Compendium of Potato Diseases - (PDF, 101 mb) - USAID

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The Disease Compendia Series 

by The American Phytopathological Society 

Soybean Diseases, 1975 

Wheat Diseases, 1977 

Alfalfa Diseases, 1979 

Corn Diseases, 1980 

Cotton Diseases, 1981 

Potato Diseases, 1981 

Elm Diseases, 1981

Compendium of Potato Diseases 

W. J. Hooker, Editor 

Published by the American Phytopathological Society 

In cooperation with: 

The Potato Association of America 

The International Potato Center, Lima, Peru 

Department of Botany and Plant Pathology, Michigan State University 

Michