5. Prime tobacco before it becomes overripe.
6. Plow under infested residue in the field.
7. Rotate tobacco with other crops.
8. Cure tobacco at a temperature of 38°C with 100% relative humidity.
Black Mildew
Cause.
The causal fungus is similar in morphology to Diporotheca rhizophila and has been found only on plants infested with the cyst nematode, Globodera spp. However,
not every plant growing in nematodeinfested soil is infected.
Distribution.
The United States (Connecticut). Black mildew is of no economic importance.
Symptoms.
Diseased tobacco roots are colonized with dark fungal mycelia.
Management.
Not necessary.

Page 821
Black Root Rot
Black root rot is also called maricume radicale, root rot, and Thielavia root rot.
Cause.
Thielaviopsis basicola (syn. Chalara elegans) survives as chlamydospores and endoconidia in soil and as saprophytes on infested residue of different plants, which
allows T. basicola to persist indefinitely in the absence of tobacco. However, Hood and Shew (1997) reported that T. basicola did not display significant saprophytic
ability and should be classified ecologically as an obligate parasite.
Thielaviopsis basicola is disseminated on roots of transplants and by any means that moves soil. Chlamydospores, considered to be the primary infective propagule,
and endoconidia germinate and form hyphae that penetrate roots. Chlamydospores and endoconidia produced in mycelium on the outside of diseased roots serve as
secondary inoculum.
Black root rot is most severe at relatively cool temperatures (17° to 23°C) and in wet soils. Plants growing in soils with a pH of 6.4 and above are more prone to
infection. Black root rot does not develop in soils with an average pH of less than 5.2.
Populations of T. basicola in field soils are directly related to the frequency of soybean and tobacco production, with the larger fungal populations occurring in soils on
which continuous tobacco is grown. Disease severity is normally positively correlated with inoculum density of T. basicola. However, some studies have reported that
inoculum density is not related to black root rot severity, and that environmental factors and cultivar resistance have a greater influence on disease development.
Distribution.
Symptoms.
Seedlings in plant beds damp off. Usually diseased plants are stunted or uneven in growth only in limited areas of affected fields. Host plants infected later in the
growing season have black lesions on roots and the leaves become yellow.
Diseased roots are partially or entirely black; small roots are completely rotted off, but larger main and lateral roots only have roughened black lesions on them.
Severely diseased plants have a few blackened, stubby roots attached to a stem. If the weather becomes warm, many diseased plants produce new roots and assume
normal growth. Leaves become yellow and wilt during the day, and plants flower prematurely.
Management
1. Grow resistant cultivars. There are two types of resistance. One type is partial resistance, which is characterized by low to moderate levels of resistance derived
from Nicotiana tabacum. The second type is a high level of monogenic resistance, which is derived from N. debneyi. Resistance is related to the presence of the
phenolic compounds scopolin and scopoletin. These compounds prevent the melanization of fungi, which is necessary for fungal growth in host tissue.

Page 822
2. Use a new bed site each year.
3. Treat soil with steam or chemicals if an old bed site is used.
4. Rotate tobacco with resistant crops, such as grass, for 3 years or longer.
5. Plow under cover crops and manure.
6. Do not apply more than 10 tons of manure per acre.
7. Maintain a soil pH of 6.0 to 6.4.
8. Fertilize according to soil tests. Avoid excessive fertilizer.
9. Avoid transplanting when soils are cold or when the air temperature is low.
Black Shank
Cause.
Phytophthora parasitica var. nicotianae (syn. P. nicotianae) or P. nicotianae var. nicotianae. Both names are considered correct but not synonymous.
Phytophthora parasitica var. nicotianae survives as chlamydospores in soil and in infested residue, and as mycelia in infested residue. Oospores are formed and
overwinter in infested tissue and soil, but their function is not known. Dissemination is on transplants, by water, or by any means that moves soil. Spread of P.
parasitica vat. nicotianae is greatest between susceptible plants and least between resistant plants.
Chlamydospores germinate and form germ tubes in which either another chlamydospore or sporangia are produced. The sporangia then germinate and form either
hyphae or zoospores. Zoospores and sporangia germinate and produce hyphae that infect plants. Zoospores encyst, germinate, and penetrate roots within I hour.
Sporulation occurs on stems near the soil surface or on infested residue. Sporangia disseminated some distance by wind and water initiate further infections on host
plants. Plants of all ages may be infected, but seedlings are most susceptible.
Black shank is most severe in wet soils at temperatures above 21°C. Thus, disease incidence is correlated with soil texture and drainage class of the parent soil.
Disease infection and severity are increased by the nematodes Meloidogyne incognita and Globodera solanacearum. Different physiologic strains of P. nicotianae
exist.
Distribution.
Africa, Asia, Australia, Caribbean, eastern Europe, North America, and South America.
Symptoms.
Symptoms initially occur in wetter areas of fields. Roots become dark brown or black, with the discoloration on the stalk extending several centimeters above the soil
line. Plants in the early stages of disease have one or more dead and blackened lateral roots but no discoloration of stems. Tops of diseased plants eventually wilt
during the day and do not recover turgidity at night. Usually plants wilt and collapse before leaves mature and can be harvested.
The collapse of diseased plants occurs very suddenly during drought stress or hot weather. The first symptom on vigorously growing plants is a

Page 823
rapid wilting of leaves, which quickly become chlorotic, hang down, die, and become brown. As disease progresses, the entire root system and base of the stalk dies
and becomes blackened,.
Older plants that become infected initially have a black discoloration on the stem that extends some distance above the soil line. Soon the leaves become chlorotic,
then brown, shrivel, and sometimes have a few small green leaves remaining at the top of the diseased plant. Such diseased plants may bloom prematurely.
One of the most characteristic symptoms of black shank is seen when the stem is split lengthwise. The pith is dry, brown to black, and separated into platelike disks.
During rainy weather, large lesions may develop on the lower leaves. At first a lesion is pale green; later it becomes brown and grows up to 8 cm in diameter.
Management.
Where black shank is present:
2. Move plant beds to an area that has not been planted in row crops.
3. Convert an infested field to permanent pasture for at least 5 years. Other alternatives include 2 to 3 years of clean fallow followed by rye grown for grain. Two or 3
years of peanuts, soybeans, and cotton are not as satisfactory but still aid in reducing the population of the pathogen. In South Africa, blue buffalo grass, Cenchrus
ciliaris, grown for 2 to 3 years in succession significantly reduced the incidence of black shank on tobacco.
4. Use good nematode control practices.
5. Leave areas or a field infested with P. nicotianae until last during tillage operations.
6. Disinfect machinery parts with fungicides after use.
7. Clean shoes after working in infested soil. Use a stomp box (a wood box with a sack in the bottom on which fungicide is poured).
8. Apply fungicides.
Where black shank is not present:
1. Grow your own plants. This prevents movement of the fungus on transplants.
2. Do not irrigate from water sources originating in infested fields.
3. Do not borrow equipment. Clean off all equipment with a fungicide solution.
Blue Mold
Blue mold is also called downy mildew.
Cause.
Peronospora tabacina (syn. P. hyoscyami f. sp. tabacina) survives as mycelia and sporangia within infested residue in geographical areas with mild winter
temperatures. Systemic mycelia overwinter in live roots of host

Page 824
plants whose aerial portion has been previously killed. Such plants produce suckers during favorable weather and become systemically infected. Wild tobacco,
Nicotiana repanda, also provides a means of overwintering and is a significant source of inoculum.
In colder tobaccogrowing areas, oospores overwinter in diseased seedlings. However, it is not known how they germinate to initiate primary infection. Therefore,
primary inoculum in cold areas may be conidia that are disseminated by wind from warmer tobaccogrowing regions.
Peronospora tabacina is primarily disseminated by wind. However, other dissemination is by any means that residue containing conidia, mycelia, and oospores can
be moved from place to place. Conidia (sporangiospores) are produced from mycelia and disseminated by wind for long distances. Conidia germinate in the presence
of moisture and produce germ tubes that penetrate a host's leaves. Conidia produced in lesions provide secondary inoculum. Oospores are also formed in diseased
tissue.
Temperatures from 15°C to 25°C and 95% or more relative humidity with intermittent rainy weather are optimum conditions for blue mold development. Availability
of moisture on leaves is an important factor for infection; consequently, disease spreads rapidly in cool, damp weather. Conversely, P. tabacina has been reported to
adapt to higher temperatures in some geographical areas. Epiphytotics have occurred during day and night temperatures up to 36° and 25°C, respectively, for 48
hours. Significantly fewer conidia are produced at these higher temperatures, but these conidia could be important as secondary inoculum for subsequent disease
development.
Young plants are more susceptible to infection than are older plants.
Distribution.
Australia, Canada, Cuba, Europe, the Mediterranean area, Mexico, the Near East, and the United States.
Symptoms.
Small diseased plants in seedbeds have erect leaves. Circular groups of larger diseased plants become yellow and the plants in the center of a group have cupped
leaves. Some cupped leaves have a bluish fungal growth consisting of mycelia, conidia, and conidiophores on the lower leaf surfaces. Diseased leaves become twisted
and turn their lower surface upward, accentuating the bluish color, especially when moisture is available. Diseased plants begin to die and turn light brown. Eventually,
the entire plant or all the leaf tissue except the growing tip is killed.
Older diseased plants in seedbeds become deformed and have partially killed leaves or leaves that are twisted and puckered. Irregularshaped necrotic lesions may
develop on leaves. Plants become stunted and roots become dark brown.
Diseased leaves on plants in the field have circular blotches that coalesce and form brown necrotic areas. Diseased leaves also become distorted and puckered and
have large areas that disintegrate. Lesions also occur on

Page 825
buds, flowers, and capsules. Diseased plants are stunted and have wilt symptoms and a vascular discoloration that is observed as brown streaks. Stems lodge and
roots become dark brown.
Management
1. Apply foliar fungicides to plants in a seedbed. Treatment must begin before disease appears.
2. Destroy beds after setting is complete.
3. Destroy any live plants remaining after harvest.
4. Locate beds in an area where they will not receive morning shade.
5. Grow resistant cultivars. Resistance may be related to the presence of the phenolic compounds scopolin or scopoletin.
Botryosporium Barn Mold
Cause.
Botryosporium longibrachiatum and B. pulchrum survive on infested residue. Host plants are apparently infected or have a latent infection at harvest time.
Secondary infection originates from bringing into the barn infested plants on which conidia are produced and spread around the building. Humid, wet conditions favor
Distribution.
Widespread.
Symptoms.
White mycelia and conidiophores are confined to lesions (120 cm long) on the midribs and on the secondary veins of lower leaves. Lesions initially are watersoaked.
Sporulation then occurs on laminae adjacent to the infected areas on the midribs and veins. Lesion development and sporulation occurs after tobacco reaches the
brown stage of curing. Eventually, sporulation spreads farther and is evident on all leaf surfaces. Lower leaves drop to the barn floor; those remaining on stalks are
severely watersoaked and decayed.
Management.
Supply supplemental heating to assist drying.
Brown Spot
Cause.
Alternaria alternata (syn. A. tenuis) survives as mycelia in woody plant residue, such as tobacco stems. During periods of wet weather, conidia are produced and
disseminated by water and wind to the lower leaves of host plants. Alternaria alternata is also disseminated by infected seed and transplants. Secondary inoculum is
conidia that are produced in lesions during moist weather and disseminated by wind to other plant hosts.
Infection and disease development occur at temperatures higher than 21.0°C but are most rapid when temperatures are higher than 26.5°C. Tobacco leaves are
infected at a late stage of plant maturity. A metabolite, AT toxin, produced by A. alternata induces the ''typical" symptoms.
Distribution.

Page 826
Symptoms.
Round brown spots occur on diseased leaves. On inoculated plants, spots are larger on old leaves than on young leaves and frequently are marked by concentric
rings. Small spots, which initially are less than 6 mm in diameter, eventually enlarge up to 25 mm in diameter during moist weather, coalesce, and kill large areas of
diseased leaves.
Spots occur on stalks late in the growing season and are smaller than on leaves but become more numerous and give diseased stalks a "speckled" appearance. There
is a significant decrease in sugar and nicotine alkaloid content in diseased tissue.
Management
1. Sow seed that is free of disease.
2. Fumigate plant beds and remove residue.
3. Rotate tobacco in fields where brown spot was present.
4. Grow tolerant cultivars. In general, burley and dark tobacco are less susceptible than flucured tobacco.
Charcoal Rot
Cause.
Macrophomina phaseolina (syn. M. phaseoli) survives as sclerotia in soil and infested residue. Sclerotia germinate and form germ tubes that penetrate the host.
Charcoal rot is more severe in dry weather at temperatures of 38°C and above and on plants to which mineral oil was applied during temperatures of 32°C and
above.
Distribution.
Wherever tobacco is grown in tropical or subtropical areas.
Symptoms.
Symptoms are associated with injury caused by mineral oil applied for sucker control. A black lesion develops from which M. phaseoli grows inward, causing pith
and wood decay, followed by plant death and lodging. Sclerotia are embedded throughout the bark and wood of diseased plants.
Management.
Fumigate the soil to kill sclerotia.
Collar Rot
Cause.
Botrytis cinerea and Sclerotinia sclerotiorum. Botrytis cinerea is discussed under "Gray Mold." Sclerotinia sclerotiorum survives as sclerotia in infested stalk
residue and soil. In the spring, sclerotia germinate and form either mycelia or apothecia. Most primary infections originate from ascospores produced on apothecia and
disseminated by wind to plants. However, infrequently infection may originate from the mycelium growing from a sclerotium.
Ascospores produced throughout the summer infect flowers that fall onto leaves and cause dead blossom leaf spot. Injury spots caused by heat and chemicals provide
additional infection courts for ascospores to germi

Page 827
nate on. Infection also occurs in wounds where the plant tops or suckers were removed. Sclerotia are then produced in the diseased stalks later in the growing season.
Collar rot is more severe during wet weather. Seedlings 35 to 53 days old are the most susceptible. Disease development is enhanced when an external source of
nutrient is present on the host leaf surface, such as clipping debris or leaf pieces. Seedlings may be infected up to transplant size.
Distribution.
Symptoms.
Tobacco transplants in greenhouses are affected. Initially, a small dark brown lesion with a welldefined margin occurs at the base of a diseased stem. After
transplanting, the lesion may circle the stem and kill the plant or become gray, have a less welldefined margin, and develop higher on the stem. A white, cottony,
mycelial growth in which small black sclerotia are present grows over a diseased area.
Management
1. Steam or fumigate plant beds.
2. Do not place plant beds in low, wet areas.
3. Provide adequate ventilation.
4. Remove debris from around transplants in the greenhouse.
Corynespora Leaf Spot
Cause.
Corynespora cassiicola survives as mycelia and chlamydospores in infested tobacco residue and soil for 2 years or more, and as a saprophyte in the residue of other
plant hosts. Conidia splashed by water and blown by wind to host leaves cause infection when free moisture is present or the relative humidity is 80% and above.
Older leaves are infected first; younger leaves are infected later in the growing season. Disease incidence increases as host plants approach harvest. Several other plant
species are hosts.
Distribution.
Nigeria.
Symptoms.
Dark brown circular spots (23 mm in diameter initially) that occur on leaves enlarge to 20 to 30 mm in diameter. Spots tend to be zonated: the dark brown center is
surrounded by a light brown zone, a thin dark brown ring, and finally a light brown margin. Spots may coalesce. Petioles and midribs have dark brown spots; later
veins become brown, starting from the midrib.
Disease causes a reduction in sugars, phenol, and nicotine alkaloid content of leaves and an increase in nitrogen content. The reduction of phenol content causes an
undesirable aroma.
Management
1. Harvest on time since mature leaves are likely to become infected.
2. Do not grow any known alternate host, such as cotton, soybean, cow

Page 828
pea, cucumbers, lupines, and watermelons, in the vicinity of tobacco fields.
Cause.
Curvularia verruculosa.
Distribution.
India.
Symptoms.
Spots that appear on diseased leaves as round to oval areas with concentric zones enlarge rapidly and affect the entire lamina. Conidia and conidiophores appear on
both leaf surfaces. Diseased leaves initially are yellow but later turn dark brown.
Management.
Do not rotate tobacco with rice.
Damping Off
Cause.
Pythium spp., including P. aphanidermatum, P. debaryanum, and P. ultimum. Other Pythium spp. may also be involved. The fungi survive in soil as oospores and
chlamydospores, which are sometimes referred to as sporangia in the literature. Although dissemination is by any means that moves soil, water is the most important.
Both structures germinate by germ tubes or form zoospores, which in turn, produce germ tubes that infect host stems and roots at or just below the soil line. Oospores
are eventually formed in diseased tissue. Damping off is more severe in watersaturated soils at temperatures below 24°C.
Distribution.
Symptoms.
Damping off is primarily a problem in plant beds. Commonly a brown, watery, soft rot that develops on hypocotyls soon girdles the hypocotyls and causes seedlings
to fall over. Roots may also be diseased and decayed.
Older seedlings become chlorotic. The roots have a soft, watery rot and the cortex eventually peels away from the wooden central cylinder. If plants are infected at
the soil line, roots are not rotted and remain white.
Transplants have brown, watery lesions that cause stems to become limp, shrivel, and disintegrate. Plants suddenly wilt and die, especially when weather is cool and
damp following setting.
Management
1. Disinfect seedbeds.
2. Avoid wet soils as plant bed sites.
3. Avoid dense stands and provide adequate ventilation during wet, humid periods.
4. Apply fungicide.
5. Disk and reset the field if loss of transplanted seedlings is high. New rows should be placed in the middle between the old diseased ones.

Page 829
Dead Blossom Leaf Spot
Cause.
Botrytis cinerea and Sclerotinia sclerotiorum. (See "Collar Rot." Botrytis cinerea is also discussed under "Gray Mold.")
Distribution.
Symptoms.
Diseased flowers fall and adhere to leaves. Small dark spots that develop on leaves where the flowers have fallen eventually become larger and brown to gray. During
wet weather, a spot may enlarge enough to cover half of a diseased leaf. If the midrib is rotted, the leaf becomes yellow and hangs down. Brown lesions several
centimeters long may occur on stems and cause all leaves above the lesion to die.
Management.
No practical management exists for dead blossom leaf spot except lateflowering cultivars are usually less affected than earlyflowering cultivars.
Frogeye
The curing phase of frogeye is called barn spot or green spot.
Cause.
Cercospora nicotianae (syn. C. apii, f. sp. nicotianae) overwinters as mycelia in infested tobacco residue and in the residue of other plant hosts. In the spring,
conidia are produced and disseminated by wind and splashing rain to host leaves. Mature leaves are most susceptible to infection; subsequent lesions usually occur on
the lower leaves. Disease development is more severe during warm, wet weather.
Distribution.
Africa, Central America, Southeast Asia, and the United States.
Symptoms.
Frogeye symptoms may occur on both seedlings and plants in the field. Lesions are small (215 mm in diameter) and brown, gray, or tan and have a "paperlike"
center. Dark dots, which are groups of conidia and conidiophores, may be found in lesions. Near harvest time, the upper leaves develop large necrotic spots,
particularly during wet weather, and are quickly destroyed. During dry weather, frogeye lesions may be only the size of a pinpoint.
Disease results in significant decreases in sugar and nicotine alkaloid content.
Management
1. Sow only seed that is free of disease.
2. Remove residue from plant beds.
3. Apply foliar fungicides before transplanting.
4. Do not overfertilize with nitrogen.
5. Prime tobacco before it becomes overripe.
6. Plow under infested residue in the field.
7. Rotate tobacco with other crops.
8. Cure at a temperature of 38°C and 100% relative humidity.

Page 830
Fusarium head blight is also called blotch and scab.
Cause.
Hymenula affinis (syn. Fusarium affine) was originally identified as Septomyxa affinis. Fusarium head blight is most severe in plant beds during wet years or in
damp, shaded areas of the plant bed. Lightcolored nitrogenstarved plants and those diseased with black root rot are more susceptible to infection by H. affinis.
Distribution.
The United States and Zimbabwe.
Symptoms.
Diseased upper leaf surfaces, petioles, and stems have olivebrown, irregularshaped blotches and streaks. During wet weather, diseased plant parts develop a soft
rot, which results in the leaves having a ragged appearance. The petioles and stems eventually decompose. Slightly diseased plants recover when they are transplanted
to the field.
Management.
Not reported.
Fusarium Wilt
Cause.
Fusarium oxysporum (syn. F. oxysporum f. sp. nicotianae) survives as chlamydospores in soil and infested residue, as mycelia in infested residue, and on roots of
symptomless hosts. Fusarium oxysporum is disseminated in tobacco transplants and by any means that moves soil. Chlamydospores germinate and form mycelia that
grow from the residue to host roots, where entry is gained into the roots through wounds. Mycelium then grows into the xylem, or waterconducting, tissue.
Wilt severity is increased in the presence of the tobacco cyst nematode, Globodera tabacum. This phenomenon is most pronounced with high nematode numbers,
low fungal population densities, and Fusariumresistant tobacco lines.
Macroconidia and microconidia are produced on the outside of moribund plant tissue. Microconidia are also formed in the vessels of xylem tissue. Mycelial cells,
macroconidia, and microconidia are converted into chlamydospores and returned to soil when the diseased tissue decomposes. Fusarium wilt is most severe at soil
temperatures from 28° to 31°C.
Distribution.
Symptoms.
Initially, leaves on one side of diseased plants are dwarfed and yellowed. Eventually, the leaves wilt and become brown. The plant top usually becomes yellow and
bends toward the affected side of the diseased plant. This condition may continue for some time before the diseased plant wilts and dies. When the soft outer bark of
the stem is removed, the surface of the exposed wood is dark chocolate brown.

Page 831
Management
2. Fumigate soil with a nematicide where nematodes are a problem.
3. Rotate tobacco with a resistant crop. Flucured, but not burley and dark, tobacco can be grown in rotation with cotton. Do not grow sweet potatoes in the same
rotation with cotton.
Gray Mold
Cause.
Botrytis cinerea, teleomorph Botryotinia fuckeliana, survives as sclerotia in soil and infested residue, and as saprophytic mycelia on the residue of several plant
hosts. Sclerotia germinate during wet weather and produce mycelia on which conidia are borne and disseminated by wind and splashing rain to tobacco. Stalkcut
tobacco is infected through wounds and injuries. Sclerotia are formed on the surface of diseased tissue.
Distribution.
Symptoms.
The first symptoms occur as spots on the lower diseased leaves when seedlings are ready to be transplanted. If the weather is dry after infection has been initiated and
subsequent disease has started, spots are limited in growth and become brown with a yellow margin. Conversely, during wet weather, a gray mycelial growth covers
the spots and diseased leaves collapse but remain attached to stems. The fungus grows from leaf petioles into the stem and causes lesions several centimeters long that
are covered with gray mycelial growth. Diseased plants usually die; however, slightly diseased plants recover during dry weather.
Management
1. Place seedbeds on a welldrained site with adequate ventilation.
Olpidium Seedling Blight
Cause.
Olpidium brassicae survives in soil and infested residue as resting sporangia. In the presence of moisture, sporangia discharge zoospores that "swim" to roots, where
they encyst. The cyst protoplast moves through the host wall and establishes itself in the host cytoplasm. Resting sporangia eventually form in roots. Olpidium seedling
blight is most severe in moist and cool soils at temperatures from 10° to 16°C.
Distribution.
Symptoms.
The aboveground portions of a diseased plant will yellow and wither. Roots have a brown decay.
Management.
Fumigate seedbeds.

Page 832
Cause.
Phyllosticta nicotiana. Nicotiana is sometimes spelled "nicotianae" in the literature. Other Phyllosticta species reported on tobacco are P. tabaci, P. capsulicola,
and P. nicotianicola.
Phyllosticta nicotiana overwinters as pycnidia in infested residue and is seedborne. Phyllosticta nicotiana is disseminated into fields on transplants. During wet
weather, pycnidiospores are produced in pycnidia and disseminated by wind and splashing rain to "stressed," dead, or dying tobacco leaves, where infection occurs.
Distribution.
Africa, the Caribbean, Europe, South America, and the United States.
Symptoms.
Leaf lesions are brown irregularshaped (110 mm in diameter) zonate spots. Lesions are dark brown in the center and lighter brown toward the lesion margin and
have a chlorotic halo that surrounds the brown or necrotic areas. Pycnidia, which appear as small black dots, are embedded in the necrotic tissue.
Other symptoms are small white spots whose centers fall out and give the diseased leaf a shothole effect. Eventually, large white blotches occur that grow up to 15
mm in diameter. Sometimes all interveinal tissue falls out, which gives a diseased leaf a skeletal appearance. Pycnidia develop in the white tissue surrounding the shot
holes.
Management.
Phyllosticta leaf spot is rarely severe enough to warrant disease management measures.
Powdery Mildew
Cause.
Erysiphe cichoracearum overwinters as perithecia on infested residue, and as mycelia in tobacco plants and weed hosts left standing in a field after harvest. Primary
inoculum is either ascospores that are released from perithecia or conidia produced on mycelia. Both spore types are disseminated by wind to host leaves. Secondary
inoculum is provided by conidia produced on leaves that are airborne to other host plants. As tobacco matures, perithecia form in fungal growth on diseased leaves
and stems.
Erysiphe cichoracearum is tolerant of a wide range of temperatures and humidities. Disease development is more severe under reduced light intensity.
Distribution.
Africa, Asia, Central America, Europe, and South America.
Symptoms.
Plants in the field do not display symptoms until approximately 6 weeks after planting. The initial feltlike patches that appear on diseased lower leaf surfaces eventually
cover the entire leaf surface. Soon, a powdery gray layer consisting of conidia, conidiophores, and mycelium covers both

Page 833
leaf surfaces. Eventually, brown spots appear on the diseased upper leaf surfaces.
Diseased leaves become thin and "papery" in texture. The black, round perithecia that form on diseased leaf surfaces can be viewed with a hand lens.
Management
2. Properly fertilize soil.
3. Plant tobacco early.
Rhizoctonia Leaf Spot
Cause.
Rhizoctonia solani AG22 and AG3, teleomorph Thanatephorous cucumeris. Rhizoctonia leaf spot is favored by cool, wet weather.
Distribution.
Brazil, Costa Pica, and the United States (North Carolina).
Symptoms.
Rhizoctonia leaf spot occurs on flucured tobacco. The initial symptom is small, circular, watersoaked spots that rapidly expand into light green to tan lesions (26 cm
in diameter) with an irregular margin. The tissue within lesions is almost transparent and often displays a pattern of concentric rings. This transparent tissue frequently
drops out and gives a shothole appearance to diseased leaves. Fungal mycelia may be present at the margins of lesions on the undersides of diseased leaves.
Occasionally a hymenial layer and the basidiospores of T. cucumeris are observed in these same locations.
Lesions are most common on the lower leaves of a diseased plant but may occur as high on a stalk as 85 cm above the soil.
Management.
Not reported.
Rhizopus Stem Rot
Cause.
Rhizopus arrhizus. Rhizopus stem rot is apparently favored by high temperatures that occur during the summer months.
Distribution.
Iraq, on Nicotiana glauca.
Symptoms.
Initially, pale green, watersoaked lesions appear on the stems immediately below the inflorescence. Disease symptoms extend upward and downward from the
original lesion and result in a slimy, wet rot of cortical tissues. Lesions may be confined to one side of the diseased stem or may completely encompass it. Leaf petioles
attached to diseased portions of the stem become flaccid and die. Diseased stem tissues appear pale to yellowbrown when dry. Frequently a flower head will topple
downward, bending over at the diseased portion of the stem but remaining attached to the

Page 834
plant, or be broken off by strong winds. Severe disease results in plant death. Fluffy mycelial growth of R. arrhizus is visible in the piths of diseased stems.
Management.
Not reported.
Rust (Puccinia substriata)
Cause.
Puccinia substriata. Aecia are produced on tobacco; uredinia and telia stages occur on various grasses, including Paspalum spp., Digitaria spp., and Setaria spp.
Puccinia substriata is a weak pathogen that infects tobacco plants during the rainy season.
Distribution.
Honduras, Nicaragua, and Zimbabwe.
Symptoms.
Diseased tobacco leaves are severely spotted. Round, raised lesions (1 cm in diameter) composed of thick, hard tissue occur on diseased upper leaf surfaces and
remain a light green after curing. Aecia, which form on the undersides of lesions, have dense concentric rings that vary in color from cream to orange. Advanced
symptoms of what is thought to be the same disease cause tissues to turn black and fall out, leaving a hole in the diseased leaf.
Management.
Not necessary.
Rust (Uredo nicotianae)
Cause.
Uredo nicotianae. Uredinia are produced on tobacco.
Distribution.
Brazil, Italy, and the United States (southern California).
Symptoms.
Brown sori are produced on diseased leaves.
Management.
Not necessary.
Sooty Mold
Cause.
Fumago vagans grows on honeydew secreted on leaves by aphids, but the fungus does not infect the tobacco plant itself.
Distribution.
Formosa, Italy, Japan, the United States, and Zimbabwe. Sooty mold rarely occurs on tobacco.
Symptoms.
The lower mature leaves are most often affected. Fungus mycelium, chlamydospores, and conidia occur as a superficial black film or sooty layer that can be easily
scraped from leaf surfaces with a fingernail.
Management.
Control aphids.

Page 835
Soreshin
Soreshin is also called canker, collar rot, blackleg, rotten stalk, stem rot, and soreshank.
Cause.
Rhizoctonia solani, teleomorph Thanatephorus cucumeris, persists as mycelia and sclerotia in soil, as a saprophyte on the residues of a large number of plant
species, and as a parasite and pathogen on the roots of weeds and other crops grown in rotation with tobacco. Thanatephorus cucumeris survives for a few weeks
as basidiospores in soil.
Roots are infected by mycelia from germinating sclerotia and basidiospores, or directly from mycelia growing in soil and from infested residue. Rhizoctonia solani is
disseminated as sclerotia and mycelia by any means that moves soil or residue. Disease development can occur over a wide temperature range in either relatively dry
or moist soils. Soreshin can occur during temperatures of 20°C and lower in a plant bed and during relatively high temperatures in the field.
Distribution.
Wherever tobacco is grown. Soreshin is generally not a serious disease.
Symptoms.
A dark brown decayed area occurs at or near the soil line on the stems of seedlings and transplants and extends upward and around the stems until the plant topples
over. If slightly diseased plants are set in a field during cool, wet weather, a poor stand will result.
A dark brown lesion occurs at or near the soil line on the stems of older diseased plants in the field and eventually girdles the stem. The canker may extend up the stem
to the lower leaves and cause them to drop off. The woody part of the diseased stalk becomes hard and brittle, and the pith is decayed, dried, and brown. Light gray
patches of mycelium may be present in the diseased stalk. The entire plant may appear stunted, yellow, and wilted.
Diseased plants are usually not noticed until the wind, or another force, topples the plant over. Roots generally remain healthy until the plant dies.
Management.
Management measures can be used in the plant bed but not in the field. Experimentally, Trichoderma harzianum added to seedbeds fumigated with methyl bromide
before seed was sown controlled R. solani. Triadimenol fungicide integrated with T. harzianum enhanced disease management.
1. Grow plants on a welldrained soil.
2. Disinfect seedbeds with steam or a fumigant.
Southern Stem and Root Rot
Southern stem and root rot is also called southern blight.

Page 836
Cause.
Sclerotium rolfsii, teleomorph Athelia rolfsii, survives as sclerotia in soil and on infested residue, and as mycelia in infested residue. Sclerotium rolfsii is
disseminated as sclerotia in seed lots and by any means that moves soil. Sclerotia germinate and form infection hyphae that penetrate the host plant stalk. Infection also
occurs by mycelium growing from precolonized host plant residue. Sclerotia are formed on the outside of diseased tissue.
Southern stem and root rot is more severe at high temperatures (30° to 35°C) and high soil moisture. Sclerotium rolfsii is killed by low temperatures.
Distribution.
Wherever tobacco is grown in warm climates.
Symptoms.
Diseased plants are usually scattered throughout a field but may occur in groups within a field. Initially, a yellowing and wilting of diseased lower leaves occurs that
gradually progresses up the plant. Eventually, leaves die and turn brown. The stem at the soil line has a dry, brown, sunken canker that completely girdles the stem.
The roots usually do not decay until the entire diseased plant dies. Under moist conditions, a white, cottonlike mycelium occurs on the canker Later, small, white to
dark brown sclerotia the size of mustard seeds appear on and in the mycelium.
Management
1. Bury infested residue at least 8 cm deep.
2. Do not place soil containing organic matter against stems when cultivating.
Target Spot
Target spot is also called Rhizoctonia leaf spot.
Cause.
Thanatephorus cucumeris, anamorph Rhizoctonia solani AG3. Disease is associated with periods of frequent rainfall and below normal temperatures of 20° to 30°
C in June and July in North Carolina. Basidiospores are produced either on diseased plants or on infested plant residue on the soil surface and disseminated by wind
to other plant hosts.
Distribution.
Brazil, Canada (Ontario), Costa Pica, South Africa, the United States (Kentucky, North Carolina, South Carolina, Tennessee, and Virginia), and Zimbabwe. Target
spot probably occurs worldwide.
Symptoms.
Plants of all ages become diseased. Target spot occurs on plants in the seedbed or greenhouse only after leaves are large enough to close the canopy. The disease
occurs in the field after plant leaves are large enough to shade the soil surface and the lower leaves of the plant.
Initially, symptoms are small (23 mm in diameter), circular, watersoaked spots. When diseased leaves on seedlings are held up to a light

Page 837
source, lesions have a ''netlike" appearance. The initial lesions usually remain distinct even as they enlarge. During high relative humidity and moderate temperature,
lesions enlarge rapidly, become light green and almost transparent, and have irregular margins and chlorotic halos. In less humid conditions, lesions expand more
slowly and develop a pattern of concentric rings similar to lesions of Alternaria brown spot. A chlorotic halo is present around many expanding lesions. The necrotic
tissue becomes brittle and often drops out, giving a shothole appearance to the diseased leaf.
Mycelium is often present at lesion margins on the top and bottom leaf surfaces. Hymenial layers with numerous basidiospores are produced on both the diseased
upper and lower leaf surfaces.
Management
1. Practice sanitation to prevent introduction of inoculum into seedling production beds or greenhouses.
2. Limit wetting of foliage in the greenhouse by proper spacing and ventilation, and by flood irrigating.
3. Eliminate primary inoculum from previously used trays with methyl bromide and steam treatments of 80°C for 0.5 to 2.0 hours.
Tobacco Stunt
Cause.
Glomus macrocarpum is an endogonaceous mycorrhizal fungus that sporulates profusely on the roots of severely stunted plants.
Distribution.
The United States (Kentucky).
Symptoms.
Diseased plants are stunted, flowering is delayed, and yield and quality are reduced. Roots do not become necrotic, and diseased plants are seldom killed. Since roots
apparently are not colonized by arbuscules or external hyphae, interference with the hormonal control of root initiation may be the mechanism of stunting rather than
competition for photosynthate.
There is a significant reduction in the number of propagules of Thielaviopsis basicola in soil.
Management.
Experimentally, tobacco stunt is managed by soil fumigation.
Verticillium Wilt
Cause.
Verticillium dahliae and V. alboatrum. Verticillium spp. survive as microsclerotia in soil and infested residue. Microsclerotia germinate and produce
chlamydospores or conidia, which in turn germinate and produce hyphae that infect host roots and grow into the xylem tissue. Microsclerotia are abundantly produced
in diseased tissue and are released into soil when residue decays. Microsclerotia and conidia are disseminated by

Page 838
wind, water, and any means that moves soil. Verticillium wilt is most severe when abundant moisture follows dry weather at temperatures of 22° to 28°C.
Distribution.
Wherever tobacco is grown. Verticillium wilt is a severe disease in New Zealand.
Symptoms.
Symptoms are not obvious until flowering time. One or more lower leaves on a diseased plant wilt, particularly during hot weather. Eventually, the interveinal areas of
lower wilted leaves turn a bright orange or orangeyellow, then become chlorotic. Eventually, the tissue dies, becomes brown, and has an orange border between the
living and dead tissue. Wilting sometimes occurs on one side of a diseased leaf or on one side of an entire plant. However, all leaves on a diseased plant eventually die.
The vascular system of leaves, petioles, and stems becomes light brown.
Management
1. Fumigate plant beds.
2. Manage nematodes.
Brown Root Rot
Cause.
Pratylenchus spp., particularly the lesion nematodes P. pratensis, P. brachyurus, and P. zeae. The nematodes overwinter as adults, eggs, or larvae in roots and soil.
Eggs are deposited in root tissue and hatch in 6 to 17 days. The resulting larvae will either continue to feed in the same root or emerge and migrate to another host
root. Eggs may also be deposited into soil by decaying roots. The larvae penetrate the root and migrate within the infected plant but mainly in the cortex.
The different lesion nematodes are favored by different soil temperatures; therefore, disease development can be expected to occur over a wide temperature range.
Although lesion nematodes are sensitive to drying, soil moisture ordinarily is not a factor in disease development.
Distribution.
Symptoms.
Symptoms usually occur in a defined area in a field, but occasionally an entire field may be affected. Diseased plants are stunted and wilt during the day, recover their
turgidity at night, but repeatedly wilt again. Eventually, the repeated wilting causes leaves in the middle and lower portions of stalks to have brown and necrotic
margins.
Roots, at first, will have colorless and watersoaked lesions. Eventually,

Page 839
cortical lesions vary from pale yellow to dark brown or black and girdle feeder roots. Lesions break open and cortical tissue sloughs off, leaving only the vascular
cylinder. Numerous adventitious roots often develop above a lesion and give a diseased root a bushy appearance. Diseased roots shrivel and die, resulting in extensive
root pruning. If pruned roots are numerous, the root system will also have a stubby appearance. Severely diseased plants can easily be pulled from the soil because of
the almost complete destruction of the root system. The surviving roots are usually grouped near the soil surface.
Management
1. There are no resistant cultivars, but some cultivars are injured less than others.
2. Crop rotation. Do not grow tobacco after timothy, rye, maize, cotton, bluegrass, and legumes since these plants support large populations of Pratylenchus spp.
Some of these plants also release toxic chemicals that may harm tobacco roots; therefore, crops should be turned over in time to allow for decomposition of residue
before planting tobacco.
Bulb and Stem
Bulb and stem is also called stem break.
Cause.
Ditylenchus dipsaci survives as the fourth larval stage in dry plant material and as larvae and eggs in the soil for several years. Eggs hatch and the resulting larvae
migrate to host plant roots and up the plant in a film of water. Larvae, which enter the stem through stomates, lenticels, and wounds, are confined to cortical tissue.
Stem break is favored by cool temperatures (15° to 20°C) and wet weather. Disease incidence is usually more severe on plants grown in moist loam or clay soils.
Ditylenchus dipsaci has a wide host range.
Distribution.
France, Germany, Holland, and Switzerland.
Symptoms.
Young plants become more severely diseased than do older ones. Initially, small, yellow swellings or galls on diseased stems may occur up to 40 cm or more above
the soil level. Older galls die, causing stems to turn black. Diseased plants stop growing and the upper leaves become yellow, while the lower ones fall off. Eventually,
stems break and plants fall over but the vascular system remains intact. Therefore, wilting usually does not occur until just before plants break over.
Management
1. Remove diseased plants from fields.
2. Rotate tobacco with resistant crops for long intervals.
3. Fumigate soil with nematicides.
4. Apply contact nematicides to plants.

Page 840
Cyst
Cause.
Globodera solanacearum (syn. G. virginiae) and G. tabacum survive as eggs in soil and as larvae in cysts. Dissemination is by any means that moves soil. Larvae
emerge from cysts and migrate to roots, where they begin to feed with their heads in the stele of the rootlet. Females become spherical and break through the root
epidermis with only their heads and necks remaining in the root. The female is fertilized by males and eggs are produced in the female body. Many eggs hatch and
reinvade rootlets. When females die, their bodies become resistant cysts containing hundreds of eggs. Injury is most severe under continuous tobacco culture.
Distribution.
The eastern United States.
Symptoms.
Diseased plants wilt; they are stunted and have a small root system. Dark brown oval cysts (0.5 mm in diameter) are attached to roots.
Management
1. Rotate to a nonhost crop. Fescue has proven successful in Virginia.
3. Grow resistant cultivars; however, these cultivars are not tolerant.
4. Practice sanitation with equipment and irrigation water.
Dagger
Cause.
Xiphinema americanum.
Distribution.
The United States (North Carolina).
Symptoms.
Diseased plants are stunted and have a reduced root system.
Management.
Not reported.
Foliar
Cause.
Aphelenchoides ritzemabosi.
Distribution.
Unknown.
Symptoms.
Aphelenchoides ritzemabosi attacks buds and foliage, causing retarded growth and small, distorted foliage. On some diseased plants, leaf spots and defoliation
occur. Symptoms on tobacco are uncertain.
Management.
Not known.
Lesion
Cause.
Pratylenchus brachyurus and P. penetrans are endoparasites. All stages of the nematode overwinter in soil and in living and dead host roots. Dissemination is by
any means that transports soil. Eggs are deposited in the

Page 841
cortex of host roots and in soil. Juveniles feed in the same root as the egg was deposited in or migrate to other roots. Eggs released into soil also hatch and the
juveniles are attracted to host roots by root exudates. The juveniles penetrate through the root cortex and feed on cells, thereby destroying them.
Distribution.
Worldwide.
Symptoms.
Diseased plants occur singly or in small groups. Plants are stunted, chlorotic, and wilt during the day. Leaves have chlorotic margins that eventually become necrotic.
Watersoaked spots that occur behind the root growing point become tan to black and may girdle the root. Cortex tissues slough off, leaving only the vascular
cylinder. Extensive root pruning may give root systems a stubby appearance. Diseased plants may be easily pulled from the soil.
Management
1. Rotate tobacco with nonhost crops.
2. Grow the most tolerant cultivars.
Reniform
Cause.
Rotylenchulus reniformis is an ectoparasite.
Distribution.
Unknown.
Symptoms.
Diseased plants are stunted and have a retarded root system.
Management.
Unknown, but it is likely that measures for managing other nematodes on tobacco will aid in managing reniform nematodes.
Root Knot
Cause.
The root knot nematodes Meloidogyne arenaria, M. hapla, M. incognita, and M. javanica survive in soil as eggs and larvae, and in galls and roots as adults and
eggs. Eggs in soil hatch and produce larvae that move through soil water and enter roots, where they remain the rest of their lives. Nematodes are disseminated by any
means that moves soil. When females are mature, eggs are produced in a sac that emerges from female genital openings prior to egg production. Eggs are released into
the soil as the diseased roots, together with the galls, decay.
Nematodes survive with difficulty at subzero temperatures. Meloidogyne arenaria, M. incognita, and M. javanica do not survive if the temperature averages below
3°C during the coldest month. Meloidogyne hapla is limited by temperatures greater than 23°C. Disease is ordinarily more severe in lighter sandy soils but may occur
in any soil type. Soil moisture is not an important factor in disease development. Different races or strains of Meloidogyne spp. exist.

Page 842
Distribution.
Symptoms.
Diseased plants occur at random throughout a field and are noticed by their stunted and yellowed appearance. Plants may occasionally be killed, especially during dry
weather. Plants may wilt during the day but recover their turgidity at night; subsequent wilting reoccurs until leaves in the middle and lower part of diseased plants
develop necrotic margins and tips.
Galls form on roots and vary in size from a pinhead to several times the thickness of the root. Galls vary in shape from irregular to spherical and are most often found
on rootlets, where they resemble beads on a string. Galls may form so close together that they resemble one large gall.
Management
1. Grow resistant cultivars. Resistance to M. incognita races 2 and 4 and moderate resistance to M. javanica have been identified.
2. Treat soil with a nematicide.
3. Rotate tobacco with resistant crops, such as small grains. Plant tobacco in the same soil only once every 3 to 4 years.
4. Plow or disk as soon after harvest as possible. Exposing roots to the drying action of the sun and air kills many nematodes. As long as tobacco stalks and root
systems are left in the field undisturbed, plants will be alive and nematodes will continue to live and reproduce in them.
Spiral
Cause.
Helicotylenchus spp.
Distribution.
Unknown.
Symptoms.
Diseased plants are stunted and have a retarded root system.
Management.
Unknown, but it is likely measures that aid in managing other nematodes on tobacco will reduce populations of spiral nematodes.
Stubby Root
Cause.
Paratrichodorus spp. and Trichodorus spp. are nematodes with a wide host range. Little is known of their life cycle, but survival likely occurs as eggs, larvae, and
adults in soil. An increase in nematode population is favored by soil temperatures of 22° to 30°C and wellaerated, light sandy soils. Trichodorus spp. are found at
depths down to 100 cm in the soil profile.
Distribution.
Throughout the world.
Symptoms.
Plant growth is retarded. Diseased plants wilt easily, even in the presence of moisture. Root tips stop growing, which results in a few short, stunted, stubby roots.

Page 843
Management.
Same as for root knot, but stubby root nematodes are more difficult to manage.
Stunt
Cause.
Merlinius spp. and Tylenchorhynchus spp. Tylenchorhynchus claytoni, the principal stunt nematode infecting tobacco, survives for several months in soil as eggs,
larvae, and adults if the soil does not become dried out. The nematode has a wide host range.
Distribution.
Canada and southeastern United States.
Symptoms.
Diseased plants are stunted and have a small root system. Diseased roots are shriveled and flaccid, do not elongate normally, and, in general, are poorly developed.
Management
2. Treat soil with a nematicide.
3. Rotate tobacco with resistant crops, such as small grains. Grow tobacco in the same soil only once every 3 to 4 years.
4. Plow or disk as soon after harvest as possible. Exposing roots to the drying action of the sun and air kills many nematodes. As long as tobacco stalks and root
systems are left in the field undisturbed, plants will be alive and nematodes will continue to live and reproduce in them.
The diseases of tobacco caused by phytoplasmas tend to be similar in symptoms and management practices.
Aster Yellows
Cause.
Aster yellows phytoplasma infects and persists in more than 175 species of plants. It is disseminated by several species of leafhoppers, including Aphrodes bicintus,
Hyalesthes obsoletus, Euscelis plebejus, Macrosteles fascifrons, M. laevis, and others. The phytoplasma multiplies in leafhoppers and overwinters in leafhopper
eggs and adults. The optimum temperature for multiplication in plant and insect tissue is 25°C. Leafhoppers may be blown by the wind or fly several hundred
kilometers.
Distribution.
Symptoms.
Diseased plants are stunted. Apical leaves are small, whitish, and curled. Older leaves have interveinal necrosis and hang close to the stem.

Page 844
Numerous small leaves are present on sucker growth. Flowers change to green leaflike structures that are intermingled with numerous short, stiff branches. The
proliferation of floral parts results in a compact, tufted growth habit.
Management
1. Eliminate weed hosts in tobacco fields and in fields adjacent to tobacco fields.
2. Plant only transplants that are free of disease.
3. Avoid growing tobacco near other host plants, such as potatoes, tomatoes, and peppers.
4. Plant when leafhopper populations are low.
5. Harvest and cure separately if only a few plants are diseased.
Bigbud
Cause.
Bigbud phytoplasma infects and persists in several species of plants. The bigbud phytoplasma overwinters in the eggs and adults of the leafhopper Orosius
argentatus. Later, the phytoplasma multiplies in and is disseminated by the same leafhopper. The leafhopper does not breed on tobacco, so transmission occurs
during periods of migration in late spring and early summer. Conditions favoring leafhopper flight are a 9:00 p.m. temperature above 27°C, high humidity, and no wind.
Distribution.
Australia.
Symptoms.
Symptoms are similar to those of aster yellows. Diseased plants are stunted. Apical leaves are small, whitish, and curled. Older leaves have interveinal necrosis and
hang close to the stem. Numerous small leaves are present on sucker growth. Flowers change to green leaflike structures that are intermingled with numerous short,
stiff branches. The proliferation of floral parts results in a compact, tufted growth habit.
Management
5. Harvest and cure separately if only a few plants are diseased.
Stolbur
Cause.
Stolbur phytoplasma overwinters primarily in the common perennial bindweed, Convolvulus arvensis, and less often in several other species of plants and in the eggs
and adults of leafhoppers. Nicotiana glauca is a symp

Page 845
tomless host. The phytoplasma is disseminated and multiplies in several species of leafhoppers that are blown or fly several hundred kilometers. Stolbur phytoplasma
strains are vectorspecific; some strains are transmitted principally by one species of leafhopper. Leafhoppers inoculate the phytoplasma directly into the phloem.
Distribution.
Europe.
Symptoms.
Younger plants become more severely diseased than plants infected later in the growing season. Symptoms are less severe during cool weather. Diseased apical
leaves are small, whitish, and curled. Other diseased leaves have interveinal necrosis and hang close to the stem. Numerous small leaves are present on sucker growth.
Cured diseased leaves are more hygroscopic than are healthy leaves. When bulked with healthy leaves, diseased leaves interfere with fermentation and decrease
quality.
Flowers are changed to green, leaflike structures that result in a compact, tufted growth habit. Diseased plants do not set seed even though the pollen is healthy.
Diseased plants in general are stunted and form numerous short, stiff branches. Internal symptoms are a degeneration of the phloem and irregularities in meiotic
processes.
Management
5. Harvest and cure separately if only a few plants are affected.
Yellow Dwarf
Cause.
Yellow dwarf phytoplasma infects and persists in several species of plants and overwinters in the eggs and adults of the leafhopper Orosius argentatus. The
phytoplasma multiplies and is disseminated only by O. argentatus. Orosius argentatus does not breed on tobacco, so transmission occurs during periods of
migration in late spring and early summer. Infection may occur at any stage of plant growth but small, rapidly growing plants are highly susceptible. Conditions favoring
leafhopper flight are a 9:00 p.m. temperature above 26°C, high humidity, and no wind.
Distribution.
Australia.
Symptoms.
Plants are yellowish and dwarfed. They grow slowly and produce small leaves that are unsuitable for commercial use. Older diseased leaves become thick and
wrinkled. Root systems remain undeveloped.

Page 846
Management
5. Harvest and cure separately if only a few plants are affected.
Nicotiana glutinosa Stunt Viroid
Cause.
Nicotiana glutinosa stunt viroid (NgSVd) is a low molecular weight RNA. NgSVd is mechanically transferred to N. clevelandii, N. debneyi, N. plumbaginifolia,
Chenopodium amaranticolor, Cucumis sativus, Luffa acutagula, Cajanus cajan, and Vigna unguiculata.
Distribution.
India.
Symptoms.
Diseased plants are characterized by an epinasty of leaves, stunting, bunchiness, and occasional necrosis.
Management.
Not reported.
Alfalfa Mosaic
Cause.
Alfalfa mosaic virus (AMV) overwinters in a wide number of hosts and is transmitted by aphids. Several strains of AMV exist and all the strains may be found in one
plant.
Distribution.
Europe, Japan, New Zealand, and the United States. AMV has not been a serious disease of tobacco.
Symptoms.
Initially, chlorotic spots and blotches occur on diseased leaves. The first leaves infected systemically have a vein clearing followed by white rings, arcs, and coalescing
line patterns of necrotic tissue. Sometimes bud leaves are distorted and have a bright yellow mosaic.
Management
1. Isolate tobacco fields from sources of inoculum.
2. Control weeds and aphids.
3. Experimentally, salicylate watered into the soil prevented systemic infection by AMV.

Page 847
4. Some cultivars of Nicotiana tabacum display more severe symptoms than others, and some Nicotiana spp. display no symptoms when infected. Nicotiana
debneyi had no symptoms and a negative ELISA reading when inoculated with two AMV isolates.
Beet Curly Top
Cause.
Beet curly top virus (BCTV) is in the geminivirus group. BCTV overwinters in more than 244 species of host plants and is transmitted by the leafhoppers Circulifer
tenellus in North America and by Agallia albidula and Agalliana ensigera in South America. BCTV can persist up to 85 days in leafhopper vectors. The
acquisition period takes up to 2 days and the latent period in leafhoppers is from 4 to 24 hours. BCTV does not multiply in vectors, which causes leafhoppers to lose
infectivity in 8 to 10 weeks.
Young plants are most susceptible to infection. Different strains of BCTV exist.
Distribution.
Symptoms.
Initially, vein clearing occurs and leaf tips and margins bend downward. Larger veins are restricted in growth, which results in a rolling and crinkling of diseased leaves
and veins that are swollen in places. Flowers may also be distorted. Diseased plants in the field are stunted and have small, rugose leaves that curl downward.
Other strains of BCTV in the United States cause similar symptoms. Plants are stunted and have rugose, warty leaves that curl downward. Leaves fully grown at the
time of infection yellow and die. Sometimes diseased plants appear to recover.
Management
1. Fumigate plant beds.
2. Control weeds and other hosts in plant beds and fields.
3. Exclude insects from plant beds by using insectproof covers.
4. Apply insecticides periodically to plants in plant bed.
5. Plow under residue and any plants left after transplanting.
Bushy Top
Cause.
A combination of two viruses: the tobacco veindistorting virus (TVDV) and the bushy top virus (BTV). TVDV is in the luteovirus group. BTV may be a strain of
tobacco mottle virus. BTV can be transmitted by aphids only if TVDV is also present in the same plant.
Distribution.
Nyasaland and Zimbabwe.
Symptoms.
Plants infected early in their growth have severe symptoms. Excessive growth of axillary buds produces numerous brittle shoots and crisp leaves. Flowers are small but
set seed.

Page 848
Management
1. Sow early before aphid populations are too large.
2. Apply systemic insecticides.
3. Control all weeds in tobacco beds and in fields adjacent to tobacco fields.
4. Destroy all plants in beds after transplanting.
Clubroot
Cause.
Clubroot virus is transmitted by grafting.
Distribution.
The United States (Kentucky, Maryland, and Tennessee). Club root is a minor disease.
Symptoms.
Disease symptoms may be confused with those caused by the rootknot nematodes. Rootknot galls are found on small and large roots. Clubroot galls of various sizes
are usually only found on older roots. Diseased plants are stunted due to a shortening of the internodes and have curled and otherwise distorted leaves. Infrequently,
veins enlarge and enations form on the undersides of diseased leaves.
Management.
Not necessary.
Cucumber Mosaic
Cause.
Cucumber mosaic virus (CMV) is in the cucumovirus group. CMV overwinters in several perennial and annual host plants. Pollen of at least four Stellaria species can
be infected with virus; consequently, CMV overwinters in the seed of these plants. Several species of aphids are vectors, with Myzus persicae and Aphis gossypii
being the two principal vectors. CMV is nonpersistent and aphids retain the virus for less than 4 hours. Different strains of CMV exist. Some strains are efficiently
transmitted by aphids and other strains are not efficiently transmitted.
Distribution.
Wherever tobacco is grown. Disease is especially severe in Japan and wherever vegetables are grown.
Symptoms.
Symptoms are similar to tobacco mosaic virus. Pale green circular spots on diseased leaves give the leaves a mottled and mosaic pattern. Systemic infection initially
appears as a slight vein clearing that is followed by a mild, general mottling of the leaf. Sometimes diseased leaves are stunted and narrow.
Mild strains cause only a faint mottling of leaves. Severe strains may cause interveinal discoloration and an ''oakleaf" pattern of necrosis on diseased lower leaves. A
burn or sun scald sometimes appears on diseased upper leaves.

Page 849
Management
1. Control weed hosts in tobacco fields and in fields adjacent to tobacco fields.
2. Plant only diseasefree or certified transplants.
3. Grow a nonhost crop to act as a barrier between the source of inoculum and tobacco.
4. Do not grow tobacco near potatoes, tomatoes, and peppers.
5. Sow tobacco when aphid populations are low.
Eggplant Mosaic
Cause.
Eggplant mosaic virus, tobacco strain (EMVT), is in the tymovirus group. EMVT is readily transmitted mechanically and by the chrysomelid beetle Diabrotica
speciosa from eggplant to other solanaceous hosts, Chenopodium quinoa and C. amaranticolor.
Distribution.
Brazil.
Symptoms.
Chlorotic and/or necrotic spots and necrotic rings that develop on diseased plant leaves 5 to 7 days after inoculation are followed by vein clearing, vein banding, and
mosaic.
Management.
At present, EMVT is not considered of economic importance and does not interfere with plant productivity.
Leaf Curl
Cause.
Tobacco leaf curl virus (TLCV) is in the geminivirus group. TLCV survives in several different species of plants and is transmitted by the whitefly Bemisia tabaci and
possibly by other insects. TLCV is also grafttransmitted but is not seed or saptransmitted. The acquisition period is from 15 to 120 minutes. TLCV persists in the
vector for at least 6 days.
Leaf curl is more severe during dry weather and warm temperatures around 30°C because of the increased whitefly activity. Several strains of TLCV exist.
Distribution.
Leaf curl is most prevalent in tropical areas of Africa, Asia, Australia, Central America, and South America. Leaf curl has been found in Russia and Switzerland.
Symptoms.
The entire diseased plant is stunted and has small, twisted and curled leaves. The most characteristic symptom is the production of leaf outgrowths up to 1 cm wide on
the veins of diseased lower leaf surfaces. Outgrowths are a dark green thickening of sections of the veins. The smaller veins have either a vein clearing or a yellow
discoloration. In some cases, veins may be greener than normal. Sometimes leaf margins are rolled downward. Flower parts are curled and deformed. The loss of
apical dominance gives a broomlike appearance to diseased plants.

Page 850
Mild strains of TLCV cause little stunting. The uppermost leaves of nearly mature plants may be curled and twisted but other leaves appear normal.
Management
1. Control weeds in and adjacent to tobacco beds and fields.
2. Do not locate tobacco beds and fields near alternate hosts.
3. Apply insecticides or mulches to control white flies in seedbeds.
4. Destroy tobacco residue after the completion of harvest.
Nicotiana velutina Mosaic
Cause.
Nicotiana velutina mosaic virus (NVMV) is in the furovirus group. NVMV is transmitted by the soilborne fungus Polymyxa betae, which survives in field soil as
cystosori. Cysts give rise to zoospores that "swim" through free soil water until they contact a host root and encyst. Encysted zoospores produce a structure called a
stachel through which zoosporic cytoplasm enters the host cell and becomes a plasmodium. (Only primary root tissue of young roots is infected; the optimum
temperature for infection is 25°C.) The host cell then becomes infected with NVMV if P. betae is viruliferous. Later, the plasmodium develops into a zoosporangium,
which releases additional zoospores that repeat the infection cycle. However, some plasmodia develop into cysts, and often nearly every cell in the small feeder roots
will contain a cyst. As root cells senesce, cysts are eventually released into the soil, where they can remain viable for years without loss of virulence.
Distribution.
Australia.
Symptoms.
A bright yellow mosaic occurs on N. velutina. Etched ringspots, followed by a mild systemic mottling, occurs on N. tabacum, a systemic chlorosis occurs on N.
glutinosa, and a mosaic and leaf malformation followed by a necrosis occurs on N. ebneyi.
Management.
Not reported.
Peanut Chlorotic Streak
Cause.
Peanut chlorotic streak virus (PClSV) is in the caulimovirus group. PClSV is mechanically transmissible to several plants in the Leguminosae and Solanaceae. Disease
is favored by the very high temperatures of the semiarid tropics. PClSV is confined primarily to inoculated leaves unless plants are grown at temperatures above 28°C.
Distribution.
India.
Symptoms.
Young leaflets display oval chlorotic streaks along the veins 3 to 4 weeks after inoculation. Streaks are not distinct in older leaflets and can be

Page 851
seen only when viewed against light. In field infections, diseased plants are stunted and have chlorotic streaks on younger leaflets.
Management.
Not reported.
Peanut Stunt
Cause.
Peanut stunt virus (PSV) is in the cucumovirus group. PSV overwinters in a large number of host plants, primarily clover species and other herbaceous perennials.
Although PSV can be transmitted mechanically, the most prevalent means of spread is by aphids. Aphis craccivora, A. spiraecola, and Myzus persicae transmit
PSV nonpersistently.
Distribution.
Japan, the eastern United States, and the state of Washington in the United States.
Symptoms.
Diseased burley tobacco is stunted. Diseased young leaves have large areas of chlorotic tissue. Older diseased leaves have chlorotic tissue that borders small veins
and large veins have spots and rings of chlorotic tissue.
Flucured tobacco is stunted. Mosaic symptoms that resemble tobacco mosaic virus and ringspot lesions are present.
Management
1. Control weed hosts in tobacco fields and in fields adjacent to tobacco fields.
Pepper Veinal Mottle
Cause.
Pepper veinal mottle virus (PVMV) is in the potyvirus group. PVMV is transmitted by sap, grafting, and the aphid Myzus persicae. PVMV is closely related to
tobacco vein mottle virus.
Distribution.
Nigeria.
Symptoms.
Irregular vein banding of diseased leaves is the primary symptom. A systemic mosaic or chlorotic mottle fades with increasing age of leaves.
Management.
Not reported.
Ringspot
Cause.
Tobacco ringspot virus (TRSV) is in the nepovirus group. TRSV survives in a wide range of host plants, including cucumbers and other vegetables, soybeans, horse
nettle, ground cherry, pokeweed, sweet clover, les

Page 852
pedeza, and alfalfa. TRSV is mechanically transmitted easily and is seedtransmitted in several plants, notably soybeans. Several vectors transmit TRSV, notably all
stages of the nematode Xiphinema americanum. Other vectors are thrips, Thrips tabaci; mites, Tetranychus sp.; grasshoppers, Melanoplus differentialis; and the
tobacco flea beetle, Epitrix hirtipennis. Different strains of TRSV exist.
Distribution.
Australia, Canada, Europe, Formosa, Japan, Nyasaland, New Zealand, Russia, South Africa, Sumatra, and the United States.
Symptoms.
Symptoms may appear on diseased plants in the plant bed or shortly after seedlings are transplanted into the field. Initially, diseased leaves have either a few or
numerous necrotic rings, which become blanched or brown after a few days. Frequently, there are line patterns that parallel veins or occur as irregular wavy lines
between larger leaf veins. Leaves on only one side of the plant may be diseased. Severely diseased plants may be dwarfed and have small leaves of poor quality.
Pollen becomes sterile.
Management
1. Control nematodes in plant beds and fields.
2. Control weeds in and adjacent to plant beds and fields.
3. Do not grow tobacco after or next to other plant hosts for TRSV.
4. Control insects in plant beds and fields.
Tobacco Etch
Cause.
Tobacco etch virus (TEV) is in the potyvirus group. TEV overwinters in tobacco roots. Plants that grow from these roots are diseased. TEV also overwinters in
several different solanaceous plants, including horse nettle, Solanum carolinense, and ground cherry, Physalis virginiana. TEV is not seedborne and does not
survive in infested residue.
TEV is a nonpersistent virus transmitted by aphids. Because the probability of transmission does not depend on the number of virus particles acquired by the aphid
vector, aphid transmission requires relatively few virus particles. Consequently, aphids that make brief acquisition probes into plants diseased by TEV are as likely to
transmit virus as aphids that make longer probes or those that feed during the acquisition access. It is hypothesized that only those virus particles retained in the
presence of a helper component in the maxillary stylets or in the foregut of the vectors are involved in transmission.
Distribution.
Canada, Germany, Japan, and the United States.
Symptoms.
Tobacco etch is most important on burley tobacco. Symptoms in the field are first noticed when plants approach the flowering stage of plant growth. Vein clearing is
the first symptom to occur, followed by line

Page 853
patterns of necrotic tissue, or etching, and mottling. Young leaves have mild mosaic symptoms but tip leaves are not mottled. On older leaves, chlorotic spots up to 6
mm in diameter occur in the interveinal area and eventually become white and necrotic. Severely diseased plants may be stunted and have fired, chlorotic, and tattered
leaves at harvest time.
Management
1. Control perennial weeds.
2. Grow only certified transplants.
3. Destroy live tobacco stalks and roots.
4. Control aphids.
Tobacco Leaf Curl
Cause.
Tobacco leaf curl virus (TLCV) is in the geminivirus group, subgroup B. TLCV is transmitted by the whitefly Bemisia tabaci.
Distribution.
Worldwide, but severe disease occurs only in tropical areas. Tobacco leaf curl has caused significant losses in Venezuela.
Symptoms.
Diseased leaves are severely crinkled, curled, and dwarfed.
Management
1. Use insecticides to control the white fly vector.
2. Plant tobacco at the time of year when the vector population is lowest.
Tobacco Mosaic
Cause.
Tobacco mosaic virus (TMV) is in the tobamovirus group. TMV overwinters in several perennial weeds, including horse nettle, Solanum carolinense, and ground
cherry, Physalis angulata. TMV also persists in airdried tobacco and in infested residue in the field in the absence of freezing, desiccation, or complete rotting.
TMV is disseminated mechanically. Workers who chew or smoke tobacco, or handle infested residue or weed hosts and then touch live tobacco plants, are primary
sources of dissemination. Other means of spread occur during tillage, suckering, or other field operations. A species of large grasshopper may mechanically transmit
the virus as well as a leaf miner fly; however, these are not efficient vectors. TMV is transported systemically in the phloem of Nicotiana tabacum cv. Xanthi nc.
plants when TMV is dually inoculated with potato leafroll virus.
Distribution.
Symptoms.
Local lesions do not form on inoculated leaves, but under high temperature and light conditions, small, circular, faintly chlorotic spots may occur. Systemic infection
first causes a vein clearing of the youngest

Page 854
diseased leaf, which eventually becomes mottled and distorted. The outer leaf edge may turn slightly upward and form a rim around the leaf. Eventually, large blisters
of green tissue and raised, or sunken, yellow areas develop along with a marked mottling of dark and light green. Considerable malformation and distortion also occur.
Frequently, the leaf lamina may be so reduced that a "shoestring" effect is produced.
Management
1. Fumigate plant bed soils with a chemical that kills weeds and inactivates the virus.
2. Control weeds in and around plant beds.
3. Do not use tobacco while working in the seedbed.
4. Spray the plant bed with milk 24 hours before pulling. Laborers should dip hands in milk every 20 minutes while working with seedlings.
5. Rotate tobacco in a field every 2 years.
6. Rogue out any diseased plants prior to the first cultivation.
7. Grow resistant cultivars. Resistance has been reported to be related to the presence of the phenolic compounds scopolin or scopoletin.
Tobacco Necrosis
Cause.
Tobacco necrosis virus A (TNVA) is in the necrovirus group. TNVA infects and persists in a large number of host plant roots but not in the resting sporangia of the
soil fungus vector Olpidium brassicae. A second virus, tobacco necrosis satellite virus (TNSV), is found only in association with TNVA. TNSV has not been
demonstrated to multiply by itself and appears to be incapable of multiplication unless associated with TNVA.
The viruses are transmitted by the soil fungus O. brassicae, which, in turn, is disseminated by any means that moves soil. Particles of both viruses leak out of diseased
roots into soil water, where they are adsorbed to the flagella and plasmalemmae of O. brassicae zoospores. When the zoospores encyst, the flagella bearing the virus
particles are pulled into the cytoplasm of the zoospores. Upon germination of the encysted zoospore, the virus particles are carried along with zoospore cytoplasm into
the host root. Root infection can also occur when wounded roots are in contact with soil water that has a high content of virus particles. Both viruses are also
mechanically transmitted. TNVA is primarily restricted to the roots of various plants that appear to be symptomless. The viruses occasionally move out of the root
into the aerial parts of the plant, but they are arrested at a point just above the soil level.
Disease symptoms are more severe during cool temperatures and low light intensities. Different strains of the virus exist.
Distribution.
Europe, Japan, New Zealand, and the United States.
Symptoms.
Tobacco necrosis only occurs in young seedlings. The first symptoms are necrotic spots that often coalesce along the midribs and veins of

Page 855
diseased lower leaves. Only the lower and oldest leaves become necrotic and dry on older plants, but the rest of the plant appears normal. Very young plants may be
killed.
Management
1. Sterilize soil to kill O. brassicae.
2. Remove tobacco residue from plant bed areas.
3. Set only healthy transplants in the field.
Tobacco Rattle
Cause.
Tobacco rattle virus (TRV) is in the tobravirus group. TRV overwinters in at least 100 different plant species and is transmitted by both adult and juvenile nematodes
of the genus Trichodorus, including T. pachydermus, T. primitivus, T. christii, and T. alii. TRV contaminates stylets and enters roots through wounds made by
nematode feeding. TRV is rarely transmitted by the seed of some weed species. Transmission is favored by temperatures of 25°C and below.
Acquisition and transmission times are 1 hour each. TRV can be retained for 20 weeks in nematodes that have not fed but does not persist through eggs or molting.
Tobacco rattle is most prevalent on sandy soils.
Distribution.
Brazil, Denmark, Germany, Holland, Japan, Scotland, and the United States.
Symptoms.
Inverted spoonshaped leaves have spots and ring or line patterns of necrotic tissue. Diseased leaves become curled, have sinuate margins, and break and rattle when
touched. Discontinuous brown to gray stripes of sunken necrotic tissue develop on stems, petioles, and leaf veins.
Leaves infected with mild strains of TRV have numerous tan lesions that form rings. Systemically infected leaves are slightly distorted and mottled but there is little stem
necrosis. Little or no plant stunting occurs. Diseased plants usually recover and produce normalappearing leaves that are somewhat elongated and pointed at the tip.
Management
1. Fumigate or use nematicides to control nematodes in the plant beds.
2. Use nematicides in the field. Experimentally, salicylate watered into soil prevented systemic infection of white burley plants. Longdistance spread was likely
prohibited.
3. Rotate tobacco with resistant crops.
Tobacco Ringspot
Cause.
Tobacco ringspot virus (TRSV) is in the nepovirus group. TRSV is seedborne and overwinters or is reservoired in a large number of legumes. TRSV is sap
transmitted by nematodes, particularly the dagger nematode, Xiphinema americanum; nymphs of thrips, Thrips tabaci; grasshoppers,

Page 856
Melanoplus differentialis; and possibly other insects. TRSV is also transmitted by root grafts.
Distribution.
Worldwide.
Symptoms.
Normally only isolated plants are diseased, but severe losses may occur in some fields. Diseased plants have chlorotic rings on leaves or chlorotic Vshaped patterns
that emanate from secondary leaf veins and give the superficial appearance of an oakleaf pattern.
Management.
Not reported.
Tobacco Rosette Disease
Cause.
A combination of two viruses: tobacco veindistorting virus (TVDV) and tobacco mottle virus (TMoV). TVDV is in the luteovirus group. TMoV overwinters in
several plant species in the Solanaceae. TMoV is mechanically transmitted and is transmitted by the aphid Myzus persicae, but only if TVDV is also present in the
plant.
TVDV also overwinters in several plant species in the Solanaceae. TVDV is transmitted by M. persicae but is not transmitted mechanically. TVDV persists in aphid
bodies for long periods.
Distribution.
Nyasaland and Zimbabwe.
Symptoms.
Tobacco rosette may occur in plant beds or fields. Midribs of young diseased leaves are twisted and distorted and form a knot in the center of the plant that looks like
a rosette. Diseased leaves curl sharply at the tip. Diseased plants are stunted.
Diseased older plants do not become distorted, but leaves droop. If plants are diseased on only one side, the flower bends over. Splitting of stems and petioles may
also occur.
Management
1. Sow early, before aphid populations are too large.
2. Apply systemic insecticides.
3. Control all weeds in tobacco beds and adjacent fields.
4. Destroy all plants remaining in beds after transplanting.
Tobacco Streak
Cause.
Tobacco streak virus (TSV) is in the ilarvirus group. TSV survives in a large number of plants, including tomato, sweet clover, cotton, peanut, and several others. TSV
is transmitted mechanically and by dodder. Insects reported to transmit TSV are Frankliniella sp., F. occidentalis, and Thrips tabaci. In Australia, transmission was
attributed to pollen from the weed Ageratum houstonianum and the insect Microcephalothrips abdominalis.
Distribution.
Asia, Australia, Canada, Europe, and the United States.

Page 857
Symptoms.
Diseased leaves are smaller than normal, narrow, and slightly crinkled. Leaves may be affected on one side only, with the midrib curling toward the affected side.
Necrotic lesions are surrounded by watersoaked lines or rings that later become brown and necrotic. Lesions spread along veins, with parallel necrotic lines
appearing in the tissue surrounding the veins. Sometimes midribs and petioles collapse.
Systemic symptoms appear as a net pattern, rings, or partial rings in leaves. These symptoms are brown at first but later become graywhite and are closely associated
with the veins and bases of young leaves. Necrotic tissue often falls out of leaves.
Management.
No management is routinely practiced. However, other hosts, particularly sweet clover, should be eliminated from the vicinity of tobacco fields before transplanting
occurs.
Tobacco Stunt
Cause.
Tobacco stunt virus (TStV) infects and persists in a large number of host plants and in the soil fungus Olpidium brassicae for long periods of time, perhaps several
years. TStV is disseminated on infected transplants and by any means that moves soil. TStV is transmitted primarily by O. brassicae and, infrequently, mechanically
and by grafts. TStV is carried into the root by the zoospore cytoplasm and then multiplies both in the cytoplasm of the tobacco cells and in the developing zoospores.
Disease severity is increased by cool temperatures and low light intensities.
Distribution.
Japan.
Symptoms.
Symptoms first appear when seedlings have five to eight leaves. The first symptom is a vein clearing; later, the veins become necrotic. Eventually, small brown to white
necrotic spots or necrotic ringlike patterns develop on the bases of the lower diseased leaves. Bud leaves become generally yellow and have surface crinkles and tips
that curl downward. Internodes fail to develop, causing diseased plants to remain in the rosette stage. A band of necrotic tissue occurs on stems at the soil level.
Transplants moved to fields remain yellow and stunted. Frequently severely diseased plants die. Plants with mild symptoms have leaves and stems that are narrow, and
flower before normal plants do.
Management
1. Sterilize soil to kill O. brassicae.
2. Remove tobacco residue from plant bed areas.
3. Set only healthy transplants in the field.
Tobacco Veinal Necrosis
Tobacco veinal necrosis caused by PVY is sometimes called vein banding.

Page 858
Cause.
Potato virus Y strain N (PVY) is in the potyvirus group. PVY overwinters in several species of plants, including potatoes, tomatoes, and peppers. PVY is
nonpersistently transmitted from overwintering hosts to tobacco on the stylet tips of Myzus persicae and several other species of aphids.
Two viral proteins are known to be involved in the transmission process: the viral CP; and a nonstructural protein, the helper component (HC). Aphids need to acquire
the HC prior to or in combination with the virions for transmission to take place. The biologically active HC is thought to be an oligomersoluble protein. The HC
differs between viral strains.
Distribution.
Africa, Canada, Europe, South America, and the United States. Disease tends to be more severe where potatoes are also grown.
Symptoms.
Symptoms vary with the tobacco cultivar that is infected. Most cultivars develop a faint mottling and vein clearing of the young expanding leaves. Larger leaves have a
slight interveinal chlorosis that leaves a band of dark green tissue along each side of the vein. Leaf epinasty and stunting may occur.
Systemic necrosis occurs in burley tobacco and may cause a complete loss of the crop. Initially, vein banding occurs when the smaller veinlets in the leaves become
necrotic, a symptom that is accompanied by a mild mosaic of the leaves. Severely diseased plants have veins that turn dark brown to black. Leaves yellow
prematurely and plants may die. Later, there may be a severe leaf necrosis that spreads to the petiole and stems. Eventually, the lower leaves collapse.
Yields and tobacco quality are reduced.
Management
1. Control weed hosts in tobacco fields and in areas adjacent to the fields.
6. Resistance has been identified.
Tobacco VeinBanding Mosaic
Cause.
Tobacco veinbanding mosaic virus (TVBMV) is in the potyvirus group. TVBMV is transmitted by aphids.
Distribution.
Taiwan and the United States (Tennessee).
Symptoms.
Veinbanding symptoms are similar to those caused by mild strains of potato virus Y. (See ''Tobacco Veinal Necrosis.")
Management.

Page 859
Tobacco Vein Mottling
Cause.
Tobacco veinmottling (or mottle) virus (TVMV) is in the potyvirus group. TVMV overwinters in the weeds dock, horse nettle, and ground cherry and also in living
tobacco roots. TVMV is transmitted nonpersistently by the green peach aphid, Myzus persicae, and other aphid species, but not mechanically under natural
conditions. TVMV is not known to be seedtransmitted.
Distribution.
The United States (Kentucky and North Carolina).
Symptoms.
Symptoms vary with time of infection and cultivar. Initially, burley types have a slight vein clearing. All diseased plants have an irregular dark green area along the veins
of some leaves. Certain cultivars develop a severe systemic necrotic spotting on leaves that becomes increasingly more severe during the season.
Plants infected early are stunted and are not as green as healthy plants. Tip leaves of these diseased plants may have light green spots.
Management
1. Control overwintering hosts in tobacco fields and in areas adjacent to tobacco fields.
2. Control insects with an insecticide application(s). However, because an aphid can transmit the virus to a healthy plant a few seconds after it starts feeding,
insecticides are often a questionable control. Repeated transmissions to several healthy plants may be reduced.
3. Grow barrier rows of maize around a tobacco field to intercept aphids reaching the field.
4. Grow resistant cultivars. No cultivar is immune, but resistance varies greatly between cultivars.
Tomato Spotted Wilt
Cause.
Tomato spotted wilt virus (TSWV) is in the tospovirus group. TSWV overwinters in several species of perennial plants in areas that have cold winter temperatures,
and in annual plants where winters are not cold enough to kill plants.
In Louisiana, virus inoculum originates from noncultivated areas. The presence of TSWV has been reported in spiny amaranthus, Amaranthus spinosus; blackseed
plaintain, Plantago rugelii; buttercup, Ranunculus spp., with R. sardous the species most often associated with natural TSWV infection; coneflower, Rudbeckia
amplexicaulis; horse nettle, Solanum carolinense; dandelion, Taraxacum officinale; spiny sowthistle, Sonchus asper; blue vervain, Verben brasiliensis; and
Lactucua spp., with L. floridana an important overwintering host.
TSWV is transmitted by several species of thrips, including potato or

Page 860
onion thrips, Thrips tabaci; blossom or cotton thrips, Frankliniella schultzei; western flower thrips, F. occidentalis; and tobacco thrips, F. fusca. The chili thrips,
T. setosus, has been shown to transmit the virus in Japan. TSWV must first be acquired by the larval form, then the subsequent adults are able to transmit TSWV.
TSWV persists in insects as long as they live, but it is not transmitted through the eggs. Tomato spotted wilt is more severe during high temperatures and abundant
moisture. Plants of all ages can be infected.
Distribution.
Symptoms.
The yellowgreen spots that initially occur on diseased young leaves later become redbrown and have concentric necrotic rings or zonate necrotic spots. Spots
frequently coalesce and form large irregularshaped areas. Young leaves infected only on one side are distorted and puckered. Necrotic streaks develop along stems,
and dark necrotic areas, or cavities, appear in the cortex and pith. Diseased plants are stunted, and apical buds droop or bend over. Severely diseased plants do not
grow for several weeks, and eventually the leaves droop and the entire plant finally dies.
Management
1. Use insecticides to control thrips in the seedbed and for a month after transplanting.
2. Eliminate overwintering hosts and deepplow all tobacco debris in a field.
Wound Tumor
Cause.
Wound tumor virus (WTV) is in the phytovirus group. WTV is transmitted by leafhoppers.
Distribution.
Widespread.
Symptoms.
Tumors or cell enlargements are produced at sites of wounding on diseased stems and roots.
Management.
Not known.
Disease Caused By Higher Plants
Broomrape
Cause.
Orobanche ramosa is a parasitic flowering plant that survives as seed in the soil for several years. Orobanche ramosa grows on the roots of tobacco.
Distribution.
Africa, Asia, Europe, and North America.

Page 861
Symptoms.
Diseased plants do not grow well, become yellow, and mature earlier than healthy plants. Large masses of blueflowered broomrape plants break through the soil
around the base of the tobacco plant.
Management
1. Do not grow tobacco in an infested field for several years.
2. Destroy broomrape plants before seed is ripe.
Selected References
Ahmed, W., and Thomas, P. E. 1991. Phloem transport of tobacco mosaic virus in Xanthi nc. tobacco induced by potato leafroll virus. (Abstr.). Phytopathology
81:1167.
Anderson, T. R., and Welacky, T. W. 1983. Barn mold of burley tobacco caused by Botryosporium longibrachiatum. Plant Dis. 67:11581159.
Anderson, T. R., and Welacky, T. W. 1988. Populations of Thielaviopsis basicola in burley tobacco field soils and the relationship between soil inoculum
concentration and severity of disease on tobacco and soybean seedlings. Can. J. Plant Pathol. 10:246251.
Barker, K. R., and Lucas, G. B. 1987. Nematode parasites of tobacco, pp. 213241. In Plant and Insect Nematodes. W. R. Nicle, ed. Marcel Dekker, New York.
Bhattiprolu, S. L. 1991. Studies on a newly recognized disease of Nicotiana glutinosa of viroid etiology. Plant Dis. 75:10681071.
Bower, L. A., Fox, J. A., and Miller, L.I. 1980. Influence of Meloidogyne incognita and Globodera solanacearum on development of black shank of tobacco.
(Abstr.). Phytopathology 70:688.
Canto, T., LopezMoya, J. J., SerraYoldi, M. T., DiazRuiz, J. R., and LopezAbella, D. 1995. Different helper component mutations associated with lack of aphid
transmissibility in two isolates of potato virus Y. Phytopathology 85:15191524.
Cole, J. S., and Zvenyika, Z. 1988. Integrated control of Rhizoctonia solani and Fusarium solani in tobacco transplants with Trichoderma harzianum and
triadimenol. Plant Pathol 37:271277.
Cornelissen, A. P. F., and van Wyk, R. J. 1987. Nicotiana tabacum breeding lines resistant to various rootknot nematodes (Meloidogyne spp.). Nematologica
33:316321.
Davis, J. M., and Main, C. E. 1984. Meteorological aspects of the spread and development of blue mold on tobacco in North Carolina. (Abstr.). Phytopathology
74:840.
Davis, J. M., Main, C. E., and Bruck, R. I. 1981. Analysis of weather and the 1980 blue mold epidemic in the United States and Canada. Plant Dis. 65:508512.
Fajola, A. O., and Alasodura, S. O. 1973. Corynespora leaf spot, a new disease of tobacco (Nicotiana tabacum). Plant Dis. Rptr. 57:375378.
St Paul, MN. 1252 pp.
Ferrin, D. M., and Mitchell, D. J. 1986. Influence of soil water status on the epidemiology of tobacco black shank. Phytopathology 76:12131217.
Fortnum, B. A., Csinos, A. S., and Dill, T. R. 1982. Metalaxyl controls blue mold in flucured tobacco seedbeds. Plant Dis. 66:10141016.

Page 862
Fortnum, B. A., Krausz, J.P., and Conrad, N. D. 1984. Increasing incidence of Meloidogyne arenaria on flucured tobacco in South Carolina. Plant Dis. 68:244
245.
Francki, R. LB., Milne, R. G., and Hatta, T. 1985. Atlas of Plant Viruses. CRC Press, Boca Raton, FL. 222 pp.
Fulton, R. W. 1980. Tobacco blackfire disease in Wisconsin. Plant Dis. 64:100.
Gayed, S. K. 1978. Tobacco Diseases. Canada Dept. Agric. Pub. 1641.
Gtebet, R. S., Klose, M. J., Teakle, D. S., and Milne, J. R. 1991. High incidence of tobacco streak virus in tobacco and its transmission by Microcephalothrips
abdominalis and pollen from Agetatum houstonianum. Plant Dis. 75:450452.
Gutierrez, W., and Shew, H. D. 1997. Factors that affect the development of collar rot disease of tobacco. (Abstr.). Phytopathology 87:S37.
Gwynn, G. R., Barker, K. R,. Reilly, J. J., Komm, D. A., Burk, L. G., and Reed, S. M. 1986. Genetic resistance to tobacco mosaic virus, cyst nematodes, rootknot
nematodes, and wildfire from Nicotiana repanda incorporated into N. tabacum. Plant Dis. 70:958962.
Hartill, W. F. T. 1967. A rust of tobacco in Rhodesia. Rhodesia Zambia Malawi J. Agric. Res. 5:189.
Hendrix, J. W., and Csinos, A. S. 1985. Tobacco stunt, a disease of burley tobacco controlled by soil fumigants. Plant Dis. 69:445447.
Herr, L. J,. and Sutton, P. 1984. Tobacco black shank control with metalaxyl and cultivars. (Abstr.). Phytopathology 74:854.
Hood, M. E., and Shew, H. D. 1997. Reassessment of the role of saprophytic activity in the ecology of Thielaviopsis basicola. Phytopathology 87:12141219.
Hopkins, J. C. F. 1956. Tobacco Diseases. Commonwealth Mycological Institute, Surrey, United Kingdom.
Ishida, Y., and Kumashiro, T. 1988. Expression of tolerance to the hostspecific toxin of Alternaria alternata (AT toxin) in cultured cells and isolated protoplasts of
tobacco. Plant Dis. 72:892895.
Johnson, M. C., Pirone, T. P., and Litton, C. C. 1982. Selection of tobacco lines with a high degree of resistance to tobacco etch virus. Plant Dis. 66:295297.
Johnson, R. R., Black, L. L., Hobbs, H. A., Valverde, R. A., Story, R. N., and Bond, W. P. 1995. Association of Frankliniella fusca and three winter weeds with
tomato spotted wilt virus in Louisiana. Plant Dis. 79:572576.
Kelman, A., and Sequeira, L. 1965. Roottoroot spread of Pseudomonas solanacearum. Phytopathology 55:304309.
Komm, D. A., Reilly, J. J., and Elliott, A. P. 1983. Epidemiology of a tobacco cyst nematode (Globodera solanacearum) in Virginia. Plant Dis. 67:12491251.
Ladipo, J. L., and Roberts, I. M. 1979. Occurrence of pepper veinal mottle virus in tobacco in Nigeria. Plant Dis. Rptr. 63:161165.
LaMondia, J. A., and Taylor, G. S. 1987. Influence of the tobacco cyst nematode (Globodera tabacum) on Fusarium wilt of Connecticut broadleaf tobacco. Plant
Dis. 71:11291132.
Latorre, B. A., and Flores, V. 1987. Wilt of tobacco in Chile caused by Verticillium dahliae. Plant Dis. 71:101.
Lucas, G. B. 1974. Diseases of Tobacco, Third Edition. Harold E. Parker & Sons Printers, FuquayVarina, NC.
McIntyre, J. L., Sands, D.C., and Taylor, G. S. 1978. Overwintering, seed disinfestation, and pathogenicity studies of the tobacco hollow stalk pathogen, Erwinia
carotovora

Page 863
var. carotovora. Phytopathology 68:435440.
Meyer, J. R., and Shew, H. D. 1991. Development of black root rot on burley tobacco as influenced by inoculum density of Thielaviopsis basicola, host resistance,
and soil chemistry. Plant Dis. 75:601605.
Meyer, J., Shew, H. D., and Shoemaker, P. B. 1989. Populations of Thielaviopsis and the occurrence of black root rot on burley tobacco in western North
Carolina. Plant Dis. 73:239242.
Modjo, H. S., and Hendrix, J. W. 1986. The mycorrhizal fungus Glomus macrocarpum as a cause of tobacco stunt disease. Phytopathology 76:688691.
Moss, M. A., and Main, C. E. 1985. Temperature tolerance of Peronospora tabacina in the U.S. (Abstr.). Phytopathology 75:1341.
Moss, M. A., and Main, C. E. 1988. The effect of temperature on sporulation and viability of isolates of Peronospora tabacina collected in the United States.
Muller, A. S., and Acedueda, H. A. 1964. Rust on tobacco discovered in Honduras. (Abstr.). Phytopathology 54:499.
Oke, O. A., 1988. Changes in chemical constituents of tobacco leaves infected with Corynespora cassiicola and Colletotrichum nicotianae. J. Phytopathol
122:181185.
Pirone, T. P., and Nesmith, W. C. 1994. Survey of Kentucky for potato virus Y strain N and other potyviruses in tobacco. Plant Dis. 78:754.
Pirone, T. P., and Thornbury, D. W. 1988. Quantity of virus required for aphid transmission of a potyvirus. Phytopathology 78:104107.
Powell, N. T., Melendez, P. L., and Batten, C. K. 1971. Disease complexes in tobacco involving Meloidogyne incognita and certain soilborne fungi.
Prasad, S. S., and Acharya, B. 1965. A new leafspot disease of tobacco. Current Sci. 34:542.
Ramachandraiah, M., Venkatarathnam, P., and Sulochana, C. B. 1979. Tobacco necrosis virus: Occurrence in India. Plant Dis. Rptr. 63:949951.
Ramachar, P., and Cummins, G. G. 1965 .The species of Puccinia on the Paniceae. Mycopathol. Mycol. Appl. 25:760.
Reddick, B. B., Christie, R. G., Gooding, G. V., Jr., and CollinsShepard, M. H. 1991. Tobacco veinbanding mosaic virus: A new virus in North America. (Abstr.).
Reeleder, R. D., Monette, S., VanHooren, D., and Sheidow, N. 1996. First report of target spot of tobacco caused by Rhizoctonia solani (AG3) in Canada. Plant
Dis. 80:712.
Reilly, J. J. 1980. Chemical control of black shank of tobacco. Plant Dis. 64:274277.
Reuveni, M., Nesmith, W. C., and Siegel, M. R. 1986. Symptom development and disease severity in Nicotiana tabacum and N. repanda caused by Peronospora
tabacina. Plant Dis. 70:727729.
Ribeiro, S. G., Kitajima, E. W., Oliveira, C. R. B., and Koenig, R. 1996. A strain of eggplant mosaic virus isolated from naturally infected tobacco plants in Brazil.
Plant Dis. 80:446449.
Richardson, M. J., and Zillinsky, F. J. 1972. A leaf blight caused by Fusarium nivale. Plant Dis. Rptr. 56:803804.
Rotem, J., and Aylor, D .E. 1984. Development and inoculum potential of Peronospora tabacina in the fall season. Phytopathology 74:309313.
Shew, H. D. 1983. Effect of host resistance level on spread of Phytophthora parasitica var. nicotianae under field conditions. (Abstr.). Phytopathology 73:505.

Page 864
Shew, H. D., and Lucas, G. B. 1991. Compendium of Tobacco Diseases. American Phytopathological Society, St. Paul, MN. 68 pp.
Shew, H. D., and Main, C. E. 1985. Rhizoctonia leaf spot of flucured tobacco in North Carolina. Phytopathology 69:901903.
Shew, H. D., and Main, C. E. 1990. Infection and development of target spot of flucured tobacco caused by Thanatephorus cucumeris. Plant Dis. 74:10091013.
Shew, H. D., and Melton, T. A. 1995. Target spot of tobacco. Plant Dis. 79:611
Shew, H. D., and Shoemaker, P. B. 1993. Effects of host resistance and soil fumigation on Thielaviopsis basicola and development of black root rot on burley
tobacco. Plant Dis. 77:10351039.
Sidebottom,J. R., and Shew, H. D. 1985. Effects of soil texture and matric potential on sporangium production by Phytophthora parasitica vat. nicotianae.
Sidebottom, J. R., and Shew, H. D. 1985. Effects of soil type and soil matric potential on infection of tobacco by Phytophthora parasitica var. nicotianae.
Spurr, H. W., Jr., Echandi, E., Haning, B. C., and Todd, F. A. 1980. Bacterial barn rot of flucured tobacco in North Carolina. Plant Dis. 64:10201022.
Stavely, J. R., and Kincaid, R. R. 1969. Occurrence of Phyllosticta leaf spot on Florida cigarwrapper tobacco. Plant Dis. Rptr. 53:837839.
Sun, M. K. C., Gooding, G. V., Jr., Pirone, T. P., and Tolin, S. A. 1974. Properties of tobacco veinmottling virus, a new pathogen of tobacco. Phytopathology
64:11331136.
Taylor, G. S. 1969. A black mildew of the genus Diporotheca found on roots of Nicotiana tabacum in Connecticut. Plant Dis. Rptr. 53:8586.
Tisdale, W. B. 1929. A disease of tobacco seedlings caused by Septomyxa affinis. (Abstr.). Phytopathology 19:90.
Wilson, K. I., AlBeldawi, A, S., and Dwazah, K. 1983. Rhizopus stem rot of Nicotiana glauca. Plant Dis. 67:526527.
Wolf, F. A. 1957. Tobacco Diseases and Decays. Duke University Press, Durham, NC.

Page 865
23.
Diseases of Wheat (Triticum Aestivum)
Bacterial leaf blight is also called bacterial leaf necrosis and bacterial blight.
Cause.
Pseudomonas syringae pv. syringae is seedborne and overwinters in infested residue, water, and soil and on the surfaces of different plant species. The bacteria can
survive as epiphytes on leaves, where they may become pathogenic under the right conditions. During wet weather and temperatures of 15° to 25°C, bacteria are
splashed and blown onto host leaves, which they enter through stomates and wounds. Bacteria may also migrate from infected or infested seed by swimming up the
seedling or by being carried along with the growing point.
Pseudomonas syringae pv. syringae is a weak pathogen that requires moist conditions during the incubation period for significant infection to occur. The presence of
P. syringae pv. syringae can increase frost damage to wheat plants grown in highaltitude areas.
Distribution.
The north central United States.
Symptoms.
Symptoms on winter wheat occur during cool, wet weather in the spring and may be confused with spots caused by other pathogens. At first, watersoaked spots
(less than 1 mm in diameter) occur on the top leaves of plants in the boot to early heading stage. Eventually, the spots grow larger and become necrotic, changing from
a dull graygreen to light brown. During wet weather, droplets of bacterial ooze develop in a spot. During continued wet weather, spots that grow together into ragged
streaks or blotches in 2 to 3 days sometimes kill the entire leaf.
Lesions on spring wheat during moist, humid weather coalesce into elongated necrotic areas that gradually expand laterally until the entire leaf is destroyed. A chlorotic
halo may be present around some lesions.

Page 866
Typical halolike symptoms caused by P. syringae have been reported from south central Colorado.
Management.
Grow resistant cultivars of spring and winter wheat.
Bacterial leaf streak and black chaff are generally considered to be two phases of the same disease. Bacterial leaf streak refers to watersoaked lesions on leaves;
black chaff refers to black lesions on glumes. Because symptom expression tends to be regarded separately in much of the literature, bacterial leaf streak and black
chaff are discussed separately in this book.
Bacterial leaf streak, bacterial stripe, black chaff, black chaff and bacterial streak, and Xanthomonas streak are names that refer to basically the same disease
syndrome.
Cause.
Xanthomonas campestris pv. translucens (syn. X. campestris and X. translucens pv. undulosa). The taxonomy of the causal organism(s) continues to be a subject
in flux. Bacterial leaf streak (and black chaff), also called bacterial blight or bacterial streak on other small grains, is considered to be caused by five of the former X.
campestris pathovars: pv. cerealis, pv. hordei, pv. secalis, pv. translucens, and pv. undulosa. These pathovars are often grouped together under the name
"translucens group" and are considered to be a single species (X. translucens) or pathovar (X. campestris pv. transtucens). Bragard et al. (1997) agreed that X.
translucens pv. translucens and X. translucens pv. hordei are true synonyms. They also reported that using restriction fragmentlength polymorphism and fatty acid
methyl esters analyses, the pathovars X. translucens pv. cerealis, X. translucens pv. translucens, and X. translucens pv. undulosa clustered in different groups and
corresponded to true biological entities.
The causal bacteria are seedborne and overwinter in infested residue, on overwintered hosts, and in soil. Primary infection is by bacteria that have been disseminated
by splashing water and insects, particularly aphids. Injuries from windblown sand and insects provide entrances for infection. Primary infection may also occur by
seedborne bacteria, but seed stored 6 months or more is not considered an important source of inoculum. However, some researchers consider seed to be the most
important source of primary inoculum. In Arkansas, infested seed is suspected to be the principal source of inoculum. Small spaces and grooves that contain water act
as a reservoir for bacteria. Secondary spread occurs by planttoplant contact, rain, and insects.
The bacteria can increase frost damage to wheat plants grown at high altitudes. Although frost is not essential to infection, susceptibility of wheat plants increases
following frost and infection spreads more rapidly in frosted tissue.

Page 867
Distribution.
Wherever wheat is grown. It is an important disease of soft red winter wheat in the southeastern United States.
Symptoms.
Symptoms usually occur after several days of damp or rainy weather. Small watersoaked spots occur on tender green leaves, sheaths of older plants, and sometimes
seedlings. The spots enlarge, coalesce, and become glossy, olivegreen, translucent stripes or streaks of various lengths that later turn yellowbrown. Stripes may
extend the length of a sheaf and are usually narrow from being limited by leaf veins. Occasionally a spot may become large and blotchlike, causing the leaf to die,
shrivel, and turn light brown. Severely diseased leaves die back from the tips. Lesions develop most rapidly in plants subjected to frost.
Droplets of milky bacterial exudate are seen on the surface of diseased spots during early morning humid conditions. The droplets dry into hard, yellowish granules that
are easily removed from the leaf surface. As plants reach maturity, brown to black stripes are produced on stems below the heads and upper joints. If a flag leaf is
diseased, the head may not emerge from the boot but may break through the side of the sheath and be distorted and blighted.
Management
1. Do not sow seed from diseased plants. Seed should be cleaned to remove lightweight infected kernels.
3. Do not rotate wheat with barley.
4. Treat seed with acidified cupric acetate. However, since germination and the resultant stand are affected, this treatment should not be used routinely except for
special cases, such as foundation seed health programs.
5. Partial resistance has been identified in diallel crosses of three genotypes.
Bacterial Mosaic
Cause.
Clavibacter michiganensis subsp. tessellarius. The species name michiganense is sometimes used in the literature. The bacterium may be seedborne.
Distribution.
Canada and the United States (Alaska, Illinois, Iowa, and Nebraska).
Symptoms.
The initial small yellow spots, which are most numerous near the midribs of diseased leaves, eventually grow together and form yellow lesions with indefinite margins.
Diseased leaves become light to dark brown; severely diseased leaves turn brown and dry up. The typical watersoaking symptoms associated with bacterial
infections are lacking.
Management.
Do not sow seed from diseased plants.

Page 868
Bacterial Sheath Rot
Cause.
Pseudomonas fuscovaginae. Disease becomes severe during high humidity and low temperatures at booting to heading stages.
Distribution.
Mexico, in the central highlands at 2249 to 2640 m above sea level.
Symptoms.
Angular, blackishbrown lesions (1020 cm in length) with gray centers and bordered by a purpleblack angular area (12 mm wide) occur on diseased leaf sheaths of
bread and durum wheat.
Management.
Not necessary, because the disease is not considered to be either widespread or severe.
Basal Glume Rot
Cause.
Pseudomonas syringae pv. atrofaciens (syn. P. atrofaciens and Phytomonas atrofaciens) is seedborne and overwinters in infested residue. Bacteria are
disseminated on dust particles, insects, and splashing water. Bacteria multiply near glume joints when water is present, but remain dormant when moisture is lacking.
Distribution.
Wherever wheat is grown.
Symptoms.
The main symptom at heading time is a browning of the bottom onethird of glumes that is more evident on the inside than the outside of the diseased glume.
Sometimes the entire glume is affected and displays symptoms. Severely diseased spikelets are slightly dwarfed and lighter than healthy ones. Sometimes the only
symptom is a dark line where the glume is attached to the spike. The base of diseased kernels has a light brown to black discoloration and seed filling is sometimes
limited.
Diseased leaves have small, dark, watersoaked spots that elongate and become yellow, then brown as diseased tissue dies.
Management
2. Sow seed that has been thoroughly cleaned.
3. Rotate wheat with resistant crops, such as legumes.
Black Chaff
Black chaff and bacterial leaf streak are generally considered to be two phases of the same disease. Bacterial leaf streak refers to watersoaked lesions on leaves;
black chaff refers to black lesions on glumes. Because symptom expression tends to be regarded separately in much of the literature, bacterial leaf streak and black
chaff are discussed separately in this book.
Black chaff is also called bacterial leaf streak, bacterial streak, bacterial stripe, black chaff and bacterial streak, and Xanthomonas streak.

Page 869
Cause.
Xanthomonas campestris pv. translucens (syn. X. campestris and X. translucens pv. undulosa). The taxonomy of the causal organism(s) continues to be a subject
in flux. Bacterial leaf streak (and black chaff) is considered to be caused by five of the former X. campestris pathovars: pv. cerealis, pv. hordei, pv. secalis, pv.
translucens, and pv. undulosa. The pathovars are often grouped together under the name ''translucens group" or are considered to be a single species (X.
translucens) or pathovar (X. campestris pv. translucens). Bragard et al. (1997) agreed that X. translucens pv. translucens and X. translucens pv. hordei are true
synonyms. They also reported that using restriction fragmentlength polymorphism and fatty acid methyl esters analyses, the pathovars X. translucens pv. cerealis, X.
translucens pv. translucens, and X. translucens pv. undulosa clustered in different groups and corresponded to true biological entities.
The causal bacteria are seedborne and overwinter in infested residue, on overwintered hosts, and in soil. Primary infection is by bacteria that have been disseminated
by splashing water and insects, particularly aphids. Injuries from windblown sand and insects provide entrances for infection. Primary infection may also occur by
seedborne bacteria, but seed stored 6 months or more is not considered an important source of inoculum. However, some researchers consider seed to be the most
important source of primary inoculum. In Arkansas, infested seed is suspected to be the principal source of inoculum. Small spaces and grooves that contain water act
as a reservoir for bacteria. Secondary spread occurs by planttoplant contact, rain, and insects.
The bacteria can increase frost damage to wheat plants grown at high altitudes. Although frost is not essential to infection, susceptibility of wheat plants increases
following frost; infection also spreads more rapidly in frosted tissue than in healthy plant tissue.
Distribution.
Wherever wheat is grown. Black chaff is an important disease of soft red winter wheat in the southeastern United States. Black chaff is also serious in wheatgrowing
areas at higher elevations. In eastern Idaho, black chaff is a serious disease in irrigated spring wheat and has caused disease losses of 30% to 40%.
Symptoms.
Symptoms usually occur after several days of damp or rainy weather but usually black chaff is not noticed until diseased plants are about twothirds grown. Diseased
plants grow slowly and may be stunted. The chaff or glumes have longitudinal, dark, somewhat sunken stripes or spots that are most abundant on the upper glumes,
where they coalesce and form larger spots or blotches. The insides of diseased glumes have brown or black spots. Beards of bearded cultivars are brown, especially
at the base. In moist weather, tiny yellow beads of bacteria ooze to the surface of dark lesions and dry as small yellow scales.
Grain is not destroyed, but it may be brown, shrunken, and carry bacteria to infect next year's crop. If a flag leaf is diseased, the head may not

Page 870
emerge from the boot but may break through the side of the sheath and be distorted and blighted.
Management
1. Do not sow seed from diseased plants. Seed should be cleaned to remove lightweight infected kernels.
3. Do not rotate wheat with barley.
4. Treat seed with acidified cupric acetate. However, because germination and the resultant stand are affected, this treatment should not be routinely used except for
special cases, such as foundation seed health programs.
5. Partial resistance has been identified in diallel crosses of three genotypes.
Pink Seed
Cause.
Erwinia rhapontici (syn. E. carotovora pv. rhapontici) infects only damaged kernels, particularly those injured by the gall midge (Cecidomyidae) or when grain is
harvested too early. It is not known how E. rhapontici survives and is disseminated to wheat, but the bacterium was isolated from plants grown under sprinkler
irrigation in Idaho. Erwinia rhapontici causes a crown rot of rhubarb, Rheum spp., its only other known host.
Distribution.
Canada, Europe, and the United States (Idaho and North Dakota). Pink seed is not serious.
Symptoms.
Seeds are pink and appear as if they had been treated with a dye. The endosperm is soft and pink.
Management.
Not necessary.
Spike Blight
Spike blight is also called gummosis.
Cause.
Clavibacter tritici (syn. Corynebacterium michiganense pv. tritici and Corynebacterium tritici) and C. iranicum. The species name iranicum is sometimes
spelled "iranicus" in the literature. Clavibacter spp. are seedborne and survive in infested organic matter in wet soils, usually in the lower areas within a field.
Dissemination within a field is primarily by the seed gall nematode, Anguina tritici. Longdistance dissemination is by seed. Nematode larvae become contaminated
with bacteria in the soil and carry them up the stem to the plant apex. Wet weather or wet, low areas in a field favor disease development.
Distribution.
Australia, Canada, China, Egypt, Ethiopia, and India. Clavibacter iranicum is reported from Iran. Spike blight is not important except in wet areas of a field.

Page 871
Symptoms.
Initially, diseased leaves may be wrinkled or misshapen as they emerge from a whorl. Heads are misshapen and covered with a sticky yellow bacterial exudate. Dried
exudate appears as white flecks that distort heads, necks, and upper leaves by inhibiting their elongation.
Management
2. Do not grow wheat in nematodeinfested soil for at least 2 years.
3. Drain any wet areas in a field.
Stem Melanosis
Cause.
Pseudomonas cichorii overwinters on several weed species found in wheat fields. Stem melanosis occurs when wheat is grown in copperdeficient soils. Wounds
facilitate the entry of bacteria. Disease occurs only with repeated infections over a 2 to 3week period that coincides with high temperatures and nightly dew
formation.
Distribution.
Canada.
Symptoms.
Symptoms initially occur at the milky ripe stage of growth. The disease pattern in a field is sharply defined, irregularshaped, dark patches that range in size from
several square meters to several hectares.
Small light brown lesions first develop on stems beneath the lower two nodes. During the following 2 weeks, coinciding with the softdough stage, lesions darken and
coalesce on stems, rachis, and peduncles and an occasional mottling of glumes occurs. The rachis and upper portions of the peduncles beneath the heads and
immediately beneath nodes turn dark brown. Diseased heads become bleached and thin and have shriveled kernels.
Copperdeficiency symptoms are a lack of plant vigor, pale stunted vegetative growth, leaf tip injury, delayed maturity, aborted or shriveled grains, head bending, and
melanism. These same symptoms occur to a limited extent on oats and barley. Pseudomonas cichorii is isolated from all melanotic tissues of wheat, but never from
barley or oats.
Management.
Stem melanosis is reduced when copper is added to copperdeficient soils.
Wheat Leaf Blight
Wheat leaf blight may be similar to bacterial leaf blight.
Cause.
Pseudomonas syringae. Many researchers consider the causal organism to be synonymous with P. syringae pv. syringae. Infection occurs during periods of heavy
rainfall.
Distribution.
Argentina.

Page 872
Symptoms.
Seedlings infiltrated with the bacterium display limited watersoaking symptoms in 7 days and complete leaf necrosis in 10 days. Watersoaking occurs at diseased leaf
margins which eventually become a confluent area of white necrosis.
Management.
Not reported.
White Blotch
Cause.
Bacillus megaterium pv. cerealis survives in soil, plant parts, seeds of susceptible cultivars, and insects. Bacteria are spread by water, insects and/or mites, and seed.
Infection is favored by high temperatures and a high light intensity.
Distribution.
United States (North Dakota) on hard red spring, hard red winter, and durum wheats.
Symptoms.
The initial small yellow or white lesions on diseased leaf blades, sheaths, and culms enlarge into white or very light tan, irregularshaped blotches and streaks. The
white blotches are often broader than the streaks symptomatic of bacterial leaf blight (bacterial leaf necrosis) and lack the initial watersoaking symptoms associated
with bacterial leaf blight.
Management.
Not reported.
Cause.
Alternaria triticina is seedborne, surviving as conidia on seed and as mycelium in seed. Alternaria triticina presumably overseasons in soil and within infested soil
residue, which probably is the source of primary inoculum. Plants are infected at about 4 weeks old when leaves in contact with soil become infected. Secondary
inoculum is provided by conidia produced in lesions and disseminated by wind to other plant hosts. Infection is favored by 10 hours or more of continued leaf wetness
and temperatures of 20° to 25°C.
Distribution.
India.
Symptoms.
Initially, small, oval, chlorotic spots occur on diseased lower leaves. Spots enlarge, become sunken, assume irregular shapes, and turn browngray. Symptoms
progress up a diseased plant and extend to the heads and leaf sheaths. During humid conditions, spots have a dark, powdery appearance due to sporulation by the
fungus.
Management
2. Apply foliar fungicides where feasible.

Page 873
3. Apply seedprotectant fungicides; however, these are frequently not effective.
Anthracnose
Cause.
Colletotrichum graminicola, teleomorph Glomerella graminicola, is a soilinhabiting fungus that is a successful saprophytic colonizer of a wide range of plant
residues. The fungus also survives as mycelia and conidia on cereals and grasses and their residues, and becomes seedborne during harvest. The optimum production
of conidia from mycelia is during wet weather and a temperature of 25°C. Conidia are disseminated by wind and water to plant hosts. Infection of all plant parts is
most severe during wet weather at 25°C. Anthracnose is most likely to occur when wheat is grown in a rotation with wheat or other cereals on coarse soils that are
low in fertility.
Distribution.
Symptoms.
Symptoms become apparent toward plant maturity as elliptical lesions (1 to 2 cm long) above and below the soil level on diseased stems. Lesions, at first, are water
soaked, then become bleached and necrotic. Diseased crowns and stem bases are bleached and later become brown. Later, when moisture is plentiful, acervuli
develop as small, black, raised spots on the surfaces of diseased lower leaf sheaths and culms, and on leaf blades of dead plants. Round to oblong lesions with
acervuli also may occur on green leaves. Plants display gross symptoms of a premature ripening or whitening, a general reduction in vigor, death, lodging, and shriveled
grain.
Management
1. Rotate wheat with a noncereal, such as a legume or grass.
Ascochyta Leaf Spot
Cause.
Ascochyta tritici. Ascochyta graminicola and A. sorghi have also been reported as pathogens. Ascochyta tritici overwinters as pycnidia and mycelia in infested
residue. During hot weather, pycnidiospores are disseminated a short distance. Factors that enhance infection are high humidity caused by weather or dense foliage,
and the contact of leaves with soil. Secondary infection occurs as pycnidiospores from pycnidia produced in older leaf spots.
Distribution.
Europe, Japan, and North America.
Symptoms.
Ascochyta leaf spot is an inconspicuous disease and can be easily overlooked or confused with other diseases, particularly glume blotch.

Page 874
Spots tend to be mostly on diseased lower leaves. Initially, spots are yellow, round to elliptical (15 mm in width). Later, spots coalesce and cause large areas of
diseased leaves to be light brown and necrotic. Pycnidia are often formed in necrotic tissue and appear as minuscule black dots because most of the fungal structure is
submerged in the diseased tissue so just the top portion is visible.
Management.
Application of foliar fungicides is somewhat effective.
Aureobasidium Decay
Cause.
Microdochium bolleyi (syn. Aureobasidium bolleyi and Gloeosporium bolleyi).
Distribution.
Widespread, but Aureobasidium decay is of little importance. Microdochium bolleyi has been reported as part of the common root rot complex in different areas.
Symptoms.
A mild necrosis of the seedling roots occurs.
Management.
Not reported.
Black Head Mold
Black head mold is also called sooty head mold.
Cause.
Several fungi, including Alternaria spp., Cladosporium spp., Epicoccum spp., Sporobolomyces spp., and Stemphylium spp. Black head mold occurs when wet
weather accompanies maturation, especially if harvest is delayed. The disease becomes more severe on heads of plants damaged from causes such as other diseases,
nutrient deficiency, or lodging.
Distribution.
Symptoms.
Greenblack molds develop on diseased heads.
Management.
Grain should be sufficiently dried before it goes into storage.
Black Point
Black point is also called kernel smudge.
Cause.
Several fungi, including Aspergillus spp.(especially A. alternata), Bipolaris spp. (especially B. sorokiniana), Chaetomium spp., Cladosporium spp., Curvularia
spp., Fusarium proliferatum, Fusarium spp., Gloeosporium spp., Helminthosporium spp., Myrothecium spp., Nigrospora spp., Penicillium spp., Plenodomus
spp., Rhizopus spp., and Stemphylium spp.
Black point is most severe at a relative humidity of 90% and higher or continuous rainfall during seed maturation. Damage will increase if grain is stored at 95% relative
humidity and 25% moisture (wet weight basis). Alternaria alternata may use pollen as a nutrient source during the infection

Page 875
process. Other exogenous sources of nutrients may account for higher disease incidence.
Irrigation of soft white spring wheat during the mid or softdough stage significantly increases the incidence of black point. Black point of the spring wheat cultivar
'Yecora Rojo' occurs more frequently in fields irrigated by centerpivot than by rill or wheel line irrigation.
Distribution.
Symptoms.
Black point describes the darkened and sometimes shriveled embryo end of diseased seed. Diseased kernels are discolored, weathered, blackpointed, or
"smudged". Germination decreases when the embryo is invaded. Discolored grain is discounted at the market.
Management
1. Treat seed with seedtreatment fungicide.
2. Store grain at 15% moisture (wet weight basis) or less.
3. Cultivars with some resistance to black point caused by B. sorokiniana may not be resistant to other diseases caused by this fungus, such as common root rot and
spot blotch.
Brown Root Rot
Cause.
Plenodomus meliloti (syn. Phoma sclerotioides).
Distribution.
Canada.
Symptoms.
Necrosis occurs where pycnidial initials are attached to roots. Pycnidial initials are greenblack, globular or flattened, and up to 0.5 mm in diameter. In the spring, they
are found attached to roots and shoot bases by a short attachment process. These stalks develop singly from adaxial surfaces of the protopycnidia, which resemble
sclerotia.
Management.
Not reported.
Cause.
Hymenula cerealis (syn. Cephalosporium gramineum) is seedborne and survives as conidia and sporodochia in infested residue in the top 8 cm of soil for up to 5
years, and as mycelia in infested host residue in soil for an indeterminate amount of time.
Maximum infection occurs when roots are wounded or broken in the presence of high concentrations of inoculum. Mechanical injuries are not absolutely required for
infection, but a higher incidence occurs when there are root wounds usually caused by soil heaving but also, in some cases, by insects.
Infection is related to root growth, root injury, and environmental factors that increase infection sites and concentrations of inoculum. High soil temperatures following
sowing make plants more susceptible to infection

Page 876
because of the increase in the size of the root system. The addition of phosphate fertilizer in drill rows further increases root growth and leads to greater disease
incidence at high temperatures but not at lower temperatures. Infection incidence and severity increase with decreasing soil pHs from 7.5 to 4.5, especially with highly
susceptible cultivars. The effect of a lower pH may be accounted for by the presence of aluminum and hydrogen ions that injure roots by causing root membranes to
leak, thereby allowing adsorbed cations to be lost. Decreases in soil pH have also been attributed to the heavy use of ammoniabased nitrogen fertilizers.
Roots are more prone to injury and breakage by heaving soil in the spring. These conditions are likely to happen when a warm autumn is followed by a cool spring and
a large number of soil freezethaw cycles are accentuated by high soil moisture during the autumn and winter. Excess soil and surface water during early winter also
favor development of sporodochia, which in turn increases both sporulation and the dispersal of conidia that serve as primary inoculum. Exudates from coldstressed
but unbroken roots also increase spore germination, conidiogenesis, and hyphal branching.
Thus the greatest amount of inoculum is produced during the winter and early spring, which coincides with a greater incidence of wounds caused by soil heaving and
freezing, and by insects. Under these circumstances, crown roots are the primary infection court for the pathogen to colonize wounded and senescent root cortical
tissue, then penetrate into the vascular system. The subcrown internode can also be infected just as seed is germinating. Severed or wounded roots have been
reported to be susceptible to infection for 16 days after wounding.
Soil freezing is not absolutely necessary for infection in all locales. When temperatures decrease and rainfall begins in the Pacific Northwest of the United States,
singlecelled conidia produced on colonized residue on or near the soil surface are liberated into the soil, where they serve as the primary inoculum and infect directly
through unbroken roots.
After infection, conidia enter xylem vessels and are systemically carried upward, where they lodge and multiply at nodes and leaves but do no further damage to roots.
The fungus prevents water movement up the plant and produces harmful metabolites.
At harvest time, C. gramineum is returned to soil in residue, where it is a successful saprophytic competitor with other soilborne microorganisms. Cephalosporium
stripe is most severe in notillage plots and decreases in minimal and conventionaltillage plots because of a threshold size for plant fragments to be infested with C.
gramineum. The optimum size of plant fragments varies between soil types because infection is influenced by total nutrients available from residue and soil.

Page 877
Distribution.
Great Britain, Japan, and most winter wheatgrowing areas of North America.
Symptoms.
Winter wheat is most severely diseased. Spring wheat is susceptible but apparently escapes the disease and usually does not show symptoms. Diseased plants are
scattered throughout a field but are usually more numerous in the lower and wetter areas.
Diseased plants are dwarfed. During jointing and heading, normally one or two, but up to four, distinct yellow stripes develop on leaf blades, sheaths, and stems and
extend the length of the plant. Thin brown lines consisting of infected veins occur in the middle of each stripe. The stripes eventually turn brown and become highly
visible on green leaves and remain noticeable even on yellow straw. Toward harvest, culms at or below diseased nodes become dark due to fungus sporulation.
Heads of diseased plants are white and contain shriveled seed or no seed.
Management
1. Grow resistant or moderately resistant cultivars. Disease declines over several seasons with monoculture of moderately resistant cultivars. Thus, higher levels of
resistance are not needed to manage Cephalosporium stripe (Shefelbine and Bockus 1989). Inoculum production is not related to the resistance response of the
cultivar.
2. Rotate wheat with a nonhost for at least 2 years. However, this recommendation conflicts with information that disease declines over several seasons with
monoculture of moderately resistant cultivars.
3. Sow later in the autumn or when the soil temperature at 10 cm below the soil surface is below 13°C. Plants under these conditions have limited root growth, thus
reducing the number of infection sites.
4. Infected residue should be plowed deeper than 8 cm.
Ceratobasidium gramineum Snow Mold
Cause.
Ceratobasidium gramineum (syn. Corticium gramineum). Snow mold occurs in welldrained, upland paddy fields but is more common on barley.
Distribution.
Japan.
Symptoms.
Diseased leaves appear "rotted" and have a dark green appearance just after snowmelt. After leaves have dried, they become pale gray to pale yellow and have
ellipsoidal lesions with a narrow brown margin. A pale gray mycelial mat grows in the center of lesions. Leaf sheaths frequently have a brownish appearance.
Symptom development ceases after snowmelt, but later in the growing season, ellipsoidal lesions are found on leaf sheaths near the soil level.
Management.
Not reported.

Page 878
Common Bunt
Common bunt is also called covered smut, European bunt, hill bunt, and stinking smut.
Cause.
Tilletia caries (syn. T. tritici) and T. laevis (syn. T. foetens and T. foetida). The specific name laevis is sometimes spelled "levis" in the literature. The two fungi are
closely related and have similar life cycles that may occur together in the same diseased plant.
Both fungi overwinter as teliospores (chlamydospores) on seed and in soil. When wheat is sown, teliospores located on or near the seed in the soil germinate in the
presence of moisture and cool temperatures (5° to 15°C). A promycelium (basidium) is formed on which eight to 16 basidiospores (sporidia) are produced. The
basidiospore fuses in the middle with a compatible basidiospore and forms an "H"shaped structure that germinates and forms yet another structure called a secondary
sporidia.
The secondary sporidia germinate and produce mycelium that infects seedlings. Mycelium grows behind the growing point or meristematic tissue of the infected plant,
invades the developing head and displaces the grain. Eventually, teliospores form inside the diseased seed. At harvest time, the diseased seed is broken and
teliospores disseminated by wind contaminate healthy host kernels and the soil.
Tilletia caries has been reported to be pathogenic for up to 10 years after being incorporated in soil. The spores have been reported to be viable after passage
through the digestive tracts of cattle and sheep, but not pigs or poultry.
Distribution.
Tilletia caries is generally distributed wherever wheat is grown but is most prevalent in the northwestern United States. Tilletia laevis is limited to areas of Europe
and North America, where it was reported from the midwestern and northwestern United States.
Symptoms.
Common bunt symptoms are more pronounced following cool soil temperatures after sowing. Wheat sown in the spring may be less severely diseased. Diseased
plants are somewhat stunted but cannot be readily distinguished from healthy plants until heading. Bunted heads are more slender than healthy heads and the glumes of
spikelets may be spread apart. A bunted head will often stay green, with a bluish cast, for a longer period of time than will a healthy head. Bunted kernels are about
the same size as healthy seed but are light brown and have a more rounded shape. The pericarp ruptures at harvest and teliospores contaminate healthy seeds, giving
them a "fishy" odor; hence, the name stinking smut. The smut balls or diseased kernels have an oily feeling when crushed.
Management

Page 879
3. Sow early in the autumn. Seedlings may be far enough advanced and less susceptible to infection by the time secondary sporidia develop.
Common Root Rot
Common root rot is also called crown rot, dry land root rot, and foot rot.
Cause.
Bipolaris sorokiniana, teleomorph Cochliobolus sativus, is considered to be the primary cause of common root rot; however, other fungi reported to cause
common root rot symptoms are Fusarium acuminatum, F. avenaceum, F. crookwellense, F. culmorum, F. graminearum group 1, and F. poae. All are
widespread fungi that survive as saprophytic mycelia in infested soil residue. Conidia of B. sorokiniana and chlamydospores of Fusarium spp. also survive for several
months in the soil and are seedborne.
Microdochium bolleyi is also a secondary invader of roots and is sometimes isolated together with B. sorokiniana and Fusarium spp. Although frequently referred
to as a minor pathogen because it does not penetrate the stele of the host plant, M. bolleyi is reported to seriously alter root function or affect shoot growth. In
Finland, M. bolleyi is reported to be commonly isolated together with B. sorokiniana and Fusarium spp. from diseased roots.
Inoculum density of B. sorokiniana in soil is related to the amount of sporulation occurring on infested residues. Some researchers have seen no significant differences
on root rot or plant yield due to tillage or straw management. Others have reported that significantly more spores were found with conventional tillage than in a
reduced tillage system in Texas. However, the distribution of spores in the soil profile was not significantly affected by the tillage system; the majority of the spores
were found in the top 10 cm of soil, regardless of tillage method. Secondary sporulation is greatest on the diseased crowns of mature wheat plants, on crown roots,
and on subcrown internodes, seed pieces, and seminal roots; the highest numbers of conidia are present on necrotic or senescent tissue.
Primary infections occur on coleoptiles, primary roots, and subcrown internodes. Plants put under stress by drought, freezing, warm temperatures, lack of nutrition,
and Hessian fly injury are most subject to infection. Under these conditions, disease severity increases with sowing depth because of an increased number of infection
sites on belowground plant tissues. Fusarium spp. infect secondary roots as they emerge from the crown. The diseased plant does not die as long as it can produce
new roots. However, early infection reduces yield potential of plants by restricting the production of tillers. Conidia are produced when disease progresses
aboveground.
Moisture is required for infection, but once initiated, disease development requires warm temperatures and moisture stress. Disease may be most severe in dry soil
when inoculum is seedborne. Infection of seedlings

Page 880
in natural soil by F. graminearum group 1 is restricted to soilwater potentials from 0.1 to 1.5MPa. A low soilwater potential predisposes wheat seedlings to
colonization and further damage by the fungus.
Crop sequence has an effect on infection: the incidence of common root rot increases under continuous cultivation. Oat stubble favors the buildup of F. culmorum in
the soil; therefore, the poor grain yields associated with an oatwheat rotation may be attributed to F. culmorum crown and root rot.
Isolates of C. sativus from fields in continuous wheat are more pathogenic to wheat than isolates from fields in firstyear wheat. Isolates of C. sativus from diseased
wheat and barley also were highly virulent on their original host species but weakly virulent on alternate host species. In Canada, spring wheat tended to be colonized
by higher levels of B. sorokiniana than winter wheat did.
Distribution.
Wherever dryland wheat is grown.
Symptoms.
Disease incidence and severity were usually significantly higher in conventional tillage plots than in reduced tillage plots in Texas. Diseased plants occur in random
patches throughout a field, are stunted, and have a lighter green color than healthy plants. Diseased plants mature early, produce few tillers, and have bronzed,
bleached, or white heads, which results in shriveled seed. Seedlings may be killed before or after emergence. The surviving seedlings have brown lesions on the
coleoptiles, roots, and culms.
Plants with diseased crowns are usually killed. Darkening of subcrown internodes is usually caused by B. sorokiniana. Fusarium spp. cause roots, culm bases, and
lower nodes to dry and darken and cause diseased plants to become brittle and break off easily near the soil line. The browning of the root system can sometimes be
seen only when adhering soil is washed from diseased roots. Winter survival of wheat is reduced, particularly when diseased by B. sorokiniana.
Management
2. Properly fertilize soil to ensure growth of new plant roots.
3. Sow winter wheat in the late autumn.
4. Grow cultivars with a degree of resistance. At least three genes have been identified that control resistance. Cultivars with some resistance to common root rot may
not be resistant to other diseases caused by B. sorokiniana, such as black point and spot blotch.
5. Leave field fallow for 3 to 4 years.
6. Winter wheat rotations incorporating canola and flax result in greater wheat survival, superior plant vigor, greater plant height, larger numbers of heads formed per
meter of row, higher grain yield, and lower levels of root disease.

Page 881
7. Tillage method. Disease incidence and severity were usually significantly higher in conventional tillage plots than in reducedtillage plots in Texas.
Cottony Snow Mold
Cottony snow mold is also called Coprinus snow mold, LTB (lowtemperature basidiomycete), SLTB (sclerotial lowtemperature basidiomycete), snow mold, and
winter crown rot.
Cause.
Coprinus psychromorbidus is the lowtemperature basidiomycete (LTB) form of cottony snow mold. The nonsclerotial form of cottony snow mold needs a
prolonged and persistent snow cover. Such a snow cover produces relatively constant soil temperatures of1°C to 5°C, which appear to be the most conducive for
development of LTB. However, a thin snow cover for a short duration appears sufficient to permit limited penetration of wheat by C. psychromorbidus and
development of the fungus within the plant, even in the absence of a persistent snow cover. Under certain conditions, microsclerotia form in diseased plant tissue and
may also be a survival mechanism.
The LTB form of cottony snow mold is the most prevalent snow mold pathogen of winter cereals in central and northern Alberta and northeastern British Columbia
and is responsible for severe mortality in most years.
Distribution.
Canada.
Symptoms.
After snowmelt, patches of dead plants normally occur where the snow was deepest in the field. Sometimes there is a sparse mycelial growth that gives diseased
plants a gray sheen; however, often little mycelium can be found. Irregularshaped gray to black sclerotia (1 mm in length) are found inside diseased leaf sheaths and
infrequently on roots and subcrown internodes. The sclerotia are loosely attached to diseased host tissues and can be easily scraped off.
Management.
Not reported.
Crater Disease
Crater disease and Rhizoctonia bare patch are similar, but their symptoms differ sufficiently to consider them as two separate diseases. A disease identified as patchy
stunting in Tanzania is possibly similar to crater disease, except crater disease occurs exclusively in black montmorillonite clay soils and patchy stunting has been
observed in clay loam, silty clay loam, and silty loam soils. Crater disease is similar to Rhizoctonia bare patch disease, but it is caused by a R. solani that does not
anastomose with AG8, the cause of Rhizoctonia bare patch.
Cause.
Rhizoctonia solani AG6. This is the same strain of R. solani that also causes patchy stunting. The umbrella thorn tree, Acacia tortilis, is a natural

Page 882
host for the fungus. Crater disease occurs only on very heavy, black montmorillonite clay soil that is 40% clay or greater and in which root growth is impeded by soil
structure. Disease is also enhanced by dry weather and early infection by R. solani. Isolates of R. solani that cause crater disease anastomose with each other but not
with any other anastomosis group tester strains and not with AG8.
Distribution.
South Africa and Tanzania.
Symptoms.
Severely stunted patches of wheat occur within a field. Under continuous cultivation of wheat, patches enlarge each year and assume an irregularshaped pattern that
tends to stretch in the direction of cultivation. Some fields display a rippling effect caused by elongated patches of less obviously stunted plants.
Initially, there is a sudden appearance of yellow areas of plants. About 3 weeks after emergence, plants wilt and the lower leaves soon become dry and white. Most
plants die as seedlings, but some survive until maturity and have reduced tillering and incomplete grain filling. Roots of stunted plants have beadlike swellings
composed of hyphae that superficially resemble sclerotia. Xylem vessels in roots are brown and occluded with a gellike material; roots break easily at these points.
Frequently the entire root is brown and rotted where the roots are broken.
Management.
Stunting is alleviated by thorough and repeated cultivation of soil.
Several experimental methods of disease management have been worked on in South Africa. Trichoderma harzianum treatments significantly increased plant growth
and reduced root infection. With the addition of a fungicide, T. harzianum and sheep manure incorporated into tilled and ''ripped" soils increased grain yield.
In other research, soil drenching with phosphorous acid at 50 g per square meter prior to sowing and a foliar application to 2weekold plants at the rate of .125 dm
(cubic) of a 10% solution per square meter significantly reduced infection of wheat by R. solani in naturally infested crater disease soil in the field.
Disease was managed by soil solarization and fumigation with methyl bromide by using deep cultivation. However, the researchers were careful to point out this was
not practical for commercial application.
Dilophospora Leaf Spot
Dilophospora leaf spot is also called twist.
Cause.
Dilophospora alopecuri (syn. D. graminis) survives as mycelia and pycnidia in infested residue, and as conidia on seed. Primary infection is caused by conidia that
are produced in pycnidia, released during wet weather, and disseminated by wind and splashing rain to host seedlings.

Page 883
Secondary infection is caused by conidia produced in pycnidia formed within the disease spots on seedling leaves during moist weather. The twist phase of the disease
is caused by secondary conidia disseminated into the whorls by larvae of the seed gall nematode, Anguina tritici, as it moves up the plant in a water film.
Distribution.
Canada, Europe, India, and the United States. Twist has not been observed for several years and is considered to be a rare disease on wheat.
Symptoms.
Initially, small, elongated, yellow spots appear only on diseased leaves. Spots become light brown with black centers that consist of stromata and pycnidia of D.
alopecuri. Diseased leaves may be killed if spots become numerous. When the whorl is colonized by the fungus, leaves do not emerge or emerge twisted, distorted,
and covered with gray mycelium. This phase of the disease rarely occurs in the absence of A. tritici. Dilophospora alopecuri dries as stromata that appear as dark
streaks on leaves and in which pycnidia are produced.
Management
1. Rotate wheat with other crops. Most cereals are not susceptible.
4. Sow certified wheat seed.
Disease Caused by Fusarium sporotrichioides
Cause.
Fusarium sporotrichioides.
Distribution.
The United States (Minnesota) on spring wheat.
Symptoms.
Foliar and glume necrosis is severe only on very young plants growing under optimum disease conditions. Leaf symptoms are variable and include the following: small
tan flecks with dark red borders; oval to elongated tan, red, or redtan lesions of different sizes that occasionally appear similar to a mechanical abrasion; tan
streaking, especially in young leaves; and tip burn. Diseased leaf sheaths occasionally kill leaves.
Head symptoms are identical to those of scab (Fusarium head blight) except kernels are not visibly affected. Diseased culms sometimes kill heads.
Management.
Not reported.
Downy Mildew
Cause.
Sclerophthora macrospora (syn. Sclerospora macrospora and Phytophthora macrospora) is seedborne as oospores and survives for years as oospores that are
embedded in infested leaf and stem tissue or are loose in soil when diseased tissues decay. Sclerophthora macrospora is an obligate parasite and cannot grow
saprophytically on dead plant tissue. Oospores are dissemi

Page 884
nated in infested soil residue by wind and water. Oospores germinate in saturated soil and produce sporangia from which zoospores are released 1 to 2 hours after
sporangia formation. In some instances, zoospore formation ceases and secondary sporangia are formed. Zoospores "swim" through soil water, settle on the
developing seedling, and produce germ tubes that penetrate the host plants. In another mode of infection, oospores survive for months in dry soil and germinate
directly and form germ tubes that penetrate hosts, or germinate indirectly by producing sporangia from which zoospores are released. Infection occurs over a wide
temperature range (7° to 31°C). Following infection, S. macrospora develops systemically in plants, particularly in meristematic tissue.
Distribution.
Wherever wheat is grown. Downy mildew is not considered a serious disease except in localized wet areas.
Symptoms.
Downy mildew occurs only in localized areas of fields where seedlings have been in flooded or waterlogged soil for 24 hours or longer. Wheat plants are dwarfed
and deformed, tiller excessively, and have several yellow leaves. Diseased plants have leathery, stiff, thickened leaves, stems, and heads. Diseased leaves, stems, and
heads are twisted and distorted, and no seeds are formed in severely diseased plants.
In less severely diseased plants, dwarfing may be slight and one or more of the upper leaves may be stiff, upright, or variously curled and twisted. Heads and stems are
not deformed. Numerous round yellowbrown oospores may be found in diseased tissue examined under magnification.
Management.
Downy mildew is ordinarily not serious enough to warrant special management measures. However, the following are some general measures that will aid in managing
disease should a serious problem occur.
1. Provide proper soil drainage.
2. Control grassy weeds that serve as hosts.
3. Sow cleaned seed from diseasefree plants.
Dry Seed Decay
Cause.
Penicillium spp. infect seed when soil is too dry for seed to germinate and seedlings to emerge.
Distribution.
Semiarid regions of the world.
Symptoms.
Diseased seed is shriveled and covered with a blue to green Penicillium growth.
Management.
Dwarf Bunt
Dwarf bunt is also called dwarf smut, short smut, stunt smut, stubble smut, and TCK smut.

Page 885
Cause.
Tilletia controversa survives as teliospores in soil and on the surfaces of infested seed. However, disease occurs only when heavily infested seed, which has an
inoculum infestation equal or greater than 1 g of teliospores per kg of seed, is sown in diseaseconducive locations. When wheat is sown in moist soil, teliospores on
or close to seed germinate under warm, dry conditions and form a promycelium on which eight to 16 basidiospores are borne. A basidiospore fuses in the middle with
a compatible basidiospore and forms an "H"shaped structure that, in turn, germinates and forms a structure called a secondary sporidium. The secondary sporidia
germinate and produce infective mycelium.
Tilletia controversa is better adapted to survive in soil and has a lower temperature range (1°5°C) for optimum germination than the common bunt fungi T. caries
and T. laevis. Protracted moist conditions and temperatures of less than 5°C in the spring induce dormancy in teliospores. The infection process occurs 35 to 105
days after germination, depending on temperature. Infection generally requires a heavy snow cover over unfrozen ground thus providing suitable conditions of moisture
and temperature at the soil surface for teliospore germination and infection of host plants. Therefore, disease is restricted to areas where wheat is grown under a
persistent snow cover.
After infection, mycelium grows behind the meristematic tissue of growing points and invades developing heads to displace grain. Eventually, teliospores form within
the seed. At harvest time, diseased seed is broken and teliospores are disseminated by wind and contaminate healthy wheat kernels or soil.
Distribution.
Canada, Europe, and the United States where a heavy snow cover is likely to occur over unfrozen ground.
Symptoms.
Dwarf bunt is limited to winter wheat and, infrequently, to winter barley. Diseased plants are generally onefourth to onehalf the size of healthy plants. Viable pollen
does not develop, the ovaries of infected florets are larger than those in healthy florets, and there are more buntinfected kernels per spikelet than seeds per spikelet on
a healthy plant.
Smut balls are smaller and rounder than common bunt, and the spore mass feels dry. Spores have a foul odor that is similar to rotten fish.
Management
1. Grow resistant cultivars in adapted areas.
Epicoccum Glume Blotch
Cause.
Epicoccum purpurascens (syn. E. nigrum).
Distribution.
India.
Symptoms.
Symptoms initially appear in the dough stage of plant develop

Page 886
ment. Purplebrown, elliptical spots, which later become gray, occur on glumes and sometimes on awns. Severely diseased glumes are entirely covered with spots that
occasionally are dotted with black spore masses. In highly susceptible cultivars, the rachis and peduncle are covered with dark brown spots and the diseased leaves
are covered with irregularshaped spots. Grain is severely shriveled.
Management.
Varying degrees of resistance exist among cultivars.
Ergot
Cause.
Claviceps purpurea, anamorph Sphacelia segetum. Claviceps purpurea survives as sclerotia in soil for about 1 year and for longer periods when mixed with grain
in storage facilities. In response to moisture and after a coldtemperature treatment, sclerotia from grasses germinate during the spring or early summer and form one
or more stalked stromata. Perithecia, which contain numerous asci in which ascospores are borne, are produced in the apex of the stromata. Ascospores are the
primary inoculum for floret infection and are disseminated by wind and splashing rain to plant hosts. Ascospores that contact a stigma germinate and penetrate the
ovary within 24 hours. In 5 days, conidia form on the ovary surface within a sweet liquid (honeydew) and serve as secondary inoculum. Conidia are disseminated to
other florets by planttoplant contact, splashing rain, and insects that have been attracted to the honeydew. Conidia production declines over time and the swollen,
convoluted ovaries enlarge and become converted from base to tip into sclerotia.
Ergot is favored by wet, cool weather that prolongs the flowering period of wheat plants. These conditions also favor honeydew formation. Florets are most
susceptible to infection just before anthesis.
Distribution.
Worldwide, but the incidence of ergot on wheat is normally low.
Symptoms.
The most conspicuous symptom is the purpleblack hornlike sclerotia or ergot bodies that replace one or more seeds in the diseased wheat head. Sclerotia protrude
from glumes and are up to 10 times larger than healthy seed. Before sclerotia are formed, the honeydew stage occurs in the form of sticky yellowish droplets that
attract insects to congregate on diseased heads. Just before sclerotia develop, infected ovaries swell and their surface becomes convoluted with a superficial layer of
conidiophores.
Wheat is considered "ergoty" if it contains more than 0.3% ergot bodies or sclerotia by weight. Sclerotia contain toxic alkaloids that affect warmblooded animals.
Consumption of infested grain or hay may cause blood vessel constriction and smooth muscle contractions. In pregnant animals, continuous doses of ergot can cause
uterine contractions that lead to spontaneous abortion. Ingesting small amounts of ergot may cause

Page 887
a reduction or complete cessation in lactation or the loss of extremities, especially ears, tails, and hooves, because of blood vessel constriction followed by the onset of
gangrene.
Management
1. Use seed that is free of sclerotia.
2. Rotate wheat with a nongrass crop.
3. Plow residue deep into the soil.
Eyespot
Eyespot is also called Cercosporella foot rot, culm rot, foot rot, stem break, strawbreaker, and strawbreaker foot rot.
Cause.
Pseudocercosporella herpotrichoides (syn. Cercosporella herpotrichoides), teleomorph Tapesia yallundae. Two other species, P. anguioides and P. aestiva,
are associated with eyespot, but their significance in the etiology of eyespot has not been established.
Pseudocercosporella herpotrichoides survives for several years as mycelia within infested residue. Apothecia are reported on wheat straw in Europe. Sporulation
occurs on infested residue and straw at the soil surface during cool, damp weather or when the humidity is near saturation and temperatures are 8° to 12°C in the
autumn or spring. Dispersal is primarily by splashing rain.
Development of epiphytotics is dependent upon the production of primary inoculum on infested residue remaining from the previous wheat crop. Winter wheat is more
likely to be infected than spring wheat. The coleoptile is most susceptible to infection during the seedling stage; however, with decay of the coleoptile, the susceptibility
of leaf sheaths increases.
Severity of both leaf sheath and stem lesions increases linearly with the amount of time host plants are subjected to favorable disease conditions. Disease severity has
been suggested to be a function of accumulated temperatures since the development of epiphytotics is often interrupted by temperatures unfavorable to disease
development. Leaf sheath penetration by P. herpotrichoides may be delayed by cold weather, and if the rate of leaf sheath death exceeds the rate of leaf sheath
penetration, lesions do not occur. The rapid death of basal leaf sheaths prevents the fungus from becoming established in stems. Secondary inoculum is not important
in the development of an epiphytotic because spores do not occur on developing lesions until later in the growing season. However, late infections add to the amount
of inoculum to infect succeeding wheat crops. On winter wheat in Ontario, some infections occurred in the autumn but the peak of infection occurred in April. Soil or
volcanic ash placed around the base of winter wheat in the spring increased disease severity in the state of Washington.

Page 888
At least two distinct morphological types, corresponding to two pathotypes of P. herpotrichoides, are present. Daniels et al. (1991) reported the two pathotypes are
designated as wheat (W) or rye (R) and are distinguished on the basis of pathogenicity to wheat seedlings, spore morphology and colony morphology, pigmentation on
maize meal agar, and isoenzyme polymorphisms. The wheat type is more pathogenic to wheat and barley than to rye and has fastergrowing, evenedged colonies in
culture. The rye type is as pathogenic to rye as to wheat and barley, and is slowergrowing in culture and has featheryedged colonies and more profuse sporulation.
Distribution.
Where wheat is grown in a cool, moist climate.
Symptoms.
Symptoms are most conspicuous near the end of the growing season, when diseased plants lodge. In the lodging that is symptomatic of eyespot, the straw falls in all
directions. In contrast, lodging caused by wind or rain causes straw to fall primarily in one direction.
Eye or ovateshaped lesions with white to tan centers and brown margins develop first on the basal leaf sheath of diseased plants. Similar spots form on stems
directly beneath those of the leaf sheath and weaken stems sufficiently to cause lodging.
Crown and basal culm tissue, but not roots, become diseased. However, a necrosis occurs around roots in the upper crown nodes. Under moist conditions, lesions
enlarge and the black, stromalike mycelium that develops over the surface of crowns and the base of culms gives diseased plant tissues a "charred" appearance.
Stems either shrivel and collapse or plants become yellowish to pale green and have heads that are reduced in size and number. When host plants are infected early in
their growth, individual culms and weaker plants are killed before maturity. White heads, which are similar to a symptom of takeall, are often present at maturity.
Management
1. Rotate wheat with noncereals.
2. Spring wheat and latesown winter wheat are less subject to infection.
3. Grow the most resistant cultivars. However, resistant cultivars often become diseased under severe disease conditions. Resistance has been determined in
accessions of Tricticum tauschii (syn. Aegilops squarrosa).
4. Apply fungicides to residue to decrease primary inoculum. Foliar fungicides reduce eyespot under experimental conditions.
5. Reduced tillage limits foot rot incidence.
Flag Smut
Cause.
Urocystis agropyri. Some researchers consider U. tritici to be a synonym. Urocystis agropyri survives as teliospores in soil for 3 years and on seed for 4 years.
Teliospores germinate and produce sporidia that germinate and infect wheat coleoptiles prior to their emergence. Infection is optimum at soil moistures of 10% to 15%
and temperatures of 10° to 20°C. Urocystis

Page 889
agropyri then overwinters as mycelium in seedlings and in the spring grows systemically in the upper portion of the plant, producing sori in which hyphal tips
differentiate into teliospores. In a few days or when wheat is harvested, the sori erupt and liberate teliospores that contaminate soil and seed.
Distribution.
Localized in most wheatgrowing areas. Commonly found in Australia and in the western and certain areas of the midwestern United States.
Symptoms.
Symptoms appear in spring and summer on a few tillers or on an entire plant. Smut lesions on leaves, sheaths, and upper parts of the diseased stem are long, light
green stripes that soon become grayblack streaks. These streaks are subepidermal smut sori that develop between the leaf veins and cause leaves to become rolled
and twisted. Splits along the sori in the diseased leaf liberate the grayblack spore masses. Diseased leaves become weakened, frayed, and split longitudinally.
Diseased plants are dwarfed, tiller excessively, and rarely head out. However, if they do head out, glumes and necks also are striped.
Management
3. Rotate wheat with a resistant host for at least 2 years and preferably for 3 years.
4. Do not sow seed deep since shallow sowing partially prevents some infection.
Fusarium Glume Spot
Cause.
Fusarium poae in close association with the mycophageous mite Siteroptes avenae. Fusarium poae occurs widely in the soils of the temperate regions and is
characterized as a saprophyte or weak parasite of grasses and herbaceous plants. Two kidneyshaped, saclike structures (sporothecae) in female mites contain
microconidia of F. poae when the mites feed on fungi. Conidia can be released from sporothecae when mites feed on plants, thereby inoculating them. Fusarium
poae is also seedborne.
Distribution.
South Africa, on winter wheat and autumnsown irrigated, spring wheat.
Symptoms.
Diseased glumes have necrotic lesions that are surrounded by dark brown borders. The borders are often more pronounced toward the base of the glume. Generally,
a few florets per spike are symptomatic.
When mature wheat plants were inoculated with a suspension of F. poae microconidia, watersoaked lesions occurred on leaves, and black chafflike symptoms and
necrosis occurred on awns.
Management.
Not reported.

Page 890
Fusarium head blight is also known as blight, Fusarium blight, head blight, pink mold, scab, tombstone scab, wheat head blight, wheat scab, and white head.
Cause.
Fusarium graminearum group 2, teleomorph Gibberella zeae; F. acuminatum; F. avenaceum, teleomorph G. avenacea; F. crookwellense; F. culmorum;
Microdochium nivale (syn. F. nivale), teleomorph Monographella nivalis (syn. Calonectria nivalis); F. equiseti; F. moniliforme; F. oxysporum; F. poae; F.
proliferatum; F. pallidoroseum (syn. F. semitectum); F. sambucinum; F. sporotrichioides; F. subglutinans; and F. tricinctum. Fusarium graminearum group
2 is considered to be the principal pathogen; however, other fungi are reported to be the principal causes in some geographical areas.
The fungi overwinter as mycelia and spores on seed, and as mycelia and perithecia in infested residue. Rainfall may be needed for perithecia and ascospores to form
and mature on crop residue, but not to trigger the actual release of ascospores. Perithecial drying during the day, followed by sharp increases in relative humidity may
provide the stimulus for release of ascospores.
In eastern Canada, ascospores were released during the first 3 weeks of July. Ascospore release during this time was a diurnal pattern beginning around 1600 to 1800
hours and reaching a peak before midnight, then declining to low levels by 0900 hours the following morning. The beginning of ascospore release was correlated with
a rise in relative humidity during the early evening hours. Ascospores produced in perithecia and conidia produced from mycelia on infested residue during warm, moist
weather are disseminated by wind to plant hosts.
Temperatures for optimum disease development differ among Fusarium species. Optimum disease development caused by F. graminearum occurs at 26.4°C, but
occurs at 13.8°C for F. crookwellense.
Infected seed causes seedling blight, and soilborne inoculum causes seedling blight and root rot. Fusarium head blight develops in warm, humid weather during the
formation and ripening of the kernels. Prolonged wet weather during and after anthesis favors infection and subsequent disease development. Conidia produced on
diseased heads serve as secondary inoculum.
Grain that becomes wet in swaths favors Fusarium head blight development. Disease is more severe when wheat follows maize, when nitrogen and phosphorous
fertilization is inadequate, and where weed density is high. Although Fusarium head blight occurs when conditions are warm and humid, disease caused by M. nivalis
is reported to occur under cool, moist conditions in the Pacific Northwest.
Fusarium graminearum group 2 readily produces perithecia in culture, but F. graminearum group 1, which is associated with crown and root rot of wheat, does
not.

Page 891
Distribution.
Symptoms.
Disease begins in flowers and spreads to other parts of the head, giving the appearance of premature ripening. One or more spikelets of emerged immature heads are
initially watersoaked, then die and become light brown, bleached, or white, beginning at the spikelet base. Eventually, hulls change from a light to dark brown
discoloration. When infection occurs late in the development of seed, only the base of the hull is brown, but in severe cases, the entire kernel may become shrunken
and brown. If the rachis is infected, the entire head is dwarfed and compressed. All spikelets above that point are closed rather than spreading, bleached, and sterile
or contain only a partially filled seed. Diseased kernels are graybrown and light in weight, and the interior of the kernel is floury and discolored. During humid or wet
weather, pink to pinkred mycelia and spores grow on diseased spikelets. Later, small black perithecia grow in the same diseased area.
Diseased grain may be harmful when fed to hogs, dogs, and humans. Mycotoxins, such as 3acetyldeoxynivalenol and deoxynivalenol (vomitoxin), may be produced
in diseased heads. Deoxynivalenol and 3acetyldeoxynivalenol affect protein synthesis at the ribosomes of susceptible wheat cultivars, which suggests these
trichothecenes are phytotoxins as well as mycotyoxins.
The fungus might survive poorly in diseased seed because the germination of seed improves after several months in storage. Researchers reported that emergence of
diseased seeds was better after storage temperatures of 10° and 20°C than at 10° and 2.5°C.
Management
1. Rotate wheat with other crops. Do not grow wheat after maize, barley, or rye. Do not grow wheat next to maize.
2. Plow under infected residue to hasten decomposition of infested residue and prevent spores from being windborne.
3. Do not spread manure that contains infected straw or maize stalks on soil where wheat is growing.
4. Sow early in the growing season to allow wheat to escape warm, moist weather.
6. Grow resistant cultivars. Resistance is characterized as being of two types: type I is resistance to the initial infection, and type II is resistance to hyphal invasion of
the plant tissue. In South Africa, differences in susceptibility to Fusarium head blight caused by F. graminearum and F. crookwellense have been reported.
A type III resistance has been suggested. Some wheat cultivars identified as resistant apparently possess the ability to degrade trichothecenes, whereas susceptible
cultivars do not have this ability. Compared to susceptible cultivars, resistant cultivars can tolerate

Page 892
101000 times the concentration of trichothecenes with no apparent effect on growth.
7. The Food and Drug Administration recommends 2 ppm and below of deoxynivalenol in wheat entering the milling process, 1 ppm for finished wheat products
destined for human consumption, and 4 ppm for wheat products to be used as animal feed.
Fusarium Leaf Blight
Cause.
Fusarium nivale (syn. Microdochium nivale).
Distribution.
Scotland.
Symptoms.
Lesions occur on diseased upper leaves at the milky ripe growth stage of plant growth. Lesions are extensive, dull, diffuse, and watersoaked and have pustules of F.
nivale sporulating through the stomata.
Management.
Not reported.
Fusarium Rot
Fusarium rot is also called Fusarium crown and foot rot.
Cause.
Fusarium culmorum and F. graminearum group 1 are most commonly cited. Fusarium graminearum group 1 does not produce perithecia in culture and is
associated with crown and root rot of wheat; F. graminearum group 2 readily produces perithecia in culture and is one of the causal fungi of Fusarium head blight.
Fusarium avenaceum, F. acuminatum, and F. tricinctum have been reported as minor components of the disease complex. Fusarium equiseti has been reported
to cause a crown rot of wheat in South Africa. A new species of Fusarium that has characteristics in common with F. longipes and F. scirpi var. filiferum has been
reported from the Orange Free State in South Africa. The symptoms caused by the new Fusarium are indistinguishable from those caused by F. graminearum group
1. However, this is possibly the same disease caused by F. equiseti.
Primary inoculum is soilborne chlamydospores and mycelia, conidia, and chlamydospores originating from infested residue in the upper 10 cm of the soil. Entry into the
crown is gained 2 to 3 cm below the soil surface through openings around crown roots or is gained by the infection of newly emerging crown roots.
Disease is severe under dry soil conditions; a 40 bar midday leaf water potential is cited as the optimum disease condition. However, infections caused by the new
Fusarium species are from an area in South Africa that has summer temperatures of 13.2° to 25.8°C, winter temperatures of 0.3° to 15.2°C, and a relatively high
rainfall that averages 638.1 mm in the summer and 168.2 mm in the winter.
Distribution.
The United States. Fusarium culmorum is widely distributed in central and eastern Washington, north central Oregon, and northern

Page 893
Idaho, Fusarium graminearum is limited to south central Washington and F. equiseti is reported from South Africa.
Symptoms.
Diseased plants rarely show outward symptoms until after heading. The crown and basal stem tissues are decayed and have a brown discoloration and a spongy
texture. Internodes become chocolate brown, but leaf sheaths remain symptomless. Pink or burgundy mycelium is seen in hollow stems. Diseased plants die
prematurely, resulting in white heads.
Symptoms caused by F. equiseti are stunted patches of wheat, a redbrown discoloration of roots and crowns, and, usually, severely rotted crowns. Inoculated
plants in the greenhouse have a lower plant mass and grain yield than do control plants.
Management.
In greenhouse trials, differences in tolerance to F. graminearum group 1 among wheat cultivars have been reported.
1. Do not rotate wheat with oat.
2. Till fields after harvest to improve water infiltration.
3. Establish a dust and stubble mulch in the spring.
4. Apply the proper amount of nitrogen.
5. Sow winter wheat in early September in North America as a compromise between early sowing, which produces larger plants and greater stress, and later sowing,
which results in lower yields.
Halo Spot
Cause.
Pseudoseptoria donacis (syn. Selenophoma donacis and Septoria donacis) overwinters as pycnidiospores, pycnidia, and mycelia in infested residue, seed, and
overwintering wheat. During cool, moist weather, pycnidiospores are exuded from pycnidia and disseminated by wind and splashing rain to plant hosts.
Distribution.
In the cool, moist climates of Great Britain, northern Europe, and the United States. Halo spot rarely causes much damage.
Symptoms.
Numerous elliptical or diamondshaped spots (less than 4 mm long) occur on leaves and sometimes the culms of winter wheat in the spring. At first, spots have purple
brown margins, but this discoloration fades as the spots age. In time, the centers of spots become gray from the presence of small black pycnidia. Sometimes spots
become so numerous that much of the diseased leaf surface is destroyed.
Management.
Not necessary. The cultivar 'Gaines' is very susceptible.
Karnal Bunt
Karnal bunt is also called partial bunt.
Cause.
Neovossia indica (syn. Tilletia indica) survives as teliospores in soil for more than 2 years and on seed. Most primary inoculum is derived from

Page 894
seedborne inoculum, but soilborne teliospores also serve as a source of inoculum. In the spring, teliospores germinate within 2 mm of the soil surface and produce
promycelia that grow to the soil surface. Sporidia are produced on promycelia and disseminated by wind to host plants, where the florets become infected. Sporidia
are disseminated a long distance by air currents and may survive up to 12 hours if the relative humidity is 95% or higher. The maximum germination of teliospores in
vitro occurs at temperatures of 15° to 20°C and in continuous light. Infection is favored by cool, wet weather.
During the early stages of infection, intercellular hyphal growth occurs among parenchyma and chlorenchyma cells in the distal to midportion, but not the basal
portion, of the glume, lemma, and palea. Hyphae are absent from the ovary, subovarian tissue, rachilla, and rachis. Later, hyphae grow intercellularly toward the floret
base to the subovarian tissue and enter the pericarp of the ovary through the funiculus. Hyphae are found in the rachis only during the later stages of infection. The
epidermis of the ovary is not penetrated, even after prolonged contact with germinating secondary sporidia. Kernels are wholly or partially converted into teliospores
that are disseminated by wind at harvest time and contaminate healthy seeds or soil.
Distribution.
Afghanistan, India, Iraq, Lebanon, Mexico, Nepal, Pakistan, Sweden, Syria, Turkey, and the United States.
Symptoms.
Normally only a few random diseased kernels per head are wholly or incompletely converted to smut sori. Symptoms first appear at the softdough stage of plant
development in the form of blackened areas that surround the bases of the grains and extend upward on the grain for various lengths. During the most severe disease,
glumes may be spread apart and expose the bunted grains, but this is not a common symptom. Most kernels are broken or partially eroded at their embryo end. On
severely diseased plants, grains are reduced to fragile black membranous sacks of teliospores and have dead, shriveled embryos. A foul odor of trimethylamine,
characteristic of the bunt fungi of wheat, accompanies diseased kernels. Infected seeds have a lower survival rate in storage than healthy seeds do.
Management
1. Grow resistant cultivars. Most durum wheats are immune.
2. Treat seed with a fungicide seed treatment; however, no chemical seed treatments can guarantee wheat seed is not carrying viable T. indica teliospores.
3. Hot water (60°80°C) with the addition of NaOCl reduces seedborne teliospores and the contamination in grain storage facilities.

Page 895
Leaf Rust
Leaf rust is also called brown rust, dwarf rust, and orange rust.
Cause.
Puccinia triticina (syn. P. recondita f. sp. tritici and P. recondita). Puccinia triticina is a heteroecious, longcycled rust fungus that has species of meadow rue,
Thalictrum spp., and, rarely, Anchusa spp. and Isopyrum spp. as alternate hosts to wheat. Because meadow rue is found primarily in Europe and is not common in
most sections of the United States, the pycnial and aecial stages of P. triticina are usually found only in Europe. Anchusa italica was reported to be an important
alternate host in Morocco.
Puccinia triticina survives the winter in the Great Plains of the United States as sporulating or dormant mycelia in live winter wheat plants and as urediniospores in
uredinia on infested dead leaves. Mycelium is apparently capable of surviving all environmental conditions that infected live host tissue can survive. Circumstantial
evidence also implies local oversummering and overwintering of certain phenotypes in Pennsylvania. Rust overwinters as urediniospores and mycelia on wheat in the
southern United States and Mexico.
Primary inoculum originates from sporulating uredinia, dormant mycelia, or viable urediniospores. These are the most important sources of inoculum for infection
because they are likely to be virulent to the cultivar. Urediniospores disseminated by wind to the northern United States and Canada in the spring infect host plants if
moisture is present. However, this source of inoculum may not be as important in initiating new infections because these urediniospores may not be virulent to the
cultivar.
A new generation of urediniospores is produced every 7 to 14 days if favorable disease conditions of heavy dews, light rains, or high humidity and temperatures of 15°
to 22°C occur. The minimum continuous dew period necessary for infection increases from 4 to 6 hours at the optimal temperatures to at least 16 hours for suboptimal
temperatures. The optimum temperature for completion of the infection process, as measured by development of appressoria, substomatal vesicles, and infection
hyphae with at least one haustorium, is 16°C. Infection occurs over a wide temperature range (5° to 25°C).
Urediniospores are winddisseminated and cause secondary infections until host plants mature. As plants near maturity, teliospores are formed. If plants are infected
near maturity, teliospores may not be produced. Teliospores in North America serve no function, but they may serve as a means of overwintering in Europe. During
late summer and autumn in North America, urediniospores in northern wheatgrowing areas that are disseminated southward by wind infect winter wheat in the
southern United States and Mexico.
Distribution.
Wherever wheat is grown. Leaf rust, which may be the most widely distributed wheat disease, is most prevalent where wheat matures late. However, infection often
occurs too late to do severe damage.

Page 896
Symptoms.
Pustules first develop on diseased lower leaves and leaf sheaths, and during moist conditions, progress up to the flag leaf. Pustules also occur on stems, and the awns
and glumes of the head. Uredinia pustules are small, round to oval, raised, orangeyellow, and contain numerous urediniospores that appear as an orange powder.
As wheat matures, telia develop as dark gray to black flattened pustules that are about the same size as uredinia but do not rupture the epidermis. Leaf rust can be
distinguished from stem rust on the basis of these pustules. Leaf rust pustules are smaller than those of stem rust, are orangeyellow rather than the brick red color
typical of stem rust pustules, and lack the jagged fragments of wheat epidermis that typically adhere to the sides of stem rust pustules.
Management
1. Grow resistant wheat cultivars. Adult plant resistance is conferred by two complementary genes: Lr 13 and Lr 34. The magnitude of gene interaction is influenced
by environment, particularly temperature. Lr 10 and an unknown gene for seedling resistance are present in some cultivars.
2. Soils should have balanced fertility. An excess of nitrogen increases the susceptibility of host plants to infection.
3. Apply a foliar fungicide if conditions warrant it.
4. Experimentally, fungicide seed treatments have proved effective.
5. Resistance is found in some species of Aegilops and Agropyron.
Leaf Spot (Ascochyta spp.)
Cause.
Ascochyta sorghi and A. graminicola have been found in association with Stagonospora nodorum (syn. Septoria nodorum).
Distribution.
The United States (Virginia).
Symptoms.
Leaf lesions that initially are elliptical to lanceolate later coalesce into irregular patterns. On diseased upper leaf surfaces, lesions are zonate, with a narrow outer
chlorotic band that encloses a light brown necrotic band and dark brown center. The dark brown center is absent on the diseased lower leaf surfaces.
Pycnidia of both fungi are present. Those of A. sorghi are goldenbrown and submerged, with only the ostiole or neck above the leaf surface. Those of S. nodorum
are dark brown and superficial.
Management.
Not necessary.
Leaf Spot (Phaeoseptoria urvilleana)
Cause
Phaeoseptoria urvilleana overwinters as pycnidiospores in pycnidia on infested residue. Free water must be present on leaves for 48 hours or longer for infection to
occur.

Page 897
Distribution.
Great Britain and the United States.
Symptoms.
In the field, irregularshaped leaf spots form on leaves of diseased plants in the late milk stage of plant development. Plants inoculated with P. nodorum have irregular
shaped, diffuse leaf spots that initially are yellow, then become tan.
Management.
Some cultivars are resistant or partially resistant.
Cause.
Phaeosphaeria herpotrichoides (syn. Leptosphaeria herpotrichoides) overwinters as mycelia in, and as ascospores in pseudothecia on, infested residue. Free
water must be present on leaves 48 hours or longer for infection to occur.
Distribution.
Canada, Europe, and the United States. Leptosphaeria leaf spot is considered a minor disease.
Symptoms.
Irregularshaped, diffuse, yellow to tan spots occur on diseased leaves.
Management.
Some cultivars are more resistant than others.
Loose Smut
Cause.
Ustilago tritici (syn. U. nuda) survives as dormant mycelia in seed embryos. When an infected seed germinates, mycelium grows systemically in the plant and
produces smutted heads filled with chlamydospores (teliospores) in place of healthy kernels. Smutted heads emerge from the boot 1 to 2 days earlier than healthy
heads and the chlamydospores are disseminated by wind to the flowers of host plants. During weather with temperatures of 16° to 22°C and moisture provided by
dews or light showers—conditions that are favorable for disease—chlamydospores germinate and form germ tubes that penetrate flower ovaries and possibly the
stigmas. Accessibility of germ tubes to embryos appears to be a limiting factor in infection. Subsequent mycelial growth occurs in the germs or embryos of developing
seeds. As seeds mature, mycelia in embryos become dormant until the following growing season. Different races of U. tritici exist.
Distribution.
Symptoms.
Diseased seed does not show outward symptoms and germination is not affected. Plants grown from diseased seed have dark green, erect leaves with chlorotic
streaks; smutted heads then emerge from boots 1 to 2 days earlier than do heads of healthy plants. The brown to dark brown spore mass is enclosed in a fragile, gray
membrane that soon ruptures, releasing spores that are disseminated by wind to healthy flowers. An erect, naked rachis that protrudes above reclining heads of healthy
plants is all that remains of a smutted head.

Page 898
Management
3. Sow certified seed known to be smutfree.
4. Hot water treatments have been used to destroy seedborne inoculum.
Microscopica Leaf Spot
Microscopica leaf spot is similar to Leptosphaeria leaf spot.
Cause.
Phaeosphaeria microscopica (syn. Leptosphaeria microscopica) survives as pseudothecia on grass and wheat stubble. Disease occurs under continuous wet
periods of 48 or more hours.
Distribution.
The United States (Minnesota and North Dakota).
Symptoms.
The symptom on diseased leaves is yellowbrown blotches.
Management.
Not necessary, since P. microscopica is considered a weak parasite.
Patchy Stunting
Cause.
Rhizoctonia solani. The R. solani that causes patchy stunting anastomoses with the R. solani that causes crater disease. The umbrellathorn tree, Acacia tortilis, is a
natural host for the fungus.
Distribution.
Tanzania.
Symptoms.
Patchy stunting is characterized by patches of stunted and chlorotic plants typical of Rhizoctonia bare patch disease. However, seminal roots of diseased plants contain
nodulose swellings and sclerotial sheaths rather than displaying the girdling and rotting symptoms that are typical of bare patch. The only difference between crater
disease and patchy stunting is that crater disease occurs exclusively in black montmorillonite clay soils. Patchy stunting has also been observed in clay loam, silty clay
loam, and silty loam soils.
Management.
Not reported.
Phialophora TakeAll
Cause.
Phialophora graminicola (syn. P. radicicola var. graminicola). Phialophora takeall occurs at soil temperatures of 24° to 29°C. Only plants in the seedling stage
are susceptible.
Distribution.
Unknown.
Symptoms.
Seminal and coronal roots of diseased plants are rotted, and culms are discolored black. Both root and shoot weights are reduced.
Management.
Not reported.

Page 899
Phoma Spot
Phoma spot is also called Phoma glume blotch.
Cause.
Phoma glomerata, P. sorghina (syn. P. insidiosa), and other Phoma spp. The Phoma spp. likely overseason as pycnidia in infested residue. Disease development
is aided by long periods of wetness.
Distribution.
India, Mexico, and South America.
Symptoms.
Symptoms caused by P. sorghina occur primarily on glumes and awns, but leaves are infected occasionally. Spots on glumes are brown and oval (2.02.5 × 5.07.0
mm). Pycnidia are present within spots.
Under humid conditions, purplebrown lesions develop on the tips of glumes of inoculated plants, then enlarge and form a gray center. No yellow halo is present.
Grain is discolored and shriveled. Inoculated leaves develop faded green streaks on the upper surfaces. Pycnidia develop in rows below the epidermis.
Phoma glomerata causes dark brown lesions on leaf sheaths.
Management.
Not reported.
Pink Snow Mold
Cause.
Microdochium nivale (syn. Fusarium nivale and Gerlachia nivalis), teleomorph Monographella nivalis, oversummers as perithecia that developed on diseased
lower leaf sheaths during cool, humid weather in the spring. During cool, wet weather in the autumn, with or without snow cover, leaf sheaths and blades that are close
to and below the soil surface are infected by ascospores and mycelia growing from residue. Saprophytic mycelial growth from residue may also provide an inoculum
source for other infections in the spring. Secondary infection occurs from conidia and ascospores that are disseminated by wind to host plants.
Distribution.
Canada, central and northern Europe, and the United States.
Symptoms.
Damage corresponds to the pattern of snow cover within a field. Pink mycelium and sporodochia are visible on living and dead plant tissue and on the soil surface after
the snow melts. When disease severity is light, lesions with strawcolored centers and dark margins occur on diseased leaves. When disease is severe, leaf sheaths,
shoots, and leaves are killed. Severely diseased leaves first become chlorotic, then necrotic, but remain intact and do not disintegrate. White or faintly pink mycelium is
sometimes present on the lower parts of diseased plants. Diseased leaves become faintly pink with mycelium when the snow cover melts and the leaves are exposed
to light and air. Unless crowns are diseased, diseased plants often recover during warm, dry weather despite extensive leaf infection.

Page 900
Management
1. Sow winter wheat later in the autumn or in the spring. Most plant growth will be during conditions that are unfavorable to fungus infection.
2. Rotate wheat with a noncereal crop, such as a legume.
3. Do not mow plants late in the autumn. Removal of clippings reduces deleterious effects of mowing.
Platyspora Leaf Spot
Cause.
Clathrospora pentamera (syn. Platyspora pentamera) survives as perithecia in infested residue. Ascospores are produced during wet, spring weather and
disseminated by wind to host plants. There must be 24 to 72 hours of continuous moisture for infection to occur. Perithecia are produced in residue as wheat matures.
Distribution.
Canada and the north central United States. Incidence of the disease is rare on wheat.
Symptoms.
While Platyspora leaf spot is rare on wheat, ascospores of C. pentamera are abundant in the air in some wheatgrowing areas. Nondescript yellowbrown spots are
randomly produced on wheat residue as plants reach maturity.
Management.
Grow resistant cultivars. Management measures listed under ''Septoria Leaf Blotch" would also be beneficial.
Powdery Mildew
Cause.
Blumeria graminis f. sp. tritici (syn. Erysiphe graminis f. sp. tritici) overwinters as cleistothecia on infested residue, and as mycelium and conidia in diseased leaf
tissue of live plants growing in geographical areas that have mild winter temperatures. Ascospores, which form in cleistothecia in the spring and are disseminated by
wind to hosts, serve as primary inoculum in northern wheatgrowing areas. Conidia are produced when mycelium becomes established on diseased leaf surfaces
during humid, cool weather but without the presence of free water. Conidia account for most of the secondary inoculum and spread of disease during the growing
season. Cleistothecia are formed on diseased leaf surfaces as plants mature.
Powdery mildew is more severe on tender, rank plants that are growing at high population densities or have had heavy applications of nitrogen fertilizer. Cool, humid,
and cloudy weather conditions are conducive to disease severity. Powdery mildew usually ceases to be a problem when weather becomes dry and warm later in the
growing season.
Winter wheat is infected in the autumn; therefore, inoculum becomes available for the initiation of spring epiphytotics. The incidence of autumn infection decreases with
later sowing.

Page 901
Distribution.
Symptoms.
Superficial mycelium, conidiophores, and conidia appear as powdery, light gray or white spots on the upper surfaces and, infrequently, the lower surfaces of diseased
leaf blades, leaf sheaths, and floral bracts. Chlorotic patches appear on leaf surfaces that are opposite the gray fungal colonies. The fungus is superficial on leaf
surfaces except for haustoria, which penetrate into epidermal cells. Later, spots enlarge, yellow, then die and turn brown as diseased plants mature. In some cultivars,
leaf tissue adjacent to mycelium becomes necrotic and turns brown. Numerous small, round, dark cleistothecia that are easily observed without magnification develop
on diseased areas. Severely diseased plants are killed.
Winter wheat infected in the autumn generally does not produce symptoms except in those autumns that have extended warm temperatures. The lowest yields occur
when plants become diseased early in autumn.
Management
1. Grow resistant cultivars. Peroxidases function in plant resistance against B. graminis f. sp. tritici.
2. Apply a foliar fungicide where economically feasible. Early applications of fungicides at plant growth stages 6 to 8 reduce powdery mildew and result in higher yield
than fungicides applied later in the season.
3. Rotate wheat with noncereal crops.
4. Plow under volunteer wheat.
5. Under experimental conditions, significant reductions in disease can be achieved in some seasons by applying potassium chloride in the spring.
6. Sow winter wheat later than recommended.
7. Apply the seedtreatment fungicide triadimenol on seed of wheat sown in the autumn.
Prematurity Blight
Prematurity blight in the Canadian prairies is a severe manifestation of common root rot and is similar to Fusarium crown rot in other wheatgrowing areas.
Cause.
Cochliobolus sativus and Fusarium culmorum. Disease is favored by moisture stress for 6 to 12 days at the flag leaf or boot stage of plant development.
Distribution.
Canada (Prairie Provinces).
Symptoms.
Bleached individual plants are scattered among healthy green plants. Usually the entire plant is bleached, but occasionally only one or two tillers are affected and the
rest of the plant remains green. Often diseased plants are slightly stunted, but since heads remain erect, the stunting is not obvious.
Brown lesions typical of common root rot usually are present on dis

Page 902
eased subcrown internodes and crowns. The brown discoloration may extend up the stem for several centimeters. Occasionally the basal discoloration is pink rather
than brown. Heads may contain severely shriveled grain or may lack seeds entirely. Infrequently diseased plants may be found with all symptoms except the
discoloration of the basal parts.
Management.
Cultivars differ in resistance.
Pythium Root Rot
Pythium root rot is also called browning.
Cause.
Several Pythium species, including P. aphanidermatum, P. aristosporum, P. arrhenomanes, P. graminicola, P. heterothallicum, P. irregulare, P. myriotylum,
P. sylvaticum, P. torulosum, P. ultimum, P. ultimum var. sporangiiferum, and P. volutum, have been associated with root rot of wheat. Pythium spp. fungi,
which are present in all agricultural soils, survive for 5 years or more in soil and infested residue as oospores. Oospores germinate and form germ tubes that infect the
host directly or form a sporangium in which 10 to 40 zoospores are produced. The zoospores "swim" through soil water to a host plant, where they rest and eventually
produce germ tubes that infect roots.
Pythium spp. infect wheat embryos within 48 hours after sowing in soil at —0.3 bar or wetter. Optimum fungal growth and infection occur during low temperatures in
wet soils in the autumn and spring. At soil temperatures of 10° to 25°C, P. ultimum is the most pathogenic of the tested Pythium spp., whereas P. irregulare is the
most pathogenic of all Pythium spp. at 5°C. Oospores are produced in diseased tissue and are returned directly to soil upon the decomposition of diseased plant
tissue or remain within the diseased, but intact, tissue.
Infection is most likely to occur in the wetter areas of fields that are deficient in phosphorous and organic matter. Wheat seedlings produced from old seed are more
susceptible to infection than seedlings produced from new seed.
Distribution.
Wherever wheat is grown. Pythium root rot occurs in patches rather than being generally distributed throughout a field.
Symptoms.
Young diseased seedlings are stunted and have chlorotic leaves that become tan. Roots lack root hairs, and fine rootlets and tips of the newest roots develop soft,
wet, light brown areas. Seedlings grow out of this condition unless low soil temperatures continue, then diseased seeds and seedlings may damp off. Diseased plants
have fewer tillers, which results in fewer heads per plant and those heads are slow to mature. Yields are reported to be only 75% to 80% of an average yield in years
of normal or above normal precipitation.

Page 903
Management
2. Maintain adequate phosphate levels in soils. This promotes root growth and allows plants to "grow away" from the disease.
3. Some cultivars are able to tolerate disease because they have a better root system than other cultivars.
Red Smudge or Pink Smudge
The names red smudge and pink smudge are used interchangeably in the literature. Pink smudge is similar to pink seed caused only by Erwinia rhapontici, where
only damaged kernels are infected, particularly those injured by the gall midge or when grain is harvested too early. The two diseases are considered separately in this
book because pink or red smudge has been reported to be caused by more than one microorganism.
Cause.
Erwinia rhapontici, Fusarium spp., and Pyrenophora triticirepentis. Discoloration by P. triticirepentis only is commonly known as red smudge. Disease occurs
during seed development and is favored by low temperatures, high rainfall, and frosts that delay maturity and ripening of the crop. Grain discoloration is favored by
high moisture during kernel development and may be more of a problem under irrigation.
Distribution.
Widespread.
Symptoms.
Symptoms are a pinkish or reddish discoloration of part or all of the kernel.
Management.
Not reported.
Rhizoctonia Bare Patch
Rhizoctonia bare patch is considered to be a form of Rhizoctonia root rot. Rhizoctonia bare patch is also called bare patch, nogrowth patches, purple patch,
Rhizoctonia patch, Rhizoctonia root rot, root rot, and stunting disease. Crater disease is similar but is caused by a R. solani that does not anastomose with AG8.
Symptoms differ sufficiently to consider Rhizoctonia bare patch (and root rot) and crater disease separate diseases.
Cause.
Rhizoctonia solani AG8, teleomorph Thanatephorus cucumeris, is generally considered the causal pathogen. However, some researchers have suggested that a
complex of fungi, rather than any one pathogen alone, is the cause of Rhizoctonia bare patch of cereals in western Australia and elsewhere. In Texas, most isolates
were found to be AG4 or AG5, due to the Texas disease possibly being different from Rhizoctonia bare patch disease in Australia. Other fungi isolated from
Rhizoctonia bare patches include a binucleate Rhizoctonia sp. AGC, Fusarium graminearum, Bipolaris sorokini

Page 904
ana, R. oryzae (teleomorph Waitea circinata), Mortierella sp., and Pythium irregulare. Other Rhizoctonias with the teleomorphs Ceratobasidium cornigerum
and Ceratobasidium spp. have been found to be mildly pathogenic to wheat.
The pathogen is possibly spread by the movement of infested residue or by mycelia growing from plant to plant along the drill row. Disease severity is greater under
conservationtillage conditions than under conventional cultivation. This may be because cultivation fragments pieces of infested residue, which in turn reduces the
propagule size and affects the ability of hyphae to ramify through the soil. Fragments of hyphae also may be more prone to attack by other soil microorganisms.
Cultivation may also prevent a buildup of organic matter that provides a substrate for the fungus to grow on. A toxin or abiotic factor may also be involved with the
stunting of plants within patches that have apparently healthy root systems.
In southern Australia, the disease occurs in highly calcareous, sandy soils; however, it has since occurred on other soil types because of the widespread use of
reducedtillage systems. In New South Wales, the disease is found on calciumdeficient and acid soils, and in western Australia, disease is most severe on plants
growing in sandy to loamy sand soils. Disease, in general, is more severe on host plants that are growing in dry soils.
In Texas, disease was observed on wheat sown in August or early September when soil temperatures were high. However, in Australia, the pathogenicity of R. solani
AG8 in artificially infested soil was greater at 12°C than at 27° and 32°C. In Oregon, root rot was more severe at low temperatures of 19° and 6°C, day and night,
respectively, than at high temperatures of 27° and 16°C, day and night, respectively.
The herbicide chlorsulfuron at 2.5 g/ha significantly increased disease.
Distribution.
Australia, Canada, England, Scotland, South Africa, and the United States (Idaho, Oregon, Texas, and Washington). The disease may not be the same in all
geographical areas. For example, the disease in Texas may be different from that in Australia.
Symptoms.
The descriptions of symptoms in the literature vary between geographical areas. The most characteristic field symptom is the occurrence within an apparently healthy
crop of stunted plants in distinct patches that vary in size from less than 30 cm in diameter to large irregularshaped areas up to 0.4 ha. Patches are sometimes circular
but are usually elongated in the direction of sowing. Patches often occur in clusters rather than randomly. Within clusters, the patches often coalesce and form larger,
irregularshaped patches. A related symptom is the killing of all wheat plants when the plants are still small so that by harvest time, the "hole" in the crop is filled with
weeds.
Patches normally have a distinct margin that forms between the stunted plants in patches and normalsized plants in the surrounding

Page 905
crop. Patches are most clearly observed at the tillering stage but can be detected 2 to 3 weeks after sowing.
Plants within the patch are stunted and display a range of symptoms associated with poor nutrition and moisture stress. Plants immediately outside the patch usually do
not display the symptoms of nutrient deficiency or moisture stress. Plants within the patch display the following symptoms: yellowing of the lower leaves, a stiff upright
leaf habit, rolled leaf blades, spindly growth, failure to produce tillers, and under cold conditions, a dark green coloration and purplish tinge of leaf blades when they
are viewed from a distance. In Texas, diseased plants lose the lower leaves and the lower leaf sheaths become dark brown and necrotic.
In some locations, stunted plants will have little or no growth during the growing season, but at other locations, plants display some growth but remain stunted or
spindly compared to the rest of the crop. Plants within patches often remain green longer than the surrounding crop, possibly due to a delay in maturity or to greater
availability of soil moisture in the patch. If plants within patches are not severely stunted, they may recover but have fewer tillers than healthy plants and produce a
poor yield.
The seminal roots of young seedlings have discrete dark brown, watersoaked lesions that are confined to one side of the diseased root or girdle the entire root and
cause the cortex to slough off, leaving the stele exposed. The stele eventually rots through and leaves a pointed stub or spear tip. The root tips are yellowish brown but
often become dark brown in older plants. Severe disease on some plants causes the entire root system to be truncated. Disease severity may vary among the different
seminal roots, and an occasional plant may have apparently healthy seminal roots but severely damaged coronal roots. Some plants within a patch have an apparently
intact root system but remain stunted like the surrounding diseased plants. Plants outside a patch may have considerable root rot but no stunting, possibly due to late
infection by R. solani AG8 or other Rhizoctonia spp.
Management
1. Application of N as ammonium sulfate, urea, or sodium nitrate reduces disease. Calcium applied to calciumdeficient soils reduces disease.
2. Practice the appropriate tillage system. Wheat sown in reducedtillage situations becomes more severely diseased than wheat sown in conventional tillage
conditions. Mixing soil deeply (5 cm or more) reduces root rot, possibly because loosened soil may allow faster root growth. Two cultivations reduce disease more
than a single cultivation. Cultivation close to sowing also reduces disease.
3. Practice proper rotation. Wheat following a medicdominant pasture has more severe root rot than wheat following a grass pasture. In Texas, do not rotate sugar
beet with wheat because R. solani AG4 is also highly virulent on sugar beet.

Page 906
Sclerotinia Snow Mold
Sclerotinia snow mold is also called snow scald.
Cause.
Myriosclerotinia borealis (syn. Sclerotinia borealis) oversummers as sclerotia in infested residue in soil near the soil surface and on the soil surface. In autumn, the
sclerotia germinate during damp, cool weather and form cupshaped apothecia. Ascospores are produced in a layer of asci on the upper portion of the apothecium
and disseminated by wind to seedlings. Snow scald occurs when cool, damp autumns are followed by a deep snow cover over unfrozen or slightly frozen soil that lasts
for 5 or more months. Myriosclerotinia borealis has been identified on cocksfoot, Dactylis glomerata.
Distribution.
Canada, Europe, Japan, Scandinavia, and the former USSR.
Symptoms.
Symptoms of snow scald occur in scattered patches throughout a field. Sparse, gray mycelia cover bleached, dead plants that are exposed to the air as the snow
melts. Diseased leaves wrinkle on exposure to light and eventually turn dark, because of the saprophytic growth of other fungi, and crumble away. Sclerotia are
globular, elongated, or flakelike (0.37.0 mm long) and are black at maturity. Sclerotia are only found in and on leaves, leaf sheaths, and the crowns of dead plants.
Management.
While there is no entirely satisfactory management of snow scald, the following measures will be of some benefit:
1. Rotate winter wheat with spring wheat, another spring cereal, or a legume to help reduce inoculum.
2. Plowing under residue will bury sclerotia and prevent them from germinating, thereby hastening their decomposition.
Septoria leaf blotch is also called leaf blotch, Septoria disease, Septoria leaf spot, Septoria tritici blotch, and speckled leaf blotch.
Cause.
Septoria tritici, teleomorph Mycosphaerella graminicola. The fungi overwinter as mycelia in diseased live wheat plants, and survive as pycnidia on infested residue
for 2 to 3 years. Residue is the primary source of inoculum. Septoria tritici is seedborne; however, seedborne inoculum is uncommon.
Disease development is dependent on temperature rather than on the growth stage of plants at infection. During temperatures of 15° to 25°C and 100% (the optimum)
relative humidity in the autumn or spring, pycnidiospores are exuded from pycnidia in a gelatinous drop, or cirrhi, that protects spores from radiation and drying out.
Pycnidiospores are disseminated to the lower leaves of host plants by splashing and blowing rain. In Indiana, primary infection takes place in the autumn before the
onset of

Page 907
cold weather; consequently, S. tritici probably overwinters as asymptomatic infections. In the absence of functional pycnidiospores in California, ascospores were
ascribed to be the primary inoculum.
Infection requires 6 or more hours of wetness; subsequent disease development is favored by temperatures of 18° to 25°C. However, response to temperature varies
with the amount of cultivar resistance. New pycnidiospores are produced in 10 to 20 days; more pycnidia are produced on susceptible cultivars than on resistant
cultivars.
Ascospores produced in pseudothecia as wheat matures in late summer or early autumn and disseminated by wind to host plants contribute to the inoculum that
initiates primary disease of wheat sown in the autumn. Mycosphaerella graminicola is readily found on residue in the United Kingdom.
Distribution.
Generally distributed wherever wheat is produced. Septoria leaf blotch can become a serious disease during environmental conditions that are conducive for disease
development.
Symptoms.
Septoria leaf blotch has two conspicuous phases: during the winter on basal leaves of wheat sown in the autumn, and during the summer on upper leaves of host
plants. Initially, small, light green to yellow spots occur between the leaf veins of lower leaves, especially if the leaves are in contact with soil. Spots rapidly elongate
and form tan to redbrown, irregularshaped lesions that are often partly surrounded by a yellow margin. Lesions age and become light brown to almost white and
have small, dark specks (pycnidia) in the center. The presence of pycnidia is a good diagnostic characteristic.
Infection of stem nodes, leaf sheaths, and the tips of glumes also occurs. Severely diseased leaves become yellow and die prematurely. Occasionally an entire plant
may be killed. Pycnidia are produced in all diseased areas of a plant. Autumn and winter infections cause a reduction in the root weight and the mass of diseased
plants.
Management
1. Sow cleaned, certified seed that is free of disease and has been treated with a seedprotectant fungicide.
3. Grow resistant wheat cultivars. Durum wheat is often reported as relatively resistant; however, durum wheats tested in Tunisia were more susceptible to the local
isolates of S. tritici than the bread wheat entries were.
4. Apply a foliar fungicide if environmental conditions favor disease development.
5. Rotate wheat with a resistant crop once every 3 to 4 years.
6. Sow winter wheat after the Hessian flyfree date.

Page 908
Sharp Eyespot
Cause.
Rhizoctonia cerealis CAG1, teleomorph Ceratobasidium cereale. Rhizoctonia solani AG4 and a binucleate species also have been reported as the causal fungi;
the strains that cause sharp eyespot differ from those that cause Rhizoctonia root rot. The strains of AG4 did not infect roots but killed seedlings in the greenhouse.
The fungi survive as sclerotia in soil and as mycelia in the infested residue of a large number of plant genera. Sclerotia germinate and form mycelia or mycelia grow
from precolonized substrates to infect roots and culms any time during the growing season, particularly in dry soils with less than 20% moistureholding capacity, and
during cool soil temperatures.
Distribution.
Symptoms.
Diseased plants are stiff, have a grayish cast, and delayed maturity. Seedlings may be killed, but older diseased plants may produce new roots to compensate for those
that rotted off. When roots are diseased, plants lodge and produce white heads.
Diamondshaped lesions that resemble those of eyespot occur on diseased lower leaf sheaths. However, sharp eyespot lesions are more superficial than eyespot
lesions. Lesions have light tan centers with dark brown margins. Frequently dark mycelium is visible on the lesions. Dark sclerotia eventually develop in lesions and
between the culms and leaf sheaths of diseased plants.
Management.
Vigorous plants growing in wellfertilized soil do not become as severely diseased as unthrifty plants.
Snow Rot
Cause.
Pythium aristosporum, P. iwayami, P. okanoganense, and P. paddicum. Pythium ultimum has also been reported as a causal fungus. Survival over the summer
is presumed to be by oospores in soil and infested residue. Oospores germinate and form sporangia in which zoospores are produced. The zoospores are released
into the soil and disseminated by snowmelt water to host plant roots. Wheat plants must be predisposed by an extended period of time under snow cover before they
become susceptible to infection. Snow rot development depends on extended periods of snow cover and nearfreezing temperatures. In Washington, disease is
confined to areas where water collects during snow and ice melt. In North Dakota, the absence of ground frost contributes to the disease syndrome.
Distribution.
Japan and the United States. In Japan, P. paddicum was the dominant pathogen isolated from poorly drained paddy fields and P. iwayami was the dominant
pathogen isolated from upland fields. Pythium iwaya

Page 909
mai, P. okanoganense, and P. paddicum were all isolated from welldrained paddy fields.
Symptoms.
As plants emerge from under a snow cover, older leaves have large, dark green, watersoaked areas. Younger leaves are distorted, watersoaked, dark green, and
flaccid. The soft tissue becomes brown or tan and the basal leaf sheaths are dark brown and filled with oospores. Leaves touching the soil are more decayed than
those in an upright position. Diseased plants are killed when fungi invade the growing point.
Root tissues are invaded when runoff water washes soil from around crowns. Stele and cortical root tissues rot and the diseased cortical tissues slough from roots.
Diseased plants develop few tillers and root systems are reduced. Inoculated plants are severely stunted.
Management.
Not reported.
Southern Blight
Southern blight is also called Sclerotium base rot and white rot.
Cause.
Sclerotium rolfsii, teleomorph Athelia rolfsii.
Distribution.
Australia and Brazil.
Symptoms.
White mycelia and sclerotia occur on the necrotic areas of diseased roots, crowns, and lower portions of stems. Diseased plants turn white and die.
Management.
Not reported.
Speckled Snow Mold
Cause.
Typhula idahoensis, T. incarnata (syn. T. itoana), T. ishikariensis, and T. ishikariensis var. T. ishikariensis overseason as sclerotia in infested residue and soil or
as parasitic growth on live plants. Saprophytic growth on dead tissue provides an inoculum source for increased disease in the spring; however, the fungi are poor
saprophytes and depend primarily on parasitism for existence. Sclerotia germinate during wet weather in the autumn and form either basidiocarps or mycelia. Optimum
infection occurs at temperatures of 1° to 5°C when basidiospores form on basidiocarps and are disseminated by wind, or mycelia directly infect host plants by
growing over the surface of the soil. Further infection occurs by mycelial growth under snow cover. Sclerotia form within necrotic tissue or in mycelium.
Bacteria described as gramnegative white colonies of fluorescent pseudomonads have been reported to be the most antagonistic to Typhula incarnata and T.
ishikariensis at temperatures of 5° to 15°C. This may be one

Page 910
reason why these fungi prevail almost exclusively under snow cover, where low temperatures inactivate most antagonists.
The growth of Typhula spp. is more closely related to snow cover than is the growth of Microdochium nivale, the cause of pink snow mold. Typhula ishikariensis
has been identified on cocksfoot, Dactylis glomerata.
Distribution.
Symptoms.
At snowmelt, graywhite mycelia are present on the leaves and crowns of diseased plants, and on soil. The numerous sclerotia in diseased plant tissues and scattered
in mycelia growing over plant surfaces give plants a ''speckled" appearance. Dead leaves are common, but unless the crowns are diseased, plants recover during
warm, dry weather but are not as vigorous as healthy plants. Dead leaves crumple easily and are covered with gray to white mycelium.
Management
1. Rotate wheat with a legume to reduce the inoculum in soil since the fungi are not good saprophytes.
2. Disease incidence was decreased in experiments by fungicide seed treatments.
Spot Blotch
Spot blotch is also called Bipolaris leaf spot and Helminthosporium leaf spot.
Cause.
Bipolaris sorokiniana (syn. Helminthosporium sativum and H. sorokinianum), teleomorph Cochliobolus sativus, survives primarily as conidia and mycelia in
infested residue. Conidia are produced from mycelium in residue and disseminated by wind to host plants. Infection occurs primarily during wet weather as host plants
approach maturity.
Distribution.
Symptoms.
Symptoms are evident after senescence. They are most frequent on the lower diseased leaves as distinct, elongated, brownblack lesions that are less than 1 cm in
length.
Following mixed inoculation with Pyrenophora triticirepentis, wheat leaves developed less necrosis than the average necrosis produced by the two pathogens
alone.
Management
1. Ensure proper soil fertility.
2. Rotate wheat with resistant crops.
3. Grow resistant cultivars. Cultivars with some resistance to spot blotch may not be resistant to other diseases, such as black point and common root rot, caused by
B. sorokiniana.

Page 911
Stagonospora Blotch
Stagonospora blotch is also called glume blotch, Septoria blotch, Septoria nodorum blotch, Septoria nodorum blotch of wheat, and Septoria nodorum leaf and
glume blotch of wheat. In some reports, Stagonospora is spelled "Stagnospora."
Cause.
Phaeosphaeria avenaria f. sp. triticea, anamorph Stagonospora avenae f. sp. triticea (syn. Septoria avenae f. sp. triticea), and Stagonospora nodorum (syn.
Septoria nodorum), teleomorph Phaeosphaeria nodorum (syn. Leptosphaeria nodorum). The causal fungi are seedborne, surviving in stored seed for more than 2
years. The fungi also overwinter as mycelia in live diseased plants, and survive for 2 to 3 years as pycnidia on infested residue. Residue is the most important source of
primary inoculum.
In the autumn or spring, pycnidiospores are exuded from pycnidia in a cirrhi, or gelatinous drop, during wet weather and temperatures of 20° to 27°C. The cirrhi
protects the spores from radiation and drying out until they are disseminated by splashing and blowing rain to the lower leaves of host plants. Infection requires 6 or
more hours of continuous wetness. Infection of the coleoptile from seedborne inoculum occurs over a wide range of soil moistures, temperatures, and planting depths.
In Indiana, primary infection takes place in the autumn before the onset of cold weather. Consequently, under these conditions S. nodorum overwinters as
asymptomatic infections in infected plants.
New pycnidiospores, which are produced in 10 to 20 days and disseminated, serve as secondary inoculum. Ascospores are produced in perithecia as wheat matures
in the late summer and early autumn. In Ireland, perithecia have been recovered from green leaves of symptomless winter wheat plants collected in January and
February.
The severity of disease on seedlings increases until 4 weeks after sowing. Thereafter, disease is usually not severe until plants near maturity. The greatest yield losses
occur when rainfall is excessive between flowering and grain harvest. Increasing nitrogen fertilizer has caused an increase in disease severity.
Several grasses are alternative hosts. Some grass isolates are associated with large lesions on wheat, but most isolates produce small lesions. Considering the potential
number of isolates available from grasses, their effect on wheat is probably less than would be expected.
Distribution.
All major wheatgrowing areas.
Symptoms.
Glumes, culms, leaf sheaths, and leaves become diseased, but usually little damage occurs until diseased plants near maturity. Two to three weeks after the heads
emerge, small, grayish or brown spots occur near the top third of glumes, then enlarge and become a chocolatebrown discoloration. Later, the centers of spots
become gray and have small black pycnidia scattered throughout them.

Page 912
Diseased nodes become brown, shrivel, and are speckled with black pycnidia. These infections often cause straw to bend over and lodge just above nodes.
Diseased leaves have light brown spots that are similar to those of Septoria leaf blotch. Brown margins surround leaf spots and pycnidia are present on both leaf
surfaces. If flag leaves are diseased, the heads are deformed. Diseased leaf sheaths have a dark brown lesion that includes most of the leaf sheath. Severely diseased
plants are stunted.
A symptom caused by an atypical form of S. nodorum was a brown discoloration at the base of coleoptiles on seedlings grown from infected seed. Inoculated leaves
developed brown lesions that were surrounded by yellowish halos.
Symptoms may be confused with those of black chaff or basal glume rot. Stagonospora blotch spots do not form streaks and are not as sharply defined or as dark
brown as those of black chaff. Stagonospora blotch does not have the watersoaked appearance of basal glume rot.
Yield losses up to 50% have been reported. Yield reductions are associated primarily with reduced kernel weight. Yields are most consistently correlated with disease
severity of the leaf below the flag leaf at the Feekes growth stage 11.1.
Management
1. Sow certified, cleaned seed that is free of disease and has been treated with a seedprotectant fungicide. Seed treatment is effective when the primary source of
inoculum is from seed, but it is ineffective when the soil is heavily infested with inoculum.
5. Rotate wheat with a resistant crop once every 3 to 4 years. However, disease development is not reduced when infected seed is used.
6. Sow winter wheat after the Hessian flyfree date.
7. Grow taller cultivars instead of shorter ones. A less favorable microclimate for disease development occurs with taller cultivars.
Stem Rust
Stem rust is also called black rust and black stem rust.
Cause.
Puccinia graminis (syn. P. graminis f. sp. tritici) is a heteroecious, longcycle rust that has the barberries Berberis canadensis, B. fendleri, B. vulgaris, and
Mahonia spp. as alternate hosts. Puccinia graminis f. sp. tritici causes stem rust of wheat by one of two life cycles: (1) During the spring and summer,
urediniospores (also called repeating spores in the literature) produced in uredinia on wheat are disseminated by wind to wheat, where they infect and produce new
(secondary) urediniospores under moist con

Page 913
ditions and moderate temperatures (15° to 25°C). Secondary urediniospores are produced in cycles every 7 to 10 days throughout the growing season until wheat
plants are mature. Urediniospores produced in northern wheatproducing areas are blown south in the summer and autumn and infect wheat in southern wheat
growing areas. The urediniospores then recycle on wheat in the southern wheatgrowing areas. Eventually, spores disseminated northward during the late winter and
spring infect wheat in the northern wheatgrowing areas.
(2) As wheat ripens, teliospores are formed that survive through the winter. In the spring, teliospores germinate and form basidiospores (sporidia) that are
disseminated by wind and infect the young leaves of barberry. Pycnia (spermogonia) form on the upper leaf surfaces of barberry and function in the exchange of
genetic material, thereby creating new races of the fungus. Each pycnium produces pycniospores and special mycelia called receptive hyphae. Pycniospores are
exuded out of the pycnium in a thick, sticky, sweet liquid (honeydew) that is attractive to insects. Pycniospores are splashed by water or carried by insects from one
pycnium to another, where they become attached to receptive hyphae. The pycniospore germinates and the nucleus from the spore enters the receptive hypha and
forms an aecium on the lower leaf surface, directly under the pycnium. Aeciospores that differ genetically from both pycniospores and receptive hyphae are produced
in the aecia, then are windborne to wheat hosts, where infection occurs. Each infection gives rise to a uredinium that produces urediniospores that serve as the
repeating stage and are repeatedly disseminated by wind to wheat, where new generations of urediniospores are formed. Telia are once again produced as diseased
wheat plants mature, thus completing the life cycle. Epiphytotics develop during moist weather but disease is not severe during dry weather.
Distribution.
Symptoms.
Uredinia and telia occur on diseased stems, leaf sheaths, leaf blades, glumes, and beards of wheat. Uredinia are redbrown oblong pustules. The plant epidermis
ruptures and is pushed back, exposing the urediniospores and giving the pustule a jagged or ragged appearance.
Just prior to plant maturation, telia appear primarily on leaf sheaths and culms. Telia are oblong to linear and dark brown to black. Teliospores are exposed by a
rupturing of the host epidermis.
Pycnia appear on barberry leaves in the spring as bright orange to yellow spots with what sometimes appears to be a drop of liquid in the middle that contains the
pycniospores and receptive hyphae. On the side of the barberry leaf opposite the pycnial spots are the aecia, which resemble raised, orange, bellshaped clusters.
Management
1. Grow resistant wheat cultivars. The hypersensitive reaction to stem rust

Page 914
is closely associated with resistance controlled by the Sr5 gene.
2. Eliminate the common barberry from wheatproducing areas. The common barberry should not be confused with the Japanese barberry, which is immune to stem
rust. There are several characteristics to differentiate between the two. The common barberry has a sawtoothed leaf edge, gray outer bark, bright yellow inner bark,
berries borne in bunches, and spines with usually three in a group. The Japanese barberry has a smooth leaf edge, redbrown outer bark, bright yellow inner bark,
berries borne in ones or twos, and usually a single spine.
3. Late sowing reduces the effectiveness of the slow rusting character that bestows tolerance to rust.
Stripe Rust
Stripe rust is also called glume rust and yellow rust.
Cause.
Puccinia striiformis f. sp. tritici (syn. P. striiformis) is a rust fungus that is not known to have an alternate host. The fungus oversummers as urediniospores on
residual green cereals and grasses during the period between harvest and the emergence of wheat sown in the autumn. Mycelia and infrequently urediniospores remain
alive over the winter in or on different hosts, such as barley, grasses, and rye. Teliospores are formed but are not known to function as overwintering spores.
Urediniospores are formed during cool, wet weather and disseminated by wind to host plants, where infection occurs. Infection is restricted to a relatively narrow
range of temperatures (5° to 12°C). Little infection occurs above 15°C. The minimum continuous dew period necessary for infection increases from 4 to 6 hours at the
optimal temperatures to at least 16 hours for suboptimal temperatures. Warmer than normal winters and cooler April temperatures favor development of stripe rust
epiphytotics.
Distribution.
Australia. In North America, stripe rust occurs at the higher elevations and cooler climates along the Pacific Coast and intermountain areas from Canada to Mexico. It
also occurs under the same circumstances in South America and in the mountainous areas of central Europe and Asia.
Symptoms.
The most severe symptoms occur during cool, wet weather in the early growth stages of wheat. Symptoms occur early in the spring before other rusts are evident,
especially in wheatgrowing areas that have mild winters. Yellow uredinia appear early in the spring on autumn foliage and new spring foliage. Uredinia coalesce and
form long stripes between the veins of diseased leaves and sheaths. Small, linear lesions occur on floral bracts. Telia develop as narrow, linear, dark brown pustules
that are covered by the leaf epidermis.
Management
1. Grow resistant wheat cultivars.

Page 915
2. Ensure soils are well fertilized. Potassium levels must be adequate.
3. Cool spring temperatures delay temperaturesensitive adult plant resistance in some cultivars.
4. Apply foliar fungicide. In Australia it is recommended to spray when 1% of leaf area is affected and predicted yield loss is sufficient to make spraying economical.
5. Experimentally, fungicide seed treatments have proven effective.
TakeAll
Takeall is also called Ophiobolus patch.
Cause.
Gaeumannomyces graminis var. tritici, G. graminis, and G. graminis var. avenae (syn. Ophiobolus graminis var. avenae) survive as mycelia in diseased plants
or as mycelia and perithecia in infested residue. Gaeumannomyces graminis var. tritici is not a good saprophyte and does not survive long in soil in the absence of a
live host. Because the competitive saprophytic ability of G. graminis var. tritici is low, roots and crowns colonized by the fungus during parasitism act as primary
inoculum. The viability of inoculum declines as soil microorganisms subsequently colonize and decompose the parasitized residue. Thus, the pathogen population is
characterized by increasing inoculum potential during the parasitic phase followed by decreasing inoculum potential during the saprophytic phase.
Seedlings become infected in the autumn or spring when roots grow in the vicinity of residue previously parasitized by G. graminis var. tritici and come in contact
with mycelia. Planttoplant spread of takeall occurs by hyphae growing through soil from a diseased plant to a healthy plant or by a diseased root coming into
contact with a healthy root. Ascospores are produced in perithecia during wet weather but are not considered important in disease spread because they are not
disseminated a great distance either by splashing water or by wind.
Disease incidence and severity depend on a number of interrelated factors. Disease occurs during low to moderate temperatures and is more severe in reducedtillage
systems than in conventional tillage systems. Tillage practices that fragment the inoculum and expose it to increased microbial degradation also can lower the inoculum
potential of the pathogen and limit disease development. Takeall is more severe with direct drilling in the Pacific Northwest due to the large size of inoculum pieces
associated with directdrill conditions.
Inoculum in the form of "propagules" builds up more under pasture than wheat because of a larger mass of fine, dense roots in the top 10 cm of soil under grasses than
under wheat. A decline in propagule numbers and infectivity in the absence of a susceptible host has been associated with the wetting of warm soils, which stimulates
the activity of competitive microorganisms. High soil moisture favors microbial activity, accelerating

Page 916
the breakdown of pathogeninfested residue and, hence, the destruction of the food base and habitat of G. graminis. vat. tritici. Conversely, some researchers have
reported a high incidence and severity of disease was associated with regular rainfall patterns.
However, disease may be more dependent on soil factors than on the number of propagules and infectivity. Disease becomes more severe at higher soil pHs.
Increased soil acidity may directly reduce the activity of the fungus or may stimulate activity of microorganisms antagonistic to G. graminis var. tritici. Host plant
predisposition may also result from inadequate supplies of certain essential plant nutrients, such as manganese, at higher pHs. Soil phosphorous and mycorrhizae affect
disease development by increasing the phosphorous status of the host. Subsequently, the leaking of exudates from roots is reduced, which in turn reduces pathogen
activity. There may also be a relationship between the form of nitrogen fertilizer and disease incidence.
Under humid, somewhat acidic soil conditions, fertilizers containing ammonium nitrogen rather than nitrate nitrogen suppress takeall or increase yield of wheat infested
with G. graminis var. tritici. Fertilizers containing chloride are effective in suppressing takeall and increasing yield of soft winter wheat grown on acidic soils in the
Pacific Northwest. Chloride may suppress takeall by decreasing the water potential in the plant or by inhibiting nitrification in unlimed acidic soils. Under alkaline soil
conditions in the northern Great Plains, the application of chloride has little effect on disease severity indices, and the nitrogen fertilizer source did not affect root
disease scores but did affect the percentage of white heads.
Distribution.
Wherever wheat is grown. Takeall is generally considered to be the most important root disease of wheat worldwide.
Symptoms.
Takeall symptoms are most severe on wheat grown in alkaline soils. The first symptoms are light brown to dark brown necrotic lesions on roots. By the time a
diseased plant reaches the jointing stage, most of its roots are brown and dead. At this point, many plants die and plants that live remain chlorotic and stunted.
Symptoms become most obvious as plants approach the heading stage of plant growth. The stand is uneven in height and plants appear to be in several stages of
maturity. Diseased plants have few tillers, ripen prematurely, and have heads that are bleached and sterile. Roots are sparse, blackened, and brittle, and when pulled
from the soil, plants easily break free of crowns. A very dark discoloration of the stem is visible just above the soil line. A mat of dark brown mycelium normally can
be seen under the lower leaf sheath between the stem and the inner leaf sheaths.
Management
1. Rotate wheat with a nonhost crop. In western Australia, a rotation with lupines, oat, or field peas reduced inoculum and suppressed growth of the pathogen in soil.

Page 917
3. Sow later in the growing season. This extends the period the fungus must survive as a saprophyte and reduces the inoculum level at planting time. The lower
temperatures associated with late sowing also favor a more vigorously growing plant.
4. Apply fertilizers containing ammonium nitrogen, phosphorous, and chloride if soils are acid.
5. Certain macronutrients, such as phosphorous, and micronutrients, such as copper, iron, manganese, and zinc, have the potential for limiting takeall by lessening
susceptibility of host tissues, promoting formation of new roots, or both.
6. Severity of takeall declines and wheat yields increase following one or two outbreaks of the disease and continuous monoculture of wheat.
7. Fluorescent pseudomonads in the rhizosphere of wheat produce phenazine antibiotics that are reported to suppress takeall.
8. Management practices that increase soil shading, such as volunteer wheat, double cropping, and no tillage, tend to prevent high soil temperatures and may promote
inoculum survival and disease.
Tan Spot
Tan spot is also called leaf spot, blight, and yellow leaf spot.
Cause.
Pyrenophora triticirepentis, anamorph Drechslera triticirepentis. Some researchers consider P. trichostoma to be synonymous with P. triticirepentis but Farr
et al. (1989) do not.
Pyrenophora triticirepentis produced on straw in the autumn and winter overwinters as mycelia and pseudothecial initials in infested residue that is primarily on the
soil surface. Pyrenophora triticirepentis is also seedborne, but airborne inoculum is the primary source of infection. Ascospores are the most important primary
inoculum, but conidia and hyphae also serve as primary inoculum. Pyrenophora triticirepentis is also isolated from several grass species. Isolates from these grass
hosts differ in their ability to cause disease symptoms on wheat, and some are as aggressive as wheat isolates. Infection and disease development are favored by
frequent rains and cool, cloudy, humid weather early in the growing season.
Conidia produced in older lesions on leaves killed by the pathogen and disseminated by wind to plant hosts serve as secondary inoculum. Infection requires a 6 to
48hour wet period, and the most infections occur in the vicinity of infested host residues. Increasing the postinoculation wet period of foliage increases lesion size.
Pseudothecial initials are produced on infected culms and leaf sheaths in the autumn.
Infection of wheat seed in the field occurs after the early dough stage and is positively correlated with tan spot severity on the flag leaf after anthesis. Disease
development is related to the initial amount of primary inoculum, despite multiple infection cycles caused by windborne secondary

Page 918
inoculum. Seed infection predominantly occurs via the lemma and palea, rather than the glume. The presence of anthers adjacent to the seed apparently enhances seed
infection.
Epiphytotics are commonly associated with conservationtillage practices because straw remaining on the soil surface supports development of abundant primary
inoculum. Pyrenophora triticirepentis survives poorly in straw that is buried or placed directly on the soil surface. In contrast, it survives well in straw that is slightly
above the soil surface, such as standing stubble or straw within a mulch layer. Disease is more severe in tall stubble than in short stubble. Residue in close contact with
soil is moist more frequently and remains moist longer than residue above the soil surface. This high moisture environment could result in more intense microbial activity
and competitive interactions detrimental to the survival and inoculum potential of P. triticirepentis.
Isolates of P. triticirepentis differ in virulence. Four pathotypes have been identified based on their ability to induce one of four symptoms: tan necrosis followed by
extensive chlorosis, tan necrosis only, extensive chlorosis only, and neither necrosis nor chlorosis on appropriate differential cultivars.
In culture, Pyrenophora triticirepentis releases a hostselective toxin designated the Ptr toxin, a protein of low molecular weight. Ptr toxin is produced by tan
necrosis isolates only and is found associated with the induction of tan necrosis in the host.
The reaction of wheat cultivars to tan spot differs from one part of the world to another. Resistance occurs first as papilla formation, then as the restriction of lesion
size and mycelial growth in the lesion. Wheat genotypes differ in their ability to restrict growth of P. triticirepentis as the period of postinoculation foliar wetness
lengthens and/or the temperature rises.
The herbicide glyphosate inhibits ascocarp formation on straw.
Distribution.
Symptoms.
Symptoms first appear in the spring on lower diseased leaves and leaf sheaths and progress to the upper leaves in the early summer. Regardless of plant growth stage
at infection, the oldest leaf is the most severely spotted and the youngest leaf is the least severely spotted. Diseased plants exhibit one of the following four symptoms:
1. Tan necrosis and extensive chlorosis begins as small brown or tan flecks or spots on both sides of seedling leaves. The flecks eventually become diamondshaped,
necrotic lesions up to 12 mm long, with a yellow border (halo) and a dark brown spot in the center that is due to sporulation by P. triticirepentis. Necrosis and/or
chlorosis often extend to cover the entire leaf. Extensive chlorosis may mask the tan necrosis.

Page 919
2. Necrotic lesions are well defined and consist of tan collapsed tissue that may coalesce and cause large areas of diseased leaves to die from the tip inward.
3. Chlorotic lesions exhibit a gradual yellow discoloration without collapsed tissue on large areas of diseased leaves. Lesions coalesce and cause large areas of
diseased leaves to die from the tip inward. Pseudothecia will eventually develop on straw as dark raised bumps.
4. Resistant symptoms are characterized by the absence or presence of slight amounts of necrosis and/or chlorosis.
A red smudge symptom on seed results in a downgrading of quality.
It has been reported that half of the total yield loss is due to disease that occurs before the boot stage. Following mixed inoculation with Bipolaris sorokiniana, wheat
leaves developed less necrosis than the average produced by each of the two pathogens alone.
Management
1. Grow resistant cultivars. Differences in resistance exist among wheat genotypes. Resistance has been attributed to polygenic or monogenic control. Resistance
decreases with leaf aging.
2. If weather conditions are wet, apply a foliar fungicide before the disease becomes severe. Fungicide sprays for tan spot management may have to be applied earlier
than for the rusts.
4. Rotate with nonhost crops. Rotation to sorghum was reported to be as effective as plowing under infested residue.
5. Nitrogen fertilizations NH4SO4 and CaNO3 reduce tan spot severity by delaying leaf senescence but do not have a direct effect on tan spot.
Tar Spot
Cause.
Phyllachora graminis, anamorph Linochora graminis, overseasons as stromata on residue. Disease is favored by moist, shaded areas.
Distribution.
Widespread. Tar spot occurs infrequently on wheat.
Symptoms.
Glossy black and somewhat sunken spots occur on diseased leaf blades and sheaths. Spots (0.10.2 × 5.0 mm) are the stromata of P. graminis.
Management.
Not necessary.
TyphulaLike Snow Mold
Cause.
A basidiomyceteous fungus similar to Typhula spp. Disease occurs under a prolonged snow cover. The fungus is considered a weak pathogen and has been identified
as OKLA1 in the literature.

Page 920
Distribution.
The United States (Oklahoma).
Symptoms.
Dead plants occur under a prolonged snow cover, especially in fields that slope northward. Small black subepidermal sclerotia, which are flatter than sclerotia of both
T. ishikariensis and T. idahoensis, are present in the basal leaf sheaths of living and dead plants.
Management.
Not reported.
Wheat Blast
Cause.
Pyricularia grisea. Confusion exists in the literature as to the nomenclature of the causal fungus. Pyricularia oryzae has been ascribed to be the causal fungus by
some researchers. However, Farr et al. (1989) state that P. oryzae is the name for the causal fungus of rice blast, but P. grisea is an older name for P. oryzae and is
the proper name for blast or gray spot of grasses. The teleomorph stage is unknown. There may be two distinct entities causing wheat blast in Brazil, and one may be
the rice blast strain.
Long periods of leaf wetness and high temperatures are needed for disease to occur. Barley, oat, and rye are also susceptible, which suggests these diseased plants
may be potential sources of inoculum. There are five known races of the wheat blast fungi.
Distribution.
Brazil.
Symptoms.
The greatest damage occurs when symptoms appear during or just after the anthesis stage of plant growth. Diseased spikes are totally or partially whitened and have
blueviolet lesions on the rachis. Yields are reduced.
Management
1. There are differences in resistance between cultivars.
2. Apply foliar fungicides. However, the application of foliar fungicides has resulted in incomplete control.
3. Apply fungicide seed treatments.
Zoosporic Root Rot
Cause.
Lagena radicicola, Ligniera pilorum, Olpidium brassicae, and Rhizophydium graminis. The fungi thrive in wet soils.
Lagena radicicola overseasons as resting spores in diseased root hairs. Resting spores give rise to zoospores that ''swim" to root epidermal cells and gain entrance by
means of a penetration peg. Once a zoospore is inside a cell, a thallus forms and attaches to the cell wall. Thalli develop into either sporangia or thickwalled resting
cells. The other fungi have similar life cycles.
Distribution.
Widespread.

Page 921
Symptoms.
The fungi are not serious pathogens but are more important as possible vectors of soilborne plant viruses.
Management.
Not necessary.
Bulb and Stem
Cause.
Ditylenchus dipsaci. Occurrence of the nematode is associated with heavy soils, high rainfall, cool growing seasons, and winter grains. Free moisture permits the
nematode to migrate to and feed on aerial plant parts. The nematode penetrates the leaves and stems.
Distribution.
Symptoms.
Cell hypertrophy and hyperplasia occur. Stunting, distortions, and swollen stems are common symptoms. In severely infested areas, growing points are destroyed and
diseased plants may die. Other plants have reduced spike growth and grain yields.
Management
Cereal Cyst
Heterodera avenae is called the cereal cyst nematode and oat cyst nematode.
Cause.
Heterodera avenae (syn. H. major). Other Heterodera species on wheat are H. bifenestra, H. hordecalis, and H. latipons. Heterodera avenae survives for a year
or more as cysts in soil. In the spring, larvae emerge from eggs within overwintered cysts, enter plant roots, and begin feeding. As eggs develop in their bodies, female
nematodes swell and break through the root surface but remain attached to the root by a thin neck. Males revert to a veriform size. Eventually, females form cysts that
detach from roots. One nematode generation from egg to adult is completed in 9 to 14 weeks. Heterodera avenae is also a pathogen of barley, oat, rye, and
numerous annual and perennial grasses.
Populations of nematodes increase in sandy soils. Other conditions, such as the death of nematodes when roots die, and nemaphagous fungi that parasitize nematodes
also cause a fluctuation in nematode populations.
Distribution.
Africa, Australia, southeastern Canada, Europe, Japan, the United States (Oregon), and the former USSR.
Symptoms.
The first symptom is poor growth of diseased plants in one or

Page 922
more areas within a field. Leaf tips of heavily infested plants are red or purple. The discolored leaves die and diseased plants become yellow. The roots are thickened
and more branched than those of healthy plants. Heavy nematode infestations cause wilting, particularly during times of water stress; stunted growth; poor root
development; and early plant death. Lemonshaped cysts are white at first, then gradually become dark brown as they harden. Cysts are visible without magnification.
Management
1. Rotate wheat with a legume crop.
2. Apply a nematicide to infested soil before sowing wheat.
3. Grow a resistant or tolerant cultivar. Tolerance has been identified in wheat cultivars grown in experimental plots. Significant differences between cultivars have been
identified for total grain weight, number of grains, number of fertile spikelets, and number of heads per plot.
4. Sow wheat in the autumn. Because plants from seed sown in the autumn develop larger root systems, they tolerate nematode infection better than wheat sown in the
spring.
Columbia Root Knot
Cause.
Meloidogyne chitwoodi.
Distribution.
Widespread.
Symptoms.
General growth of diseased plants is reduced. There are less tillers per plant of winter wheat, and the dry shoot weight may be reduced in some cultivars.
Management.
Not reported.
Dagger
Cause.
Xiphinema americanum is an external parasite that prefers feeding on young succulent roots.
Distribution.
Widespread. Damage on wheat is likely not very severe.
Symptoms.
Moderate swelling occurs on young diseased roots. Severely diseased plants have clusters of short, stubby root branches, and small roots shrivel at their points of
attachment. The most obvious symptom is one or several necrotic flecks, which vary from light brown to dark brown or black, on diseased roots.
Management.
Not necessary.
Grass Cyst
Cause.
Punctodera punctata (syn. Heterodera punctata). The life cycle is similar to that of H. avenae. (See "Oat Cyst Nematode" in Chapter 11.)

Page 923
Distribution.
Symptoms.
The first symptom is poor growth of diseased plants in areas within a field. Leaf tips of severely diseased plants are red or purple. The discolored leaves die and plants
generally become yellow. Diseased roots are thickened and more branched than those of healthy plants. Heavy infestations cause wilting, particularly during times of
water stress; stunted growth; poor root development; and early plant death. Lemonshaped cysts are white at first, then gradually become dark brown as they harden.
Cysts are visible without magnification.
Management.
Not reported, but presumably disease management is similar to that for the cereal cyst nematode.
Lesion
Cause.
Pratylenchus species, including P. minyus, P. neglectus, and P. thornei. Nematodes live free in soil as migratory endoparasites and overwinter as eggs, larvae, or
adults in diseased host tissue and in soil. Both larvae and adults penetrate roots and move through cortical cells, where the females deposit eggs as they migrate. Older
diseased roots are abandoned and new roots are sought as sites for penetration and feeding.
Distribution.
Symptoms.
Diseased plants in areas of a field will appear yellow and moisturestressed. Roots and crowns will be rotted when Rhizoctonia solani infects host plants through
nematode wounds. Diseased roots become dark and stunted, and there is a loss in grain yield.
Management
1. Sow wheat in autumn when soil temperatures are below 13°C.
2. Use soil fumigants where the high costs warrant them.
3. Application of nitrogen and phosphorous reduced populations of P. thornei on roots; however, this occurs to a greater extent in wheat in a rotation than in
monoculture.
Ring
Cause.
Criconemella spp. are ectoparasites.
Distribution.
Not reported.
Symptoms.
Disease symptoms on wheat are not well known. The feeding of Criconemella spp. on the roots of other plant species does not result in necrosis.
Management.
Not reported.

Page 924
Root Gall
The root gall nematode is also called the grass root gall nematode.
Cause.
Subanquina radicicola (syn. Ditylenchus radicicola and Anguillulina radicicola) is an endoparasite that survives in host roots. Larvae penetrate roots and develop
in the cortical tissue and form a root gall within 2 weeks. Mature females begin egg production in galls that eventually weaken and release larvae to establish secondary
infections. Each generation is completed in about 60 days.
Distribution.
Symptoms.
Diseased seedlings frequently have reduced top growth and a general chlorosis. Galls on roots tend to be inconspicuous and vary in diameter from 0.5 to 6.0 mm. At
the center of the larger galls is a cavity filled with nematode larvae. Roots may be bent at the gall site.
Management.
Rotate wheat with noncereal crops.
Root Knot
Cause.
Meloidogyne spp. are endoparasitic nematodes that overwinter as eggs in the soil. The three species most commonly found on wheat are M. arenaria, M. incognita,
and M. naasi. Meloidogyne arenaria and M. incognita do not survive if the soil temperature averages below 3°C during the coldest month of the year. In the spring,
larvae hatch from eggs but enter host roots at any time. By the middle of summer, females inside the rootknot tissue release eggs into the soil.
Distribution.
Symptoms.
Root knots are found on diseased roots in spring and summer. They are swellings, or thickenings, comprised of swollen cortical cells and the bodies of nematodes
containing egg masses. When root knots are cut open, egg masses turn dark.
Management
1. Sow wheat in the autumn.
2. Rotate wheat with root crops.
Seed Gall
Seed gall is also called wheat gall.
Cause.
Anguina tritici survives for several years as larvae in seed galls. Longrange dissemination is by seed galls that are mixed in with grain. When galls are sown together
with seed, larvae released into the moist soil move up host plants in a water film, eventually reaching the flower primordia.

Page 925
Mature nematodes copulate and produce eggs. Seed galls develop from undifferentiated flower tissue that has been infected by the nematodes. If gall development is
retarded, larvae may be present in healthyappearing seed. Galls are mixed with normal seed or fall to the ground, where the nematodes become dormant under dry
conditions.
Distribution.
Eastern Asia, parts of Europe, India, and southeastern United States.
Symptoms.
Prior to the heading stage of plant growth, wheat plants are swollen near the soil level and diseased leaves are twisted, wrinkled, or rolled. After heading, the
distortions are not as obvious, but diseased plants are stunted and mature slowly. Heads are small and the dark, seedlike gall forces the glumes to spread apart. Galls
are dark brown and do not have the brush or embryo markings of healthy seed.
Management
1. Sow clean seed.
2. Seed may be soaked for 10 minutes at 54°C.
3. Grow nonhost crops for 2 years in a rotation.
Spiral
Cause.
Distribution.
Not reported.
Symptoms.
Symptoms on wheat are not well known. Small necrotic flecks on roots and a general decline in plant vigor have been suggested.
Management.
Not reported.
Stubby Root
Cause.
Paratrichodorus species, principally Paratrichodorus minor (syn. P. christiei and Trichodorus christiei) survives in soil or on diseased roots as eggs, larvae, and
adults. These nematodes are migratory ectoparasites that move relatively rapidly through soil at 5 cm per hour, especially in fine sandy soils, and feed only on the
outside of wheat roots. Feeding is confined to epidermal and external cortical cells of the host roots. Wheat sown early in the autumn in sandy soils is most severely
diseased.
Distribution.
Symptoms.
Diseased roots are thickened, short, and stubby and have brown lesions on the root tips. The tops of plants grow poorly and the entire plant is easily pulled from soil
due to a lack of a fibrous root system.
Management.
No practical management is available.

Page 926
Stunt
Cause.
Merlineus brevidens survives in soil and in association with host tissue as different morphological stages of the nematode. Merlineus brevidens is an ectoparasite that
feeds on the outside of wheat roots, often in association with the fungus Olpidium brassicae.
Distribution.
Presumed to be indigenous to most soils, but the nematode is rarely found at high populations.
Symptoms.
The most severe damage occurs on winter wheat that is growing in wet soils. The lower leaves die, and a few short tillers with small seed form on diseased plants.
Roots of diseased seedlings are short, dark, and shriveled.
Management
1. Apply nematicides or soil fumigants to infested soils.
2. Grow cultivars that tolerate stunting.
Aster Yellows
Cause.
The aster yellows phytoplasmalike organism (PLO) survives in several biennial or perennial dicotyledonous plants and in leafhoppers. The aster yellows phytoplasma
is transmitted primarily by the aster leafhopper, Macrosteles fascifrons, and less commonly by the leafhoppers Athysanus argentarius, Elymana sulphurella,
Endria inimica, and M. laevis. Leafhoppers first acquire the phytoplasma by feeding on diseased plants and then transmit the phytoplasma by flying to healthy plants
and feeding on them.
Canadian wheat cultivars were not infected by a strain of aster yellows from Oklahoma, which suggests the possibility of different PLO strains or leafhopper biotypes
in the two regions.
Distribution.
Generally distributed throughout eastern Europe, Japan, and North America. However, aster yellows is rarely severe.
Symptoms.
Symptoms become most obvious at temperatures of 25° to 30°C. Diseased seedlings either die 2 to 3 weeks after infection or are stunted. Diseased leaves are yellow
or have yellow blotches, and the heads are sterile and have distorted awns.
Infection of older plants causes leaves to become somewhat stiff and discolored shades of yellow, red, or purple from the tip or margin inward. Root systems may not
be well developed.
Management.
Not reported.

Page 927
Seedborne Wheat Yellows
Cause.
Seedborne wheat yellows viroid (SWTV). SWTV is seedborne and is thought to be mechanically transmitted.
Distribution.
China.
Symptoms.
Chlorotic spots initially occur on the upper and middle portions of diseased seedling leaves and, subsequently, on new leaves as they emerge. Spots coalesce and form
large chlorotic areas that, in turn, become necrotic.
Management.
Sow pathogenfree seed.
Cause.
African cereal streak virus (ACSV). The natural virus reservoir is native grasses. ACVS is transmitted by the planthopper Toya catilina, but it is not mechanically or
seedtransmitted. ACSV is limited to the phloem of the plant host, where it induces a necrosis. Disease development is aided by high temperatures of 20°C and
above.
Distribution.
East Africa, specifically Kenya and possibly Ethiopia.
Symptoms.
Initially, faint, broken, chlorotic streaks begin near the base of the diseased leaf and extend upward. Later, definite alternate yellow and green streaks develop along
the entire leaf blade, and eventually diseased leaves become almost completely yellow. New diseased leaves tend to develop a shoestring habit and die.
Plants infected when young become chlorotic and severely stunted, and die. Plants infected when older have distorted yellow heads. Diseased plants become soft,
flaccid, and almost velvety to the touch. Yield is almost completely suppressed in diseased plants.
Management.
Not reported.
Agropyron Mosaic
Agropyron mosaic is also called Agropyron green mosaic, streak mosaic, and yellow mosaic.
Cause.
Agryopyron mosaic virus (AgMV) is in the potyvirus group. AgMV is reservoired in quackgrass and other grass hosts, including Elymus smithii, Bothriochloa
laguroides, Aristida sp., and Sorghastrum nutans; therefore, dis

Page 928
ease tends to occur near these virus sources. AgMV is transmitted by the mite Abacarus hystix and is saptransmissible between gramineous hosts.
Distribution.
Canada, northern Europe, and the northern United States and Oklahoma. Agropyron mosaic is generally not considered to be an important disease.
Symptoms.
Symptoms occur as patches of diseased plants within a field or at the edges of fields along grassy borders. Initially, pale green or yellow mosaics, streaks, or dashes
occur on leaf blades. Moderate stunting may occur. With the exception of stunting, symptoms become less conspicuous as diseased plants mature.
Management
1. Grow tolerant cultivars.
2. Eliminate volunteer wheat and grasses.
3. Sow winter wheat later in the autumn.
Cause.
American wheat striate mosaic virus (AWSMV) is in the rhabdovirus group. AWSMV overwinters in wheat and grasses in association with the painted leafhopper,
Endria inimica, which overwinters as eggs. AWSMV is transmitted mainly by E. inimica and occasionally by the leafhopper Elymana virenscens. Leafhopper
adults are migratory, and all leafhopper stages are dispersed by wind. Symptom development is favored by warm temperatures (25° to 33°C). Disease is associated
with heavy infestations of leafhoppers.
Distribution.
South central Canada and north central United States.
Symptoms.
Diseased leaves have obvious striations consisting of thin, yellow to white, parallel streaks that are more severe on the abaxial leaf surface. Streaks may spread over
the entire leaf and become necrotic. Older leaves are stunted and chlorotic, then become necrotic. On some wheat cultivars, AWSMV causes a brown necrotic
streaking of culms and glumes.
Management.
Not reported.
Australian Wheat Streak Mosaic
Australian wheat streak mosaic is also called chloris striate mosaic.
Cause.
Australian wheat streak mosaic virus (AWSMV) is in the geminivirus group. AWSMV is transmitted by the leafhoppers Nesoclutha obscura and N. pallida, but it is
not saptransmissible. AWSMV is introduced into the mesophyll by the vectors. Barley, maize, and oat are also susceptible.
Distribution.
Australia. The disease is not considered important.

Page 929
Symptoms.
Diseased plants are dwarfed. Leaves have broken yellow streaks and fine, grayish striping.
Management.
Not necessary.
Cause.
Barley stripe mosaic virus (BSMV) is in the hordeivirus group. BSMV is transmitted through seed, sap, and pollen. BSMV can remain viable in seed for up to 8
years, but seed transmission is relatively uncommon in wheat. When an infected seed germinates, the resulting seedling is diseased. BSMV is disseminated through
plant sap when a diseased leaf rubs against a healthy leaf. BSMV can be transmitted by infected pollen but not by insects or other means.
Distribution.
Southern Asia, Australia, Europe, Japan, western North America, and the former USSR.
Symptoms.
Diseased leaves have yellow mottling or spots that are either narrow or wide, numerous or few, and continuous or broken. The spots may be light green, tan,
yellowish, or bleached white, while the rest of the leaf is green. Normally, chlorotic stripes develop on leaves and become increasingly yellow or brown. Virulent
strains of the virus cause brown stripes that are either continuous or broken and have irregular margins. Diseased plants are dwarfed, rosetted, and excessively tillered.
Plants infected by BSMV through sap develop acute and localized symptoms on subsequent leaves. Within a few days, symptoms disperse throughout the plant as a
mild systemic mosaic. Symptoms are best expressed in diseased plants grown at temperatures of 22° to 30°C.
Management.
Do not rotate wheat with barley.
Barley Yellow Dwarf
Cause.
Barley yellow dwarf virus (BYDV) is in the luteovirus group. BYDV survives in autumnsown small grains, such as barley, oat, and wheat, and in annual and perennial
grasses. However, in general, local grasses, winter wheat, and maize are of little importance as primary sources of BYDV.
BYDV is transmitted by several species of aphids but is not transmitted through eggs, newborn aphids, seed, and soil, or by mechanical means. Once an aphid
acquires BYDV, it is capable of transmitting the virus for the rest of its life. Some strains of BYDV are transmitted equally well by all species of aphids; others display
a high degree of vector specificity. Aphid flights are local or are assisted by wind and extend for hundreds of kilometers, causing virus inoculum to be carried by aphids
for a long distance. Thus, the major source of aphids in the spring may be from distant plants, but in the autumn, viruliferous aphids are both distant and local. In sus

Page 930
ceptible wheat cultivars, BYDV induces physiological changes that improve their acceptability to the English grain aphid, Sitobion avenae, and enhance the vector's
effectiveness.
Epiphytotics occur during cool temperatures (10° to 18°C) and moist seasons that favor grass and cereal growth as well as aphid multiplication and migration.
Infections occur through the growing season but are most numerous in areas that support populations of aphids.
Distribution.
Africa, Asia, Australia, Europe, New Zealand, North America, and parts of South America.
Symptoms.
Symptoms are not striking and tend to be confused with nutritional disorders or weatherrelated problems but become more pronounced at cool temperatures (16° to
20°c) and on cloudless days. Single plants or groups of plants are discolored yellow and stunted. Seedling infection slows plant maturity and causes older diseased
leaves to become bright yellow. Leaves tend to be stiff and discolored in various shades of yellow, red, or purple, starting from the leaf blade edge. A later infection
causes the flag leaf to turn yellow or red. Frequently, the feeding of some vectors produces tiny, brownblack spots on leaves and culms, with adjacent tissues first
turning yellow, then tan. Diseased roots are not well developed, and phloem tissues are darkened. The cold hardiness of diseased winter wheat plants is reduced.
Management
1. Grow tolerant wheat cultivars.
2. Sow winter wheat later in the autumn.
Barley Yellow Streak Mosaic
Cause.
Barley yellow streak mosaic virus (BaYSMV) is a novel virus transmitted by the brown wheat mite, Petrobia latens. Petrobia latens is a nonwebspinning spider
mite that is generally believed to reproduce parthenogenetically. The mite deposits eggs on debris located on the soil surface near a host plant. BaYSMV particles are
extremely large for a plant virus (64 × 1000 nm) and appear to be enveloped in and contain singlestranded RNA. BaYSMV has been transmitted mechanically to
Nicotiana benthamiana and Chenopodium quinoa.
Distribution.
Canada (Alberta) and the United States (Idaho and north central Montana).
Symptoms.
Diseased leaf symptoms consist of a yellowgreen mosaic, streaking, color banding, and severe necrosis.
Management.
Not reported.

Page 931
Barley Yellow Striate Mosaic
Cause.
Barley yellow striate mosaic virus (BYSMV) is in the rhabdovirus group. BYSMV is reservoired in volunteer diseased wheat plants and is transmitted by the
planthopper Laodelphax striatellus.
Distribution.
Italy, but the incidence and severity are very low.
Symptoms.
A mild yellow mottling occurs on diseased basal leaves and striations occur on upper leaves.
Management.
Not reported.
Barley Yellow Stripe
Cause.
The causal agent is not known for certain, but it is transmitted by the leafhopper Euscelis plebejus. Disease tends to occur along field borders and near grassy
reservoirs of E. plebjus.
Distribution.
Italy.
Symptoms.
Fine, continuous stripes that occur on diseased leaves sometimes are followed by yellowing and death.
Management.
Not reported.
Brome Mosaic
Cause.
Brome mosaic virus (BMV) is in the bromovirus group. BMV survives in cereals, perennial grasses, and dry leaf tissues and is seedborne. BMV is primarily sap
transmitted, but the virus is inefficiently transmitted by the nematodes Xiphenema coxi and X. paraelongatum in Europe and by the Russian wheat aphid, Diuraphis
noxia, in North America. Transmission also occurs through plant contact and any means that transfers sap.
BMV infects plant embryos and traces of the virus are occasionally found in seed coats. Plants infected early in the growing season have the highest incidence of
seedborne infection.
Distribution.
North America, Northern Europe, South Africa, the former USSR, and Yugoslavia.
Symptoms.
Seedborne virus affects germination. Initially, a streaklike, yellowgreen mosaic occurs on diseased leaves, but it becomes less prominent as diseased plants age. Mild
stunting and head deformation may also occur. Some cultivars are symptomless carriers.
Management.
Control grassy weeds.

Page 932
Cause.
Cereal chlorotic mottle virus is a rhabdovirus transmitted by cicadellids.
Distribution.
Australia and northern Africa.
Symptoms.
Severe necrotic and chlorotic streaks occur on diseased leaves.
Management.
Not reported.
Cereal Tillering
Cause.
Cereal tillering virus (CTV) is in the reovirus group. CTV is transmitted by the planthoppers Laodelphax striatellus and Dicranotropis hamata. CTV is limited to
the phloem and is similar to oat sterile dwarf virus, rice blackstreaked dwarf virus, and maize rough dwarf virus.
Distribution.
Italy and Sweden.
Symptoms.
Diseased plants are dwarfed and excessively tillered, and have a general dark green discoloration and poor grain yields. Infrequently, leaves become malformed and
have serrated edges.
Management.
Not reported.
Cocksfoot Mottle
Cause.
Cocksfoot mottle virus (CFMV) is in the sobemovirus group. CFMV is saptransmitted and also is spread by the cereal leaf beetles Oulema melanopa and O.
lenchenis.
Distribution.
Great Britain.
Symptoms.
The initial mottling of diseased leaves is followed by a general yellowing and, finally, death.
Management.
Not reported.
Cucumber Mosaic
Cause.
Cucumber mosaic virus (CMV) is in the cucumovirus group. CMV is reservoired in diseased vegetables and is transmitted to wheat by windborne aphids. CMV has
been detected in seed.
Distribution.
South Africa.
Symptoms.
Symptoms are first noticed at the heading stage of plant growth. An uneven elongation of shoots occurs, with a subsequent appearance of sterile, yellowwhite heads.
Leaves become chlorotic, and severely diseased plants die.
Management.
Not reported.

Page 933
Eastern Wheat Striate
Cause.
Eastern wheat striate virus (EWSV) is transmitted by the leafhopper Cicadulina mbila, but is not transmitted by sap, seed, soil, or aphids. EWSV overseasons in
perennial naraenga grass.
Distribution.
India.
Symptoms.
Fine chlorotic stripes on diseased leaves and leaf sheaths become necrotic and more pronounced as diseased plants age. Diseased plants are variously stunted.
Stunting and striate symptoms are more pronounced in barley than in wheat, and in plants infected when young. Plants infected while young usually die. Diseased
plants produce partially filled heads with shriveled seed of poor quality.
Management.
Not reported.
Enanismo
Enanismo is also called cereal dwarf.
Cause.
One or more unidentified viruses and a toxin from the leafhopper Cicadulina pastusae. Leafhopper adults and nymphs of both sexes transmit the virus or viruses in a
circulative mode. Females pass the virus(es) transovarially and are more efficient vectors than males. Barley and oat are also hosts.
Distribution.
Colombia and Ecuador.
Symptoms.
Diseased seedlings are killed or stunted. Later infections result in less stunting, but diseased leaves have blotches and earlike enations or galls. Galls appear on the
newest leaves formed on an infected plant 1 to 3 weeks after leafhopper feeding, rather than appearing on the leaves that were fed upon. Plants infected at heading
time produce distorted heads and incompletely filled seeds.
Management
1. Sow wheat later in the spring after vector activity declines.
European Wheat Striate Mosaic
European wheat striate mosaic is also called oat striate, red disease, wheat striate, and wheat striate mosaic.
Cause.
European wheat striate mosaic virus (EWSMV) is in the tenuivirus group. EWSMV is passed through eggs and is transmitted persistently by the planthopper
Javesella pellucida and sometimes by J. dubia. Nymphs are more efficient vectors than adults. Symptoms occur 2 to 4 weeks after feeding.

Page 934
Distribution.
Central Europe, Great Britain, and Scandinavia.
Symptoms.
Diseased seedlings die. Older plants are severely stunted and do not head out. Plants infected near the heading stage of plant growth mature early, develop yellow
white leaf stripes, and have white heads with shrunken seed.
Management.
Sow wheat later in the autumn or in the spring to avoid exposure to vectors.
Flame Chlorosis
Cause.
The likely disease agent or its replicative intermediate is doublestranded RNAs that range in size from 900 to 2800 base pairs and are present in vesicles rather than
virions. The causal agent is soiltransmitted and has been transmitted by growing host plants in soil where diseased plants had grown.
The grassy weeds green foxtail, Setaria viridis, and barnyard grass, Echinochloa crusgalli are also hosts.
Distribution.
Canada (Manitoba) on spring wheat.
Symptoms.
A striking flamelike pattern of leaf chlorosis and severe stunting occur in spring wheat. Chloroplasts and mitochondria of diseased cells are hypertrophied and contain
an extensive proliferation of fibrilcontaining vesicles that form within the organellar envelope. Diseased plants continued to produce leaves with symptoms after they
were transferred to sterile potting medium.
Management.
Not reported.
High Plains Disease
Cause.
High Plains virus (HPV) is transmitted by the wheat leaf curl mite, Aceria tosichella, which also transmits wheat streak mosaic virus (WSMV) and results in a mixed
infection by these two viruses. HPV is associated with a 32kDa protein that resembles tenuiviruses. However, some researchers have suggested that there is also
some resemblance to tospoviruses.
HPV is also transmitted to barley and maize.
Distribution.
The midwestern United States (Colorado, Idaho, Kansas, Nebraska, Texas, and Utah).
Symptoms.
The first symptom is small, chlorotic spots on diseased leaves. The spots rapidly expand into a mosaic and then into a general yellowing of the entire diseased plant.
Severely diseased plants become necrotic. Field infections very often are mixed infections of WSMV and HPV.
Management.
Not reported.

Page 935
Indian Peanut Clump
Cause.
Indian peanut clump virus.
Distribution.
India.
Symptoms.
Diseased plants are severely stunted, have dark green leaves, and show mosaic symptoms on the youngest leaves.
Management.
Not reported.
Maize Dwarf Mosaic
Cause.
Maize dwarf mosaic virus (MDMV) is in the potyvirus group. MDMV is transmitted from maize to wheat by several aphid species. Infections occur on plants grown
near diseased maize.
Distribution.
The United States (New York). However, infection of wheat is rare.
Symptoms.
Diseased leaves have a mild mottling.
Management.
Not necessary.
Maize Streak
Cause.
Maize streak virus (MSV) is in the geminivirus I group. MSV is transmitted circulatively by five species of Cidaulina leafhoppers, especially Cidaulina mbila. All
stages of leafhoppers transmit MSV. Wheat is most likely to become infected when grown in association with maize.
Distribution.
Africa and Southeast Asia.
Symptoms.
Diseased leaves are shortened and curled and have fine, linear, chlorotic streaks. Diseased plants are excessively tillered, are sterile, and have shortened culms.
Management
2. Sow winter wheat later in the autumn than the normal time to sow.
3. Do not grow wheat in the vicinity of maize.
Maize White Line Mosaic
Maize white line mosaic is also called white line mosaic and stunt.
Cause.
Maize white line mosaic virus (MWLMV) is not mechanically transmitted but has been transferred to healthy roots from diseased roots placed in sterile soil together
with zoospores of an Olpidiumlike fungus that is considered to be the likely vector. Infection by MWLMV is associated with the time of the growing season rather
than plant age. Maize white line mosaic often occurs locally in poorly drained areas of a field and along edge

Page 936
rows. A satellite virus serologically related to a satellitelike particle associated with maize dwarf ringspot virus is associated with MWLMV.
Distribution.
The United States (Michigan, New York, Ohio, Vermont, and Wisconsin).
Symptoms.
Inoculated wheat plants displayed a mild mosaic, but no necrotic lesions, on the leaves.
Management.
Not reported.
Maize Yellow Stripe
Cause.
leafhopper Cicadulina chinai. Acquisition and inoculation threshold times are 30 minutes each with a latent period of 4.5 to 8.0 days, depending on temperatures
from 14°C (minimum) to 25°C (maximum). The maximum retention period is 27 days.
Barley, sorghum, and graminaceous weeds are winter hosts. Different strains of MYSV exist.
Distribution.
Egypt.
Symptoms.
Symptoms on wheat are unclear. Three symptom types exist on maize: fine stripe, coarse stripe, and chlorotic stunt. Each type may represent different MYSV strains.
Experimentally, fine stripes appeared on the first leaves and coarse stripes on younger leaves; however, some leaves have both symptom types.
Management.
Not Reported.
Mal De Rio Cuarto
Cause.
Mal de Rio Cuarto virus (MRCV) is in the fijivirus group. MRCV is transmitted in a persistent, propagative way by the planthopper Delphacodes kuscheli. The
insects develop mainly on oat and wheat, then migrate to maize during their first stages of growth. Disease is most severe when infection takes place during the early
stages of plant development and during periods of high rainfall. MRCV has been detected in 12 species of weeds in the families Poaceae and Cyperaceae.
Distribution.
Argentina. Mal de Rio Cuarto is the most important disease of maize in Argentina.
Symptoms.
Diseased plants have deformed leaves, spikes, and spikelets; shortened internodes; and leaves with serrated borders. Spikelets may be sterile.
Management.
Not reported.

Page 937
Cause.
Northern cereal mosaic virus (NCMV) is in the rhabdovirus group. NCMV is transmitted by the planthopper Laodelphax striatellus. The insects Unkanodes
sapporonus and Delphacodes spp. have also been reported as vectors. The wheat rosette stunt virus (WRSV) reported from northern China may be the same virus.
Barley, oat, rice, and rye are also hosts.
Distribution.
China (if WRSV and NCMV are the same), Japan, and Korea.
Symptoms.
Symptoms on diseased leaves are a yellow mosaic and chlorotic leaf streaks. Diseased plants are stunted.
Management.
Oat Sterile Dwarf
Oat sterile dwarf is also called oat base tillering disease and oat dwarf tillering disease.
Cause.
Oat sterile dwarf virus (OSDV) is in the reovirus group. OSDV is transmitted persistently by planthoppers, especially Javesella pellucida and Dicranotropis
hamata. Barley, grasses, maize, millet, and oat are also susceptible.
Distribution.
Eastern and northern Europe.
Symptoms.
Diseased plants are stunted, excessively tillered, and sterile and have helical leaf twisting.
Management
2. Avoid growing wheat adjacent to oat.
Orchardgrass Mosaic
Cause.
Orchardgrass mosaic virus is mechanically transmitted. Orchardgrass is a source of inoculum.
Distribution.
Canada (Quebec).
Symptoms.
Typical mosaic symptoms occur on diseased leaves. Diseased plants are severely stunted and have reduced or delayed heading.
Management.
Not reported.
Cause.
Rice blackstreaked dwarf virus (RBSDV) is in the reovirus group. RBSDV is transmitted by the planthoppers Laodelphax striatellus, Unkanodes

Page 938
sapporonus, and U. albifascia. RBSDV is retained from season to season in all stages of the planthoppers, but it is not transmitted through planthopper eggs.
Distribution.
Japan.
Symptoms.
Diseased plants are severely stunted. Leaves are twisted and have waxy, veinal swellings on their undersides and on the culms.
Management.
Do not grow wheat adjacent to rice.
Rice Hoja Blanca
Rice hoja blanca is also called white leaf, white spike, and white tip.
Cause.
Rice hoja blanca virus (RHBV) is in the tenuivirus group. RHBV is transmitted persistently by planthoppers, especially Sogata cabana and S. orizicola. RHBV is
circulative and passes through eggs for up to 10 generations.
Distribution.
The Caribbean, Central and South America, and the southern United States.
Symptoms.
Upper diseased leaves and the spike have a graywhite discoloration, while other leaves are mottled, striped, and chlorotic. Diseased plants become sterile and die.
Management.
Do not grow wheat in association with susceptible rice cultivars.
Russian Winter Wheat Mosaic
See ''American Wheat Striate Mosaic."
Cause.
Winter wheat mosaic virus (WWMV) is disseminated by the leafhoppers Psammotettix striatus and Macrosteles laevis. Psammotettix striatus carries WWMV
through all life cycle stages, transovarially passing the virus to successive generations. Barley, rye, and some grasses are also hosts.
Distribution.
Eastern Europe, Russia, and Ukraine.
Symptoms.
Diseased leaves have mosaic and streak mosaic patterns. Plants are mildly stunted and have distinct yellow dashes and streaks that are oriented parallel to leaf veins.
Severe disease results from seedling infections and includes severe stunting, tillering, and necrosis. Surviving seedlings exist as rosettes and have typical leaf mosaic
symptoms.
Management.

Page 939
Tobacco Mosaic
Cause.
Tobacco mosaic virus (TMV) is in the tobamovirus group. TMV is associated with wheat soilborne mosaic virus.
Distribution.
Symptoms.
Inoculated plants of cultivar 'Pawnee' incubated at 30°C and in bright sunlight developed faint, chlorotic, local lesions that rapidly disappeared, leaving symptomless
plants. A faint, transient mosaic occurred on inoculated leaves of 'Pawnee,' 'Arthur,' and 'Michigan Amber' wheats and 'Reno' barley.
Management.
Not needed.
Wheat (Cardamom) Mosaic Streak
Cause.
A virus transmitted through sap and the aphids Brachycaudus helichrysi and Rhopalosiphum maidis. Infection occurs near reservoirs of virus in cardamom plants
growing in close proximity to wheat.
Distribution.
India.
Symptoms.
Diseased plants are mildly stunted and predisposed to infection by Bipolaris sorokiniana. Leaves have chronic yellowgreen mosaic symptoms.
Management
2. Grow wheat apart from cardamom.
Wheat Chlorotic Streak
Cause.
Wheat chlorotic streak virus (WCSV) is in the rhabdovirus group. WCSV is presumed to be reservoired in Agropyron repens, which also maintains the planthopper
vector Laodelphax striatellus. WCSV is disseminated in a persistent and transovarial manner.
Distribution.
France. Wheat chlorotic streak occurs infrequently on wheat.
Symptoms.
The growth and yield of diseased individual plants are reduced.
Management.
Not reported.
Wheat Dwarf
Cause.
Wheat dwarf virus (WDV) is in the geminivirus I group. WDV is transmitted by the leafhoppers Psammotettix alienus and Macrosteles laevis. Nymphs, which are
more efficient vectors than adults, must acquire WDV from diseased plants since the virus is not passed through eggs.

Page 940
Wheat dwarf occurs in association with heavy infestations of leafhoppers, and disease results from the combined effects of leafhopper feeding and virus infection.
Distribution.
The former Czechoslovakia, Russia, Sweden, and Ukraine.
Symptoms.
Diseased plants infected as seedlings are severely dwarfed and do not head out. If host plants are infected later, dwarfing is less severe but emerged heads contain
little seed or the seed is shriveled. Diseased leaves develop scattered, fine, light green to yellowbrown spots and blotches that coalesce and cause prominent
yellowing and necrosis.
Management.
Grow resistant cultivars. Softwheat cultivars are less susceptible than hardwheat cultivars.
Wheat Rosette Stunt
Cause.
Wheat rosette stunt virus (WRSV) is the rhabdovirus group. WRSV is a strain of northern cereal mosaic virus.
Distribution.
China.
Symptoms.
A yellow mosaic and/or chlorotic leaf streaks occur on diseased leaves. Diseased plants are stunted.
Management
1. Sow wheat later in the growing season.
2. Eliminate alternate grassy weed hosts.
Wheat Soilborne Mosaic
Wheat soilborne mosaic is also called eastern wheat mosaic, green mosaic, mosaic rosette, soilborne mosaic, soilborne wheat mosaic, and yellow mosaic.
Cause.
Wheat soilborne mosaic virus (WSBMV) is in the furovirus group. WSBMV survives in soil in Polymyxa graminis, a soilborne plasmodiophoraceous fungus that is
an obligate parasite in roots of many higher plants. When soil is watersaturated and at low soil temperatures (10° to 20°C), P. graminis enters root hairs and
epidermal cells of roots as motile zoospores. Once inside the plant, P. graminis replaces plant cell contents with plasmodial bodies that either segment into additional
zoospores or develop into thickwalled resting spores 2 to 4 weeks after infection.
WSBMV is spread by any method that disseminates infested soil. Disease is most common in lowlying areas of fields that tend to be wet. Autumnsown wheat is
most severely diseased because abundant plant growth occurs during the low temperatures that favor dissemination and infection by P. graminis.
WSBMV combined with wheat spindle streak mosaic virus (WSSMV)

Page 941
causes disease in plants that are resistant to WSBMV. The ratio of WSBMV and WSSMV in infected plants is about 20:1, respectively.
Different strains, labeled the yellow and green strains, have been reported.
Distribution.
Argentina, Brazil, Egypt, Italy, Japan, and the United States. Soilborne wheat mosaic is considered a major virus disease of hard red winter wheat in the plains states
of the United States.
Symptoms.
Two phases, mosaic and mosaicrosette, are caused by yellow and green strains, respectively. Symptoms are light green to yellow leaf mosaics that are most
prominent on diseased lower leaves in the spring. The youngest diseased leaves and leaf sheaths are mottled and develop parallel spots or streaks. Diseased plants are
slightly to severely stunted. Warm weather prevents development of disease symptoms.
Symptoms of the combined WSBMV and WSSMV infection are a yellowing and overall bronze appearance to the field and plants that are stunted, have a mosaic
appearance, and have reduced tillering. Symptoms are most obvious on plants growing in the lower portions of fields. During warm weather in the late spring, diseased
plants lose disease symptoms except for the stunting.
Large, brown, vacuolate inclusions in epidermal cells stained with calcomineorange and Luxol brilliant green can be seen with a light microscope.
Management
2. Sow wheat later in the autumn.
3. Grow resistant cultivars. Expression of resistance may involve an inhibition of virus movement from roots to foliage. The mechanisms of resistance to WSBMV may
involve a reduction in rates of virus particle assembly, movement, and/or replication.
Wheat Spindle Streak Mosaic
Wheat spindle streak mosaic is also called Ontario soilborne wheat mosaic, wheat variegation, and wheat yellow mosaic. (See "Wheat Yellow Mosaic.")
Cause.
Wheat spindle streak mosaic virus (WSSMV) is in the bymovirus group. WSSMV is transmitted by the soil fungus Polymyxa graminis and can survive for several
years in soil in association with the fungus. Resting spores (cystosori) of P. graminis form in the root cortex and can remain dormant for many years. Virus is thought
to remain infectious in cystosori for over 10 years in the absence of the virus's plant host. Some researchers regard WSSMV as a distinct strain of wheat yellow
mosaic virus.
WSSMV is a coolweather disease; the temperature for optimum virus

Page 942
transmission in the soil is 15°C. During favorable temperatures for virus transmission, high soil moisture is also needed for the release of infective zoospores of P.
graminis. Infection does not occur above 20°C, and disease development does not occur above 18°C. Although symptom expression occurs in the spring, infection
probably occurs in the autumn. Optimum disease development is at air or soil temperatures from 5° to 13°C for 60 days.
WSSMV combined with wheat soilborne mosaic virus (WSBMV) causes a disease of plants resistant to WSBMV. The ratio of WSBMV and WSSMV in infected
plants is about 20:1, respectively.
Distribution.
Canada (southern Ontario), France, India, and the United States. WSSMV is a prevalent and damaging pathogen of winter wheat in central and eastern North
America. It is likely that wheat spindle streak mosaic occurs throughout the world.
Symptoms.
Symptoms occur on lower, older leaves during cool spring weather and tend to occur on diseased plants uniformly distributed throughout a field. Warmer weather
(18°C or more) prevents symptom development on younger leaves. The first leaves produced in the spring have yellowgreen mottling, dashes, or streaks. Streaks are
oriented parallel with leaf veins and have tapered ends that resemble spindles. As the leaves mature, brown areas replace the yellowgreen areas and leaf tips or entire
leaves may die. As warm weather continues, new symptomless leaves hide diseased lower leaves.
Diseased plants remain stunted, and their tillering capacity is reduced or lost, which is the major reason yields are reduced. Because both shoot and root growth are
reduced and the stress of low temperatures is greater, plants have less coldhardiness. Milling and baking qualities may also be reduced. Maturity may be delayed,
which results in an increase in other foliar diseases, such as leaf rust.
Symptoms of the combined WSBMV and WSSMV infection are a yellowing and overall bronze appearance to a field and plants that are stunted, have a mosaic
appearance, and have reduced tillering. Symptoms are most obvious on diseased plants growing in the lower portions of fields. During warm weather in late spring,
diseased plants lose their disease symptoms except for the stunting.
Management
2. Sow wheat later in the autumn. Spring wheat tends to be unaffected by WSSMV.
3. Crop rotation is of some help, but WSSMV remains infective in soil for several years.

Page 943
Wheat Spot Mosaic
Wheat spot mosaic is also called wheat spot, and wheat spot chlorosis.
Cause.
The causal agent, wheat spot mosaic virus (WSpMA), is thought to be a virus transmitted by the wheat curl mite Eriophyes tulipae. WSpMA is retained through
mottling but not through the egg stage. WSpMA is not saptransmissible.
Distribution.
Canada (Alberta) and the United States (Ohio). A similar disease has been reported from North Dakota.
Symptoms.
About 3 to 8 days after mites have fed, light green spots (0.51.0 mm in diameter) develop on the youngest diseased leaves. The spots become necrotic, enlarge,
coalesce, and form yellowish areas that may cover entire leaves. Later, diseased plants may develop severe mottling, chlorosis, leaf tip necrosis, and stunting, then die,
especially if the wheat streak mosaic virus is present.
Following transmission of WSpMA and incubation periods of 12 to 15 days at the optimum temperature of 20°C, doublemembranebound bodies (0.10.2 m in
diameter) are scattered or found as large aggregates in the cytoplasm of epidermal cells, subepidermal parenchyma cells, and phloem elements.
Management
1. Destroy all volunteer wheat and grasses in adjoining fields 2 weeks before sowing and 2 to 4 weeks before using the sowing field.
2. Sow wheat as late as practical after the Hessian flyfree date. The flyfree date is a guide that assumes mite populations have also been reduced. Wheat often
escapes infection if it emerges in October or later.
3. Resistant cultivars are being developed. Some cultivars are tolerant.
Wheat Streak Mosaic
Cause.
Wheat streak mosaic virus (WSMV) is in the rymovirus group of the Potyviridae. WSMV is transmitted by the wheat curl mites Aceria tulipae and A. tosichella and
survives in several annual and perennial grasses. No active virus has been detected in dead plants or seed. Mites are also able to retain the virus for several weeks
after they have acquired it. Neither the mite nor the virus can survive longer than 1 to 2 days in the absence of a living plant. In many wheatgrowing areas, volunteer
wheat is the major source of both WSMV and the vector. Maize is an oversummering host for both WSMV and A. tulipae.
As winter wheat plants mature, mites migrate to nearby volunteer wheat, grasses, or maize plants and infect them with WSMV. Later, mites move from volunteer
wheat to earlysown wheat. Mites are disseminated by wind for a distance of at least 2.4 km and possibly farther. Some grasses

Page 944
are hosts for mites but not for WSMV, and vice versa. Some grasses are susceptible to both mites and WSMV, and some grasses are resistant to both.
Only young mites acquire WSMV by feeding 15 or more minutes on diseased plants. Infection depends on three factors: the population of the mites; the nearness of
infected plants, especially volunteer wheat; and enough moisture to keep wheat vigorously growing where mites attain maximum reproduction.
Serologically, different strains of WSMV occur.
Distribution.
Eastern Europe, western and central North America (particularly the Great Plains), and the former USSR.
Symptoms.
Winter wheat is commonly infected in the autumn, but symptoms ordinarily do not appear until the following spring. The greatest losses occur in plants infected early in
the autumn. WSMV is most severe in earlysown wheat; conversely, late sowing decreases symptoms of WSMV. In Oklahoma, red winter wheat cultivars, except
'Rail,' were more severely diseased when they had been inoculated in the autumn. 'Rail' displayed some resistance when it was sown in the autumn during the time
recommended for north central Oklahoma. Spring inoculation of wheat sown early in the autumn (September or October) did not consistently resuit in symptoms.
However, spring inoculation of wheat sown late in the autumn (November) resulted in symptoms. Thus, the maturity of plants at the time of infection may affect the
severity of symptoms. Wheat sown in November was less mature (Feekes growth stage 5) than wheat sown in September or October (Feekes growth stage 6).
The first symptoms consist of light green to light yellow blotches, dashes, or streaks parallel to leaf veins. As diseased plants mature, yellowstriped leaves turn brown
and die. Feeding mites often cause leaf edges to curl tightly in toward the upper midvein. Diseased plants become stunted, have a general yellow mottling, and develop
an abnormally large number of tillers that vary considerably in height. Diseased stunted plants may remain standing after harvest at the same height or shorter than
stubble. Heads may be sterile or partially sterile and have shriveled seed. In severe cases, diseased plants die before maturity.
Systemic infection of wheat by WSMV interferes with chloroplast development. Synergistic effects that are suspected between wheat streak mosaic virus and other
viruses, such as barley yellow dwarf virus, make field identification difficult.
Management
1. Destroy all volunteer wheat and grasses in adjoining fields 2 weeks before sowing and 2 to 4 weeks before using the field.
2. Sow wheat as late as practical after the Hessian flyfree date. The flyfree date is a guide for assuming mite populations have been reduced. Wheat often escapes
infection if it emerges in October or later.
3. Resistant cultivars are being developed. Some cultivars are tolerant.

Page 945
Wheat Yellow Leaf
Cause.
Wheat yellow leaf virus (WYLV) is in the closterovirus group. WYLV is transmitted in a semipersistent manner by the aphid Rhopalosiphum maidis. Barley is also a
host.
Distribution.
Japan.
Symptoms.
Diseased leaves become discolored yellow and blighted. Diseased plants often die or ripen prematurely.
Management.
Not reported.
Wheat Yellow Mosaic
Cause.
Wheat yellow mosaic virus (WYMV) is in the potyvirus group. WYMV is soilborne and sometimes is associated with wheat soilborne mosaic virus. WYMV is also
saptransmitted.
Distribution.
Japan.
Symptoms.
Diseased leaves have a yellow mosaic.
Management.
Unknown Virus
Cause.
An unknown virus that is possibly in the tenuivirus group.
Distribution.
Symptoms.
Diseased plants are stunted, and leaves are mottled and streaked. Symptoms are similar to those of wheat streak mosaic.
Management.
Not reported.
Diseases Caused By Unknown Factors
Physiologic Leaf Spot
Physiologic leaf spot is also called noname disease.
Cause.
Unknown. Leaf spot is observed to be more severe in conservation tillage than in lowresidue tillage systems, especially when wheat is sown early and grown in a
monoculture. Disease is less severe as the date of sowing is delayed and as the rate of nitrogen fertilization increases. Disease is more severe in annual wheat than in
rotations of wheat with fallow or peas.
Foliar application of urea plus calcium chloride reduces leaf spot severity and increases grain yield. However, the application of urea plus micronutrients does not
reduce disease.

Page 946
Distribution.
On winter and spring wheat in the northwestern United States, particularly the semiarid regions of the inland Pacific Northwest.
Symptoms.
Symptoms vary among cultivars. Initially, brown spots appear on some cultivars, necrotic lesions appear on other cultivars, and enlarged necrotic lesions with chlorotic
halos appear on yet other cultivars. Diseased lower leaves often become necrotic and senesce early. Up to 60% of the flag leaf area becomes necrotic soon after the
flag leaves become fully extended. Grain production is reduced by 10%.
Leaf spots of similar description include Alternaria leaf blight, Septoria leaf blotch, tan spot, and bacterial leaf blight.
Management.
Disease severity can be reduced by the management of wheat cultivar selection, crop rotation, sowing date, and plant nutrition.
Unknown
This disease may be the same as wheat spot mosaic reported from Canada (Alberta) and the United States (Ohio).
Cause.
Unknown, but it is associated with the wheat curl mite Aceria tulipae. The disease was found in association with wheat streak mosaic. Membranebound ovoid
bodies (130 to 220 nm in diameter) were observed in the mesophyll cells of diseased plants.
Distribution.
The United States (eastern North Dakota).
Symptoms.
Spotting, mosaic, and yellowing of diseased leaves.
Management.
Not reported.
Selected References
Anderegg, J. C., and Murray, T. D. 1988. Influence of soil matric potential and soil pH on Cephalosporium stripe of winter wheat in the greenhouse. Plant Dis.
72:10111016.
Arneson, E., and Stiers, D. L. 1977. Cephalosporium gramineum: A seedborne pathogen. Plant Dis. Rptr. 61:619621.
Azad, H., and Schaad, N. W. 1988. The relationship of Xanthomonas campestris pv. translucens to frost and the effect of frost on black chaff development in
wheat. Phytopathology 78:95100.
Babadoost, M., and Hebert, T. T. 1984. Factors affecting infection of wheat seedlings by Septoria nodorum. Phytopathology 74:592595.
Babadoost, M., and Hebert, T. T. 1984. Incidence of Septoria nodorum in wheat seed and its effects on plant growth and grain yield. Plant Dis. 68:125129.
Bailey, J. E., Lockwood, J. L., and Wiese, M. V. 1982. Infection of wheat by Cephalosporium gramineum as influenced by freezing of roots. Phytopathology
72:13241328.
Bailey, K. L., Knott, D. R., and Harding, H. 1988. Heritability and inheritance of resistance to common root rot (Cochliobolus sativus) in wheat (Triticum
aestivum). Can. J. Plant Pathol. 10:207214.

Page 947
Bateman, G. L. 1988. Pseudocercosporella anguioides, a weakly pathogenic fungus associated with eyespot in winter wheat at a site in England. Plant Pathology
37:291296.
Beddis, A. L., and Burgess, L. W. 1992. The influence of plant water stress on infection and colonization of wheat seedlings by Fusarium graminearum Group 1.
Bockus, W. W. 1983. Effects of fall infection by Gaeumannomyces graminis var. tritici and triadimenol seed treatment on severity of takeall in winter wheat.
Bockus, W. W., O'Connor, J. P., and Raymond, P. J. 1983. Effect of residue management method on incidence of Cephalosporium stripe under continuous winter
wheat production. Plant Dis. 67:13231324.
Bockus, W. W., Davis, M. A., and Norman, B. L. 1994. Effect of soil shading by surface residues during summer fallow on takeall of winter wheat. Plant Dis.
78:5054.
Bonde, M. R. 1987. Possible dissemination of teliospores of Tilletia indica by the practice of burning wheat stubble. (Abstr.) Phytopathology 77:639.
relevance. Phytopathology 87:11111117
Brakke, M. K., Estes, A. P., and Schuster, M. L. 1965. Transmission of soilborne wheat mosaic virus. Phytopathology 55:7986.
Bretag, T. W. 1985. Control of ergot by a selective herbicide and stubble burning. Trans. Brit. Mycol. Soc. 85:341343.
Broscious, S. C., and Frank, J. A. 1986. Effects of crop management practices on common root rot of winter wheat. Plant Dis. 70:857859.
Brown, J. S., and Holmes, R.J. 1983. Guidelines for use of foliar sprays to control stripe rust of wheat in Australia. Plant Dis. 67:485487.
Brown, W. M., Perotti, L. E., and Hill, J. P. 1985. Wheat takeall in Colorado high country irrigated spring wheat. (Abstr.) Phytopathology 75:1296.
Bruehl, G. W., and Cunfer, B. 1971. Physiologic and environmental factors that affect the severity of snow mold of wheat. Phytopathology 61:792799.
Bruehl, G. W., and Machtmes, R. 1984. Effects of "dirting" on strawbreaker foot rot of winter wheat. Plant Dis. 68:868870.
Bruehl, G. W., Peterson, C. J., Jr., and Machtmes, R. 1974. Influence of seeding date, resistance and benomyl on Cercosporella foot rot of winter wheat. Plant Dis.
Rptr. 58:554558.
Bruehl, G. W., Machtmes, R., and Murray, T. 1982. Importance of secondary inoculum in strawbreaker foot rot of winter wheat. Plant Dis. 66:845847.
Campbell, W. P. 1958. A cause of pink seeds in wheat. Plant Dis. Rptr. 42:1272.
Carling, D. E., Meyer, L., and Brainard, K. A. 1996. Crater disease of wheat caused by Rhizoctonia solani AG6. Plant Dis. 80:1429.
Carlson, R. R., and Vidaver, A. K. 1981. Bacterial mosaic of wheat: Distribution and hosts. (Abstr.) Phytopathology 71:207.
Carlson, R. R., and Vidaver, A. K. 1982. Bacterial mosaic, a new corynebacterial disease of wheat. Plant Dis. 66:7679.
Cashion, N. L., and Luttrell, E. S. 1988. Hostparasite relationships in Karnal bunt of wheat. Phytopathology 78:7584.
Chamswarng, C., and Cook, R. J. 1985. Identification and comparative pathogenicity of Pythium species from wheat roots and wheat field soils in the Pacific
Northwest. Phytopathology 75:821827.

Page 948
Clement, D. K., Lister, R. M., and Foster, J. E. 1986. ELISAbased studies on the ecology and epidemiology of barley yellow dwarf virus in Indiana.
Conner, R. L. 1990. Interrelationship of cultivar reactions to common root rot, black point, and spot blotch in spring wheat. Plant Dis. 74:224227.
Conner, R. L., and Atkinson, T. G. 1989. Influence of continuous cropping on severity of common root rot in wheat and barley. Can. J. Plant Pathol. 11:127132.
Conway, K. E., and Williams, E., Jr. 1986. Typhulalike snow mold on wheat in Oklahoma. Plant Dis. 70:169170.
Cook, R. J. 1980. Fusarium foot rot of wheat and its control in the Pacific Northwest. Plant Dis. 64:10611066.
Cook, R. J., and Hering, T. F. 1986. Infection of wheat embryos by Pythium and seedling response as influenced by age of seed. (Abstr.) Phytopathology 76:1061.
Cook, R. J., and Waldher, J. T. 1977. Influence of stubblemulch residue management on Cercosporella foot rot and yields of winter wheat. Plant Dis. Rptr. 61:96
100.
Cook, R. J., Sitton, J. W., and Haglund, W. A. 1987. Influence of soil treatments on growth and yield of wheat and implications for control of Pythium root rot.
Cook, R. J., and Zhang, B. X. 1985. Degrees of sensitivity to metalaxyl within the Pythium spp. pathogenic to wheat in the Pacific Northwest. Plant Dis. 69:686
688.
Cook, R. J., Slitton, J. W., and Waldher, J. T. 1980. Evidence for Pythium as a pathogen of directdrilled wheat in the Pacific Northwest. Plant Dis. 64:102103.
Cook, R. J., Sitton, J. W., and Haglund, W. A. 1987. Influence of soil treatments on growth and yield of wheat and implications for control of Pythium root rot.
Cotterill, P.J., and Sivasithamparam, K. 1988. Reduction of takeall inoculum by rotation with lupine, oats or field peas. J. Phytopathol. 121:125134.
Cotterill, P. J., and Sivasithamparam, K. 1988. Effect of sowing date on takeall of wheat in Western Australia. Phytophylactica 20:1114.
Cotterill, P.J., and Sivasithamparam, K. 1988. Inoculum of the takeall fungus in rotations of wheat and pasture: Relationships to disease and yield of wheat. Trans.
Brit. Mycol. Soc. 91:6372.
Cox, D. J., and Hosford, R. M., Jr. 1987. Resistant winter wheats compared at differing growth stages and leaf positions for tan spot severity. Plant Dis. 71:883886.
Cronje, C. P. R., and Whitlock, V. H. 1987. The effect of germination and seed transmission of brome mosaic virus (BMV) in wheat seeds (CV. Betta). (Abstr.)
Phytophylactica 19:128.
Cunfer, B. M., Demski, J. W., and Bays, D. C. 1988. Reduction in plant development, yield, and grain quality associated with wheat spindle streak mosaic virus.
da Luz, W. C., and Bergstrom, G. C. 1987. Interactions between Cochliobolus sativus and Pyrenophora triticirepentis on wheat leaves. Phytopathology
77:13551360.
Damsteegt, V. D., and Hewings, A. D. 1988. The Russian wheat aphid, Diuraphis noxia, confirmed as vector of brome mosaic virus in North America. Plant Dis.
72:79.
Daniels, A., Lucas, J. A., and Peberdy, J. F. 1991. Morphology and ultrastructure of W and R pathotypes of Pseudocercosporella herpotrichoides on wheat
seedlings. Mycol. Res. 95:385397.
Deacon, J. W., and Scott, D. B. 1985. Rhizoctonia solani associated with crater disease (stunting) of wheat in South Africa. Trans. Brit. Mycol. Soc. 85:319327.

Page 949
Dehne, H. W., and Oerke, E. C. 1985. Investigations on the occurrence of Cochliobolus sativus on barley and wheat. 1. Influence of pathogen, host plant and
environment on infection and damage. Zeitschrift fur Pflazenkrankheiten und Pflanzenschutz 92:270280.
Delfosse, P., Reddy, A. S., Devi, P. S., Murthy, A. K., Wesley, S. V., Naidu, R. A., and Reddy, D. V. R. 1995. A disease of wheat caused by Indian peanut clump
de VallavieillePope, C., Huber, L., Leconte, M., and Goyeau, H. 1995. Comparative effects of temperature and interrupted wet periods on germination, penetration,
and infection of Puccinia recondita f. sp. tritici and P. striiformis on wheat seedlings. Phytopathology 85:409415.
Dewan, M. M., and Sivasithamparam, K. 1987. First report of Sclerotium rolfsii on wheat in Western Australia. Plant Dis. 71:1146.
Diehl, J. A., Tinline, R. D., Kochhan, R. A., Shipton, P. J., and Rovira, A. D. 1982. The effect of fallow periods on common root rot of wheat in Rio Grande do Sul,
Brazil. Phytopathology 72:12971301.
Duczek, L. J. 1989. Relationship between common root rot (Cochliobolus sativus) and tillering in spring wheat. Can. J. Plant Pathol. 11:3944.
Duczek, L. J. 1990. Sporulation of Cochliobolus sativus on crowns and underground parts of spring cereals in relation to weather and host species, cultivar, and
Duveiller, E., and Maraite, H 1990. Bacterial sheath rot of wheat caused by Pseudomonas fuscovaginae in the highlands of Mexico. Plant Dis. 74:932935.
Edwards, M. C., and McMullen, M. P. 1988. A newly discovered wheat disease of unknown etiology in eastern North Dakota. Plant Dis. 72:362.
Engel, R. E., and Mathre, D. E. 1988. Effect of fertilizer nitrogen source and chloride on takeall of irrigated hard red spring wheat. Plant Dis. 72:393396.
Eversmeyer, M. G., Kramer, C. L., and Browder, L. E. 1988. Winter and early spring survival of Puccinia recondita on Kansas wheat during 19801986. Plant
Dis. 72:10741076.
Eversmeyer, M. G., Kramer, C. L., and Hassan, Z. M. 1988. Environmental influences on the establishment of Puccinia recondita infection structures. Plant Dis.
72:409412.
Eyal, Z., Scharen, A. L., Huffman, M. D., and Prescott, J. M. 1985. Global insights into virulence frequencies of Mycosphaerella graminicola. Phytopathology
75:14561462.
Ezzahiri, B., and Roelfs, A. P. 1989. Inheritance and expression of adult plant resistance to leaf rust in Era wheat. Plant Dis. 73:549551.
Ezzahiri, B., Diouri, S., and Roelfs, A. P. 1992. Anchusa italica as an alternate host for wheat leaf rust in Morocco. Plant Dis. 76:1185.
Fernandes, J. M., and Picinini, E. C. 1989. Pyricularia oryzae, a new pathogen of wheat in Brazil. (Abstr.) Can. J. Plant Pathol. 11:189.
Fernandez, J. A., Wofford, D. S., and Horton, J. L. 1985. Interactive effects of freezing and common root rot fungi on winter wheat. Phytopathology 75:845847.
Fernandez, M. R., Clark, J. M., DePauw, R. M., Krvine, R. B., and Knox, R. E. 1994. Black point and red smudge in irrigated durum wheat in southern
Saskatchewan in 19901992. Can. J. Plant Pathol. 16:221227.

Page 950
Fitt, B. D. L., and White, R. P. 1988. Stages in the progress of eyespot epidemics in winter wheat crops. Z. Pfl. Krankh. Pfl. Schutz. 95:3545.
Forster, R. L. 1990. Pink seed of wheat caused by Erwinia rhapontici in Idaho. Plant Dis. 74:81.
Forster, R. L., and Schaad, N. W. 1988. Control of black chaff of wheat with seed treatment and a foundation seed health program. Plant Dis. 72:935938.
Frank, J. A. 1985. Influence of root rot on winter survival and yield of winter barley and winter wheat. Phytopathology 75:10391041.
Frank, J. A., Cole, H., Jr., and Harley, O. E. 1988. The effect of planting date on fall infections and epidemics of powdery mildew on winter wheat. Plant Dis.
72:661664.
Fried, P. M., and Meister, E. 1987. Inheritance of leaf and head resistance of winter wheat to Septoria nodorum in a diallel cross. Phytopathology 77:13711375.
Fryda, S. J., and Otta, J. D. 1978. Epiphytotic movement and survival of Pseudomonas syringae on spring wheat. Phytopathology 64:10641067.
Gardner, W. S. 1981. Relationship of corn to the spread of wheat streak mosaic virus in winter wheat. (Abstr.) Phytopathology 71:217.
Gaudet, D. A., Bhalla, M. K., Clayton, G. W., and Chen, T. H. H. 1989. Effect of cottony snow mold and low temperatures on winter wheat survival in central and
northern Alberta. Can. J. Plant Pathol. 11:291296.
Goates, B. J. 1988. Histology of infection of wheat by Tilletia indica, the Karnal bunt pathogen. Phytopathology 78:14341441.
Goel, R. K., and Gupta, A. K. 1979. A new glume blotch disease of wheat in India. Plant Dis. Rptr. 63:620.
Gough, F. J., and Lee, T. S. 1985. Moisture effects on the discharge and survival of conidia of Septoria tritici. Phytopathology 75:180182.
Gough, F. J., and Merkle, O. G. 1977. The effect of speckled leaf blotch on root and shoot development of wheat. Plant Dis. Rptr. 61:597599.
Graham, J. H., and Menge, J. A. 1982. Influence of vesiculararbuscular mycorrhizae and soil phosphorous on takeall disease of wheat. Phytopathology 72:9598.
Grey, W. E., Mathre, D. E., Hoffman, J. A., Powelson, R. L., and Fernandez, J. A. 1986. Importance of seedborne Tilletia controversa for infection of winter
wheat and its relationship to international commerce. Plant Dis. 70:122125.
Griffin, G. D. 1990. Effect of Meloidogyne chitwoodi on the growth of wheat. (Abstr.) Phytopathology 80:1006.
Haber, S., and Chong, J. 1993. Flame chlorosis induces vesiculations in chloroplasts and mitochondria: What does it mean? (Abstr.) Can. J. Plant Pathol. 15:57.
Haber, S., and Hardener, D. E. 1992. Green foxtail (Setaria viridis) and barnyard grass (Echinochloa crusgalli), new hosts of the viruslike agent causing flame
HalfonMeiri, A., and Kulik, M. M. 1977. Septoria nodorum infection of wheat seeds produced in Pennsylvania. Plant Dis. Rptr. 61:867869.
Hannukkala, A., and Koponen, H. 1988. Microdochium bolleyi, a common inhabitant of barley and wheat roots in Finland. Karstenia 27:3136.
Herrman, T., and Weise, M. V. 1985. Influence of cultural practices on incidence of foot rot in winter wheat. Plant Dis. 69:948950.
Hess, D. E., and Shaner, G. 1987. Effect of moisture and temperature on development of Septoria tritici blotch in wheat. Phytopathology 77:215219.

Page 951
Higgins, S., and Fitt, B. D. L. 1984. Production and pathogenicity to wheat of Pseudocercosporella herpotrichoides conidia. Phytopathol. Zeitschr. 111:222231.
Hiruki, C. 1989. Characterization of the disease agent of wheat spot mosaic disease in western Canada. (Abstr.) Can. J. Plant Pathol. 11:190.
Hoffman, J. A., and Goates, B. J. 1981. Spring dormancy of Tilletia controversa teliospores. (Abstr.) Phytopathology 71:881.
Hoffman, J. A., and Sisson, D. V. 1987. Evaluation of bitertanol and thiabendazole seed treatment and PCNB soil treatment for control of dwarf bunt of wheat. Plant
Dis. 71:839841.
Holmes, R. J., and Dennis, J. I. 1985. Accessory hosts of wheat stripe rust in Victoria, Australia. Trans. Brit. Mycol. Soc. 85:159160.
Hosford, R. M., Jr. 1971. A form of Pyrenophora trichostoma pathogenic to wheat and other grasses. Phytopathology 61:2832.
Hosford, R. M., Jr. 1975. Platyspora pentamera, a pathogen of wheat. Phytopathology 65:499500.
Hosford, R. M., Jr. 1978. Effects of wetting period on resistance to leaf spotting of wheat, barley and rye by Leptosphaeria herpotrichoides. Phytopathology
68:591594.
Hosford, R. M., Jr. 1978. Effects of wetting period on resistance to leaf spotting of wheat by Leptosphaeria microscopica with conidial stage Phaeoseptoria
urvilleana. Phytopathology 68:908912.
Hosford, R. M., Jr. 1982. White blotch incited in wheat by Bacillus megaterium pv. cerealis. Phytopathology 72:14531459.
Hosford, R. M., Jr., Hogenson, R. O., Huguelet, J. E., and Kiesling, R. L. 1969. Studies of Leptosphaeria avenaria f. sp. triticea on wheat in North Dakota. Plant
Dis. Rptr. 53:378381.
Hosford, R. M., Jr., Jordahl, J. G., and Hammond, J. J. 1990. Effect of wheat genotype, leaf position, growth stage, fungal isolate, and wet period on tan spot lesions.
Plant Dis. 74:385390.
Huber, D. M. 1987. Immobilization of Mn predisposes wheat to takeall. (Abstr.) Phytopathology 77:1715.
Huber, D. M., and Hankins, B. J. 1974. Effect of fall mowing on snow mold of winter wheat. Plant Dis. Rptr. 58:432434.
Inglis, D. A., and Cook, R. J. 1981. Calonectria nivalis causes scab in the Pacific Northwest. Plant Dis. 65:923924.
Ingram, D. M., and Cook, R. J. 1987. Influence of temperature and plant residues on pathogenicity of Pythium spp. on wheat barley, peas and lentils. (Abstr.)
Jacobs, D. L., and Bruehl, G. W. 1986. Saprophytic ability of Typhula incarnata, T. idahoensis, and T. ishikariensis. Phytopathology 76:695698.
Jacobsen, B. J. 1977. Effect of fungicides on Septoria leaf and glume blotch, Fusarium scab, grain yield, and test weight of winter wheat. Phytopathology 67:1412
1414.
Jardine, D. J., Bowden, R. L., Jensen, S. G., and Seifers, D. L. 1994. A new virus of corn and wheat in western Kansas. (Abstr.). Phytopathology 84:1117.
Jenkyn, J. F., and King, J. E. 1988. Effects of treatments to perennial ryegrass on the development of Septoria spp. in a subsequent crop of winter wheat. Plant
Pathology 37:112119.
Jensen, S. G., Lane, L. C., and Seifers, D. L. 1996. A new disease of maize and wheat in the High Plains. Plant Dis. 80:13871390.
Kane, R. T., Smiley, R. W., and Sorrells, M. E. 1987. Relative pathogenicity of selected Fusar

Page 952
ium species and Microdochium bolleyi to winter wheat in New York. Plant Dis. 71:177181.
Kemp, G. H. J., Pretorius, Z. A., and Wingfield, M. J. 1996. Fusarium glume spot of wheat: A newly recorded miteassociated disease in South Africa. Plant Dis.
80:4851.
Khokhar, L. K., and Pacumbaba, R. P. 1985. Additional alternative grass hosts of Leptosphaeria nodorum. (Abstr.) Phytopathology 75:1295.
Krupinsky, J. M. 1985. Leaf Spot diseases of wheat related to stubble height. (Abstr.) Phytopathology 75:1295.
Krupinsky, J. M. 1992. Grass hosts of Pyrenophora triticirepentis. Plant Dis. 76:9295.
Krupinsky, J. M. 1997. Aggressiveness of Stagonospora nodorum isolates from perennial grasses on wheat. Plant Dis. 81:10321036.
Lai, P., and Bruehl, G. W. 1966. Survival of Cephalosporium gramineum in naturally infected wheat straws in soil in the field and in the laboratory. Phytopathology
56:213218.
Lamari, L., and Bernier, C. C. 1991. Genetics of tan necrosis and extensive chlorosis in tan spot of wheat caused by Pyrenophora triticirepentis. Phytopathology
81:10921095.
Lamari, L., Bernier, C. C., and Smith, R. B. 1991. Wheat genotypes that develop both tan necrosis and extensive chlorosis in response to isolates of Pyrenophora
triticirepentis. Plant Dis. 75:121122.
Latin, R. X., Harder, R. W., and Wiese, M. V. 1982. Incidence of Cephalosporium stripe as influenced by winter wheat management practices. Plant Dis. 66:229
230.
Lawn, D. A., and Sayre, K. D. 1989. Effects of crop rotation, tillage and straw management on common root rot of wheat. (Abstr.) Phytopathology 79:1142.
Lawton, M. B., Burpee, L. L., and Goulty, L. G. 1987. Seed treatments control gray snow mold of winter wheat. (Abstr.) Can. J. Plant Pathol. 9:281.
Lipps, P. E., and Bruehl, G. W. 1978. Snow rot of winter wheat in Washington. Phytopathology 68:11201127.
Lipps, P. E., and Herr, L. J. 1982. Etiology of Rhizoctonia cerealis in sharp eyespot of wheat. Phytopathology 72:15741577.
Lipps, P. E., and Madden, L. V. 1989. Effect of fungicide application timing on control of powdery mildew and grain yield of winter wheat. Plant Dis. 73:991994.
Lockhart, B. E. L. 1986. Occurrence of cereal chlorotic mottle virus in northern Africa. Plant Dis. 70:912915.
Lommell, S. A., Willis, W. G., and Kendall, T. L. 1986. Identification of wheat spindle streak mosaic virus and its role in a new disease of winter wheat in Kansas.
Plant Dis. 70:964968.
Loria, R., Weise, M. V., and Jones, A. L. 1982. Effect of free moisture, head development and embryo accessibility on infection of wheat by Ustilago tritici.
Los, O., van Wyk, P. S., and Marasas, W. F. O. 1987. A new species of Fusarium causing crown rot of wheat in South Africa. (Abstr.) Phytophylactica 19:29.
Love, C. S. 1985. Effect of soil pH on infection of wheat by Cephalosporium gramineum. Phytopathology 75:1296.
Love, C. S., and Bruehl, G. W. 1987. Effect of soil pH on Cephalosporium stripe in wheat. Plant Dis. 71:727731.
Luke, H. H., Pfahler, P. L., and Barnett, R. D. 1983. Control of Septoria nodorum on wheat with crop rotation and seed treatment. Plant Dis. 67:949951.
Luke, H. H., Barnett, R. D., and Pfahler, P. L. 1985. Influence of soil infestation, seed in

Page 953
fection, and seed treatment on Septoria nodorum blotch of wheat. Plant Dis. 69:7476.
Luz, W. C. D., and Hosford, R. M., Jr. 1980. Twelve Pyrenophora trichostoma races for virulence to wheat in the central plains of North America. Phytopathology
70:11931196.
Luzzardi, G. C., Luz, W. C., and Perobom, C. R. 1983. Podridas branca dos cereais causada por Sclerotium rolfsii no Brazil. Fitopatologia Brasileira 8:371375
(in Portugese).
Maas, E. M. C., and Kotze, J. M. 1985. Fusarium equiseti crown rot of wheat in South Africa. Phytophylactica 17:169170.
MacNish, G. C. 1985. Methods of reducing Rhizoctonia patch of cereals in Western Australia. Plant Pathol. 34:175181.
MacNish, G. C., and Neate, S. M. 1996. Rhizoctonia bare patch of cereals: An Australian perspective. Plant Dis. 80:965971.
Madariaga, R. B., and Gilchrist, D. G. 1990. Phenology of ascospore release by Mycosphaerella graminicola from wheat stubble in relation to crop cycle, and
other associated fungi. (Abstr.) Phytopathology 80:1006.
Maloy, O. C., and Specht, K. L. 1988. Black point of irrigated wheat in central Washington. Plant Dis. 72:10311033.
Manisterski, J., Segal, A., Levy, A. A., and Feldman, M. 1988. Evaluation of Israeli Aegilops and Agropyron species for resistance to wheat leaf rust. Plant Dis.
72:941944.
Martin, J. M., Johnston, R. H., and Mathre, D. E. 1989. Factors affecting the severity of Cephalosporium stripe of winter wheat. Can. J. Plant Pathol. 11:361367.
Mathieson, J. T., Rush, C. M., Bordovsky, D., Clark, L. E., and Jones, O. R. 1990. Effects of tillage on common root rot of wheat in Texas. Plant Dis. 74:1006
1008.
Matsumoto, N., and Tajimi, A. 1987. Bacterial flora associated with the snow mold fungi, Typhula incarnata and T. ishikariensis. Ann. Phytopathol. Soc. Japan
53:250253.
McBeath, J. H. 1981. Bacterial mosaic disease on spring wheat and triticale in Alaska. (Abstr.) Phytopathology 71:893.
McBeath, J. H. 1985. Pink snow mold on winter cereals and lawn grasses in Alaska. Plant Dis. 69:722723.
Meyer, L., Wehner, F. C., Kuwite, C. A., and Piening, L. 1996. Crater disease and patchy stunting of wheat caused by the same strain of Rhizoctonia solani. Plant
Dis. 80:1079.
MihutaGrimm, L., and Forster, R. L. 1989. Scab of wheat and barley in southern Idaho and evaluation of seed treatments for eradication of Fusarium spp. Plant
Dis. 73:769771.
Modawi, R. S., Heyne, E. G., Brunetta, D., and Willis, W. G. 1982. Genetic studies of field reaction to wheat soilborne mosaic virus. Plant Dis. 66:11831184.
Moore, K. J., and Cook, R. J. 1984. Increased takeall of wheat with direct drilling in the Pacific Northwest. Phytopathology 74:10441049.
Nagaich, B. B., and Sinha, R. C. 1974. Eastern wheat striate: A new viral disease. Plant Dis. Rptr. 58:968970.
Nelson, K. E., and Sutton, J. C. 1988. Epidemiology of eyespot on winter wheat in Ontario. Phytoprotection 69:921.
Nema, K. G., Dave, G. S., and Khosla, H. K. 1971. A new glume blotch of wheat. Plant Dis. Rptr. 55:95.
Nguyen, H. T., and Pfeifer, R. P. 1980. Effects of wheat spindle streak mosaic virus on winter wheat. Plant Dis. 64:181184.

Page 954
Nyvall, R. F., and Kommedahl, T. 1973. Competitive saprophytic ability of Fusarium roseurn f. sp. cerealis 'Culmorum' in soil. Phytopathology 63:590597.
O'Reilly, P., Bannon, E., and Downes, M. J. 1988. Leptosphaeria nodorum on wheat in Ireland. Plant Pathol. 37:153154.
Otta, J. A. 1974. Pseudomonas syringae incites a leaf necrosis on spring and winter wheats in South Dakota. Plant Dis. Rptr. 58:10611064.
Paliwal, Y. C. 1982. Role of perennial grasses, winter wheat and aphid vectors in the disease cycle and epidemiology of barley yellow dwarf virus. Can. J. Plant
Pathol. 4:367374.
Paliwal, Y. C., and Andrews, C. J. 1979. Effects of barley yellow dwarf and wheat spindle streak mosaic viruses on cold hardiness of cereals. Can. J. Plant Pathol.
1:7175.
Palmer, L. T., and Brakke, M. K. 1975. Yield reduction in winter wheat infected with soilborne wheat mosaic virus. Plant Dis. Rptr. 59:469471.
Patykowski, J., Urbanek, H., and Kaczorowska, T. 1988. Peroxidase activity in leaves of wheat cultivars differing in resistance to Erysiphe graminis DC. J.
Paulitz, T. C. 1996. Diurnal release of ascospores by Gibberella zea in inoculated wheat plots. Plant Dis. 80:674678.
Paulsen, A., Niblett, C. L., and Willis, W. G. 1975. Natural occurrence of tobacco mosaic virus in wheat. Plant Dis. Rptr. 59:747750.
Peterson, J. F. 1989. A cerealinfecting virus from orchardgrass. Can. Plant Dis. Surv. 69:1316.
Pfender, W., and Wootke, S. 1985. Overwintering microbial populations in wheat straw infested with Pyrenophora triticirepentis. (Abstr.) Phytopathology
75:1350.
Pfender, W., and Wootke, S. 1987. Production of pseudothecia and ascospores by Pyrenophora triticirepentis in response to macronutrient concentrations.
Piening, L. J., MacPherson, D. J., and Malhi, S. S. 1989. Stem melanosis of some wheat, barley, and oat cultivars on a copperdeficient soil. Can. J. Plant Pathol.
11:6567.
Piening, L. J., Orr, D. D., and Bhalla, M. 1990. Survival of Coprinus psychromorbidus under continuous cropping. Can. J. Plant Pathol. 12:217218.
Pool, R. A. F., and Sharp, E. L. 1969. Some environmental and cultural factors affecting Cephalosporium stripe of winter wheat. Plant Dis. Rptr. 53:898902.
Prabhu, A. S., and Prasada, R. 1966. Pathological and epidemiological studies of leaf blight of wheat caused by Alternaria triticina. Indian Phytopathol. 19:95112.
Pumphrey, F. V., Wilkins, D. E., Hane, D. C., and Smiley, R. W. 1987. Influence of tillage and nitrogen fertilizer on Rhizoctonia root rot (bare patch) of winter
wheat. Plant Dis. 71:125127.
Puning, L. J., and MacPherson, D. J. 1985. Stem melanosis, a disease of spring wheat caused by Pseudomonas cichorii. Can. J. Plant Pathol. 7:168172.
Raemaekers, R. H., and Tinline, R. D. 1981. Epidemic of diseases caused by Cochliobolus sativus on rainfed wheat in Zambia. Can. J. Plant Pathol. 3:211214.
Rakotondradona, R., and Line, R. F. 1984. Control of stripe rust and leaf rust of wheat with seed treatments and effects of treatments on the host. Plant Dis. 68:112
117.
Rao, A. S. 1968. Biology of Polymyxa graminis in relation to soilborne wheat mosaic virus. Phytopathology 58:15161521.
Reis, E. M., and Wunsche, W. A. 1984. Sporulation of Cochliobolus sativus on residues of winter crops and its relationship to the increase of inoculum density in
soil. Plant Dis. 68:411412.

Page 955
Reis, E. M., Cook, R. J., and McNeal, B. L. 1982. Effect of mineral nutrition on takeall of wheat. Phytopathology 72:224229.
Reis, E. M., Cook, R. J., and McNeal, B. L. 1983. Elevated pH and associated reduced tracenutrient availability as factors contributing to increased takeall of
wheat upon soil liming. Phytopathology 73:411413.
Rewal, H. S., and Jhooty, J. S. 1986. Physiological specialization of loose smut of wheat in the Punjab state of India. Plant Dis. 70:228230.
Richardson, M. J., and Noble, M. 1970. Septoria species on cerealsA note to aid their identification. Plant Pathol. 19:159163.
Rivoal, R., and Sarr, E. 1987. Field experiments on Heterodera avenae in France and implications for winter wheat performance. Nematologica 33:460479.
Roane, C. W., Roane, M. K., and Starling, T. M. 1974. Ascochyta species on barley and wheat in Virginia. Plant Dis. Rptr. 58:455456.
Roberts, F. A., and Sivasithamparam, K. 1987. Effect of interaction of Rhizoctonia spp. with other fungi from cereal bare patches on root rot of wheat. Trans. Brit.
Mycol. Soc. 89:256259.
Rodriguez Pardina, P. E., Gimenez Pecci, M. P., Laguna, I. G., Dagoberto, E., and Truol, G. 1998. Wheat: A new natural host for the Mal de Rio Cuarto virus in the
endemic disease area, Rio Cuarto, Cordoba Province, Argentina. Plant Dis. 82:149152.
Rovira, A. D. 1986. Influence of crop rotation and tillage on Rhizoctonia bare patch of wheat. Phytopathology 76:669673.
Rovira, A. D., and McDonald, H. J. 1986. Effects of the herbicide chlorsulfuron on Rhizoctonia bare patch and takeall of barley and wheat. Plant Dis. 70:879882.
Rowe, R. C., and Powelson, R. L. 1973. Epidemiology of Cercosporella foot rot of wheat: Disease spread. Phytopathology 63:984988.
Rowe, R. C., and Powelson, R. L. 1973. Epidemiology of Cercosporella foot rot of wheat: Spore production. Phytopathology 63:981984.
Rush, C. M., Carling, D. E., Harveson, R. M., and Mahieson, J. T. 1994. Prevalence and pathogenicity of anastomosis groups of Rhizoctonia solani from wheat and
sugar beet in Texas. Plant Dis. 78:349352
Russell, C. C., and Perry, V. G. 1966. Parasitic habit of Trichodorus christiei on wheat. Phytopathology 56:357358.
Scardaci, S. C., and Webster, R. K. 1982. Common root rot of cereals in California. Plant Dis. 66:3134.
Schafer, J. F., and Long, D. L. 1986. Evidence for local source of Puccinia recondita on wheat in Pennsylvania. Plant Dis. 70:892.
Scharen, A. L., and Krupinsky, J. M. 1971. Ascochyta tritici on wheat. Phytopathology 61:675680.
Schilder, A. M. C., and Bergstrom, G. C. 1992. The process of wheat seed infection by Pyrenophora triticirepentis. (Abstr.). Phytopathology 82:1072.
Scott, D. B., Visser, C. P. N., and Rufenacht, E. M. C. 1979. Crater disease of summer wheat in African drylands. Plant Dis. Rptr. 63:836840.
Scott, P. R., Benedikz, P. W., Jones, H. G., and Ford, M. A. 1985. Some effects of canopy structure and microclimate on infection of tall and short wheats by
Septoria nodorum. Plant Pathol. 34:578593.
Scott, P. R., Sanderson, F. K., and Benedikz, P. W. 1988. Occurrence of Mycosphaerella graminicola, teleomorph of Septoria tritici, on wheat debris in the U.
K. Plant Pathol. 37:285 290.
Seifers, D. L., Harvey, T. L., and Bowden, R. L. 1995. Occurrence and symptom expression

Page 956
of American wheat striate mosaic virus in wheat in Kansas. Plant Dis. 79:853858.
Seifers, D. L., Harvey, T. L., Martin, T. J., and Jensen, S. G. 1997. Identification of the wheat curl mite as the vector of the High Plains virus of corn and wheat. Plant
Dis. 81:11611166.
Sellam, M. A., and Wilcoxson, R. D. 1976. Bacterial leaf blight of wheat in Minnesota. Plant Dis. Rptr. 60:242245.
Shane, W. W., and Baumer, J. S. 1987. Population dynamics of Pseudomonas syringae pv. syringae on spring wheat. Phytopathology 77:13991405.
Shane, W. W., Baumer, J. S., and Teng, P. S. 1987. Crop losses caused by Xanthomonas streak on spring wheat and barley. Plant Dis. 71:927930.
Shaner, G., and Buechley, G. 1995. Epidemiology of leaf blotch of soft red winter wheat caused by Septoria tritici and Stagonospora nodorum. Plant Dis. 79:928
938.
Shaner, G., and Powelson, R. L. 1973. The oversummering and dispersal of inoculum of Puccinia striiformis in Oregon. Phytopathology 63:1317.
Shefelbine, P. A., and Bockus, W. W. 1989. Decline of Cephalosporium stripe by monoculture of moderately resistant winter wheat cultivars. Phytopathology
79:11271131.
Shefelbine, P. A., and Bockus, W. W. 1990. Host genotype effects on inoculum production by Cephalosporium gramineum from infested residue. Plant Dis. 74:
238240.
Sherwood, J. L., Myers, L. D., and Hunger, R. M. 1991. Replication and movement of wheat soilborne mosaic virus (WSBMV) in hard red winter wheat. (Abstr.)
Phytopathology 81: 1216.
Shipton, P. J. 1975. Takeall decline during cereal monoculture, pp. 137144. In Biology and Control of Soilborne Plant Pathogens, G. W. Bruehl, ed. American
Phytopathological Society, St. Paul, MN. 216 pp.
Sinha, R. C., and Benki, R. M. 1972. American Wheat Striate Mosaic Virus. Descriptions of Plant Viruses. Set 6, No. 99. Commonwealth Mycological Institute.
Slykhuis, J. T. 1970. Factors determining the development of wheat spindle streak mosaic caused by a soilborne virus in Ontario. Phytopathology 60:319331.
Slykhuis, J. T., and Barr, D. J. S. 1978. Confirmation of Polymyxa graminis as a vector of wheat spindle streak mosaic virus. Phytopathology 68:639643.
Smilanick, J. L., Hoffmann, J. A., and Royer, M. H. 1985. Effect of temperature, pH, light and desiccation on teliospore germination of Tilletia indica.
Smiley, R. W., Fowler, M. C., and Reynolds, K. L. 1986. Temperature effects on takeall of cereals caused by Phialophora graminicola and Gaeumannomyces
graminis. Phytopathology 76:923931.
Smiley, R. W., GillespieSasse, L.M., Uddin, W., Collins, H. P., and Stoltz, M. A. 1993. Physiologic leaf spot of winter wheat. Plant Dis. 77:521527.
Smiley, R. W., Uddin, W., Zwer, P. K., Wysocki, D. J., Ball, D. A., Chastain, T. G., and Rasmussen, P. E. 1993. Influence of crop management practices on
physiologic leaf spot of winter wheat. Plant Dis. 77:803810.
Smith, E. M., and Wehner, F. C. 1987. Biological and chemical measures integrated with deep soil cultivation against crater disease of wheat. Phytophylactica 19:87
90.
Smith, J. D. 1981. Snow molds of winter cereals: Guide for diagnosis, culture and pathogenicity. Can. J. Plant Pathol. 3:1525.

Page 957
Spadafora, V. J., Cole, H., Jr., and Frank, J. A. 1987. Effects of leaf and glume blotch caused by Leptosphaeria nodorum on yield and yield components of soft red
winter wheat in Pennsylvania. Phytopathology 77:13261329.
Stack, R. W. 1989. A comparison of the inoculum potential of ascospores and conidia of Gibberella zeae. Can. J. Plant Pathol. 11:137142.
Stack, R. W., and McMullen, M. P. 1985. Head blighting potential of Fusarium species associated with spring wheat heads. Can. J. Plant Pathol. 7:7982.
Stack, R. W., Jons, V. L., and Lamey, H. A. 1979. Snow rot of winter wheat in North Dakota. (Abstr.) Phytopathology 69:543.
Stanton, J. M., and Fisher, J. M. 1987. Field assessment of factors associated with tolerance of wheat to Heterodera avenae. Nematologica 33:357360.
Stiles, C. M., and Murray, T. D. 1996. Infection of fieldgrown winter wheat by Cephalosporium gramineum and the effect of soil pH. Phytopathology 86:177
183.
Sturz, A. V., and Bernier, C. C. 1987. Incidence of pathogenic fungal complexes in the crowns and roots of winter and spring wheat relative to cropping practice.
Sturz, A. V., and Bernier, C. C. 1989. Influence of crop rotations on winter wheat growth and yield in relation to the dynamics of pathogenic crown and root rot
fungal complexes. Can. J. Plant Pathol. 11:114121.
Takamatsu, S. 1989. A new snow mold of wheat and barley caused by foot rot fungus, Ceratobasidium gramineum. Ann. Phytopathol. Soc. Japan 55:233237.
Takamatsu, S., and Ichitani, T. 1987. Detection of Pythium snow rot fungi in diseased leaves of wheat and barley grown in paddy fields and upland fields. Ann.
Phytopathol. Soc. Japan 53:5659.
Taylor, R. G., Jackson, T. L., Powelson, R. L., and Christensen, N. W. 1983. Chloride, nitrogen form, lime, and planting date effects on takeall root rot of winter
wheat. Plant Dis. 67:11161120.
Teich, A. H., and Nelson, K. 1984. Survey of Fusarium head blight and possible effects of cultural practices in wheat fields in Lambton County in 1983. Can. Plant
Dis. Surv. 64:1113.
Teyssandier, E., and Sands, D. C. 1987. Wheat leaf blight caused by Pseudomonas syringae in Argentina. (Abstr.) Phytopathology 77:1766.
Tinline, R. D. 1981. Effect of depth and rate of seeding on common root rot of wheat in Saskatchewan. (Abstr.) Phytopathology 71:909.
Tinline, R. D. 1994. Etiology of prematurity blight of hard red spring wheat and durum wheat in Saskatchewan. Can. J. Plant Pathol. 16:8792.
Traquair, J. A., and Smith, J. D. 1982. Sclerotial strains of Coprinus psychromorbidus, a snow mold basidiomycete. Can. J. Plant Pathol. 4:2636.
Trione, E. J., Stockwell, V. O., and Latham, C. J. 1989. Floret development and teliospore production in buntinfected wheat, in plants and in cultured spikelets.
Urashima, A. S., Igarashi, S., and Kato, H. 1993. Host range, mating type, and fertility of Pyricularia grisea from wheat in Brazil. Plant Dis. 77:12111216.
Usugi, T., and Saito, Y. 1979. Relationship between wheat yellow mosaic virus and wheat spindle streak mosaic virus. Ann. Phytopathol. Soc. Japan 45:397400.
van Wyk, P. S., Los, O., and Kloppers, F. J. 1986. Crown rot of wheat caused by Fusarium crookwellense. Phytophylactica 18:9192.

Page 958
van Wyk, P. S., Los, O., and Marasas, W. F. O. 1988. Pathogenicity of a new Fusarium sp. from crown rot of wheat in South Africa. Phytophylactica 20:7375.
Vargo, R. H., and Baumer, J. S. 1986. Fusarium sporotrichioides as a pathogen of spring wheat. Plant Dis. 70:629631.
Vargo, R. H., Baumer, J. S., and Wilcoxson, R. D. 1981. Fusarium tricinctum as a pathogen of spring wheat. (Abstr.) Phytopathology 71:910.
Velasco, V. R, Ishimaru, C. A., and Brown W. M., Jr. 1991. Halo blight of spring wheat caused by Pseudomonas syringae. (Abstr.) Phytopathology 81:1159.
yon Wechmar, M. B. 1987. Cucumber mosaic virus causes wheat disease. (Abstr.) Phytophylactica 19:126.
Wallwork, H., and Spooner, B. 1988. Tapesia yallundae—The teleomorph of Pseudocercosporella herpotrichoides. Trans. Brit. Mycol. Soc. 91:703705.
Wang, Y. Z., and Miller, J. D. 1988. Effects of Fusarium graminearum metabolites on wheat tissue in relation to Fusarium head blight resistance. J. Phytopathology
122:118125.
Warham, E. J. 1990. Effect of Tilletia indica infection on viability, germination, and vigor of wheat seed. Plant Dis. 74:130132.
Weller, D. M., Cook, R. J., MacNish, G., Bassett, E. N., Powelson, R. L., and Petersen, R. R. 1986. Rhizoctonia root rot of small grains favored by reduced tillage
in the Pacific Northwest. Plant Dis. 70:7073.
Weste, G. 1972. The process of root infection by Ophiobolus graminis. Trans. Brit. Mycol. Soc. 59:133147.
Wiese, M. V. 1987. Compendium of Wheat Diseases, Second Edition. American Phytopathological Society, St. Paul, MN.
Wilcoxson, R. D., Kommedahl, T., Ozmon, E. A., and Windels, C. E. 1988. Occurrence of Fusarium species in scab by wheat from Minnesota and their
pathogenicity to wheat. Phytopathology 78:586589.
Wilkie, J. P. 1973. Basal glume rot of wheat in New Zealand. New Zealand J. Agric. Res. 16:155160.
Wilkinson, H. T., Cook, R. J., and Alldredge, J. R. 1985. Relation of inoculum size and concentration to infection of wheat roots by Gaeumannornyces graminis
var. tritici. Phytopathology 75:98103.
Zhang, W., and Pfender, W. F. 1992. Effect of residue management on wetness duration and ascocarp production by Pyrenophora triticirepentis in wheat residue.
Zhang, L., Zitter, T. A., and Lulkin, E.J. 1991. Artificial inoculation of maize white line mosaic virus into corn and wheat. Phytopathology 81:397400.

Page 959
24.
Diseases of Wild Rice (Zizania palustris)
Bacterial Brown Spot
Cause.
Pseudomonas syringae pv. syringae.
Distribution.
The United States (Idaho and Minnesota).
Symptoms.
Diseased leaves initially have small watersoaked spots or short streaks that later become chestnut or tan and are surrounded by a diffuse greenbrown halo with a
dark brown margin. Watersoaked areas frequently become translucent spots or slits in the centers of lesions and fall out of older lesions, giving leaves a ''shothole"
appearance. Small or narrow lesions are uniformly dark brown. Although typical lesions are roughly elliptical or spindleshaped (110 × 2100 mm or more), some
lesions may be irregularshaped or diffuse. White exudate rarely is present in the centers of lesions.
Management.
Not reported.
Bacterial leaf streak is also called bacterial streak.
Cause.
Xanthomonas campestris and Pseudomonas syringae pv. zizaniae.
Distribution.
Symptoms.
Initially, the watersoaked, dark green lesions on leaves are narrow (12 cm long), linear, and parallel to veins. Later, lesions become necrotic and dark brown to
black, then dry up and are covered with a glistening crust of bacterial exudate.
Management.
Not reported.

Page 960
Anthracnose
Cause.
Colletotrichum graminicola (syn. C. sublineola). The species name "sublineola" is sometimes spelled "sublineolum" in the literature.
Distribution.
The United States (Minnesota).
Symptoms.
Initially, small (12 mm in diameter), dark greenbrown, watersoaked lesions occur on diseased leaves of aerial plants and on floating leaves of young plants. Later,
lesions become elliptical to fusiform in shape (0.11.5 × 0.10.6 cm) and have light tan centers and dark brown margins. Lesions contain numerous, black, setose,
veinlimited acervuli covered with orangepink masses of conidia.
Management.
Not reported.
Ergot
Cause.
Claviceps zizaniae overwinters as sclerotia. When wild rice flowers are forming in early summer, sclerotia germinate and produce stalks on which stroma are
produced. Perithecia containing ascospores form in stromatic heads. Ascospores are disseminated by wind to wild rice flowers and infect them. After infection, insects
are attracted to a sweet, sticky liquid containing conidia that is exuded from flowers. Insects then disseminate conidia as secondary inoculum to healthy flowers.
Eventually, hard sclerotia form in place of grain, drop into water, and wash to shore, where they survive unfavorable periods.
Distribution.
Wherever wild rice is grown, but ergot is rare in commercial wild rice paddies.
Symptoms.
Large ergot bodies or sclerotia replace kernels. Initially, sclerotia are pink to purple, when growing on plants, but become black and hard when they mature and dry
up. Sclerotia vary in size (36 × 320 mm). Prior to formation of sclerotia, drops of the sweet liquid and insects may be seen on plant heads.
Yield losses are minimal. Ergot bodies may be harmful if consumed, but because of their larger size, they are easily separated from grain.
Management.
Remove sclerotia from grain during the cleaning process. Chips and pieces of ergot bodies that remain in grain can be floated out with water.
Fungal Brown Spot
Fungal brown spot is also called brown spot, Helminthosporium brown spot, and Helminthosporium blight.

Page 961
Cause.
Bipolaris oryzae infrequently overwinters as mycelium in infested whole stems that are not flooded, and in reed canarygrass. It is also seedborne, but this is likely not
a factor in disease development. Conidia are produced in summer and are disseminated by wind to wild rice plants, where infection occurs beginning at the flowering
stage of plant growth. Secondary infection is by conidia produced in new lesions and disseminated by wind to host plant tissue.
Infection and disease development are optimum at temperatures of 25 to 30°C and continuous wet periods of 16 to 28 hours. Disease development is greatest
between the flowering stage of plant growth and harvest.
Distribution.
Symptoms.
Symptoms do not become evident until flowering or later in the growing season. Where environmental conditions are conducive to disease development, symptoms
will increase in incidence and severity until harvest time. All plant parts are diseased.
The first symptoms, which are found on leaves, are tiny, brown or purple lesions that develop into different shapes and may be limited by veins. Some lesions remain 1
mm or less in diameter and retain a very dark brown to purpleblack color. Frequently, lesions will expand and develop brown centers with chlorotic margins. Some
lesions retain a discrete shape and a size of 6 to 10 mm, whereas others lengthen to 3 to 4 cm. As lesions become larger and more numerous, leaves turn brown to
yellowbrown and die.
Stem and sheath lesions develop similarly to those on leaves. Large necrotic areas develop on stems, frequently causing them to weaken and break. Infected spikes
are bleached and florets and caryopses fail to develop, which results in a reduced number of seeds or no seeds being produced. Yields suffer slight to total (100%)
losses.
Management
2. Paddies should be isolated from each other by 1.63.2 km.
4. Remove infested crop residue from paddy.
5. Plow paddy soil.
6. Grow wild rice for 2 successive years in the same soil followed by fallow soil or an alternative crop for at least 1 year.
Fusarium head blight is also called scab.
Cause.
Several Fusarium spp., but F. graminearum is the dominant species. Fungi overwinter as mycelia and spores on crop residue and other plant hosts. The fungi
spread to plants by windborne spores. Infection of wild rice is thought to occur under wet environmental conditions.

Page 962
Distribution.
Unknown. It is presumed to be generally distributed wherever wild rice is grown.
Symptoms.
Diseased spikelets are light brown. Diseased seed is light in weight and poorly developed. Diseased seed generally "shatters" from the head and falls to the soil
surface. The fungi are then destroyed upon flooding of the paddy.
Management.
Flooding paddies controls local sources of inoculum. However, conidia are likely disseminated by wind from other host plants and infested residue.
Phytophthora Crown and Root Rot
Cause.
Phytophthora erythroseptica. Onset of symptoms coincides with hot, windy weather, which possibly predisposes host plants to disease. This is the only known
example of a species of Phytophthora causing a serious disease of a mature grass host.
Distribution.
Symptoms.
Disease distribution is relatively uniform in some fields and patchy in others, appearing to be confined to a portion of a field. Not all plants in an affected area are
diseased. Healthy plants can grow adjacent to diseased ones and can compensate for diseased ones so that severely affected areas appear to be normal at the end of
the growing season.
Plants ranging in age from the earlytillering to the grainfilling stages are killed. Initially, the disease progresses rapidly in the field but after 3 to 4 weeks, disease
incidence and severity slows dramatically and few additional plants show symptoms.
Typically, diseased plants within fields show drought symptoms even though they are growing in flooded conditions. Leaves of diseased plants are gray to graygreen,
then become tan or strawcolored, dry, and brittle. The crown, first internode, portions of leaf sheaths surrounding the internode, and many adventitious roots
become necrotic; crowns typically show the most severe necrosis. Crowns frequently become so rotted that tillers separate from them and float to the water surface,
leaving roots embedded in the soil.
Management.
Not known.
Smut
The resultant galls are known as gausun and kahpehsung and are sold as vegetables. This hostpathogen combination is intentionally cultivated throughout the Orient
for this purpose.
Cause.
Ustilago esculenta.

Page 963
Distribution.
Asia and the United States (California on Manchurian wild rice, Zizania latifolia).
Symptoms.
Culms enlarge and form galls up to 3 cm in diameter. Dark sori (1 × 510 mm) filled with teliospores are present inside galls.
Management.
Practice sanitation.
Spot Blotch
Cause.
Bipolaris sorokiniana overwinters primarily as mycelia on grasses growing adjacent to cultivated wild rice fields and within infested residue of several plant host
species. Conidia are produced on residue or grasses in the spring and early summer and disseminated to host plants, where infection occurs on the first aerial leaves
and infrequently on the floating leaves.
Distribution.
Symptoms.
All plant parts are infected. The first symptoms are tiny brown or purple lesions on the first aerial leaves and infrequently on the floating leaves. Spots develop into
different shapes that are sometimes limited by veins. Some spots remain 1 mm or less in diameter and retain a very dark brown to purpleblack color. Some retain a
discrete shape and size of 6 to 10 mm, whereas other spots lengthen to 3 to 4 cm. As spots become larger and more numerous, leaves turn brown to yellowbrown
and die.
Stem and sheath spots develop similarly to those on leaves. Large necrotic areas develop on stems, frequently causing them to weaken and break. Infected spikes are
bleached, and florets and caryopses fail to develop, which results in a reduced number of seeds or no seeds being produced.
Management
2. Paddies should be isolated from each other by 1.63.2 km.
4. Remove infested crop residue from paddy.
5. Plow paddy soil.
6. Grow wild rice for 2 successive years followed by fallow soil or an alternative crop for at least 1 year.
Stem Rot
Cause.
Sclerotium sp. and Nakataea sigmoidea (syn. Helminthosporium sigmoideum). These two fungi, or similar fungi, also cause a stem rot on white rice, Oryzae
sativa. On white rice, the sclerotial stage is S. oryzae and the conidial stage is N. sigmoidea. On wild rice, both N. sigmoidea and Scle

Page 964
rotium sp. produce sclerotia that differ morphologically but are likely different stages of the same causal fungus, as in white rice.
The fungi overwinter as sclerotia in infested residue, paddy water, and soil. Optimum survival is in the residue on top of the soil, but numerous sclerotia can be
observed floating on top of the water after paddies have been flooded. Sclerotia of Sclerotium sp. are also produced in lesions of white water lily, Nymphaea
odorata, which serves as a site for overwintering and an increase of inoculum.
The fungi are disseminated from wild rice paddy to paddy primarily by infested residue and paddy water and infrequently by seed lots contaminated with sclerotia.
Sclerotia germinate and produce conidia that are disseminated by wind or sclerotia that float to host plants, where they germinate and produce infective mycelium.
Plants are infected at the water level or at the soil level and crowns when water is removed from paddies. Disease development is slow until water is removed, then
increases rapidly if the weather stays dry and temperatures are above 24°C. Sclerotia form in culms, leaf sheaths, and floating leaves that were cut from plants during
thinning operations in the spring or early summer.
Distribution.
Symptoms.
Initially, purplish lesions develop on stems at the water level and on floating leaves and the first, and infrequently the second, aerial leaves. Black, round sclerotia (less
than 2 mm in diameter) occur in lesions and on senescent plants. Later, as paddies are drained, brown lesions develop in crowns and the lower 15 cm of stems.
Diseased stems become necrotic, dry, and brittle and break easily at the soil line. Diseased culms and leaf sheaths are partially or wholly destroyed and contain masses
of black sclerotia embedded in white mycelium. Heads are poorly filled with seed that is light in color and underdeveloped.
Management
1. Remove plant residue from paddies.
2. Paddy soil should be plowed.
3. Paddies should be left fallow for at least 1 year.
Stem Smut
Cause.
Entyloma lineatum.
Distribution.
Wherever wild rice is grown.
Symptoms.
Symptoms do not occur until plants are almost mature. Glossy black lesions occur on stems, culms, and heads due to numerous chla

Page 965
mydospores produced under the surface of diseased stems and leaves. As plants mature and dry, lesions elongate, coalesce, and girdle stems near the head and
change color from black to lead gray. Stem and leaf infections do not cause much damage, but head infection reduces seed production.
Management.
Differences in resistance exist among individual breeding lines and selections.
Zonate Eyespot
Cause.
Drechslera gigantea survives in volunteer wild rice plants when paddies are fallow. Smooth brome, Bromus inermis; quackgrass, Agropyron repens; and reed
canarygrass, Phalaris arundinacea, serve as alternate hosts. Zonate eyespot is associated with dense stands and infested residue from the previous crop. Disease
occurs following 72 hours of 90% to 100% relative humidity and temperatures of at least 30°C.
Distribution.
Symptoms.
Initial symptoms on leaves are small (1 mm in diameter), watersoaked, graygreen lesions with welldefined brown margins. As lesions enlarge, they become tan to
brown in the center and secondary lesions that form around the primary lesions produce typical zonate eyespot lesions. Lesions typically are 0.8 to 1.5 cm long but
may enlarge to 1 to 2 cm in length. Lesions coalesce and cover the entire leaf area of susceptible cultivars. Under humid conditions, white, prostrate mycelial strands
grow outward from the lesion margins.
Management.
Not reported.
Miscellaneous Fungi
Diplodia oryzae was isolated from dead culms.
Doassansia zizaniae causes a stem smut.
Mycosphaerella zizaniae causes a leaf spot.
Ophiobolus oryzinus causes a culm rot and is reported to be synonymous with Gaeumannomyces graminis.
Phaeoseptoria sp. causes a leaf spot.
Sclerotium hydrophilum was isolated from stem and foliar lesions.
Miscellaneous Nematodes
Radopholus gracilis was isolated from the cortex of roots.
Hirschmanniella gracilis was isolated from paddy soil.

Page 966
Disease Caused by Viruses
Wheat Streak Mosaic
Cause.
Wheat streak mosaic virus wild rice isolate (WSMVWR) is in the potyvirus group. The life cycle of WSMVWR is unclear. Dissemination is likely by the mite
Aceria tulipae, which is disseminated by wind for long distances and is commonly found on wild rice. Aceria tulipae retains WSMVWR for several days.
Distribution.
Symptoms.
Diseased plants have typical streak symptoms. As disease symptoms progress for 10 days, chlorotic areas on the lower diseased leaves become necrotic. The
necrotic areas eventually coalesce and cause the death of diseased leaves.
Management.
Not reported.
Selected References
Bean, G. A., and Schwartz, R. 1961. A severe epidemic of Helminthosporium brown spot disease on cultivated wild rice in northern Minnesota. Plant Dis. Rptr.
45:901.
Berger, P. H., Percich, J. A., and Ransom, J. K. 1981. Wheat streak mosaic virus in wild rice. Plant Dis. 65:695696.
Bowden, R. L., and Eschen, D. J. 1986. First report of wild rice diseases in Idaho. Plant Dis. 70:800.
Bowden, R. L., and Percich, J. A. 1981. Bacterial leaf streak of wild rice. (Abstr.) Phytopathology 71:204.
Bowden, R. L., and Percich, J. A. 1981. Bacterial leaf streak of wild rice caused by Xanthomonas campestris and Pseudomonas syringae. (Abstr.)
Bowden, R. L., and Percich, J. A. 1983. Etiology of bacterial leaf streak of wild rice. Phytopathology 73:640645.
Bowden, R. L., and Percich, J. A. 1983. Bacterial brown spot of wild rice. Plant Dis. 67:941943.
Bowden, R. L., Kardin, M. K., Percich, J. A., and Nickelson, L. J. 1984. Anthracnose of wild rice. Plant Dis. 68:6869.
Brantner, J., Malvick, D., Percich, J., and Nyvall, R. F. 1994. Variation in sensitivity to propiconazole in Bipolaris oryzae and B. sorokiniana, causal organisms of
fungal brown spot of wild rice. (Abstr.) Phytopathology 84:1139.
Brantner, J. A., Nyvall, R. F., and Percich, J. A. 1995. Overwintering sites of Bipolaris oryzae and B. sorokiniana causing fungal brown spot of wild rice. (Abstr.)
Gunnell, P. S., and Webster, R. K. 1988. Crown and root rot of cultivated wild rice in Call

Page 967
fornia caused by Phytophthora erythroseptica sensu lato. Plant Dis. 72:909910.
Johnson, D. A., Stewart, E. L., and King, T. H. 1976. A Sclerotium species associated with water lilies in Minnesota. Plant Dis. Rptr. 60:807808.
Johnson, D. R., and Percich, J. A. 1989. Detection of ophiobolin in culture filtrates of Bipolaris oryzae and use in a wild rice root elongation assay. (Abstr.).
Kardin, M. K., Bowden, R. L., Percich, J. A., and Nickelson, L. J. 1981. Zonate eyespot of wild rice in Minnesota. (Abstr.) Phytopathology 71:885.
Kardin, M. K., Bowden, R. L., Percich, J. A., and Nickelson, L. J. 1982. Zonate eyespot on wild rice caused by Drechslera gigantea. Plant Dis. 66:737739.
Kernkamp, M. F., Kroll, R., and Woodruff, W. C. 1976. Diseases of cultivated wild rice in Minnesota. Plant Dis. Rptr. 60:771775.
Kernkamp, M. F., Kroll, R., and Woodruff, W. C. 1977. Wild rice infected by Sclerotium sp. isolated from white water lily. Plant Dis. Rptr. 61:187188.
Kohls, C. L., Percich, J. A., and Huot, C. M. 1987. Wild rice yield losses associated with growthstagespecific fungal brown spot epidemics. Plant Dis. 71:419
422.
Moffat, A., Nyvall, R., and Percich, J. 1997. Host range of Bipolaris oryzae, cause of fungal brown spot on cultivated wild rice. (Abstr.). Phytopathology 87:S67.
Morrison, R. H., and King, T. H. 1971. Stem rot of wild rice in Minnesota. Plant Dis. Rptr. 55:498500.
Nyvall, R. F., and Percich, J. 1992. Control of fungal brown spot of cultivated wild rice with propiconazole. (Abstr.) Phytopathology 82:1068.
Nyvall, R. F., Percich, J. A., and Brantner, J.R. 1994. Fungal brown spot of cultivated wild rice is two different diseases. (Abstr.) Phytopathology 84: 1102.
Nyvall, R. F., Percich, J. A., Porter, R. A., and Brantner, J. R. 1994. Comparison of fungal brown spot severity to incidence of seedborne Bipolaris oryzae and B.
sorokiniana and infected floral sites on cultivated wild rice. Plant Dis. 78:249250.
Nyvall, R. F., Porter, R. A., and. Percich, J. A. 1995. First report of scab on cultivated wild rice in Minnesota. Plant Dis. 79:82.
Pantidou, M. E. 1959. Claviceps from Zizania. Can. J. Bot. 37:12331236.
Percich, J. A., and Huot, C. M. 1989. Comparison of propiconazole and mancozeb applied individually or sequentially for management of fungal brown spot of wild
rice. Plant Dis. 73:257259.
Percich, J. A., and Nickelson, L. J. 1982. Evaluation of several fungicides and adjuvant materials for control of brown spot of wild rice. Plant Dis. 66:10011003.
Percich, J. A., Bowden, R. L., Kardin, M. K., and Hotchkiss, E. S. 1983. Anthracnose of wild rice caused by a Colletotrichum sp. (Abstr.) Phytopathology
73:843.
Percich, J. A., Nyvall, R. F., Malvick, D. K., and Kohls, C. L. 1997. Interaction of temperature and moisture on infection of wild rice by Bipolaris oryzae in the
growth chamber. Plant Dis. 81:11931195.
Watson, T. 1991. Smut of Manchurian wild rice caused by Ustilago esculenta in California. Plant Dis.75:1075.

Page 969
Index
Abacarus hystix, 928
Abutilon mosaic virus, 219
Aceratagallia calcaris, 728
Aceria tosichella
barley, 91
maize, 315
millet, 365
oat, 399
sorghum, 615
wheat, 934, 943944
Aceria tulipae
barley, 95
maize, 330331
rye, 555
wheat, 943944, 946
wild rice, 966
Acetylneosolaniol, 706
Achaparramiento, 310311
Achene blemish syndrome, 785786
Achlya spp, 500
Acidovorax avenae
maize, 247
millet, 344
oat, 369
rice, 479480
sorghum, 575
Acremonium spp.
maize, 258, 261
sorghum, 578
soybean, 628
sunflower, 788
Acrocalymma medicaginis, 7
Acrocylindrium oryzae, 497
Acrosternurn hilare, 668
Actinomyces scabies, 697
Acyrthosiphon pisum, 30, 3739, 173, 471, 680
Aecidium clematidis, 535536
Aerial blight
peanut, 404
soybean, 655656
Aerolate mildew, cotton, 185
Aflatoxin, 257
African cereal streak virus
barley, 85
oat, 393
rice, 505
rye, 553
wheat, 927
Agallia albidula, 847
Agallia ensigera, 847
Aggregate sheath spot, rice, 482
Agriotes mancus, 252
Agrobacterium biovar 1, 183
Agrobacterium radiobacter, 184185
Agrobacterium root rot and wilt, cotton, 183
Agrobacterium tumefaciens
alfalfa, 5
canola, 108
sugar beet, 697
sunflower, 784785
tobacco, 813814
Agryopyron mosaic virus, 927928
Albugo candida, 123124
Albugo tragopogonis, 802
Alfalfa (Medicago stiva), 339
bacterial diseases, 37
alfalfa sprout rot, 3
crown gall, 5
dwarf, 6
leaf spot, 34
root and crown rot complex, 67
stem blight, 45
wilt, 4
fungal diseases, 733
Acrocalymma root and crown rot, 7
anthracnose, 78
Aphanomyces root rot, 8
black patch, 9
black root rot, 9
brown root rot, 9

Page 970
Alfalfa (Medicago stiva) (continued)
corky root rot, 10
crown wart, 1011
Cylindrocarpon root rot, 11
Cylindrocladium root and crown rot, 11
damping off, 1112
downy mildew, 1213
forked foot disease, 13
Fusarium crown and root rot, 1314
Fusarium wilt, 14
leaf spot, common, 10
lepto leaf spot, 15
Marasmius root rot, 15
Mycoleptodiscus crown and root rot, 1516
Mycothecium root rot, 16
Oidiopsis powdery mildew, 16
Oidium powdery mildew, 1617
Phoma root rot, 17
Phymatotricum root rot, 1718
Phytophthora root rot, 1819
powdery mildew, 19
Rhizoctonia foliage blight, 1920
Rhizoctonia root rot, 20
Rhizoctonia stem blight, 2021
Rhizopus sprout rot, 21
root and crown rot complex, 2122
rust, 2223
Sclerotinia crown and stem rot, 2324
southern blight, 24
spring black stem, 25
Stagonospora leaf spot, 2526
Stagonospora root rot, 2627
Stemphylium leaf spot, 2728
summer black stem, 2829
Verticillium wilt, 2931
violet root rot, 31
winter crown rot, 3132
yellow leaf blotch, 3233
nematodecaused diseases
alfalfa stem, 33
cyst, 33
dagger, 34
pin, 34
reniform, 34
root knot, 3435
root lesion, 35
spiral, 35
stubby root, 35
stunt, 36
phytoplasmal diseases, 3637
aster yellows, 36
witches' broom, 3637
vital diseases, 3739
alfalfa enation, 37
alfalfa latent, 37
alfalfa mosaic, 3738
bean leaf roll, 38
Lucerne transient streak, 3839
Alfalfa enation virus, 37
Alfalfa latent virus, 37
Alfalfa mosaic virus
alfalfa, 3738
red clover, 469
safflower, 570
soybean, 674
tobacco, 846847
Alfalfa sprout rot, 3
Alfalfa stem disease, 33
Alfalfa weevils (Hypera postica), 30
Almond leaf scorch, 6
Alsike clover mosaic virus, 469470
Alternaria alternata
barley, 62
bean, 139, 146
buckwheat, 102
canola, 110, 117, 119
cotton, 187188, 194195
maize, 253254
peanut, 404
red clover, 460
safflower, 560
soybean, 628629
sugar beet, 698
sugarcane, 742
sunflower, 785786, 786787
tobacco, 812, 825826
Alternaria arachidis, 404
Alternaria atrans, 628
Alternaria black spot, canola, 109110
Alternaria brassicae, 109110, 698
Alternaria carthami, 560
Alternaria circinans, 229230
Alternaria flower and stem blight, flax, 233
Alternaria gossypina, 186187
Alternaria helianthi, 785786
Alternaria leaf blight
maize, 253254
peanut, 404
sunflower, 786787
wheat, 872873
Alternaria leaf spot
bean, 139
canola, 110
cotton, 186187
crambe, 229230
peanut, 404
safflower, 560
soybean, 628629
sugar beet, 698
sugarcane, 742
Alternaria lini, 233
Alternaria linicola, 235
Alternaria macrospora, 187188
Alternaria padwickii, 499
Alternaria seedling blight, flax, 235
Alternaria spot and veinal necrosis, peanut,

Page 971
404
Alternaria spp.
canola, 123
safflower, 563
sorghum, 611
soybean, 628629
sunflower, 786787
wheat, 874875
Alternaria stem blight and leaf spot, cotton, 187188
Alternaria tenuissima, 404, 628
Alternaria triticina, 872873
Alternaria zinniae, 786787
Amblysellus grex, 317
American wheat striate mosaic virus
barley, 85
maize, 312, 331
oat, 393394
wheat, 928
Anguillulina radicicola, 924
Anguina tritici
rye, 528529, 552
wheat, 870, 883, 924925
Angular black spot, 140
Angular leaf spot
bean, 140
sorghum, 588
tobacco, 811812
Angular leaf spot nematode, 163
Anther mold, red clover, 451452
Anthocyanosis, cotton, 219
Anthracnose
alfalfa, 78
barley, 4849
bean, common, 141143
canola, 110
cotton, 188190
flax, 233234
maize, 254256
oat, 371372
peanut, 405
red clover, 458
rye, 525
safflower, 561
sorghum, 579580, 594, 597
soybean, 629630
tobacco, 819
wheat, 873
wild rice, 960
Apantesis blakei, 30
Aphanomyces cochlioides, 8, 700
Aphanomyces euteiches
alfalfa, 8
bean, common, 143
red clover, 452
Aphanomyces raphani, 113, 230
Aphanomyces root rot
alfalfa, 8
bean, 143
crambe, 230
red clover, 452
Aphasmatylenchus straturatus, 431
Aphelenchoides arachidis, 435
Aphelenchoides besseyi, 503
Aphelenchoides ritzemabosi, 163, 840
Aphids. See also specific species
alfalfa, 30, 3739
buckwheat, 104105
canola, 126128
cotton, 219220, 222
crambe, 231232
maize, 316, 319321, 327328
millet, 364
oat, 394
peanut, 436438, 443445
red clover, 469471
rye, 554
safflower, 570571
sorghum, 609610, 614
soybean, 674, 678680, 683
sugar beet, 723724, 726729
tobacco, 848, 851852, 856, 858859
wheat, 929932, 939, 945
Aphis craccivora, 37, 436437, 851
Aphis fabae, 683
Aphis glycines, 678
Aphis gossypii
cotton, 219220
sorghum, 609
sugarcane, 775
tobacco, 848
Aphis idiosacchari, 772
Aphis indica, 350
Aphis maidis, 772
Aphis rumicis, 470
Aphis sacchari, 772
Aphis spiraecola, 851
Aphrodes bicintus, 843
Apical chlorosis, sunflower, 783
Aplanobacter insidiosum, 4
Arachis hypogaea. See Peanut (Arachis hypogaea)
Arkansas foot rot, 487488
Arthrinium arundinis, 49, 62
Ascochyta blight, cotton, 190191
Ascochyta boltshauseri, 158
Ascochyta fagopyri, 101
Ascochyta gossypii, 190191
Ascochyta graminicola, 873, 896
Ascochyta hordei var. americana, 49
Ascochyta imperfecta, 17, 25
Ascochyta ischaemi, 304305
Ascochyta leaf blight, buckwheat, 101
Ascochyta leaf spot
alfalfa, 25
barley, 49

Page 972
Ascochyta leaf spot (continued)
bean, 143144
canola, 111
soybean, 630
sunflower, 787
tobacco, 820
wheat, 873874, 896
Ascochyta lethalis, 455
Ascochyta oryzae, 487
Ascochyta phaseolorum, 143144, 820
Ascochyta sorghi, 598, 873, 896
Ascochyta spp.
canola, 111
maize, 256
soybean, 630
sunflower, 787
Ascochyta tritici, 873
Ashbya fiber stain, 191
Ashbya gossypii, 191
Ashen spot, cotton, 190191
Ashy stem, cotton, 195196
Ashy stem blight, bean, 144145
Aspergillus boll rot, 191
Aspergillus crown rot, peanut, 405406
Aspergillus flavus
cotton, 191192
maize, 256258, 296
millet, 352
peanut, 430431
Aspergillus fumigatus, 698699
Aspergillus glaucus, 256257
Aspergillus melleus, 631
Aspergillus nidulans, 145
Aspergillus niger
cotton, 192
maize, 256257
peanut, 405406
Aspergillus parasiticus, 430431
Aspergillus pulverulentus, 405406
Aspergillus seedling blight, soybean, 631
Aspergillus spp.
canola, 123
maize, 256258
wheat, 874875
Aster leafhopper (Macrosteles fascifrons), 84, 93, 244, 392, 396, 553
Aster yellows
alfalfa, 36
barley, 84
canola, 126
flax, 244
oat, 392393
rye, 553
sunflower, 805
tobacco, 843844
wheat, 926
Athelia rolfsii
cotton, 209210
red clover, 462
sugarcane, 763
sunflower, 801
tobacco, 836
wheat, 909
Athysanus argentarius, 926
Aulacorthum solani, 173, 471, 680
Aureobasidium bolleyi, 381
Aureobasidium caulivorum, 458
Aureobasidium decay, wheat, 874
Aureobasidium lini, 235236
Aureobasidium zeae, 272
Australian maize stripe virus
maize, 312
sorghum, 608
Australian wheat streak mosaic virus, 928929
Australian wheat striate virus, 85
Avena sativa. See Oat (Avena sativa)
Awl nematode
bean, common, 162
maize, 306
sorghum, 604605
Bacillus cereus
alfalfa, 19
tobacco, 814
Bacillus megaterium, 872
Bacillus subtilis, 252, 621
Bacterial diseases
alfalfa, 37
barley, 4548
canola, 107109
cotton, 183186
crambe, 229
maize, 247253
millet, 343345
oat, 369371
peanut, 403404
red clover, 451
rice, 475481
rye, 523524
safflower, 559560
sorghum, 575578
soybean, 621628
sugar beet, 695698
sugarcane, 737742
sunflower, 783785
wheat, 865872
wild rice, 959
Bacterium melleum, 818
Bacterium pseudozoogloae, 813
Bajra streak virus, 363
Bakanae disease, 482483
Balansia sp., 752
Baldulus tripsaci, 310, 322
Banana streak virus, 773
Banded leaf and sheath blight, sorghum, 580

Page 973
Banded leaf and sheath spot, maize, 258
Banded sclerotial leaf disease, sugarcane, 742
Banks grass mite (Oligonychus pratensis), 262, 277
Bare patch, barley, 7071
Barley (Hordeum vulgate), 4596
basal glume rot, 4748
basal kernel blight, 47
blight, 4546
leaf blight, 46
stripe, 4647
anthracnose, 4849
Arthrinium arundinis kernel blight, 49
Ascochyta leaf spot, 49
barley stripe, 5051
blast, 51
Cephalosporium stripe, 52
Ceratobasidium gramineum snow mold, 5253
covered smut, 5455
crown rust, 55
downy mildew, 5556
dwarf bunt, 56
ergot, 57
eyespot, 5758
false loose smut, 5859
Fusarium head, 6061
Gibberella seedling blight, 61
gray snow mold, 6162
halo spot, 62
kernel blight, 62
leaf rust, 6263
leaf speckle, 6364
leaf spot, 6465
Leptosphaeria leaf spot, 65
loose smut, 6566
net blotch, 6668
pink snow mold, 68
powdery mildew, 69
Pythium root rot, 6970
root rot, common, 5354
scald, 7172
Sclerotinia snow mold, 72
Septoria speckled leaf blotch, 7273
sharp eyespot, 7374
southern blight, 74
speckled snow mold, 7475
spot blotch, 7576
Stagonospora blotch, 7677
stem rust, 7779
stripe rust, 79
takeall, 7980
Verticillium disease, 80
wirrega blotch, 8081
yellow leaf spot, 81
nematodecaused diseases, 8284
cereal cyst, 82
root gall, 8283
root knot, 83
root lesion, 8384
stunt, 84
African cereal streak, 85
American wheat striate mosaic, 85
Australian wheat, 85
brome mosaic, 8990
cereal chlorotic mottle, 90
cereal tillering, 90
eastern wheat striate, 90
enanismo, 9091
flame chlorosis, 91
high plains virus, 9192
hordeum mosaic, 92
maize yellow stripe, 92
mosaic, 86
northern cereal mosaic, 9293
oat blue dwarf, 93
oat pseudorosette, 93
oat sterile dwarf, 93
rice blackstreaked dwarf, 94
rice stripe, 94
Russian winter wheat mosaic, 94
soilborne wheat mosaic, 9495
stripe mosaic, barley, 86
wheat dwarf, 95
wheat streak mosaic, 9596
wheat yellow leaf, 96
yellow dwarf, 87
yellow mosaic, 88
yellow streak mosaic, 8889
yellow striate mosaic, 89
yellow stripe, 89
Barley mosaic virus, 86
Barley stripe, 50
Barley stripe mosaic virus
barley, 86
maize, 312
wheat, 929
Barley yellow dwarf virus
barley, 8788
maize, 312313
oat, 394395
rice, 505
rye, 531, 554
wheat, 929930
Barley yellow mosaic virus, 88
Barley yellow streak mosaic virus
barley, 8889
wheat, 930
Barley yellow striate mosaic virus
barley, 89
wheat, 931

Page 974
Barley yellow stripe, 89, 931
Barn rot, tobacco, 812
Barn spot, tobacco, 820
Basal glume rot
barley, 4748
wheat, 868
Basal kernel blight, barley, 47
Basal node rot, rice, 483
Basal stem blight, flax, 234235
Bassus stigmaterus, 754
Bean (Phaseolus vulgaris), 133175
blight, common, 135136
brown spot, 133
Erwinia nulandii leaf spot, 136
fuscous blight, 136137
halo blight, 137139
Pseudomonas blatchfordae leaf spot, 139
wildfire, 134
wilt, 134
Alternaria leaf spot, 139
angular black spot, 140
angular leaf spot, 140141
anthracnose, 141143
Aphanomyces root and hypocotyl rot, 143
Ascochyta blight, 143144
ashy stem blight, 144145
Aspergillus nidulans disease, 145
Bipolaris sorokiniana, 145
black node disease, 145146
black pod disease, 146
black root rot, 147
Cercospora leaf blotch, 147148
Chaetoseptoria leaf spot, 148
floury leaf spot, 148
Fusarium root rot, 148150
Fusarium yellows, 150
gray leaf spot, 151
gray mold, 151152
Phyllosticta leaf spot, 152
Phymatotrichum root rot, 152153
pink pod rot, 153
pod rot, 153
powdery mildew, 154
Pythium root and hypocotyl rot, 154155
Pythium wilt, 155
Rhizoctonia root rot/damping off, 155156
rust, 156157
smut, 157158
southern blight, 158
speckle disease, 158
stem rot, 159
web blight, 159160
white leaf spot, 160
white mold, 160162
awl, 162
bulb and stem, 162
cyst, 162
dagger, 162
lance, 163
lesion, 163
pin, 163
reniform, 164
ring, 164
root knot, 164
spiral, 165
sting, 165
stubby root, 165
stunt, 165
machismo, 165
witches' broom, 165
calico mosaic, 166
clover yellow vein, 171172
common mosaic, 167168
cowpea mild mottle, 172
cowpea severe mosaic, 172
cucumber mosaic, 172
curly dwarf mosaic, 168, 172
curly top, 173
dwarfing disease, 173
dwarf mosaic, 168
golden mosaic, 168169
mild mosaic, 169
peanut mottle, 173174
peanut stunt, 174
pod mottle, 169
red node, 169170
rugose mosaic, 170
southern bean mosaic, 174
southern mosaic, 170
soybean yellow shoot, 174175
stipple streak, 175
yellow mosaic, 170171
yellow stipple virus, 171
Bean calico mosaic virus, 166
Bean common mosaic virus, 167168
Bean curly dwarf mosaic virus, 168, 172
Bean dwarf mosaic virus, 168
Bean golden mosaic virus, 168169
Bean leaf beetle (Ceratoma ruicornis), 471
Bean leaf beetle (Ceratoma trifurcata), 471, 628, 674
Bean leaf roll virus, 38
Bean mild mosaic virus, 169
Bean pod mottle virus
bean, common, 169
soybean, 644, 648, 674675
Bean rugose mosaic virus, 170
Bean southern mosaic virus, 170
Bean yellow mosaic virus
bean, common, 170

Page 975
peanut, 436
red clover, 470
Bean yellow stipple virus, 171
Beauvericin, 275, 491
Beet, sugar. See Sugar beet (Beta vulgaris)
Beet crinkle, 721
Beet curly top virus
sugar beet, 721722
tobacco, 847
Beet distortion mosaic virus, 722
Beet lace bug (Piesma quadratum), 720
Beet latent rosette, 720
Beet leaf curl virus, 722723
Beet leafhopper (Circulifer tenellus), 244245
Beetles. See also specific species
maize, 252253, 274, 280, 318
red clover, 471
rice, 512
sorghum, 610
soybean, 628, 674, 676677
tobacco, 849
wheat, 932
Beet mild yellowing virus, 723
Beet mosaic virus, 723724
Beet necrotic yellow vein virus, 730732
Beet pseudoyellows virus, 724
Beet ring mottle virus, 724725
Beet savoy virus, 732
Beet soilborne mosaic virus, 725726
Beet soilborne virus, 725
Beet western yellows virus
canola, 128
crambe, 231
sugar beet, 726727
Beet yellow net virus, 727728
Beet yellow stunt virus, 728
Beet yellows virus, 728729
Beet yellow vein, 728
Belonolaimus gracilis, 672
Belonolaimus longicaudatus
bean, common, 165
cotton, 217218
maize, 309
oat, 392
sorghum, 607
soybean, 672
Belonolaimus spp., 434
Bemisia gossypipderda, 678
Bemisia tabaci, 677678, 680
Beniowskia sphaeroidea, 351, 585
Beta vulgaris. See Sugar beet (Beta vulgaris)
Bigbud, tobacco, 844
Bipolar cookei, 603
Bipolaris leaf spot, millet, 345
Bipolaris maydis, 300301, 602
Bipolaris nodulsa, 353
Bipolaris oryzae, 486
Bipolaris rostrata, 295
Bipolaris sacchari, 753
Bipolaris setariae, 345
Bipolaris sorokiniana
barley, 5354, 62
bean, common, 145
buckwheat, 102
oat, 378379
rye, 527528, 543
wheat, 879880, 910
wild rice, 963
Bipolaris spicifera, 411, 751
Bipolaris stenospila
millet, 354
sugarcane, 744
Bipolaris turcica, 288
Bipolaris urochloae, 346
Bipolaris victoriae, 387388
Bipolaris zeicola, 289290
Bipolar oryzae, 961
Bipolar turcica, 590
Black bean aphid (Aphid fabae), 728729
Black blight, canola, 120121
Black blotch, red clover, 461
Black boll rot, cotton, 192
Black bundle disease, maize, 258
Black chaff
alfalfa, 4546
oat, 370371
Black chaff, wheat, 868870
Black cowpea aphid (Aphis craccivora), 438, 443
Blackfire, tobacco, 811812
Black head mold, wheat, 874
Blackhull, peanut, 406
Black kernel, rice, 483484
Black kernel rot, maize, 259
Blackleg
canola, 111113
sugar beet, 707
tobacco, 813, 835
Black mildew, tobacco, 820
Black mold rot, canola, 113
Black node disease, bean, 143, 145146
Black patch disease
alfalfa, 9
red clover, 452
Black pod disease, bean, 146
Black point
barley, 62
wheat, 874875
Black root
canola, 113
sugar beet, 700
Black root canker, 20
Black root rot
alfalfa, 9
bean, 147
cotton, 192193

Page 976
Black root rot (continued)
peanut, 406
red clover, 452453
tobacco, 821822
Black rot
canola, 107
sugarcane, 743
Black rust
cotton, 194195
tobacco, 813
Black shank, tobacco, 822823
Black smut, barley, 5859
Black stripe, sugarcane, 743
Blade blight, oat, 369370
Blast
barley, 51
millet, 345346
oat, 400
rice, 484485
wheat, 920
Blight. See also Blight, bacterial; specific crop or disease
bean, 135136
buckwheat, 101
Blight, bacterial
barley, 4546
cotton, 183184
crambe, 229
millet, 343
oat, 369370
rice, 475477
safflower, 559
soybean, 621
Blind staggers, 276
Blue disease, cotton, 220
Blueeye, 290
Blue mold, 823825
Blumeria graminis, 382, 539, 900901
Boil smut, 263264
Boll rot. See Cotton, fungal diseases
Borde blanco, 259
Botryodiplodia phaseoli, 261
Botryodiplodia theobromae, 193, 259
Botryosphaeria festucae, 267268, 292
Botryosphaeria zeae, 282
Botryosporium barn mold, tobacco, 825
Botryosporium longibrachiatum, 825
Botryosporium pulchrum, 825
Botryotinia fuckeliana
bean, 151152
safflower, 561
tobacco, 831
Botrytis anthophila, 451
Botrytis blight, peanut, 407
Botrytis cinerea, 101102, 700701, 787
bean, 151152
canola, 118
flax, 237
peanut, 407
safflower, 561
tobacco, 812, 826827, 829, 831
Botrytis head rot, sunflower, 787788
Botrytis rot, buckwheat, 101102
Botrytis storage rot, sugar beet, 700701
Brachycaudus helichrysi, 939
Bract necrosis, sunflower, 806
Bradysia impatiens, 30
Brassica spp. See Canola (Brassica)
Brazilian bud blight, 675
Brazilian corn streak, 322
Brazilian maize mosaic, 314
Bremia lactucae, 563
Brevi coryne, 126
Brevicoryne brassicae, 232
Broadbean wilt virus
buckwheat, 104105
red clover, 472
Broccoli necrotic yellows virus, 128
Brome mosaic virus
barley, 8990
maize, 313
sorghum, 608609
wheat, 931
Broomrape, 860861
Brown blotch, rice, 485486
Brown girdling root rot, 113114, 128
Browning, wheat, 902903
Browning root rot, barley, 6970
Brown leaf spot, millet, 346
Brown root rot
alfalfa, 9
red clover, 453
tobacco, 838839
wheat, 875
Brown rot
peanut, 404405
sugar beet, 711713
sugarcane, 743744
Brown spot
bean, 133134
maize, 259260
rice, 486487
soybean, 631632
sugarcane, 744
tobacco, 825826
wild rice, 959, 960961
Brown stem blight, flax, 235
Brown stem rot, soybean, 632633
Brown stripe, sugarcane, 744745
Brown stripe downy mildew, 260261
Brown wheat mite (Petrobia latens), 8889, 930
Buckwheat (Fagopyrum esculentum), 101105
Ascochyta leaf blight, 101
blight, 101
Botrytis rot, 101102

Page 977
chlorotic leaf spot, 102
downy mildew, 102103
Fusarium wilt, 103
leaf spot, 103
powdery mildew, 104
Pythium palingeries disease, 104
ring spot, 104
viral diseases, 104105
broad bean wilt, 104105
turnip mosaic, 105
Bud blight, soybean, 675676
Bulb and stem nematode, 33
bean, common, 162
maize, 306
oat, 388
red clover, 465466
tobacco, 839
wheat, 921
Bulmeria graminis, 69
Bunt
barley, 56
rice, 491492
rye, 525526, 530, 534535
wheat, 878879, 884885, 893894
Burkholderia glumae, 480
Burkholderia plantarii, 481
Burrowing nematode, 306
Bushy top virus, 847848
Caloglyphus rodionovi, 422
Calonectria crotalariae, 654
Calonectria ilicicola, 409
Canker
canola, 111
flax, 245
red clover, 455456
Rhizoctonia, 2021
Canola (Brassica), 107129
black rot, 107
crown gall, 108
pod rot, 107
seedling root rot, 109
soft rot, 107108
wilt and rot, 108
Xanthomonas leaf spot, 109
brown girdling root rot, 128
Alternaria black spot, 109110
anthracnose, 110
blackleg, 111113
black mold rot, 113
black root, 113
brown girdling root rot, 113114
Cercospora leaf spot, 114
charcoal rot, 114
clubroot, 115
damping off, 115116
downy mildew, 116
foot rot, 116117
Fusarium seed infection, 117
Fusarium wilt, 117118
gray mold, 118
leaf spot, 118
light leaf spot, 118119
pod drop, 119
powdery mildew, 119
Rhizoctonia crown rot, 120
ring spot, 120121
Sclerotinia stem rot, 121122
smut, root gall, 122
storage molds, 123
white blight, 123
white rust, 123124
winter decline syndrome, 124125
wirestem, 125
yeast infection of seed, 125
pollen necrosis, 128
cauliflower mosaic, 126
crinkle, 127
mosaic, 127
phyllody, 127
rai mosaic, 127
yellows, 128
Capnodium spp., 767
Cardamom mosaic streak virus, 939
Carolinaia cyperi, 775
Carthamus tinctorius. See Safflower (Carthamus tinctorius)
Cauliflower mosaic virus, 126
Cephalosporium acremonium
canola, 123
maize, 258, 261
sorghum, 578
sunflower, 788
Cephalosporium gramineum
barley, 52
oat, 372373
rye, 526527
wheat, 875877
Cephalosporium gregatum, 632
Cephalosporium kernel rot, maize, 261
Cephalosporium maydis, 286287
Cephalosporium sacchari, 769
Cephalosporium stripe
barley, 52
oat, 372373
rye, 526527
wheat, 875877

Page 978
Cephalosporium wilt, sunflower, 788
Ceratobasidium cereale
rye, 542
wheat, 908
Ceratobasidium gramineum
barley, 5253
wheat, 877
Ceratobasidium oryzaesativae, 482
Ceratocystis adiposa, 743
Ceratocystis paradoxa, 760
Ceratoma ruicornis, 471
Ceratoma trifurcata, 471, 628, 674
Cercospora albida, 160
CercosporaAlternaria leaf blight complex, cotton, 194195
Cercospora arachidicola, 411412, 415
Cercospora atrofiliformis, 743
Cercospora beticola, 701
Cercospora bidentis, 788
Cercospora brassicicola, 114
Cercospora canescens, 147148
Cercospora carthami, 561
Cercospora castellanii, 151
Cercospora fagopyri, 104
Cercospora fusimaculans, 590
Cercospora gossypina, 193195
Cercospora helianthi, 788
Cercospora janseana, 493
Cercospora kikuchii, 633634, 650652
Cercospora koepkei, 770
Cercospora leaf blotch, bean, 147148
Cercospora leaf spot
canola, 114
cotton, 193194
maize, 261, 282283
millet, 346347
rice, 493
safflower, 561562
soybean, 633634
sugar beet, 701
sunflower, 788
Cercospora longipes, 744
Cercospora medicaginis, 2829
Cercospora nicotianae, 820, 829
Cercospora oryzae, 485
Cercospora pachypus, 788
Cercospora penniseti, 346347
Cercospora rubropurpurea, 761
Cercospora seed decay, soybean, 634
Cercospora sojina, 634, 638639
Cercospora sorghi, 283, 588
Cercospora spp. in maize, 261
Cercospora vaginae, 764
Cercospora vanderysti, 151
Cercospora zeaemaydis, 283
Cercospora zebrina, 464
Cercosporella brassicae, 123
Cercosporella foot rot, oat, 376
Cercosporella herpotrichoides
barley, 58
rye, 531532, 547
wheat, 887888
Cercosporidium graminis
oat, 383
rye, 536537
Cereal chlorotic mottle virus
barley, 90
maize, 313
oat, 395
wheat, 932
Cereal cyst nematode
barley, 82
oat, 389390
rye, 550
wheat, 921922
Cereal dwarf, barley, 9091
Cereal leaf beetle (Oulema lenchenis), 932
Cereal leaf beetle (Oulema melanopa), 89, 318, 610, 932
Cereal root nematode, 605
Cereal tillering disease virus
barley, 90
maize, 313
wheat, 932
Cerebella volkensii, 584
Cerotoma arcuata, 677
Cerotoma ruficornis, 677
Cerotoma spp., 170171
Cerotoma trifurcata, 676
Chaetocnema denticulata, 252
Chaetocnema pulicaria, 252, 318, 610
Chaetomium spp. in wheat, 874875
Chaetoseptoria wellmanii, 148
Chalara elegans, 452, 821
Chalara paradoxa, 760
Charcoal rot
bean, 144145
canola, 114
cotton, 195196
maize, 261262
peanut, 407408
safflower, 562
sorghum, 580581
soybean, 634636
sugar beet, 702
sunflower, 788789
tobacco, 826
Chilli mosaic virus, 570
Chlorotic leaf spot, 102
Choanephora cucurbitarum, 196
Choanephora infundibulifera, 636
Choanephora leaf blight, soybean, 636
Choanephora leaf spot, peanut, 408
Choanephora mold, cotton, 196
Choanephora spp. in peanut, 408
Chocolate spot, 249

Page 979
Cicadulina bimaculata, 326
Cicadulina bipunctella, 326, 330
Cicadulina bipunctella zeae, 776
Cicadulina chinai, 92, 327, 612, 936
Cicadulina mbila
barley, 90
maize, 321, 324, 325, 327
millet, 363364
sorghum, 612
sugarcane, 776
wheat, 933, 935
Cicadulina pastusae, 9091, 933
Circulifer tenellus, 173, 721722, 847
Cladochytrium alfalfae, 1011
Cladosporium cladosporioides
canola, 123
maize, 285
sunflower, 789
Cladosporium herbarum
barley, 62
maize, 285
Cladosporium leaf spot, sunflower, 789
Cladosporium rot, maize, 285
Cladosporium spp.
canola, 119
sunflower, 785786
wheat, 874875
Clamp rot, sugar beet, 700701
Clathrospora pentamera
rye, 538539
wheat, 900
Clavibacter iranicum, 870
Clavibacter michiganense
alfalfa, 45
maize, 249250
sugar beet, 697
wheat, 867
Clavibacter tritici, 870
Clavibacter xyli, 740741
Claviceps africana, 583584
Claviceps fusiformis, 350351
Claviceps gigantea, 271272
Claviceps purpurea
barley, 57
oat, 376
rye, 531
sugarcane, 752
wheat, 886887
Claviceps pusilla, 752
Claviceps sorghi, 583584
Claviceps zizaniae, 960
Clover, red. See Red clover (Trifolium pratense)
Clover cyst nematode
red clover, 466
sugar beet, 716
Clover root curculio, 13, 14
Clover scorch, 458
Clover yellow mosaic virus, 470
Clover yellow vein virus, 171
Clubroot, 115
Clubroot virus, 848
Clyindrocladium crotalariae, 21
Clypeoporthe iliau, 754
Cobb's disease of sugarcane, 738739
Cob rot, 271
Cochliobolus bicolor, 581
Cochliobolus carbonum, 289290
Cochliobolus heterostrophus, 300301, 602
Cochliobolus leaf spot
cotton, 196
sorghum, 581
Cochliobolus lunatus, 483
Cochliobolus miyabeanus, 486, 494
Cochliobolus sativus
barley, 53
rye, 527528, 543
wheat, 879880, 901, 910
Cochliobolus spicifer, 196
Cochliobolus stenospilus, 744
Cocksfoot mottle virus, 932
Coleosporium helianthi, 803
Coleosporium pacificum, 803
Collar rot
peanut, 408409
rice, 487
sugarcane, 745
tobacco, 826827
Colletotrichum arachidis, 405
Colletotrichum capsici
cotton, 188189, 196197
safflower, 561
soybean, 629
Colletotrichum dematium, 405
Colletotrichum destructivum
alfalfa, 78
tobacco, 819
Colletotrichum falcatum, 762
Colletotrichum gloeosporioides, 110, 141143, 409, 629
Colletotrichum gossypii, 188189, 198
Colletotrichum graminicola
barley, 4849
maize, 254256
oats, 371372
rye, 525
sorghum, 579, 594, 597
wheat, 873
wild rice, 960
Colletotrichum leaf spot, peanut, 409
Colletotrichum lindemuthianum, 141143
Colletotrichum lini, 233234
Colletotrichum mangenoti, 405
Colletotrichum orbiculare, 563
Colletotrichum stem rot, safflower, 563
Colletotrichum trifolii, 78, 461462
Colletotrichum truncatum, 629

Page 980
Columbia lance nematode, 307, 668669
Columbia root knot nematode, 922
Common bean. See Bean (Phaseolus vulgaris)
Common leaf spot
alfalfa, 10
red clover, 453
Common pea mosaic virus, 470471
Common root rot, barley, 5354
Coniothyrium minitans, 162, 799
Coniothyrium phyllachorae, 303
Coprinus psychromorbidus
alfalfa, 3132
red clover, 465
rye, 528
wheat, 881
Corchosis, 10
Corkey root rot, 10
Corn. See Maize (Zea mays)
Corn chlorotic vein banding virus, 314
Corn cyst nematode, 307
Corn earworms, 290
Cornespora cassiicola, 827828
Corn flea beetle (Chaetocnema pulicaria), 252, 318, 610
Corn leaf aphid (Rhopalosiphum maidis)
barley, 8687, 96
maize, 316317, 320
millet, 364
oat, 394
sorghum, 609610
sugarcane, 775
wheat, 939, 945
Corn lethal necrosis, 314
Corn rootworms, 313, 318, 610
Corn stunt, 310311
Corticium ear rot, maize, 264
Corticium gramineum, 5253, 877
Corticium sasakii, 264
Corticium sp. in sugarcane, 743
Corynebacterium fascians, 816
Corynebacterium flaccumfaciens, 134, 624625
Corynebacterium michiganense, 4, 249250
Corynebacterium sepedonicum, 697
Corynespora cassiicola, 197, 665
Corynespora leaf spot, cotton, 197
Cotton (Gossypium), 183224
Agrobacterium root rot and wilt, 183
blight, 183184
crown gall, 184185
Erwinia internal necrosis, 185
lint discoloration, 184
Pantoea agglomerans cotton lint rot, 185
Pseudomonas leaf spot, 185186
aerolate mildew, 186
Alternaria stem blight, 187188
anthracnose, 188190
Ascochyta blight, 190191
Ashbya fiber stain, 191
Aspergillus boll rot, 191192
black boll rot, 192
black root rot, 192193
Botryodiplodia seedling blight and boll rot, 193
CercosporaAlternaria leaf blight complex, 194195
charcoal rot, 195196
Choanephora mold, 196
Cochliobolus leaf spot, 196
Colletotrichum boll rot, 196197
Corynespora leaf spot, 197
Cylindrocladium black rot, 197
Diplodia boll rot, 198
escobilla, 198199
Fusarium boll rot, 199
Fusarium damping off, 199200
Fusarium nygami root colonization, 200
Fusarium seed infection, 200
Helminthosporium leaf spot, 201
Myrothecium leaf spot, 201202
Nematospora boll stain, 202
Nigrospora lint rot, 203
Phomopsis leaf spot, 203
Phytophthora boehmeriae boll rot, 205206
Phytophthora parasitica boll rot, 205
powdery mildew, 206
Pythium damping off, 206207
ramulose, 207
Rhizoctonia leaf spot, 207208
Rhizopus boll rot, 208
rust, 208
Sclerotium boll rot, 209
Sclerotium stem and root rot, 209210
soreshin, 210
southwestern cotton rust, 211
Stemphylium leaf spot, 211
tropical cotton rust, 212
dagger, 214
lance, 214215
lesion, 215
pin, 215
reniform, 216
ring, 216
root knot, 216217
Scutellonema spp., 217
spiral, 217
sting, 217218
stubby root, 218

Page 981
stunt, 218
abutilon mosaic, 219
anthcyanosis, 219
blue disease, 220
leaf crumple, 220
leaf curl, 221222
leaf mottle, 222
leaf roll, 222
mosaic, 222
psylosis, 222223
small leaf, 220221
terminal stunt, 221, 223
tobacco streak, 223
veinal mosaic, 223224
vein clearing, 223
Cotton anthocyanosis virus, 219
Cotton leaf crumple virus, 220
Cotton leaf curl virus, 221222
Cotton root rot
alfalfa, 1718
bean, 152153
sunflower, 794
Cotton small leaf virus, 220221
Cotton terminal stunt virus, 221
Cottony snow mold
rye, 528
wheat, 881
Cotyledon spot, soybean, 636
Covered kernal smut, sorghum, 581582
Covered smut
barley, 5455
oat, 373
sugarcane, 746748
Cowpea aphid (Aphis craccivora), 37, 436437, 831
Cowpea chlorotic mottle virus
bean, common, 171
peanut, 436
soybean, 676
Cowpea mild mottle virus
bean, 172
peanut, 436437
soybean, 677
Cowpea mosaic virus
red clover, 471
soybean, 677
Cowpea severe mosaic virus
bean, 172
soybean, 677
Crambe (Crambe abyssinica), 229232
bacterial blight, 229
beet western yellows virus, 231
fungal disease, 229231
Fusarium wilt, 230
turnip mosaic virus, 232
Crater disease, wheat, 881882
Crazy top, sorghum, 582
Crazy top downy mildew, maize, 265
Criconemella ornata
millet, 362
peanut, 432
soybean, 670
Criconemella spp.
cotton, 216
oat, 390
red clover, 467
sorghum, 606
wheat, 923
Criconemoides citui, 308309
Criconemoides ornata, 308309
Criconemoides ovantus, 164
Crinkle, canola, 127
Crinkle leaf, soybean bacterial, 623
Cristulariella moricola, 431
Crown gall
alfalfa, 5
canola, 108
cotton, 184185
sugar beet, 697
sunflower, 784785
tobacco, 813814
Crown rot, alfalfa, 2122
Crown rust
barley, 55
oat, 374375
Crown sheath rot, rice, 487488
Crown wart
alfalfa, 1011
red clover, 456
sugar beet, 699
Cucumber mosaic virus
bean, 172
maize, 314315
peanut, 437
red clover, 471
safflower, 570
sorghum, 609
sugar beet, 729730
sunflower, 806
tobacco, 848849
wheat, 932
Culmicolous smut, sugarcane, 746748
Culm rot
barley, 5758
wheat, 887888
Curly top virus
bean, common, 173
flax, 244245
Curtobacterium flaccumfaciens, 134, 624625
Curvularia kernal rot, sorghum, 583
Curvularia leaf blight, red clover, 453454

Page 982
Curvularia leaf spot
maize, 265
millet, 347
sugarcane, 749
sunflower, 789
tobacco, 828
Curvularia lunata
millet, 352
rice, 483
sorghum, 583
soybean, 636
sugarcane, 749
sunflower, 789
Curvularia penniseti, 347
Curvularia spp.
maize, 265
rice, 494
wheat, 874875
Curvularia trifolii, 453
Curvularia verruculosa, 828
Cuscuta campestris, 720
Cylindrocarpon magnusianum, 11, 454
Cylindrocarpon root rot
alfalfa, 11
red clover, 454
Cylindrocladium black rot
cotton, 197
peanut, 409411
Cylindrocladium clavatum, 654
Cylindrocladium crotalariae
alfalfa, 11
cotton, 197
red clover, 454
soybean, 654
Cylindrocladium leaf spot, peanut, 411
Cylindrocladium parasiticum, 409411
Cylindrocladium root and crown rot
alfalfa, 11
red clover, 454
Cylindrocladium scoparium, 411
Cylindrocopturus adsperus, 788
Cylindrosporium concentricum, 118119
Cymadothea trifolii, 461
Cynodon chlorotic streak virus, 315
Cyst nematode
alfalfa, 33
bean, common, 162
millet, 361
oat, 388
soybean, 663665, 671672
tobacco, 840
Cystopus tragopogonis, 802
Cytospora sacchari, 767
Dactuliophora elongata, 347
Dagger nematode
alfalfa, 34
bean, common, 162
cotton, 214
maize, 307
millet, 361
oat, 388389
peanut, 432
red clover, 466
sorghum, 605, 609
soybean, 675, 681
sunflower, 803
tobacco, 840, 855
wheat, 922
Dalbulus elimatus, 310311, 322
Dalbulus maidis, 310311, 317, 322
Damping off
alfalfa, 1112
canola, 115116
cotton, 199, 206207
peanut, 421
safflower, 563
soybean
Pythium, 653654
Rhizoctonia, 656657
tobacco, 828
Dead blossum leaf spot, tobacco, 829
Dead head, barley, 7980
Dead tiller syndrome, 488
Deightoniella papuana, 768
Delphacodes albifascia, 328
Delphacodes kuscheli, 327, 936
Deoxynivalenol, 280, 706, 891892. See also Vomitoxin
Diabrotica longicornis, 610
Diabrotica speciosa, 849
Diabrotica spp., 170171
Diabrotica undecimpunctata, 313, 610, 676
Diabrotica undecimpunctata howartii, 252
Diabrotica virgifera, 313, 610
Diaporthe helianthi, 793794
Diaporthe phaseolorum, 643644, 648, 660661, 666
Dicladispa gestroi, 512
Dicranotropis hamata, 90, 313, 328, 398, 932, 937
Didymella exitialis, 266
Didymella leaf spot, maize, 266
Didymosphaeria arachidicola, 430
Didymosphaeria taiwanensis, 755
Diente de caballo, 271272
Dilophospora alopecuri
rye, 528529
wheat, 882883
Dilophospora leaf spot
rye, 528529
wheat, 882883
Dimeriella sacchari, 762
Diplodia boll rot, cotton, 198
Diplodia frumenti, 267268
Diplodia gossypina, 408409

Page 983
Diplodia macrospora, 268
Diplodia maydis, 266270
Diplodia oryzae, 965
Diplodia spp.
maize
ear rot, 266267
ear rot and stalk rot, 267268
leaf spot, 268
seedling blight, 268269
stalk rot, 269271
peanut, 411
Dirty panicle disease, 478479
Ditylenchus africanus, 434
Ditylenchus augustus, 503
Ditylenchus dipsaci
alfalfa, 33
maize, 306
oat, 388
red clover, 465466
rye, 550
soybean, 672
sugar beet, 718
tobacco, 839
wheat, 921
Ditylenchus radicicola, 924
Ditylenchus spp., 162
Diuraphis noxia, 87, 89, 394, 931
Doassansia zizaniae, 965
Dolichodorus heterocephalus, 162, 306
Dolichodorus spp., 604605
Downy mildew
alfalfa, 1213
barley, 5556
in buckwheat, 102103
canola, 116
maize
brown stripe, 260261
crazy top, 265
green ear, 284
Java, 286
Philippine, 291292
sorghum, 299300
spontaneum, 302
sugarcane, 302303
millet
Plasmopara penniseti, 349350
Sclerospora graminicola, 347348
Sclerospora macrospora, 349
oat, 375376
red clover, 454
rice, 488489
rye, 529530
safflower, 563
sorghum, 600601
soybean, 636637
sugarcane, 749751, 759
sunflower, 789790
tobacco, 823825
wheat, 883884
Draeculacephala portola, 615, 773
Drechslera avenacea, 379380
Drechslera blight, soybean, 637
Drechslera dematioidea, 350
Drechslera gigantea, 489, 965
Drechslera glycini, 637
Drechslera graminea, 50
Drechslera halodes, 295
Drechslera hawaiiensis, 790791
Drechslera leaf spot
millet, 350
peanut, 411
sunflower, 790791
Drechslera maydis, 300, 602
Drechslera rostrata, 295
Drechslera sacchari, 753
Drechslera setariae, 354355
Drechslera sorokiniana, 378379
Drechslera spicifera, 411, 751
Drechslera teres, 6668
Drechslera triticirepentis, 549, 917919
Drechslera turcica, 288, 590
Drechslera wirreganensis, 8081
Dry ear rot, 271
Dry rot canker, sugar beet, 703704
Dry seed decay, wheat, 884
Dry top rot, sugarcane, 751752
Dwarf
alfalfa, 6
rice, 506507
sugarcane, 774
Dwarf bunt
barley, 56
rye, 530
wheat, 884885
Dwarfing disease, bean, 173
Ear and tassel smut, 284285
Early leaf spot, peanut, 411412
Eastern wheat striate virus
barley, 90
wheat, 933
Echinochloa spp. See Millet
Eggplant mosaic virus, 849
Elephant grass mosaic virus
maize, 315
sorghum, 609
Eleusine coracana. See Millet
Elsinoe sacchari, 769
Elymana sulphurella, 926
Elymana virenscens, 312, 393, 928
Enanismo
barley, 9091
wheat, 933
Endria inimica, 126, 312313, 393, 553, 926, 928
English grain aphid (Sitobion avenae), 87, 394, 930

Page 984
Entochamiento, rice, 511
Entyloma lineatum, 964965
Entyloma oryzae, 493
Entyloma petuniae, 157158
Epicoccum glume blotch, wheat, 885886
Epicoccum nigrum, 295
Epicoccum purpurascens, 885
Epicoccum spp. in wheat, 874875
Epitrix hirtipennis, 852
Equine leucoencephalomalcia (ELEM), 276
Ergot
barley, 57
maize, 271272
millet, 350351
oat, 376
rye, 531
sorghum, 583585
sugarcane, 752
wheat, 886887
wild rice, 960
Eriophyes tulipae, 943
Erratomyces patelli, 140
Erwinia amylovora, 21
Erwinia carotovora
canola, 107108, 108
maize, 248
safflower, 559560
sugar beet, 696
sunflower, 785
tobacco, 812, 813, 815816
Erwinia chrysanthemi
alfalfa sprout rot, 3
maize, 248
rice, 480
sorghum, 577
Erwinia herbicola
cotton, 185
millet, 344345
Erwinia internal necrosis, cotton, 185
Erwinia nulandii, 136
Erwinia rhapontici, 870, 903
Erwinia soft rot
sorghum, 577578
sugar beet, 696697
Erwinia stewartii, 252
Erysiphe cichoracearum
safflower, 565
sunflower, 795
tobacco, 832833
Erysiphe commonis, 104
Erysiphe cruciferarum, 119
Erysiphe graminis
barley, 69
oat, 382
rye, 539
wheat, 900901
Erysiphe polygoni
alfalfa, 19
bean, 154
canola, 119
flax, 239
red clover, 458
sugar beet, 709
Escobilla, 198199
Essex disease, 638
European corn borer (Ostrinia nubilalis), 255, 274
European wheat striate mosaic virus, 933934
Euscelis plebejus, 89, 126, 843, 931
Euschistus impictiventris, 185
Euschistus spp., 668
Exserohilum leaf blight, millet, 351
Exserohilum oryzae, 486
Exserohilum rostratum
maize, 295
millet, 351
rice, 491
sorghum, 591, 597
sugarcane, 753, 764
Exserohilum turcicum, 288, 590
Eyespot
barley, 5758
maize, 272
oat, 376377, 383
peanut, 437
rice, 489
rye, 531532, 542, 547
sugarcane, 753
wheat, 887888
Fagopyrum esculentum. See Buckwheat (Fagopyrum esculentum)
False cinch bug, 125
False loose smut, barley, 5859
False mildew, sorghum, 585
False root knot nematode, 307, 717
False smut
maize, 272273
rice, 489490
Fascination, 816
Fiji disease, 774775
Flag smut, wheat, 888889
Flame chlorosis
barley, 91
oat, 396
wheat, 934
Flax (Linum usitatissimum), 233245
aster yellows, 244
environmentalrelated problems
boll blight, 245
heat canker, 245
top dieback, 245
Alternaria flower and stem blight, 233
anthracnose, 233234
basal stem blight, 234235

Page 985
browning and stem break, 235236
brown stem blight, 235
die back, 236
Fusarium secondary rot, 236237
gray mold, 237
pasmo, 237238
powdery mildew, 239
Rhizoctonia seedling blight and root rot, 239
rust, 240
scorch, 241
seed rot, 241
stem mold and rot, 242
Thielaviopsis root and rot, 242243
wilt, 243
crinkle, 244
curly top, 244245
Flax fire, 241
Flea beetle (Systena frontalis), 318, 610
Flexibacter sp., 21
Floury leaf spot, 148
Foliar nematode, 840
Foot rot
barley, 5758, 74
canola, 116117
flax, 234235
millet, 359360
peanut, 428429
rice, 480
Forked foot disease, 13
Frankliniella fusca, 441, 860
Frankliniella occidentalis, 441, 785, 856, 860
Frankliniella schultzei, 441, 860
Freckles, 249250
Frenching, 814
Frogeye, tobacco, 829
Frogeye leaf spot, soybean, 638639
Fumago spp.
sugarcane, 767
tobacco, 834
Fumonisins, 275276, 491, 585586
Fungal diseases. See also specific diseases
alfalfa, 733
barley, 4881
buckwheat, 101104
canola, 109125
cotton, 186214
crambe, 229231
flax, 233243
maize, 253305
millet, 345361
oat, 371388
peanut, 404431
red clover, 451465
rice, 482500
rye, 525550
safflower, 560569
sorghum, 578604
soybean, 628668
sugar beet, 698716
sugarcane, 742771
sunflower, 785803
tobacco, 819838
wheat, 872921
wild rice, 960965
Fungus gnats (Bradysia impatiens), 30
Fusarenone, 280
Fusarium acuminatum, 1112
Fusarium affine, 830
Fusarium associated diseases
alfalfa
crown and root rot, 1314, 21
wilt, 14
barley
Fusarium patch, 68
head blight, 6061
bean, common
pod rot, 153
root rot, 148150
wilt, 150
yellows, 150
buckwheat, 103
canola
foot rot, 116117
seed infection, 117
wilt, 117118
cotton
boll rot, 199
damping, 199200
root colonization, 200
seed infection, 200
wilt, 200201
crambe, 230
flax
Fusarium secondary rot, 236237
wilt, 243
maize
F. avenaceum stalk rot, 273
F. globossum kernal infection, 273
F. scirpi in grain, 276277
F. thapsinum infection, 278279
Gibberella ear rot, 279281
Gibberella stalk rot, 281282
kernal rot, 273276
leaf spot, 276
stalk rot, 277278
oat
foot rot, 377
head blight, 378
peanut
peg and root rot, 412413
stem canker, 413
wilt, 413414

Page 986
Fusarium associated diseases (continued)
red clover, 454455
rice
leaf blotch, 490
sheath rot, 491
rye
head blight, 533534
root rot, 527528, 534
safflower, 563564
sorghum
Fusarium thapsinum infection, 587588
head blight, 585586
pokkah boeng, 595596
root and stalk rot, 586587
soybean
pod and collar rot, 649
root rot, 640641
seed infection, 639640
sudden death syndrome, 662665
wilt, 641
sugar beet
root rot, 704705
tip rot, 705
yellows, 705706
sugarcane
sett and stem rot, 754
wilt, 769700
sunflower, 791792
tobacco
head blight, 830
wilt, 830831
wheat
black point, 874875
Fusarium sporotrichioides, 883
glume spot, 889
head blight, 890892
leaf blight, 892
pink smudge, 903
pink snow mold, 899900
prematurity blight, 901902
rot, 892893
wild rice, 961962
Fusarium avenaceum, 273
Fusarium crookwellense, 279
Fusarium culmorum
barley, 6465
oat, 377
rice, 490
rye, 534
wheat, 879880, 892, 901
Fusarium equiseti
rice, 490
wheat, 892893
Fusarium globosum, 273
Fusarium graminearum
barley, 6061
maize, 279282
oat, 378
rye, 533
soybean, 639
wheat, 879880, 890, 892893
wild rice, 961962
Fusarium javanicum, 705
Fusarium martii, 413414
Fusarium moniliforme
maize, 273279, 296
millet, 352
rice, 482483, 491
sorghum, 585587
sugarcane, 754, 761
sunflower, 791
Fusarium napiforme, 585586
Fusarium nivale
rice, 490
wheat, 890, 892, 899
Fusarium nygamai, 351352
Fusarium oxysporum
alfalfa, 14
bean, 150
canola, 117118
cotton, 200
crambe, 230
flax, 243
peanut, 413414
rice, 483
safflower, 563
soybean, 638, 639641
sugar beet, 704706
sunflower, 791
tobacco, 830
Fusarium pallidoroseum
bean, 153
soybean, 640, 649
Fusarium poae, 889
Fusarium proliferatum
maize, 273277
rice, 491
sorghum, 585586
Fusarium roseum, 113114, 116117
Fusarium sacchari, 769
Fusarium scirpi, 276277
Fusarium semitectum, 490
Fusarium solani
bean, 148150
peanut, 413
rice, 490
soybean, 638, 640, 662664
Fusarium sporotrichioides, 883
Fusarium spp.
barley, 53, 6061, 62
buckwheat, 103
canola, 115
cotton, 199200
flax, 236237
peanut, 412414

Page 987
red clover, 455
rye, 527528
safflower, 563
wheat, 874875, 890893
wild rice, 961962
Fusarium subglutinans
maize, 273278
millet, 360
sorghum, 585586, 595
Fusarium tabacinum, 791792
Fusarium thapsinum, 278279, 587588
Fuscous blight, bean, 136137
Gaeumannomyces graminis
barley, 79
maize, 298
oat, 387
rice, 487
rye, 548549
wheat, 915917
wild rice, 965
Giallume disease, 505506
Gibberella fujikuroi
maize, 273278
sorghum, 585586
sugarcane, 754, 761
Gibberella seedling blight, 61
Gibberella subglutinans, 754, 761
Gibberella thapsina
maize, 278279
sorghum, 587588
Gibberella zeae
barley, 61
maize, 279282, 296
oat, 378
rye, 533
Glischrochilus quadrisignatus, 280
Globodera solanacearum, 822, 840
Globodera tabacum, 830, 840
Gloeocercospora sorghi
maize, 305
millet, 360361
sorghum, 604
sugarcane, 770
Gloeosporium bolleyi, 381
Gloeosporium carthami, 561
Gloeosporium spp. in wheat, 874875
Glomerella cingulata, 110, 141143
Glomerella gossypii, 188189, 198
Glomerella graminicola
oats, 371372
rye, 525
sorghum, 579, 594
wheat, 873
Glomerella lindemuthiana, 141143
Glomerella tucumanensis, 762
Glomus macrocarpum, 837
Glume blight, rice, 480
Glume blotch
barley, 7677
rice, 477
rye, 544545
wheat, 911912
Glume rot, barley, 4748
Glume rust
barley, 79
wheat, 914915
Gnomonia iliau, 754
Goss's bacterial wilt and blight, 249250
Grain rot, rice, 480
Graminella nigrifrons, 310, 317, 322, 398, 610
Graminella sonora, 317, 329, 610, 614
Graminicola downy mildew, 284
Granville wilt, 815
Grapes, Pierce's disease of, 6
Grass cyst nematode, 922923
Grasshoppers
alfalfa, 30
soybean, 675
tobacco, 852853, 855856
Grassy shoot, sugarcane, 772
Grassy stunt B, 505506
Grassy stunt Y, 506
Gray ear rot, 282
Gray leaf spot
bean, 151
maize, 282283
red clover, 463464
sorghum, 588
Gray mold
bean, 151152
canola, 118
flax, 237
safflower, 561
sunflower, 787788
tobacco, 831
Gray snow mold
oat, 385
rye, 543
wheat, 909910
Gray stem, canola, 120121
Gray stem canker, red clover, 455456
Greenbug (Schizaphis graminum), 87, 327328, 364, 394, 610, 775
Green ear, sorghum, 589
Green ear downy mildew, 284
Green peach aphid. See Myzus persicae
Green petal disease, canola, 126
Green smut, 489490
Groundnut crinkle virus, 437
Groundnut eyespot virus, 437438
Groundnut leaf blight, 416
Groundnut rosette virus, 438439
Groundnut streak virus, 439

Page 988
Guignardia fulvida, 235236
Guinea grass mosaic virus, 364
Gumming disease, 738739
Gummosis, wheat, 870871
Halo blight
bean, 137139
oat, 369370
rice, 477
rye, 524525
Halo spot
alfalfa, 15
barley, 62
rye, 534
wheat, 893
HC toxin, 289
Head blight
barley, 6061
oat, 378379
Head mold, millet, 352
Head smut
maize, 284285
millet, 352353
sorghum, 589590
Helicobasidium brebissonii
alfalfa, 31
red clover, 465
sugar beet, 715716
Helicotylenchus dihysteria, 165
Helicotylenchus spp.
alfalfa, 35
cotton, 217
maize, 309
oat, 391
sorghum, 607
soybean, 672
sugarcane, 771
sunflower, 805
tobacco, 842
wheat, 925
Helminthosporiosis, millet, 353
Helminthosporium cookei, 603
Helminthosporium dematiodea, 350
Helminthosporium frumentacei, 355
Helminthosporium giganteum, 489
Helminthosporium gossypii, 201
Helminthosporium gramineum, 5051
Helminthosporium helianthi, 792
Helminthosporium leaf blight, sunflower, 792
Helminthosporium leaf spot
cotton, 201
millet, 354
rice, 491
Helminthosporium maydis, 602
Helminthosporium nodulosum, 353
Helminthosporium rostratum, 351, 491, 591, 597, 764
Helminthosporium sacchari, 753
Helminthosporium sativum, 910
Helminthosporium seedling blight, 379
Helminthosporium sigmoideum, 963
Helminthosporium spicifera, 751
Helminthosporium spp.
maize, 288289, 295, 300
millet, 352
oat, 378380, 387
rye, 543
sugarcane, 768
wheat, 874875
Helminthosporium stenospilum, 354
Helminthosporium triticirepentis, 549
Helminthosporium turcicum, 590
Hemicycliophora spp., 391
Hendersonina sacchari, 745
Hessian fly injury, 53
Heterodera avenae
maize, 307
oat, 389390
wheat, 921922
Heterodera gambiensis, 361
Heterodera glycines, 162, 663664
Heterodera schachtii, 719720
Heterodera spp.
barley, 82
oat, 388
Heterodera trifolii
alfalfa, 33
peanut, 466
sugar beet, 716
Heterodera zeae, 307
High plains virus
barley, 9192
maize, 315316
wheat, 934
Hirschmanniella gracilis, 965
Hirschmanniella oryzae, 501
Hoja blanca, 325, 508
Holcus spot, 250251
Hollow stalk, tobacco, 815816
Homoeosoma electellum, 796
Honeydew, 583584. See also Ergot
Hoplolaimus columbus, 307, 668669, 771
Hoplolaimus galeatus, 307, 669
Hoplolaimus indicus, 277, 307, 362
Hoplolaimus spp., 163, 215, 466
Hordeum vulgare. See Barley (Hordeum vulgare)
Hormodendrum cladosporioides, 285
Hormodendrum ear rot, 285
Horse's tooth, 271272
HT2 toxin, 706
Hyalesthes obsoletus, 843
Hyalothyridium maydis, 285286
Hylemyia cilicrura, 252
Hylemyia spp., 108, 813
Hymenula affinis, 830

Page 989
Hymenula cerealis
barley, 52
oat, 372373
rye, 526527
wheat, 875
Hypera postica, 30
Hysteroneura setariae, 775
Inazuma dorsalis, 503
Indian peanut clump virus, 439440, 935
Indonesian soybean dwarf virus, 678
Isariopsis griseola, 140141
Java downy mildew, 286
Javesella discolor, 328, 398
Javesella dubia, 398, 933
Javesella obscura, 328, 398
Javesella pellucida, 328, 398, 933, 937
Johnsongrass mosaic virus
maize, 316317
sorghum, 609610
Kabatiella caulivora, 458
Kabatiella zeae, 272
Kalahasti malady, 432
Karnal bunt
rye, 534535
wheat, 893894
Kernel blight, barley, 47, 49, 62
Kernel smudge, wheat, 874875
Kernel smut
millet, 354
rice, 491492
Kernel spotting, 493494
Kopfsalat, 721
Kresek, 475477
Krok, 8283
Lacebug (Piesma quadratum), 721722
Ladder leaf spot, sorghum, 590
Ladodelphax striatellus, 90, 9294
Lagena radicicola, 920
Lance nematode
bean, common, 163
cotton, 214215
maize, 307308
millet, 362
red clover, 466
soybean, 669
sugarcane, 771
Laodelphax striatellus
maize, 313, 323, 328329
rice, 506, 510
sorghum, 612613
wheat, 931932, 937, 939
Lasiodiptodia theobromae
cotton, 193, 198
maize, 259
peanut, 408409
Late leaf spot, peanut, 414415
Late wilt, maize, 286287
Leaf and stem nematode, 550551
Leaf blast, sugarcane, 755
Leaf blight, bacterial
barley, 46
maize, 247
sorghum, 575
wheat, 8650866
Leaf blight, fungal
sorghum, 590591
sugarcane, 755
Leaf curl
sugar beet, 721
tobacco, 849850
Leafcutter bee (Megachile rotundata), 30
Leaf gall
maize, 330
red clover, 456
tobacco, 816
Leafhoppers
alfalfa, 6, 36
barley, 8487, 8996
canola, 126
cotton, 218
flax, 244
maize, 310313, 317318, 321322, 324327, 329330
millet, 363364
oats, 392393, 396, 398
peanut, 435436
red clover, 468469
rice, 503504, 507, 509, 511
rye, 553
safflower, 569
sorghum, 610, 612, 614
soybean, 673674
sugar beet, 720721, 728
sunflower, 805
tobacco, 843847, 860
wheat, 926, 928, 933, 935936, 939940
Leaf mottle virus, 222
Leaf roll virus, 222
Leaf rust
barley, 6263
rye, 535536
wheat, 895896
Leaf scald
rice, 492
sugarcane, 739740
Leaf scorch
canola, 118119
sugarcane, 756
Leaf smut, rice, 493
Leaf speckle, barley, 6364

Page 990
Leaf spot. See also specific crop or disease
alfalfa, 10
barley, 6465
buckwheat, 103
canola, 118
safflower, 559
sorghum, 591
wheat, 896897
Leaf spot, bacterial
alfalfa, 34
maize, 248
red clover, 451
sorghum, 575576
sugar beet, 695
sunflower, 783784
Leaf streak, bacterial
millet, 343344
rice, 478
sorghum, 576
wheat, 866867
wild rice, 959
Leaf streak, rye, 536537
Leaf stripe, bacterial
millet, 344
sorghum, 577
Legume yellows virus, 38
Leptodiscus terrestris, 1516, 456
Lepto leaf spot, 15
Leptosphaeria avenaria, 384
Leptosphaeria bicolor, 756
Leptosphaeria herpotrichoides
barley, 65
rye, 537
wheat, 897
Leptosphaeria leaf spot
barley, 65
maize, 287
rye, 537
Leptosphaeria lindquistii, 793
Leptosphaeria maculans, 111113, 117
Leptosphaeria mayis, 287
Leptosphaeria microscopia, 898
Leptosphaeria nodorum, 544, 911
Leptosphaeria pratensis
leaf spot, alfalfa, 2526
red clover, 463
root rot, alfalfa, 2627
Leptosphaeria sacchari, 765
Leptosphaeria taiwanensis, 755
Leptosphaeria zeamaydis, 291
Leptosphaerulina briosiana, 641
Leptosphaerulina crassiasca, 417418
Leptosphaerulina leaf spot, soybean, 641642
Leptosphaerulina trifolii, 15, 459, 641
Leptotrochila medicaginis, 3233
Lesion nematode
bean, common, 163
cotton, 215
maize, 308
oat, 389
red clover, 466
rice, 501
sorghum, 605
soybean, 669
sugarcane, 771
sunflower, 803804
tobacco, 840841
wheat, 923
Lettuce chlorosis virus, 730
Lettuce infectious yellows virus, 730
Lettuce mosaic virus, 571
Leuconostoc mesenterioides, 698
Leveillula compositarum, 795
Leveillula taurica, 206, 795
Light leaf spot, canola, 118119
Ligniera pilorum, 920
Ligniera vascularum, 751
Linochora graminis, 919
Linum usitatissimum. See Flax (Linum usitatissimum)
Lipaphis erysimi, 127
Longidorus africans, 215
Longidorus africanus, 605606
Longidorus attenuatus, 717
Longidorus breviannulatus, 308
Longidorus caespiticola, 717
Longidorus cohni, 389
Longidorus leptocephalus, 717
Longidorus macrosoma, 313
Long smut
millet, 355
sorghum, 592
Loose kernal smut, sorghum, 592
Loose smut
barley, 6566
oat, 380381
rye, 537538
wheat, 897898
Lucerne transient streak virus, 3839
Machismo
bean, common, 166
soybean, 673
Macrophoma spp. in peanut, 415416
Macrophoma zeae, 282
Macrophomina phaseolina
canola, 114
cotton, 195196
maize, 261262
peanut, 407408
safflower, 562
sorghum, 580581
soybean, 635, 666
sugar beet, 702

Page 991
sunflower, 788789
tobacco, 826
Macrosiphum euphorbiae, 437
Macrosiphum gei, 683
Macrosiphum granarium, 327328
Macrosiphum pisi, 470472, 683
Macrosiphum solanifolii, 683
Macrosteles fascifrons, 805, 843, 926
Macrosteles laevis
barley, 9495
rye, 553
tobacco, 843
wheat, 926, 938939
Macrosteles quadrilineatus, 435
Magnaporthe grisea, 484
Magnaporthe salvinii, 499500
Maize (Zea mays), 247332
black bundle disease, 258
black kernal rot, 259
chocolate spot, 249
Goss's bacterial wilt and blight, 249250
holcus spot, 250251
leaf blight and stalk rot, 247
leaf spot, 248
Pseudomonas fuscovaginae disease, 251
purple leaf sheath, 251252
seed rot and seedling blight, 252
stalk and top rot, 248
Stewart's wilt, 252253
stripe, 248249
Alternaria leaf blight, 253254
anthracnose stalk rot, 254255, 255256
Ascochyta leaf and sheath spots, 256
Aspergillus ear rot, 256258
banded leaf and sheath spot, 258
borde blanco, 259
brown spot and stalk rot, 259260
Cephalosporium kernal rot, 261
Corticium ear rot, 264
Curvularia leaf spot, 265
Didymella leaf spot, 266
Diplodia
ear rot, 266267
ear rot and stalk rot, 267268
leaf spot, 268
stalk rot, 269271
downy mildew
crazy top, 265
Java, 286
Philippine, 291292
sorghum, 299300
spontaneum, 302
sugarcane, 302303
dry ear rot, 271
ergot, 271272
eyespot, 272
Fusarium
F. avenaceum stalk rot, 273
F. globosum kernal infection, 273
F. scirpi, 276277
F. thapsinum infection, 278279
kernal rot, 273276
leaf spot, 276
stalk rot, 277278
gray ear rot, 282
gray leaf spot, 282283
Hormodendrum ear rot, 285
Hyalothyridium leaf spot, 285286
late wilt, 286287
Nigrospora stalk rot, 287
northern leaf blight, 287289
northern leaf spot, 289290
Penicillium rot, 290
Phaeocytostroma stalk infection, 291
Phaeosphaeria leaf spot, 291
Phomopsis seed rot, 292
Physalospora ear rot, 292
Pyrenochaeta stalk rot, 292
Pythium
root rot, 293
seed and seedling blight, 293294
stalk rot, 294
red kernal disease, 295
Rhizoctonia ear rot, 295
Rhizoctonia root rot and stalk rot, 295
rostratum leaf spot, 295296
rust
common corn, 262263
southern corn, 301302
tropical corn, 304
Sclerotium ear rot, 296
seed and seedling blight, 296297
Selenophoma leaf spot, 297
Septoria leaf blotch, 297
sheath blight, 297298
sheath rot, 298
shuck rot, 298
silage mold, 298
smut
common, 263264
false, 272273
head, 284285
Sordaria fimicola stalk infection, 299
southern corn leaf blight, 300301
tar spot, 303304
Trichoderma ear rot and root rot, 304

Page 992
Maize (Zea mays) (continued)
yellow leaf blight, 304305
zonate leaf spot, 305
awl, 306
bulb and stem, 306
burrowing, 306
Columbia lance, 307
corn cyst, 307
dagger, 307
false root knot, 307
lance, 307
lesion, 308
needle, 308
ring, 308
root knot, 308309
spiral, 309
sting, 309
stubby root, 309310
stunt, 310
North Queensland stripe, 332
corn stunt, 310311
maize bushy stunt, 311
Australian maize stripe, 312
barley stripe mosaic, 312
barley yellow dwarf, 312313
brome mosaic, 313
cereal tillering mottle, 313
corn chlorotic mottle, 314
corn lethal necrosis, 314
cynodon chlorotic streak, 315
elephant grass mosaic, 315
high plains, 315316
Johnsongrass mosaic, 316317
maize chlorotic dwarf, 317318
maize chlorotic mottle, 318319
maize dwarf mosaic, 319
maize leaf streak, 320
maize line, 320
maize mosaic, 320321
maize mottle, 321
maize necrotic lesion, 321
maize pellucid ringspot, 321
maize rayado fino, 322
maize raya gruesa, 322
maize red stripe, 322323
maize ring mottle, 323
maize Rio Cuarto, 323
maize rough dwarf, 323
maize sterile stunt, 323324
maize streak, 324325
maize stripe, 325
maize tassel abortion, 325
maize vein enation, 325326
maize wallaby ear, 326
maize white line mosaic, 326327
mal de Rio Cuarto, 327
millet red leaf, 327328
oat pseudorosette, 328
rice stripe, 329
sorghum stunt mosaic, 329
sugarcane Fiji disease, 329
sugarcane mosaic, 329330
vein enation, 330
wheat spot mosaic, 330
wheat striate mosaic, 331
Maize bushy stunt phytoplasma (MBSP), 311
Maize chlorotic dwarf virus, 317318, 610
Maize chlorotic mottle virus, 314, 318319, 610
Maize Colombian stripe, 322
Maize dwarf mosaic virus
maize, 314, 319
millet, 364
oat, 396
sorghum, 610612
wheat, 935
Maize leaf fleck virus, 320
Maize line virus, 320
Maize mosaic virus, 320
Maize necrotic lesion virus, 321
Maize pellucid ringspot virus, 321
Maize rayado fino virus, 322
Maize raya gruesa virus, 322
Maize red stripe virus, 322323
Maize ring mottle virus, 323
Maize rough dwarf virus, 323, 612
Maize sterile stunt virus, 323
Maize streak virus
maize, 321, 324325
millet, 364
sorghum, 612
sugarcane, 776777
wheat, 935
Maize stripe virus, 325, 612
Maize tassel abortion virus, 325
Maize vein enation virus, 325
Maize wallaby ear virus, 326
Maize white line mosaic virus, 326327, 935936
Maize yellow stripe virus
barley, 92
maize, 327
sorghum, 612613
wheat, 936
Malaxodes farinosus, 325
Mal de Rio Cuarto virus, 327, 936

Page 993
Manchado de grano, 478479
Mancha gris, 151
Marasmiellus spp., 259, 756
Marasmius root rot, 15
Marasmius sheath and shoot blight, sugarcane, 756757
Marasmius spp., 15
Marasmius stenophyllus, 756
Marble leaf virus, 723
Marginal necrosis, peanut, 440
Marsonia secalis, 7172
Matsumuratettix hiroglyphicus, 772
May beetle (Phyllophaga) sp., 252
Meadow nematode, 433
Medicago stiva. See Alfalfa (Medicago stiva)
Megachile rotundata, 30
Melampsora lini, 240
Melanoplus differentialis, 675, 852, 856
Melanopsichium eleusinis, 358359
Melanosis, peanut, 416
Meloidogyne arenaria, 432433
Meloidogyne chitwoodi
oat, 391
wheat, 922
Meloidogyne hapla, 432
Meloidogyne incognita
cotton, 216217
maize, 277
millet, 362
tobacco, 822
Meloidogyne javanica, 277
Meloidogyne naasi
barley, 83
sorghum, 605
Meloidogyne spp.
bean, common, 164
canola, 125126
maize, 309
red clover, 467
rice, 501502
rye, 551
safflower, 569
sorghum, 606
soybean, 670
sugar beet, 718
sugarcane, 771
sunflower, 804805
tobacco, 841842
wheat, 924
Medinius brevidens
barley, 84
sorghum, 607
wheat, 926
Medinius spp.
bean, common, 165
cotton, 218
oat, 392
tobacco, 843
Metasphaeria maydis, 291
Metribuzin herbicide, 647
Meuterianella fairmairei, 328
Mexican bean beetle, 172
Microcephalothrips abdominalis, 856
Microdochium bolleyi
barley, 53
oat, 381
wheat, 874, 879
Microdochium nivale
barley, 68
oat, 381382
rye, 538
wheat, 890, 892, 899
Microdochium oryzae, 492, 494
Microdochium root rot, oat, 381
Microscopia leaf spot, wheat, 898
Microsphaera diffusa, 650
Midvein spot, red clover, 456
Mildew. See Downy mildew; Powdery mildew
Mildew, aerolate, 186
Millet, 343365
blight, 343
leaf streak, 343344
leaf stripe, 344
Pantoea agglomerans leaf spot, 344345
spot, bacterial, 344
stripe, bacterial, 344
brown leaf mottle, 365
Bipolaris leaf spot, 345
blast, 345346
brown leaf spot, 346
Dactuliophora leaf spot, 347
Drechslera leaf spot, 347, 354355
ergot, 350351
Exserohilum leaf blight, 351
false mildew, 351
Fusarium nygamai disease, 351352
head mold, 352
head smuts, 352353
Helminthosporiosis, 353
kernel smuts, 354
long smut, 355
Phyllosticta leaf blight, 356
Pyricularia leaf spot, 356357
rust, 358
smut, 358359
top rot, 360

Page 994
Millet (continued)
burrowing, 361
cyst, 361
dagger, 361
lance, 362
ring, 362
root knot, 362
root lesion, 362
sting, 362363
stubby root, 363
stunt, 363
red leaf spot, 365
Bajra streak, 363
Guinea grass mosaic, 364
maize streak, 364
panicum mosaic, 364365
Millet red leaf virus, 327328
Milo disease, 593
Mites
barley, 8889, 91, 9596
bean, common, 156
cotton, 203
maize, 277, 315, 330331
millet, 365
oats, 399
peanut, 422
rye, 555
wheat, 889, 928, 930, 932, 943944, 946
wild rice, 966
Moesziomyces penicillariae, 355
Monascus spp., 298
Moniliformin, 275276, 491
Monographella maydis, 303
Monographella nivalis
barley, 6465
oat, 381
wheat, 899
Mosaic, wheat bacterial, 867
Mosaic viruses. See specific crop or disease
Mottle, sugarcane, 737738
Mottled stripe, sugarcane, 740741
Mung bean yellow mosaic virus, 678
Musca domestica, 350
Mustard. See Canola (Brassica)
Mycoleptodiscus crown and root rot
alfalfa, 1516
red clover, 456457
Mycoleptodiscus root rot, soybean, 642
Mycoleptodiscus terrestris, 1516, 456, 642
Mycosphaerella arachidis, 411412
Mycosphaerella areola, 186
Mycosphaerella berkeleyi, 414415
Mycosphaerella brassicicola, 120121
Mycosphaerella carinthiaca, 456
Mycosphaerella cruenta, 147148
Mycosphaerella gossypina, 193
Mycosphaerella graminicola, 541, 906907
Mycosphaerella linicola, 237238
Mycosphaerella striatiformans, 750
Mycosphaerella zeaemaydis, 304
Mycosphaerella zizaniae, 965
Mycotoxins. See also specific toxins
maize, 275276, 280
rice, 491
rye, 533
sugar beet, 706
wheat, 886887, 891892
Mycovellosiella koepkei, 770
Mycovellosiella phaseoli, 148
Mycovellosiella vaginae, 764
Myriogenospora aciculispora, 757
Myriosclerotinia borealis
barley, 72
rye, 542
wheat, 906
Myrothecium disease, soybean, 642643
Myrothecium gramineum, 298
Myrothecium leaf blight, peanut, 416
Myrothecium leaf spot
cotton, 201202
millet, 356
red clover, 457
sunflower, 792
Myrothecium root rot, red clover, 456
Myrothecium roridum
alfalfa, 16
canola, 118
cotton, 201
millet, 356
peanut, 416
red clover, 457
soybean, 642
sunflower, 792
Myrothecium spp.
alfalfa, 21
wheat, 874875
Myrothecium verrucaria
alfalfa, 16
red clover, 457
sunflower, 792
Myzus persicae
alfalfa, 39
canola, 126128
crambe, 231232
maize, 320
peanut, 443
red clover, 470
safflower, 570571
soybean, 683
sugar beet, 723, 726728
tobacco, 848, 851, 856, 858

Page 995
Naccobus aberrans, 717
Naccobus dorsalis, 307, 717
Nakataea sigmoidea, 499, 963964
Naked smut, oat, 380381
Nanismo ruvido, 323
Narrow brown leaf spot, 493
Nebraska root gall nematode, 717
Necrotic mosaic disease, rice, 508509
Nectria haematococca, 662
Needle nematode
cotton, 215
maize, 308
oat, 389
sorghum, 605606
sugar beet, 717
Nematodecaused diseases
alfalfa, 3336
barley, 8284
canola, 125126
cotton, 214218
maize, 306310
millet, 361363
oat, 388392
peanut, 431435
red clover, 465468
rice, 501503
rye, 550552
safflower, 569
sorghum, 604607
soybean, 668673
sugar beet, 716720
sugarcane, 771772
sunflower, 803805
tobacco, 838843
wheat, 921926
wild rice, 965
Nematospora coryli, 202, 668
Nematospora gossypii, 202
Nematospora nagpuri, 202
Nematospora sinecauda, 125
Neoaliturus fenestratus, 569
Neocosmospora root rot, peanut, 416417
Neocosmospora stem rot, soybean, 643
Neocosmospora vasinfecta, 416417, 643
Neovossia indica, 534535, 893894
Nephotettix spp., 504, 507, 511, 513514
Nesodutha obscura, 928
Nesodutha pallida, 313, 326, 928
Net blotch
barley, 6668
peanut, 417
Nezara viridula, 668
Nicotiana glutinosa stunt viroid, 846
Nicotiana velutina mosaic virus, 850
Nigra loose smut, barley, 5859
Nigrospora oryzae, 203, 271, 287
Nigrospora spp. in wheat, 874875
Nigrospora stalk rot, maize, 287
Nilaparvata lugens, 505506, 508, 509, 515
Nivalenol, 280
Noname disease, wheat, 945946
Northern anthracnose, red clover, 458
Northern cereal mosaic virus
barley, 9293
maize, 328
wheat, 937
Northern corn rootworm (Diabrotica longicornis), 318
Northern leaf blight
maize, 287289
sorghum, 590591
Northern leaf spot, maize, 289290
Northern poor root syndrome, sugarcane, 757758
North Queensland stripe, 332
Nothocriconemella mutabilis, 390
Nysius niger, 125
Oat (Avena sativa), 369400
aster yellows, 392393
black chaft, 370371
blight, 369370
stripe blight, 370
blast, 400
anthracnose, 371372
covered smut, 373
crown rust, 374375
ergot, 376
eyespot, 376377
Fusarium foot rot, 377
Fusarium head blight, 378
head blight, 378379
Helminthosporium seedling blight, 379
leaf blotch and crown rot, 379380
loose smut, 380381
Microdochium root rot, 381
powdery mildew, 382
Pythium seed and seedling rot, 382383
Scoliocotrichum leaf blotch, 383
sharp eyespot, 383
speckled blotch, 384
stem rust, 385386
takeall, 387
Victoria blight, 387388
bulb and stem, 388
cyst, 388
dagger, 388389
lesion, 389

Page 996
Oat (Avena sativa) (continued)
needle, 389
oat cyst, 389390
ring, 390
root gall, 390391
root knot, 391392
sheath, 392
spiral, 392
sting, 392
stubby root, 392
stunt, 392
blue dwarf, oat, 396
flame chlorosis, 396
golden stripe, oat, 397
mosaic, oat, 397
necrotic mottle, oat, 397398
orchardgrass mosaic, 399
soilborne mosaic, oat, 398
sterile dwarf, oat, 398
striate mosaic, oat, 398399
Oat birdcherry aphid (Rhopalosiphum padi), 87, 320, 394, 775
Oat blue dwarf virus
barley, 93
flax, 244
oats, 396
Oat cyst nematode, 389390
Oat golden stripe virus, 397
Oat mosaic virus, 397
Oat necrotic mottle virus, 397398
Oat pseudorosette virus
barley, 93
maize, 328
Oat soilborne mosaic virus, 398
Oat sterile dwarf virus
barley, 93
maize, 328
oat, 398
wheat, 937
Oat striate mosaic virus, 398399
Oidiopsis sp., 16
Oidium arachidis, 420421
Oidium asterispunicei, 795
Oidium latisporum, 795
Oidium lini, 239
Oidium powdery mildew, 1617
Oidium sicula, 795
Oidium spp., 1617
Oidium tenellum, 352
Olpidium brassicae
peanut, 417
tobacco, 831, 854, 857
wheat, 920, 926
Olpidium root rot, peanut, 417
Olpidium seedling blight, tobacco, 831
Ontario soilborne wheat mosaic virus, 941942
Ophiobolus graminis, 915917
Ophiobolus oryzinus, 965
Ophiobolus patch, wheat, 915917
Orange rust
sugarcane, 758
wheat, 895896
Orchardgrass mosaic virus, 399, 937
Orobanche ramosa, 860861
Orosius albicinctus, 127
Orosius argentatus, 674, 844845
Orosius orientalis, 166, 674
Orosius spp. in cotton, 218
Ostrinia nubilalis, 255, 274
Oulema lenchenis, 932
Oulema melanopa, 89, 318, 610, 932
Oval leaf spot, sorghum, 593594
Ozonium omnivorum, 1718
Pachymetra chaunorhiza, 757759
Pachymetra root rot, sugarcane, 758759
Painted leafhopper. See Endria inimica
Palay lalake, 482483
Panicle blight, rice, 515
Panicum miliaceum. See Millet
Panicum mosaic virus, 364
Pantoea agglomerans
cotton, 185
millet, 344345
Pantoea stewartii, 252253
Paratamus exitiosus, 720
Paratrichodorus christiei, 165
Paratrichodorus minor
millet, 363
oat, 392
sorghum, 607
Paratrichodorus spp.
alfalfa, 35
cotton, 218
maize, 309
rye, 552
sugar beet, 719
tobacco, 842843
wheat, 925
Paratylenchus hamatus, 34
Paratylenchus projectus, 804
Paratylenchus spp.
bean, common, 163
cotton, 215
red clover, 467
sorghum, 606
Pasmo, 237238
Patchy stunting, wheat, 898
Pea aphid (Acyrthosiphon pisum)
alfalfa, 30, 3739
bean, common, 173
red clover, 471

Page 997
soybean, 680
Pea aphid (Macrosiphum pisi)
red clover, 470472
soybean, 683
Pea leaf roll virus, 38
Peanut (Arachis hypogaea), 403446
bacterial wilt, 403404
aerial blight, 404
Alternaria spot and veinal necrosis, 404
anthracnose, 405
Aspergillus corn rot, 405406
blackhull, 406
Botrytis blight, 407
Choanephora leaf spot, 408
collar rot, 408409
Colletotrichum leaf spot, 409
Cylindrocladium black rot, 409411
Cylindrocladium leaf spot, 411
Diplodia infection, 411
Drechslera leaf spot, 411
early leaf spot, 411412
Fusarium peg and root rot, 412413
Fusarium stem canker, 412
late leaf spot, 414415
Macrophoma leaf spot, 415416
melanosis, 416
Myrothecium leaf blight, 416
Neocosmospora root rot, 416417
net blotch, 417
Olpidium root rot, 417
pepper spot and scorch, 417418
Pestalotia leaf spot, 418
Pestalotiopsis leaf spot, 418
Phanerochaete omnivorum association, 419
Phomopsis foliar blight, 419
Phyliosticta leaf spot, 419420
pod wart, 420
powdery mildew, 420421
Pythium pod rot, 421422
Pythium wilt, 422423
Rhizoctonia diseases, 423424
Rhizopus seed rot, 424425
rust, 425426
scab, 426
Sclerotinia blight, 426427
Sclerotinia leaf spot, 427
web blotch, 430
yellow mold, 430431
Aphasmatylenchus straturatus, 431
dagger, 432
pod lesion (Kalahasti malady), 432
ring, 432
root knot, 432433
root lesion, 433434
seed and pod, 434
spiral, 434
sting, 434435
testa, 435
peanut yellows, 435
rugose leaf curl, 436
bean yellow mosaic, 436
bud necrosis, 440441
chlorotic ringspot, peanut, 442
chlorotic streak, peanut, 442
cowpea chlorotic mottle, 436
eyespot, 437
green mosaic, peanut, 442
groundnut crinkle, 437
groundnut eyespot, 437438
groundnut rosette, 438439
groundnut streak, 439
Indian peanut clump, 439440
marginal necrosis, 440
mild mottle, peanut, 442443
mottle, peanut, 443
stripe, peanut, 443445
stunt, peanut, 445
yellow mottle, peanut, 445
witches' broom, 435
Peanut bud necrosis virus, 440441
Peanut chlorotic ringspot virus, 442
Peanut chlorotic streak virus
peanut, 442
tobacco, 850851
Peanut clump virus
peanut, 439440
sorghum, 613
sugarcane, 778
Peanut green mosaic virus, 442
Peanut mild mottle virus, 442443
Peanut mottle virus
peanut, 443
soybean, 678
Peanut stripe virus
peanut, 443445
soybean, 679
Peanut stunt virus
bean, common, 174
soybean, 679
tobacco, 851
Peanut yellows, 435
Pearl millet smut, 355
Pea streak virus, 37

Page 998
Pecky rice, 493494
Pectobacterium carotovorum, 737
Pellicularia rolfsii, 763
Pellicularia sasakii, 742
Penicillium rot, maize, 290
Penicillium spp.
canola, 123
maize, 290
safflower, 563
wheat, 874875, 884
Penicillium storage rot, sugar beet, 706
Penicillium vermiculatum, 799
Pennisetum glaucum. See Millet
Pepper spot, alfalfa, 15
Pepper spot and burn, red clover, 459
Pepper spot and scorch, peanut, 417418
Pepper veinal mottle virus, 851
Peregrinus maidis
maize, 312, 314, 320, 322, 325
sorghum, 608, 612
Periconia circinata, 593
Perkinsiella saccharicida, 329, 615, 774
Perkinsleila vastatrix, 329, 774
Peronosclerospora maydis, 286
Peronosclerospora miscanthi, 750751
Peronosclerospora philippinensis, 291, 759
Peronosclerospora sacchari, 302303, 749750
Peronosclerospora sorghi, 600602
Peronosclerospora spontanea, 302, 750
Peronospora ducometi, 102103
Peronospora manshurica, 636637, 639
Peronospora parasitica, 116
Peronospora tabacina, 823825
Peronospora trifoliorum, 1213, 454
Pestalotia arachidicola, 418
Pestalotia leaf spot, peanut, 418
Pestalotiopsis arachidis, 418
Pestalotiopsis leaf spot, peanut, 418
Pestalotiopsis versicolor, 487
Petrobia latens, 8889, 930
Phaeocytostroma ambiquum, 291
Phaeocytostroma iliau, 754
Phaeocytostroma sacchari, 765
Phaeoisariopsis griseola, 140141
Phaeoisariopsis personata, 412, 414415
Phaeoramularia fusimaculans, 590
Phaeoseptoria spp. in wild rice, 965
Phaeoseptoria urvilleana, 896897
Phaeosphaeria avenaria
barley, 63
wheat, 911
Phaeosphaeria herpotrichoides
barley, 65
wheat, 897
Phaeosphaeria leaf spot, maize, 291
Phaeosphaeria maydis, 291
Phaeosphaeria microscopia, 898
Phaeosphaeria nodorum, 911
Phakopsora gossypii, 212
Phakopsora meibomiae, 657
Phakopsora pachyrhizi, 657
Phanerochaete omnivorum, 419
Phaseolus vulgaris. See Bean (Phaseolus vulgaris)
Phaseosphaeria herpotrichoides, 537
Phaseosphaeria nodorum, 544
Phialophora asteris, 792
Phialophora graminicola, 898
Phialophora gregata, 632633
Phialophora takeall, wheat, 898
Phialophora yellows, sunflower, 792
Philippine bacterial leaf spot, tobacco, 817
Philippine downy mildew
maize, 291292
sugarcane, 759
Phoma arachidicola, 430
Phoma betae, 701, 706707
Phoma black stem, sunflower, 793
Phoma exigua
flax, 234235
sunflower, 793
Phoma glomerata, 494
Phoma leaf blight, sunflower, 793
Phoma leaf spot
sorghum, 595
sugar beet, 706707
Phoma lingam, 111113
Phoma macdonaldii, 793
Phoma medicaginis, 17, 25
Phoma meliloti, 2527
Phoma pinodella, 463
Phoma root rot, alfalfa, 17
Phoma sclerotioides
alfalfa, 9
red clover, 453, 465
wheat, 875
Phoma seedling blight, rice, 494
Phoma sorghina, 595
Phoma spot, wheat, 899
Phoma spp.
maize, 291
wheat, 899
Phoma terrestri, 292
Phomopsis brown stem canker, sunflower, 793794
Phomopsis foliar blight, peanut, 419
Phomopsis helianthi, 793794
Phomopsis leaf spot, cotton, 203
Phomopsis longicolla, 643, 648
Phomopsis phaseoli
peanut, 419
soybean, 648649, 660661, 666
Phomopsis seed rot
maize, 292
soybean, 643645
Phomopsis spp.

Page 999
cotton, 203
maize, 292
soybean, 643644, 648
Phyllachora graminis, 919
Phyllachora maydis, 303
Phyllachora sacchari, 603, 768
Phyllody
cotton, 218
red clover, 468
safflower, 569570
Phyllosticta arachidishypogaea, 419420
Phyllosticta brassicae, 118
Phyllosticta carthami, 564
Phyllosticta hawaiiensis, 759
Phyllosticta leaf blight, millet, 356
Phyllosticta leaf spot
bean, common, 152
cotton, 203
peanut, 419420
safflower, 564
soybean, 645
sugarcane, 759
tobacco, 832
Phyllosticta maydis, 304305
Phyllosticta nicotiana, 832
Phyllosticta penicillariae, 356
Phyllosticta phaseolina, 152
Phyllosticta pod rot, soybean, 645646
Phyllosticta polyconorum, 103
Phyllosticta sojicola, 419420, 645
PhylIosticta spp.
cotton, 203
sugarcane, 765
Phyllosticta stomaticola, 62
Phymatotrichopsis omnivora
alfalfa, 1718
cotton, 203205
peanut, 420
soybean, 646
sugar beet, 708
sunflower, 794
Phymatotrichum root rot
alafalfa, 1718
bean, 152153
cotton, 203205
peanut, 420
soybean, 646
sugar beet, 708
sunflower, 794
Physalospora ear rot, maize, 292
Physalospora tucumanensis, 762
Physalospora zeae, 282
Physalospora zeicola, 292
Physiologic leaf spot, wheat, 945946
Physoderma alfalfae, 1011
Physoderma leproides, 699
Physoderma maydis, 259260
Physoderma trifolii, 456
Physopella pallescens, 304
Physopella zeae, 304
Phytomonas alfalfae, 34
Phytomonas medicaginis, 4
Phytophthora aphanidermatum, 238239
Phytophthora boehmeriae, 205206
Phytophthora crown and root rot, wild rice, 962
Phytophthora cryptogea
sugar beet, 708709
sunflower, 795
Phytophthora drechsleri
alfalfa, 1819
sugar beet, 708
sunflower, 795
Phytophthora erythroseptica
sugarcane, 759
wild rice, 962
Phytophthora macrochlamydospora, 646
Phytophthora macrospora
maize, 265
wheat, 883884
Phytophthora megasperma
alfalfa, 1819
soybean, 646647
sugar beet, 708
sugarcane, 759
Phytophthora nicotianae
flax, 239
tobacco, 822823
Phytophthora parasitica
buckwheat, 101
cotton, 205
tobacco, 822
Phytophthora root and stem rot
safflower, 564565
soybean, 646647
Phytophthora root rot
alfalfa, 1819
flax, 238239
sugar beet, 708709
Phytophthora rot, sugarcane, 759760
Phytophthora spp.
canola, 115
safflower, 563, 564
Phytophthora stem rot, sunflower, 795
Phytoplasmal diseases
alfalfa, 3637
barley, 84
bean, common, 166
canola, 126
cotton, 218219
flax, 244
maize, 310311
oat, 392393
peanut, 435
red clover, 468469

Page 1000
Phytoplasmal diseases (continued)
rice, 503504
rye, 553
safflower, 569570
sorghum, 608
soybean, 673674
sugar beet, 720
sugarcane, 772773
sunflower, 805
tobacco, 843846
wheat, 926
Pierce's disease of grape, 6
Piesma quadratum, 720
Pigweed bug (Piesma cinerea), 732
Pin, alfalfa, 34
Pineapple disease, sugarcane, 760
Pink pod rot, bean, 153
Pink seed, wheat, 870
Pink smudge, wheat, 903
Pink snow mold
barley, 68
oat, 381382
rye, 538
wheat, 899900
Pink sugarcane mealybug (Saccharicoccus sacchari), 773, 777
Pin nematode
bean, common, 163
cotton, 215
oat, 389
red clover, 467
sorghum, 606
sunflower, 804
Pith canker, sunflower, 791792
Pithomyces chartarum, 494
Pithomyces glume blotch, rice, 494
Plamopara penniseti, 349350
Planicephalus flavicostatus, 317
Planthoppers
barley, 89, 90, 9294, 93
maize, 312315, 320, 322323, 325, 327329
oats, 393, 398
rice, 505508, 510, 514515
rye, 553
sorghum, 608, 612613
wheat, 927, 931933, 936939
Plasmodiophora brassicae, 115
Plasmopara halstedii, 789790
Plasmopara helianthi, 789790
Platyspora leaf spot
rye, 538539
wheat, 900
Platyspora pentamera
rye, 538539
wheat, 900
Plectosphaerella cucumerina, 791792
Plenodomus meliloti
red clover, 453
wheat, 875
Plenodomus root rot, alfalfa, 9
Plenodomus spp. in wheat, 874875
Pleosphaerulina briosiana, 15
Pleospora betae, 706707
Pleospora sp., 2728
Pleospora tarda, 464
Pocket, bacterial, 695696
Pod and stem rot, soybean, 648649
Pod drop, canola, 119
Pod rot, canola, 107
Pod wart, peanut, 420
Pokkah boeng
millet, 360
sorghum, 595596
sugarcane, 761
Polymyxa betae
oat, 397
sugar beet, 722, 725726, 730732
tobacco, 850
Polymyxa graminis
barley, 88, 95
oat, 397398
peanut, 439
peanut clump virus, 613
rice, 509
rye, 554555
sugarcane, 778
wheat, 940942
Polysora rust, 301302
Polythrincium trifolii, 461
Poor root syndrome, sugarcane, 757758
Potato virus Y strain, 858859
Powdery mildew
alfalfa
Erysiphe sp., 19
Oidiopsis sp., 16
Oidium sp., 1617
barley, 69
bean, common, 154
in buckwheat, 104
canola, 119
cotton, 206
flax, 239
oat, 382
peanut, 420421
red clover, 458459
rye, 539
safflower, 565
soybean, 650
sugar beet, 709
sunflower, 795796
tobacco, 832833
wheat, 900901
Pratylenchus brachyurus, 277, 840841
Pratylenchus hexincisus
maize, 256
sorghum, 605

Page 1001
sunflower, 803804
Pratylenchus penetrans
alfalfa, 35
bean, common, 149, 163
red clover, 466467
tobacco, 840841
Pratylenchus spp.
barley, 8384
cotton, 215
maize, 308
millet, 362
oat, 389
peanut, 433
rice, 501
rye, 551552
soybean, 669
sugarcane, 771
tobacco, 838839
wheat, 923
Pratylenchus zeae
maize, 277
sorghum, 605
Prematurity blight, wheat, 901902
Proliferation, red clover, 468
Protomycopsis patelii, 140
Psammotettix alienus, 95, 939
Psammotettix striatus, 9495, 938
Pseudocercospora albida, 160
Pseudocercospora cruenta, 147148
Pseudocercospora rubropurpurea, 761
Pseudocercosporella capsellae, 123
Pseudocercosporella herpotrichoides
barley, 58
oat, 376377
rye, 531532, 547
wheat, 887888
Pseudomonas aeruginosa, 817
Pseudomonas andropogonis
maize, 248249
sorghum, 577
Pseudomonas avenae, 741742
Pseudomonas blatchfordae, 139
Pseudomonas cichorii, 783, 871
Pseudomonas fuscovaginae
maize, 251
rice, 481
sorghum, 578
wheat, 868
Pseudomonas marginalis
alfalfa, 21
canola, 107108
Pseudomonas rp2, 109
Pseudomonas rubrisubalbicans, 740
Pseudomonas solanacearum
peanut, 403404
soybean, 626
sunflower, 784
tobacco, 815
Pseudomonas spp.
cotton, 184
maize, 253
millet, 345
sorghum, 575578
Pseudomonas syringae
alfalfa, 4
barley
glume rot, 4748
kernel blight, 47
leaf blight, 46
stripe, 4647
bean, 133134, 137139
canola, 107
cotton, 185186
maize, 249251
millet, 344
oat, 369
red clover, 451
rice, 477, 479, 481
safflower, 559
sorghum, 575
soybean, 621623, 626627
sugar beet, 695
sunflower, 783784
tobacco, 811812, 817818
wheat, 865866, 868, 871
wild rice, 959
Pseudomonas viridiflava, 67
Pseudopeziza leaf spot, 10
Pseudopeziza medicaginis, 10
Pseudopeziza sp., 3233
Pseudopeziza trifolii, 10, 453
Pseudoplea leaf spot, red clover, 459
Pseudoplea spp., 15
Pseudoplea trifolii, 459
Pseudoplusia includens, 661
Pseudoseptoria donacis
rye, 534
wheat, 893
Psylosis, cotton, 222
Puccinia arachidis, 425
Puccinia cacabata, 211
Puccinia calcitrapae, 566567
Puccinia coronata
barley, 55
oat, 374375
Puccinia graminis
barley, 7778
oat, 385386
rice, 495
rye, 546
wheat, 912914
Puccinia helianthi, 797
Puccinia hordei, 63
Puccinia kuehnii, 758
Puccinia melanocephala, 745746
Puccinia polysora, 301302

Page 1002
Puccinia purpurea, 599
Puccinia recondita, 535536
Puccinia schedonnardi, 208
Pucdnia sorghi, 262263
Puccinia striiformis
barley, 79
rye, 548
wheat, 914915
Puccinia subnitens, 715
Puccinia substriata
millet, 358
tobacco, 834
Puccinia triticina, 895896
Puccinia xanthi, 797
Punctodera chalcoensis, 307, 388
Punctodera punctata, 922923
Purple leaf sheath, 251252
Purple patch, barley, 7071
Purple spot of sugarcane, 761
Purple stain, soybean, 650652
Pustule, bacterial, 623624
Pyrenochaeta glycines, 652
Pyrenochaeta leaf spot, soybean, 652653
Pyrenochaeta oryzae, 497
Pyrenochaeta stalk rot, maize, 292293
Pyrenochaeta terrestris, 292293
Pyrenopeziza brassicae, 118119
Pyrenophora avenae, 380
Pyrenophora graminea, 5051
Pyrenophora teres, 6668
Pyrenophora triticirepentis, 81, 549, 903, 917919
Pyricularia grisea
millet, 356357
rice, 484485
wheat, 920
Pyricularia oryzae, 51
Pyricularia setariae, 345
Pythium aphanidermatum
bean, 155
sugar beet, 710
Pythium blight, red clover, 461
Pythium damping off
cotton, 206207
rice, 494495
safflower, 565
soybean, 653654
sugar beet, 710
Pythium graminicola, 757
Pythium hypocotyl rot, 154155
Pythium arrhenomanes, 596597
Pythium megalacanthum, 241
Pythium myriotylum
peanut, 422423
sugarcane, 757758
Pythium palingenes, 104
Pythium root rot
barley, 6970
safflower, 565566
sorghum, 596
sugar beet, 710711
sugarcane, 761762
wheat, 902903
Pythium seed and seedling rot, 382383
Pythium spp.
alfalfa, 1112
barley, 6970
canola, 115, 117
cotton, 206207
flax, 241
maize, 293294
oat, 382
peanut, 421423
red clover, 461
rice, 494495, 500
safflower, 563, 565566
sorghum, 596597
soybean, 653654
sugar beet, 710711
sugarcane, 761762
tobacco, 812, 828
wheat, 902903, 908909
Pythium ultimum
alfalfa, 13
canola, 113114
Pythium wilt, bean, 155
Q.28 disease, 740741
Quinisulcius acutus, 165, 309, 805
Quinisulcius capitatus, 392
Quinisulcius spp. in sorghum, 607
Radopholus gracilis, 965
Radopholus similis, 306, 361
Ragged leaf spot, tobacco, 820
Rai mosaic virus, 127
Ramularia beticola, 711
Ramularia carthami, 566
Ramularia leaf spot
safflower, 566
sugar beet, 711
Ramularia oryzae, 500
Ramularia phaseoli, 148
Ramulispora sorghi, 600
Ramulispora sorghicola, 593
Ramulose, 207
Rapeseed. See Canola (Brassica)
Ratoon stunting disease, 740741
Rayado fino, 322
Recilia dorsalis, 503504, 507
Red clover (Trifolium pratense), 451472
bacterial leaf spot, 451

Page 1003
anther mold, 451452
black patch disease, 452
brown root rot, 453
common leaf spot, 453
Curvularia leaf blight, 453454
Cylindrocarpon root rot, 454
Cylindrocladium root and crown rot, 454
downy mildew, 454
gray stem canker, 455456
leaf gall, 456
midvein spot, 456
Mycoleptodiscus crown and root rot, 456457
Myrothecium root rot, 457
northern anthracnose, 458
Pseudoplea leaf spot, 459
rust, 459460
Sclerotinia crown and root rot, 460
seed mold, 460
seed rot and damping off, 461
sooty blotch, 461
southern anthracnose, 461462
spring black stem and leaf spot, 463
Stagnospora leaf spot, 463464
summer black stem, 464
target spot, 464465
violet root rot, 465
winter crown rot, 465
bulb and stem, 465466
clover cyst, 466
dagger, 466
lance, 466
lesion, 466467
pin, 467
ring, 467
root knot, 467
spiral, 468
phyllody, 468
proliferation, 468
witches' broom, 468
yellow edge, 469
alfalfa mosaic, 469
alsike clover mosaic, 469470
bean yellow mosaic, 470
clover yellow mosaic, 470
common pea mosaic, 470471
cowpea mosaic, 471
dwarf, 471
ringspot, 472
streak, 472
vein mosaic, red clover, 471472
wilt, 472
Red clover vein mosaic virus, 39, 471472
Red crown rot, soybean, 654655
Red ear rot, 279281
Red kernel disease, 295
Red leaf blotch, soybean, 652653
Red leaf mottle, sugarcane, 778
Red leaf spot
sorghum, 579580
sugarcane, 762
Red node, bean, 169
Red root rot, 292
Red rot
sorghum, 597
sugarcane, 762764
Red smudge, wheat, 903
Red spider mites (Tetranychus cinnabarinus), 89
Red spot
sorghum, 597598
sugarcane, 764
Red stripe
sorghum, 613
sugarcane, 741742
Reniform nematode
alfalfa, 34
bean, 164
cotton, 216
sorghum, 606
soybean, 669670
sunflower, 804
tobacco, 841
Rfs gene, soybean, 664
Rhizoctonia bare patch, wheat, 903905
Rhizoctonia bataticola
peanut, 407408
safflower, 562
Rhizoctonia blight
millet, 357
safflower, 566
sorghum, 580
Rhizoctonia cerealis
barley, 7374
oat, 383
rye, 542
wheat, 908
Rhizoctonia crocorum
alfalfa, 31
red clover, 465
sugar beet, 715716
Rhizoctonia crown rot
canola, 120
sugar beet, 711713
Rhizoctonia ear rot, 295

Page 1004
Rhizoctonia foliage blight
alfalfa, 1920
sugar beet, 713
Rhizoctonia leaf spot
cotton, 207208
tobacco, 833
Rhizoctonia leguminicola
alfalfa, 9
red clover, 452
Rhizoctonia oryzae, 498
Rhizoctonia oryzaesativae, 482
Rhizoctonia root rot
alfalfa, 20
barley, 7071
rye, 542
sugar beet, 711713
Rhizoctonia sheath and shoot rot, sugarcane, 764765
Rhizoctonia solani
alfalfa, 1112, 1921
barley, 7071
bean, common, 155156, 159160
canola, 113117, 120121, 123, 125
cotton, 207208, 210
flax, 239240
maize, 258, 295, 296, 297298
millet, 357
peanut, 404, 423424
rice, 495496
rye, 551
safflower, 566
sorghum, 580, 598
soybean, 638, 655657
sugar beet, 703704, 711713
sugarcane, 764765
tobacco, 833, 835837
wheat, 881882, 898, 903905, 908
Rhizoctonia stalk rot, sorghum, 598
Rhizoctonia stem blight, 2021
Rhizoctonia stem canker, safflower, 566
Rhizoctonia zeae
maize, 295
millet, 357
Rhizomania disease, 730732
Rhizophydium graminis, 920
Rhizopus arrhizus
peanut, 424
sugar beet, 714
tobacco, 812, 833834
Rhizopus head rot, sunflower, 796
Rhizopus nigricans, 208
Rhizopus oryzae, 796
Rhizopus root rot, sugar beet, 714
Rhizopus spp. in wheat, 874875
Rhizopus sprout rot, 21
Rhizopus stem rot, tobacco, 833834
Rhizopus stolonifer
alfalfa, 21
canola, 113
peanut, 424
sugar beet, 714
Rhodococcus fascians, 816
Rhopalosiphum maidis. See Corn leaf aphid (Rhopalosiphum maidis)
Rhopalosiphumpadi, 87, 320, 394, 775
Rhopalosiphum rufiabdominelis, 87, 394
Rhynchosporium oryzae, 492, 494
Rhynchosporium secalis, 7172, 539540
Ribautodelphax albifascia
maize, 328329
rice, 506, 510
sorghum, 613
Rice (Oryzae sativa), 475516
blight, 475477
foot rot, 480
glume blotch, 477
grain rot, 480
halo blight, 477
leaf streak, 478
sheath brown rot, 478479, 481
sheath stripe, 479
stripe, 479480
aggregate sheath spot, 482
bakanae disease, 482483
basal node rot, 483
black kernel, 483484
blast, 484485
brown blotch, 485486
brown spot, 486
collar rot, 487
crown sheath rot, 487488
dead tiller syndrome, 488
eyespot, 489
false smut, 489490
Fusarium leaf blotch, 490491
Fusarium sheath rot, 491
kernel smut, 491492
leaf scald, 492
leaf smut, 493
narrow brown leaf spot, 493
pecky rice, 493
Phoma seedling blight, 494
Pithomyces glume blotch, 494
rust, 495
sheath blight, 495496
sheath blotch, 497
sheath rot, 497498
sheath spot, 498
stackburn disease, 499
stem rot, 499500

Page 1005
water mold disease, 500
white leaf streak, 501
lesion, 501
rice root, 501
root knot, 501502
stem, 502503
summer crimp, 503
panicle blight, 515
rice orange leaf, 503504
rice yellow dwarf, 504
sekiguchi lesion, 515516
straighthead, 516
African cereal streak virus, 505
giallume disease, 505
grassy stunt B, 505506
grassy stunt Y, 506
rice black streak dwarf, 506
rice dwarf, 506507
rice gall dwarf, 507
rice grassy stunt, 507508
rice hoja bianca, 508
rice necrotic mosaic, 508509
rice ragged stunt, 509510
rice stripe, 510
rice stripe necrosis, 511
rice transitory yellowing, 511512
rice wilted stunt, 514
nce yellow mottle, 512
tungro, 512514
waika disease, 514515
wilted stunt, 515
Rice blackstreaked dwarf virus
barley, 94
maize, 328329
rice, 506
wheat, 937938
Rice dwarf virus, 507
Rice gall dwarf virus, 507
Rice grassy stunt virus, 507508
Rice hoja bianca virus, 508, 938
Rice necrotic mosaic virus, 509
Rice orange leaf disease, 503504
Rice ragged stunt virus, 509510
Rice root aphid (Rhopalosiphum rufiabdominelis), 87, 394
Rice root nematode, 501
Rice stripe necrosis virus, 511
Rice stripe virus
barley, 94
maize, 329
rice, 510
sorghum, 613614
Rice transitory yellowing virus, 511512
Rice waika virus, 514515
Rice yellow mottle virus, 512
Rickettsial diseases
peanut, 436
sugar beet, 720721
Rind disease, sugarcane, 765
Ring nematode
bean, 164
cotton, 216
maize, 308
millet, 362
oat, 390
peanut, 432
red clover, 467
sorghum, 606
wheat, 923
Ring spot
buckwheat, 104
canola, 120121
red clover, 464465
sugarcane, 765766
tobacco, 851852
Rio Cuarto disease, 323
Rio Grande corn stunt, 310311
Root and crown rot complex, alfalfa, 67, 2122
Root gall nematode
barley, 8283
oat, 390391
rye, 551
wheat, 924
Root knot nematode
alfalfa, 5, 14, 18, 3435
barley, 83
bean, common, 164
canola, 125126
cotton, 216217
maize, 309
millet, 362
oat, 391
peanut, 432433
red clover, 467
rice, 501502
rye, 551
safflower, 569
sorghum, 606
soybean, 670
sugar beet, 718
sugarcane, 771
sunflower, 804805
tobacco, 841842
wheat, 924
Root lesion nematode
alfalfa, 35
barley, 8384
millet, 362
peanut, 433434
rye, 551552
Root rot. See specific crop or disease
Rosette
peanut, 438439

Page 1006
Rosette (continued)
sugar beet, 720
Rotten neck, rice, 484485
Rotylenchulus reniformis
bean, 164
cotton, 216
soybean, 669670
sunflower, 804
tobacco, 841
Rotylenchulus spp.
alfalfa, 34
sorghum, 606
sugarcane, 771
Rough leaf spot, sorghum, 598599
Russian wheat aphid (Diuraphis noxia), 87, 89, 394, 931
Rust
alfalfa, 2223
barley
crown, 55
leaf, 6263
stem, 7779
stripe, 79
beet, 699
canola, 116, 123124
cotton, 194195, 208, 211, 212
flax, 240
maize
common, 262263
southern corn rust, 301302
tropical corn, 304
millet, 358
oat, 374375, 385386
peanut, 425426
red clover, 459460
rice, 495
rye, 535536, 546547, 548
safflower, 566567
sorghum, 599
soybean, 657658
sugar beet, 715
sugarcane
common, 745746
orange, 758
sunflower, 797, 802803
tobacco, 813, 834
wheat
leaf, 895
stem, 912914
stripe, 914915
Rxp gene, soybean, 623
Rye (Secale cereale), 523556
aster yellows, 553
halo blight, 524525
streak, 523524
anthracnose, 525
bunt, 525526
common root rot, 527528
Dilophospora leaf spot, 528529
dwarf bunt, 530
ergot, 531
eyespot, 531532
halo spot, 534
kernel bunt, 534535
leaf rust, 535536
loose smut, 537538
pink snow mold, 538
Platyspora leaf spot, 538539
powdery mildew, 539
scald, 539540
Septoria tritici leaf blotch, 541
sharp eyespot, 542
snow scald, 542543
spot blotch, 543544
Stagnospora blotch, 544545
stalk smut, 545546
stem rust, 546547
strawbreaker, 547548
stripe rust, 548
takeall, 548549
tan spot, 549550
cereal cyst, 550
leaf and stem, 550551
root gall, 551
root knot, 551
root lesion, 551552
seed gall, 552
stubby root, 552
soilborne mosaic, 554555
Saccharicoccus sacchari, 773, 777
Saccharum officinarum. See Sugarcane (Saccharum officinarum)
Safflower (Carthamus tinctorius), 559572
leaf spot and stem blight, 559
stem soft rot, 559560
anthracnose, 561

Page 1007
Botrytis head rot, 561
charcoal rot, 562
Colletotrichum stem rot, 563
damping off, 563
downy mildew, 563
Phytophthora root and stem rot, 564565
powdery mildew, 565
Ramularia leaf spot, 566
Rhizoctonia blight and stem canker, 566567
rust, 566567
Sclerotinia stem rot and head blight, 568
Septoria leaf spot, 568
phyllody, 569570
root knot nematode, 569
alfalfa mosaic, 570
chilli mosaic, 570
lettuce mosaic and necrosis, 571
tobacco mosaic, 571
turnip mosaic and necrosis, 571572
Salminia malachrae, 206
Sap beetles (Glischrochilus quadrisignatus), 280
Sarocladium oryzae, 494, 497498
Savoy, sugar beet, 732
Scab
barley, 6061
oat, 378
peanut, 426
rye, 533534
soybean, 658
sugar beet, 697698
wheat, 890892
wild rice, 961962
Scald
barley, 7172
rye, 539540
Scaphytopices fulginosus, 166
Scaphytopius acutus, 673
Scaphytopius fuliginosus, 673
Schizaphis graminum, 87, 327328, 364, 394, 610, 775
Sclerophthora disease, sugarcane, 766
Sclerophthora macrospora
maize, 265
oat, 375376
rice, 488
rye, 529530
sorghum, 582
sugarcane, 766
wheat, 883884
Sclerophthora rayssiae
barley, 55
maize, 260261
Sclerospora graminicola
maize, 284
millet, 347348
sorghum, 589
Sclerospora macrospora, 349
Sclerospora maydis, 286
Sclerospora miscanthi, 750751
Sclerospora philippinensis, 291
Sclerospora sacchari, 302303, 749750
Sclerospora sorghi, 600
Sclerospora spontanea, 302, 750
Sclerotinia basal stalk rot and wilt, sunflower, 798799
Sclerotinia blight, peanut, 426427
Sclerotinia borealis
barley, 72
rye, 542
wheat, 906
Sclerotinia crown and root rot, red clover, 460
Sclerotinia crown and stem rot, alfalfa, 2324
Sclerotinia homoeocarpa, 427
Sclerotinia minor
peanut, 426427
soybean, 658
sunflower, 798799
Sclerotinia sclerotiorum
alfalfa, 2324
canola, 121122
crambe, 230231
flax, 242
safflower, 568
soybean, 658
sunflower, 798800
tobacco, 812, 826827, 829
Sclerotinia snow mold
barley, 72
rye, 542543
wheat, 906
Sclerotinia spermophila, 451
Sclerotinia stem rot
canola, 121122
crambe, 230231
soybean, 658659
Sclerotinia stem rot and head blight, safflower, 568
Sclerotinia trifoliorum, 2324, 460
Sclerotinia white mold, sunflower, 798800
Sclerotium basal stalk rot and root rot, sunflower, 801
Sclerotium bataticola
maize, 261
safflower, 562
Sclerotium cinnamomi, 431
Sclerotium hydrophilum, 965

Page 1008
Sclerotium oryzae, 499
Sclerotium rolfsii
alfalfa, 24
barley, 74
bean, common, 158
canola, 122
cotton, 209210
maize, 296
millet, 359360
peanut, 428429
red clover, 462
sorghum, 602
sugar beet, 714715
sugarcane, 763
sunflower, 801
tobacco, 836
wheat, 909
Sclerotium root rot, sugar beet, 714715
Sclerotium spp.
soybean, 666
wild rice, 963964
Scoliocotrichum graminis
oat, 383
rye, 536537
Scorch, flax, 241
Scutellonema cavenessi
peanut, 434
Scutellonema spp.
cotton, 217
sugarcane, 771
Secale cereale. See Rye (Secale cereale)
Seedborne wheat yellows viroid, 927
Seed corn maggot (Hylemyia cilicrura), 252
Seed gall nematode
rye, 528529, 552
wheat, 924925
Seedling blight, rice, 481
Seed mold, red clover, 460
Seed rot
maize, 252
red clover, 461
Sekiguchi lesion, 515516
Selenophoma donacis
barley, 62
rye, 534
Selenophoma leaf spot, maize, 297
Selenophoma linicola, 236
Selenophoma spp. in maize, 297
Septoria avenae, 6364
Septoria carthami, 568
Septoria carthamicola, 568
Septoria donacis, 62
Septoria glycines, 631
Septoria helianthi, 801
Septoria leaf blotch
maize, 297
rye, 540541
wheat, 906907
Septoria leaf spot
safflower, 568
sunflower, 801
Septoria linicola, 237
Septoria nodorum, 544
Septoria passerinii, 6364, 7273
Septoria secalis, 540
Septoria speckled leaf blotch, 7273
Septoria spp.
barley, 7677
maize, 297
Septoria tritici
rye, 541
wheat, 906907
Serratia marcescens, 21
Sesame leaf spot, 486
Sesamum phyllody virus, 127
Sesselia pusilla, 512
Setaria italica. See Millet
Setosphaeria rostrata, 295
Setosphaeria turcica, 288, 590591
Sharp eyespot
barley, 7374
oat, 383
rye, 542
wheat, 908
Sheath blight
maize, 297298
rice, 495496
Sheath blotch, rice, 497
Sheath brown rot, rice, 478479, 481
Sheath nematode
oat, 391
soybean, 671
Sheath rot
maize, 298
rice, 497
sugarcane, 767
wheat, 868
Sheath spot, rice, 498
Sheath stripe, rice, 479
Shuck rot, 298
Silage mold, 298
Siteroptes avenae, 889
Siteroptes reniformis, 203
Sitobion avenae, 87, 394, 930
Sitona hispidulus. See Clover root curculio
Sleepy disease, 759
Slime disease, peanut, 404405
Smut
barley
covered, 5455
false loose, 5859
loose, 6566
canola, 122
maize
common, 263264

Page 1009
false, 272273
head, 284285
millet, 358359
head, 352353
kernel, 354
long, 355
oat
covered, 373
loose, 380381
rice
false, 489490
kernal, 491492
leaf, 493
rye
loose, 537538
stalk, 545546
sorghum
covered kernel smut, 581582
head, 589590
long, 592
loose kernel, 592593
sugarcane
covered, 746
Culmicolous, 746748
wheat
common bunt, 878879
dwarf bunt, 884885
flag smut, 888889
karnal bunt, 893894
loose smut, 897898
wild rice, 962965
Snow mold
alfalfa, 3132
barley
Ceratobasidium gramineum, 5253
gray, 6162
pink, 68
Sclerotinia, 72
speckled, 7475
oat, 381382, 385
rye, 538, 542543
wheat
Ceratobasidium gramineum, 877
cottony, 881
pink, 899900
Sclerotinia, 906
speckled, 909910
Typhulalike, 919920
Snow mold, cottony, 528, 881
Snow mold, gray. See Gray snow mold
Snow mold, pink. See Pink snow mold
Snow mold, speckled. See Speckled snow mold
Snow rot, wheat, 908909
Snow scald
rye, 542543
wheat, 906
Soft rot, canola bacterial, 107108
Sogata cabana, 938
Sogata orizicola, 938
Sogatodes oryzicola, 508
Soilborne wheat mosaic virus, 9495
Sooty blotch, red clover, 461
Sooty head mold, wheat, 874
Sooty mold
sugarcane, 767
tobacco, 834
Sooty stripe, sorghum, 600
Sordaria fimicola, 299
Soreshin
cotton, 210
tobacco, 835
Sorghum (Sorghum bicolor), 575616
Erwinia soft rot, 577578
leaf blight, 575
leaf spot, 575576
leaf streak, 576
leaf stripe, 577
Pseudomonas fuscovaginae infection, 578
Acremonium wilt, 578579
anthracnose, panicle and grain, 594
anthracnose leaf blight, 579580
Cochliobolus leaf spot, 581
covered kernal smut, 581582
crazy top, 582
Curvularia kernal rot, 583
ergot, 583585
false mildew, 585
Fusarium root and stalk rot, 586587
Fusarium thapsinum infection, 587588
gray leaf spot, 588
green ear, 589
head smut, 590
ladder leaf spot, 590
leaf blight, 590591
leaf spot, 591
long smut, 592
loose kernal smut, 592593
milo disease, 593
oval leaf spot, 593594
Phoma leaf spot, 595
pokkah boeng, 595596
Pythium seed and seedling blight, 596597
red rot, 597
red spot, 597598
Rhizoctonia stalk rot, 598
rough leaf spot, 598599
rust, 599
sooty stripe, 600
southern leaf blight, 602

Page 1010
Sorghum (Sorghum bicolor) (continued)
southern sclerotial rot, 602603
target leaf spot, 603
tar spot, 603
awl, 604605
cereal root knot, 605
dagger, 605
lesion, 605
needle, 605606
pin, 606
reniform, 606
ring, 606
root knot, 606
spiral, 607
sting, 607
stubby root, 607
stunt, 607
Australian maize streak, 608
brome mosaic, 608609
elephant grass mosiac, 609
maize chlorotic dwarf, 610
maize chlorotic mottle, 610
maize dwarf mosaic head blight, 611612
maize rough dwarf, 612
maize streak, 612
maize stripe, 612
peanut clump, 613
red stripe disease, 613
rice stripe, 613614
sorghum mosaic, 614
sorghum stunt mosaic, 614615
sorghum yellow banding, 615
sugarcane chlorotic streak, 615
sugarcane Fiji disease, 615
weak neck, 616
yellow sorghum stunt, 608
Sorghum downy mildew, maize, 299300
Sorghum mosaic virus, 614
Sorghum stunt mosaic virus
maize, 329
sorghum, 614
Sorghum yellow banding virus, 615
Sorosphaera vascularum, 751
Sour smell, sugarcane, 765
Southern anthracnose, 461462. See also Anthracnose
Southern bean mosaic virus, 174
Southern blight
alfalfa, 24
barley, 74
bean, common, 158
canola, 112
cotton, 209210
maize, 296, 300301
millet, 359360
peanut, 428429
red clover, 462
soybean, 659660
sunflower, 801
tobacco, 835836
wheat, 909
Southern corn leaf blight, 300301
Southern corn rootworm (Diabrotica undecimpunctata), 318
Southern corn rust, 301302
Southern leaf blight, sorghum, 602
Southern root rot, sugar beet, 714715
Southern sclerotial rot, sorghum, 602603
Soybean (Glycine max), 621683
blight, 621622
crinkle leaf, 623
pustule, 623624
seed decay, Bacillus, 621
seed decay, Pseudomonas, 626627
tanspot, 624
wildfire, 627628
wilt, 625626
Acremonium wilt, 628
anthracnose, 629630
Aspergillus seedling blight, 631
brown spot, 631632
brown stem rot, 632633
Cercospora leaf spot and blight, 633634
Cercospora seed decay, 634
Choanephora leaf blight, 636
collar rot, 649
cotyledon spot, 636
Drechslera blight, 637
Essex disease, 638
frogeye leaf spot, 638639
Fusarium graminearum seed infection, 639
Fusarium oxysporum seed infection, 639640
Fusarium pallidoroseum seed infection, 639
Leptosphaerulina leaf spot, 641642
Mycoleptodiscus root rot, 642
Myrothecium disease, 642643
Neocosmospora stem rot, 643
Phomopsis seed rot, 643645
Phyllosticta pod rot, 645646
Phytophthora root and stem rot, 646647
pod and stem rot, 648649
pod rot, 649

Page 1011
powdery mildew, 650
purple stain, 650652
Pyrenochaeta leaf spot, 652653
Pythium damping off and rot, 653654
red crown rot, 654655
Rhizoctonia aerial blight, 655656
Rhizoctonia damping off and rot, 656657
rust, 657658
scab, 658
stem canker, 660662
Stemphylium leaf blight, 662
sudden death syndrome, 662665
target spot, 665
Thielaviopsis root rot, 665666
top dieback, 666
twin stem abnormality disease, 666667
Verticillium pod loss, 667
yeast spot, 668
Columbia lance, 668669
lance, 669
lesion, 669
reniform, 669670
ring, 670
root knot, 670
sheath, 671
soybean cyst, 671672
spiral, 672
stem, 672
sting, 672673
machismo, 673
soybean bud proliferation, 673674
witches' broom, 674
pod necrosis, 683
alfalfa mosaic, 674
bean pod mottle, 674675
Brazilian bud blight, 675
bud blight, 675676
cowpea chlorotic mottle, 676
cowpea mild mottle, 677
cowpea mosaic, 677
cowpea severe mosaic, 677
delayed maturity, 677
Indonesian soybean dwarf, 678
mung bean yellow mosaic, 678
peanut mottle, 678
peanut stripe, 679
peanut stunt, 679
soybean chlorotic mottle, 679
soybean crinkle leaf, 680
soybean dwarf, 680
soybean mosaic, 680681
soybean severe stunt, 681682
soybean yellow shoot, 682
tobacco mosaic, 682
tobacco necrosis, 682
yellow mosaic, 683
Soybean bud proliferation, 673674
Soybean chlorotic mottle virus, 679
Soybean cyst nematode (Heterdera glycines), 635
Soybean dwarf virus
bean, common, 173
red clover, 471
soybean, 680
sugar beet, 732
Soybean mosaic virus, 680681
Soybean severe stunt virus, 681682
Soybean yellow mosaic virus, 683
Soybean yellow shoot virus
soybean, 682
Speckled blotch
barley, 6364
oat, 384
Speckle disease, bean, 158
Speckled leaf blotch
rye, 541
wheat, 906907
Speckled snow mold
barley, 7475
oat, 385
rye, 543
wheat, 909910
Sphacelia segetum
rye, 531
wheat, 886887
Sphacelia sorghi, 583584
Sphacelia sp., 271272
Sphaceloma arachidis, 426
Sphaceloma glycines, 658
Sphaceloma sacchari, 769
Sphacelotheca cruenta, 592
Sphacelotheca macrospora, 746
Sphacelotheca reiliana, 284285
Sphaerotheca fuliginea, 795
Sphaerulina maydis, 291
Spike blight, wheat, 870871
Spiral nematode
alfalfa, 35
bean, common, 165
cotton, 217
maize, 309
oat, 391
peanut, 434
sorghum, 607
soybean, 672
sugarcane, 771
sunflower, 805
tobacco, 842
wheat, 925
Spiroplasma kunkelii, 310311
Spittlebugs, 6
Spontaneum downy mildew, 302

Page 1012
Sporisorium cruentum, 592
Sporisorium destruens, 352353
Sporisorium holcisorghi, 284285, 589590
Sporisorium neglectum, 354
Sporisorium sorghi, 581582
Sporobolomyces spp. in wheat, 874875
Spot blotch
rye, 543544
wheat, 910
wild rice, 963
Spot mosaic virus, 943, 946
Spotted cucumber beetle, 172, 676
Spring black stem, alfalfa, 17, 25
Spring black stem and leaf spot, red clover, 463
Spring leaf spot, 25
Stackburn disease, 499
Staghead, 116, 123124
Stagonospora avenae, 384
barley, 6364, 7273
wheat, 911
Stagonospora blotch
barley, 7677
rye, 544545
wheat, 911912
Stagonospora leaf spot
alfalfa, 25
red clover, 463464
Stagonospora meliloti, 2526
Stagonospora nodorum
barley, 7677
rye, 544
wheat, 896, 911912
Stagonospora recedens, 463
Stagonospora sacchari, 756
Stagonospora taiwanensis, 755
Stagonosporopsis hortensis, 158
Stalk and top rot, maize, 248
Stalk rot, bacterial
canola, 107108
maize, 247248
Stalk smut, rye, 545546
Stem and bulb nematode, 718
Stem blight, alfalfa bacterial, 4
Stem canker
canola, 111
soybean, 660662
Stem melanosis, wheat, 871
Stem nematode
rice, 502503
soybean, 672
Stemphylium botryosum, 416, 464
Stemphylium leaf spot
alfalfa, 2728
cotton, 211
Stemphylium sarciniforme, 464
Stemphylium spp.
alfalfa, 2728
cotton, 211
wheat, 874875
Stem rot
bean, common, 159
rice, 499500
wild rice, 963964
Stem rust
barley, 7778
oat, 385386
rye, 546547
wheat, 912914
Stem smut, wild rice, 964965
Stem soft rot, safflower, 559560
Stenocarpella macrospora, 268
Stenocarpella maydis, 269270, 296
Sting nematode
bean, common, 165
cotton, 217218
maize, 309
millet, 362363
oat, 392
peanut, 434435
sorghum, 607
soybean, 672673
Stinkbugs
cotton, 185
soybean, 668
Stinking smut, rye, 525526
Stipple spot, 102
Stipple streak, bean, 175
Stirellus bicolor, 317, 322
Stolbur, tobacco, 844845
Straighthead, rice, 516
Strawbreaker
barley, 5758
rye, 531532, 547
wheat, 887888
Streak, rye bacterial, 523524
Streptomyces scabies, 697
Streptornyces spp. in peanut, 417, 420
Stripe, bacterial
barley, 4647
maize, 248249
oat, 370
rice, 479
Stripe rust
barley, 79
rye, 548
wheat, 914915
Stubble decline, sugarcane, 767768
Stubby root nematode
bean, common, 165
cotton, 218
maize, 309310
millet, 363
rye, 552
sorghum, 607
sugar beet, 719
tobacco, 842843

Page 1013
wheat, 925
Stunt nematode
alfalfa, 36
barley, 84
bean, common, 165
cotton, 218
maize, 310
millet, 363
sunflower, 805
tobacco, 843
wheat, 926
Stunt root nematode, sorghum, 607
Subanguina radicicola
barley, 8283
oat, 390391
rye, 551
wheat, 924
Subterranean clover red leaf virus, 680, 732
Sudden death syndrome, soybean, 662665
Sugar beet (Beta vulgaris), 695732
Corynebacterium infection, 697
crown gall, 697
leaf spot, 695
pocket, 695696
scab, 697698
vascular necrosis and soft rot, 696697
Aspergillus fumigatus storage rot, 698699
beet tumor, 699
black root, 700
Botrytis storage rot, 700701
charcoal rot, 702
downy mildew, 703
dry rot canker, 703704
Fusarium tip rot, 705
Penicillium storage rot, 706
Phoma leaf spot, 706707
Phoma root rot, 707
powdery mildew, 709
Ramularia leaf spot, 711
Rhizoctonia crown and root rot, 711713
Rhizoctonia foilage blight, 713
Rhizopus root rot, 714
rust, 699, 715
Sclerotium root rot, 714715
seedling rust, 715
violet root rot, 715716
clover cyst, 716
false root knot, 717
Nebraska root gall, 717
needle, 717
root knot, 718
stem and bulb, 718
stubby root, 719
sugar beet, 719
rickettsial diseases
beet latent rosette, 720
yellow wilt, 720721
rosette disease, 720
beet crinkle, 721
beet distortion mosaic, 722
beet leaf curl, 722723
beet mild yellowing, 723
beet mosaic, 723724
beet pseudoyellows, 724
beet ring mottle, 724725
beet soilborne, 725
beet soilborne mosaic, 725726
beet western yellows, 726727
beet yellow net, 727728
beet yellows, 728729
beet yellow stunt, 728
beet yellow vein, 728
curly top, 721722
lettuce chlorosis, 730
lettuce infectious yellows, 730
marble leaf, 723
rhizomanic disease, 730732
savoy, 732
yellows, 732
Sugar beet nematode, 719720
Sugarcane (Saccharum officinarum), 737779
gumming disease, 738739
leaf scald, 739740
mottle, 737738
mottled stripe, 740
ratoon stunting disease, 740741
red stripe, 741742
top rot, 741742
banded sclerotial leaf disease, 742743
black rot, 743
black stripe, 743
brown rot, 743744
brown spot, 744
collar rot, 745
covered smut, 746
Culmicolous smut, 746748
Curvularia leaf spot and seedling blight, 749

Page 1014
Sugarcane (Saccharum officinarum) (continued)
Drechslera seedling blight and leaf spot, 751
dry top rot, 751752
ergot, 752
eyespot, 753
foliage blight of seedlings, 753
Fusarium stem rot, 754
iliau, 754755
leaf blast, 755
leaf blight, 755
leaf scorch, 756
Marasmius sheath and shoot blight, 756757
Myriogenospora leaf binding, 757
northern poor root syndrome, 757758
Pachymetra root rot, 758759
Philippine downy mildew, 759
Phytophthora rot of cuttings, 759760
pineapple disease, 760
pokkah boeng, 761
purple spot, 761
red leaf spot, 762
red rot, 762764
red spot, 764
Rhizoctonia sheath and shoot rot, 764765
rind disease, 765
ring spot, 765766
rust, common, 745746
rust, orange, 758
Sclerophthora disease, 766
sheath rot, 767
smut, 746748
sooty mold, 767
stubble decline, 767768
target blotch, 768
tar spot, 768
veneer blotch, 768769
white rash, 769
wilt, 769770
yellow spot, 770
lance, 771
lesion, 771
root knot, 771
spiral, 771772
grassy shoot, 772
white leaf, 772773
banana streak, 773
chlorotic streak, 773774
dwarf, 774
Fiji disease, 774775
mosaic, 775776
red leaf mottle, 778
sereh, 776
streak disease, 776777
striate mosaic, 777
sugarcane bacilliform, 777
sugarcane mild mosaic, 777778
yellow leaf disease, 778
yield decline, 778779
Sugarcane bacilliform virus, 777
Sugarcane borer (Diatraea saccharalis), 754
Sugarcane chlorotic streak virus
sorghum, 615
sugarcane, 773774
Sugarcane downy mildew, 302303
Sugarcane dwarf virus, 774
Sugarcane Fiji disease
maize, 329
sorghum, 615
sugarcane, 774775
Sugarcane mild mosaic virus, 777778
Sugarcane mosaic virus
maize, 329330
sorghum, 613
sugarcane, 775776
Sugarcane sereh disease virus, 776
Sugarcane striate mosaic virus, 777
Sugarcane yellow leaf diseaseassociated virus, 778
Suleima helianthana, 785
Summer black stem
alfalfa, 2829
red clover, 464
Summer crimp nematode, 503
Sunflower (Helianthus annus), 783806
aster yellows, 805
apical chlorosis, 783
crown gall, 784785
Erwinia stalk and head rot, 785
leaf spot, 783784
wilt, 784
bract necrosis, 806
achene blemish syndrome, 785786
Botrytis head rot, 787788
Cephalosporium wilt, 788
Cladosporium leaf spot, 789
Drechslera leaf spot, 790791
Fusarium moniliforme wilt, 791
Fusarium oxysporum wilt, 791
Fusarium pith canker, 791792

Page 1015
Helminthosporium leaf blight, 792
Myrothecium leaf and stem spot, 792
Phialophora yellows, 792
Phoma black stem, 793
Phoma leaf blight, 793
Phomopsis brown stem canker, 793794
Phytophthora stem rot, 795
Rhizopus head rot, 796
rust, 797
rust, white, 802803
rust, yellow, 803
Sclerotinia basal stalk rot and wilt, 798
Sclerotinia head rot, 799800
Sclerotinia white mold, 798800
Sclerotium basal stalk rot and root rot, 801
Septoria leaf spot, 801
stunt, 805
white rust, 802803
yellow rust, 803
dagger, 803
lesion, 803804
pin, 804
reniform, 804
root knot, 804805
spiral, 805
vital diseases, 806
mosaic, 806
yellow leaf spot mosaic, 806
Sunflower budworm (Suleima helianthana), 785
Sunflower moth (Homoeosoma electellum), 796
Sunflower stem weevil (Cylindrocopturus adsperus), 788
Sunflower virus, 806
Systena frontalis, 318, 610
Takeall
barley, 7980
oat, 387
rye, 548549
wheat, 898, 915917
Talaromyces flavus, 799
Tan spot
barley, 81
rye, 549550
soybean, 624
wheat, 917919
Tapesia yallundae
rye, 531532
wheat, 887
Target blotch, sugarcane, 768
Target leaf spot, 603
Target spot
alfalfa, 2728
red clover, 464465
soybean, 665
tobacco, 836837
Tar spot
maize, 303304
sorghum, 603
sugarcane, 768
wheat, 919
Terminal stunt, cotton, 223
Testa, 435
Tetranychus sp., 852
Tetranychus urticae, 156, 262, 277
Texas root rot
alfalfa, 1718
sugar beet, 708
Thanatephorus cucumeris
cotton, 207, 210
maize, 264
peanut, 423424
rice, 495496
safflower, 566
sorghum, 580
soybean, 656
sugar beet, 711713
sugarcane, 742
tobacco, 833, 835837
wheat, 903
Thichothecium roseum, 153
Thielaviopsis basicola, 9, 147, 666
alfalfa, 21
cotton, 192193
flax, 242243
peanut, 406
red clover, 452
tobacco, 821
Thielaviopsis paradoxa, 760
Thielaviopsis root rot
flax, 242243
soybean, 665666
Thrips
bean, common, 169
maize, 318
peanut, 441
tobacco, 852, 855856, 859860
Thrips setosus, 441, 860
Thrips tabaci
peanut, 441
soybean, 675
tobacco, 852, 855856, 860
Tikka, 411412, 414415
Tilletia barclayana, 491492
Tilletia caries
rye, 525526
wheat, 878
Tilletia controversa
barley, 56
rye, 530
wheat, 885

Page 1016
Tilletia indica
rye, 534535
wheat, 893894
Tilletia laevis
rye, 525526
wheat, 878
Tobacco (Nicotiana tabacum), 811861
barn rot, 812
black rust, 813
crown gall, 813814
frenching, 814
Granville wilt, 815
hollow stalk, 815816
leaf gall, 816
Philippine bacterial leaf spot, 817
wildfire, 817818
Wisconsin bacterial leaf spot, 818819
broomrape, 860861
anthracnose, 819
Ascochyte leaf spot, 820
barn spot, 820
black mildew, 820
black shank, 822823
blue mold, 823825
Botryosporium barn mold, 825
brown spot, 825826
charcoal rot, 826
collar rot, 826827
Corynespora leaf spot, 827828
damping off, 828
dead blossom leaf spot, 829
frogeye, 829
gray mold, 831
Olpidium seedling blight, 831
Rhizoctonia leaf spot, 833
Rhizopus stem rot, 833834
rust, 834
sooty mold, 834
soreshin, 835
southern stem and root rot, 835836
target spot, 836837
tobacco stunt, 837
brown root rot, 838839
bulb and stem, 839
cyst, 840
dagger, 840
foliar, 840
lesion, 840841
reniform, 841
root knot, 841842
spiral, 842
stubby root, 842843
stunt, 843
Nicotiana glutinosa stunt viroid, 846
aster yellows, 843844
bigbud, 844
stolbur, 844845
yellow dwarf, 845846
alfalfa mosaic, 846847
beet curlytop, 847
bushy top, 847848
clubroot, 848
eggplant mosaic, 849
leaf curl, 849850
Nicotiana velutina mosaic virus, 850
peanut chlorotic streak, 850851
peanut stunt, 851
pepper veinal mottle, 851
ringspot, 851852
tobacco etch, 852853
tobacco mosaic, 853854
tobacco necrosis, 854855
tobacco rattle, 855
tobacco ringspot, 855856
tobacco rosette disease, 856
tobacco streak, 856857
tobacco stunt, 857
tobacco veinal necrosis, 858859
tobacco veinbanding mosaic, 858
tobacco vein mottling, 857858
tomato spotted wilt, 859860
wound tumor, 860
Tobacco etch virus, 852853
Tobacco flea beetle (Epitrix hirtipennis), 852
Tobacco leaf curl virus, 849850, 853
Tobacco mosaic virus
safflower, 571
soybean, 682
sunflower, 806
tobacco, 853854
wheat, 939
Tobacco mottle virus, 856
Tobacco necrosis virus
bean, common, 175
soybean, 682
tobacco, 854
Tobacco rattle virus, 855
Tobacco ringspot virus
red clover, 472
soybean, 675676
tobacco, 851852, 855856
Tobacco rosette disease, 856

Page 1017
Tobacco streak virus
cotton, 223
red clover, 472
soybean, 675
tobacco, 856857
Tobacco stunt virus, 857
Tobacco veinal necrosis, 857858
Tobacco veinbanding mosaic virus, 858
Tobacco veindistorting virus, 847848, 856
Tobacco veinmottling virus, 859
Tolyposporium ehrenbergii, 592
Tomato spotted wilt virus, 440441, 859860
Toothed flea beetle (Chaetocnema denticulata), 252
Top dieback, soybean, 666
Top rot, millet, 360
Toya catilina, 85, 325, 393, 505, 553, 927
Toya propinqua, 315
Trichoderma harzianum, 835, 882
Trichoderma viride, 304
Trichodorus christiei, 309
Trichodorus spp.
sugar beet, 719
tobacco, 842843, 855
Trifluralin herbicide, 640, 647
Trifolium pratense. See Red clover (Trifolium pratense)
Triticum aestivum. See Wheat (Triticum aestivum)
Tropical corn rust, 304
Tsai's disease, 325
T2 toxin, 706
Tungro, 512514
Turnip crinkle virus, 127
Turnip mosaic virus
buckwheat, 105
canola, 127
crambe, 232
safflower, 571572
Twelvespotted cucumber beetle (Diabrotica undecimpunctata howartii), 252
Twin stem abnormality disease, soybean, 666667
Twist, 528529, 882883
Twospotted spider mite (Tetranychus urticae), 156, 262, 277
Tylenchorhynchus brevilineatus, 432
Tylenchorhynchus nudus, 805
Tylenchorhynchus spp.
alfalfa, 36
barley, 84
bean, common, 165
cotton, 218
maize, 310
millet, 363
oat, 392
sorghum, 607
tobacco, 843
Tylenchorhynchus vulgaris, 277
Typhula incarnata, 6162
Typhula ishikariensis, 7475
Typhula spp.
oat, 385
red clover, 465
rye, 543
wheat, 909910, 919920
Ufra disease, 502503
Ulocladium atrum, 785786
Unkanodes albifascia, 94, 938
Unkanodes sapporonus
barley, 94
maize, 328329
rice, 506, 510
sorghum, 613
wheat, 937938
Uredo glumarum, 548
Uredo nicotianae, 834
Urocystis agropyri, 888889
Urocystis brassicae, 122
Urocystis occulata, 545
Uromyces appendiculatus, 156157
Uromyces betae, 699
Uromyces junci, 797
Uromyces striatus, 2223
Uromyces trifoliirepentis, 459
Urophlyctis alfalfae, 1011
Urohlyctis trifolii, 456
Urophylyctis leproides, 699
Ustilaginoidea virens
maize, 272273
rice, 489490
Ustilago avenae, 380381
Ustilago crameri, 354
Ustilago eleusinis, 358359
Ustilago esculenta, 962963
Ustilago hordei, 5455
Ustilago nigra, 5859
Ustilago nuda, 59, 65
Ustilago reiliana, 284285
Ustilago scitaminea, 746748
Ustilago segetum, 373
Ustilago trichophora, 352353
Ustilago tritici
rye, 537538
wheat, 897898
Ustilago zeae, 262264
Veinal mosaic virus, 223224
Vein enation, maize, 330
Veneer blotch, sugarcane, 768769
Verticillium alboatrum
alfalfa, 2931
sugar beet, 715
sunflower, 802
tobacco, 837838

Page 1018
Verticillium dahliae
barley, 80
cotton, 212214
peanut, 429
safflower, 567, 568
sunflower, 802
tobacco, 837838
Verticillium nigrescens, 667
Verticillium wilt
alfalfa, 2931
canola, 123
cotton, 212214
peanut, 429
safflower, 568569
soybean, 667668
sugar beet, 715
sunflower, 802
tobacco, 837838
Victoria blight, oat, 387388
Violet root rot
alfalfa, 31
red clover, 465
sugar beet, 715716
Viral diseases. See also specific viruses
barley, 8596
buckwheat, 104105
canola, 126128
cotton, 219224
crambe, 231232
flax, 244245
maize, 312331
millet, 363365
oat, 393400
peanut, 436446
red clover, 469472
rye, 553556
safflower, 570572
sorghum, 608616
soybean, 674683
sugar beet, 721732
sugarcane, 73778
sunflower, 806
tobacco, 846860
wheat, 927945
wild rice, 966
Viroids, 846, 927
Viruela, 411412, 414415
Virus producing mild mottle, 442443
Vomitoxin
maize, 280
rye, 533
soybean, 639
wheat, 891892
Waika disease, 514515
Waitea circinata, 295
Wallemia sebi, 123
Water mold disease, 500
Weak neck, sorghum, 616
Web blight
alfalfa, 1920
Web blotch, peanut, 430
Western corn rootworm (Diabrotica virgifera), 274, 318
Western flower thrips (Frankliniella occidentalis), 785
Wet foot disease, 1819
Wheat (Triticum aestivum), 865946
aster yellows, 926
basal glume rot, 868
black chaff, 868870
leaf blight, 865866
leaf streak, 866867
mosaic, 867
pink seed, 870
sheath rot, 868
spike blight, 870871
stem melanosis, 871
wheat leaf blight, 871872
white blotch, 872
anthracnose, 873
Aureobasidium decay, 874
black head mold, 874
black point, 874875
blast, 920
brown root rot, 875
bunt, common, 878879
bunt, dwarf, 884885
bunt, karnal, 893894
Ceratobasidium gramineum snow mold, 877
cottony snow mold, 881
crater disease, 881882
Dilophospora leaf spot, 882883
dry seed decay, 884
dwarf bunt, 884885
Epicoccum glume blotch, 885886
ergot, 886887
eyespot, 887888
flag smut, 888889
Fusarium glume spot, 889
Fusarium leaf blight, 892
Fusarium rot, 892893
Fusarium sporotrichioides disease, 883
halo spot, 893
karnal bunt, 893894
leaf rust, 895896
leaf spot, 896897

Page 1019
loose smut, 897898
Microscopica leaf spot, 898
patchy stunting, 898
Phialophora takeall, 898
Phoma spot, 899
pink smudge, 903
Platyspora leaf spot, 900
prematurity blight, 901902
red smudge, 903
Rhizoctonia bare patch, 903905
rust, stem, 912914
rust, stripe, 914915
Sclerotinia snow mold, 906
sharp eyespot, 908
snow rot, 908909
spot blotch, 910
Stagnospora blotch, 911912
stem rust, 912914
stripe rust, 914915
takeall, 915917
tan spot, 917919
tar spot, 919
Typhulalike snow mold, 919920
zoosporic root rot, 920921
bulb and stem, 921
cereal cyst, 921922
Columbia root knot, 922
dagger, 922
grass cyst, 922923
lesion, 923
ring, 923
root gall, 924
root knot, 924
seed gall, 924925
spiral, 925
stubby root, 925
stunt, 926
physiologic leaf spot, 945946
seedborne wheat yellows viroid, 927
agryopyron mosaic, 927928
Australian wheat streak mosaic, 928929
barley stripe mosaic, 929
barley yellow streak mosaic, 930
barley yellow striate mosaic, 931
barley yellow stripe, 931
brome mosaic, 931
cereal tillering, 932
cocksfoot mottle, 932
eastern wheat striate, 933
enanismo, 933
European wheat striate, 933934
flame chlorosis, 934
high plains disease, 934
Indian peanut clump, 935
maize streak, 935
maize white line mosaic, 935936
mal de Rio Cuarto, 936
orchardgrass mosaic, 937
rice hoja blanca, 938
tobacco mosaic, 939
wheat chlorotic streak, 939
wheat dwarf, 939940
wheat mosaic streak, 939
\wheat rosette stunt, 940
wheat soilborne mosaic, 940941
wheat spindle streak mosaic, 941942
wheat spot mosaic, 943, 946
wheat yellow leaf, 945
wheat yellow mosaic, 945
Wheat chlorotic streak virus, 939
Wheat curl mite (Aceria tosichella), 91, 315, 365, 399, 615, 934, 943944
Wheat cuff mite (Aceria tulipae), 95, 330331, 555, 943944, 946
Wheat curl mite (Eriophyes tulipae), 943
Wheat dwarf disease, barley, 95
Wheat dwarf virus, 939940
Wheat leaf blight, 871872
Wheat mosaic streak virus, 939
Wheat rosette stunt virus, 940
Wheat soilborne mosaic virus
rye, 554555
wheat, 940941
Wheat spindle streak mosaic virus, 941942
Wheat spot mosaic virus, 330
Wheat streak mosaic virus
barley, 9596
maize, 331
millet, 365
oat, 399400
rye, 55566
sorghum, 615
wheat, 943944
wild rice, 966
Wheat striate mosaic, 933934

Page 1020
Wheat yellow leaf virus
barley, 96
wheat, 945
Wheat yellow mosaic virus, 945
Whetzelinia sclerotiorum, 658
White blast, maize, 287289
White blight, canola, 123
White blister, sunflower, 802803
White blotch, wheat, 872
White border, maize, 259
White ear rot, 266267
Whitefly (Bemisia tabaci)
bean, common, 166, 168
cotton, 219222
peanut, 436
soybean, 677678, 680
sugar beet, 730
tobacco, 849850, 853
Whitefly (Trialeurodes vaporariorum), 724
White head
barley, 7980
oat, 387
White leaf, sugarcane, 772773
White leaf spot
bean, common, 160
canola, 120121, 123
White leaf streak, rice, 500
White mold
peanut, 428429
White rash, sugarcane, 769
White rot
barley, 74
wheat, 909
White rust
canola, 116, 123
sunflower, 802803
White stalk, rice, 482483
White star, oat, 400
White tip, rice, 503
Wildfire
bean, 134
soybean, 627628
tobacco, 817818
Wild rice (Zizania palustris), 959966
brown spot, 959
leaf spot, 959
anthracnose, 960
brown spot, fungal, 960961
ergot, 960
Phytophthora crown and root rot, 962
smut, 962963
smut, stem, 964965
spot blotch, 963
stem rot, 963964
zonate eyespot, 965
vital disease, 966
Wilt. See Wilt, bacterial; specific crop or disease
Wilt, bacterial
alfalfa, 45
bean, 134
canola, 108
maize, 249250, 252253
peanut, 403404
soybean
Curtobacterium, 626
Pseudomonas, 626
sunflower, 784
Winter crown rot
alfalfa, 3132
red clover, 465
rye, 528
Winter decline syndrome, canola, 124125
Winter wheat mosaic virus
barley, 94
wheat, 938
Wirestem, canola, 125
Wireworm (Agriotes mancus), 252
Wirrega blotch, barley, 8081
Wisconsin bacterial leaf spot, tobacco, 818819
Witches' broom
alfalfa, 3637
bean, common, 166
cotton, 198199, 207
peanut, 435
red clover, 468
soybean, 674
sugar beet, 720
Woolly bears (Apantesis blakei), 30
Wound tumor, tobacco, 860
Wound tumor virus, 860
Xanthomonas albilineans, 739740
Xanthomonas beticola, 695
Xanthomonas campestris
alfalfa, 34
bean, 135137
canola, 107, 109
cotton, 183184
crambe, 229
maize, 248
millet, 343344
oat, 370371
rye, 523524
sorghum, 576
soybean, 623
sugarcane, 738739
wheat, 866, 869870
wild rice, 959
Xanthomonas oryzae, 475477, 478
Xanthomonas translucens, 4546

Page 1021
Xiphenema coxi, 931
Xiphinema americanum
alfalfa, 34
bean, common, 162
cotton, 214
maize, 307
millet, 361
oat, 388389
peanut, 432
red clover, 466
sorghum, 605
soybean, 675, 681
sunflower, 803
tobacco, 852, 840, 855
wheat, 922
Xiphinema coxi, 313, 609
Xiphinema diversicaudatum, 313, 432
Xiphinema mediterraneum, 307
Xiphinema paraelongatum, 609
Xylaria sp., 10
Xylella fastidiosa, 6
Yaikaho, 508509
Yeast infection of seed, canola, 125
Yeast spot, soybean, 668
Yellow dwarf
rice, 504
tobacco, 845846
Yellow dwarf virus, barley, 8788
Yellow edge, red clover, 469
Yellow leaf blight, maize, 304305
Yellow leaf blotch
alfalfa, 3233
maize, 253
millet, 345
sorghum, 575578
Yellow leaf disease, sugarcane, 778
Yellow leaf spot, barley, 81
Yellow leaf spot mosaic, sunflower, 806
Yellow mold, peanut, 430431
Yellow net virus, 727728
Yellow rust
barley, 79
sunflower, 803
wheat, 914915
Yellows
canola, 117118, 128
sugar beet, 732
Yellow sorghum stunt, 608
Yellow spot, sugarcane, 770
Yellow wilt
rice, 488489
sugar beet, 720721
Zea mays. See Maize (Zea mays)
Zearalenone, 60, 280, 639, 706
Zizania palustris. See Wild rice (Zizania palustris)
Zonate eyespot. See also Eyespot
millet, 351
wild rice, 965
Zonate leaf spot
maize, 305
millet, 360361
peanut, 431
red clover, 464465
sorghum, 604
sugarcane, 770771
Zoosporic root rot, wheat, 920921

Field Crop Diseases

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Field Crop Diseases

Uploaded by

Copyright:

Available Formats

Page iii

You might also like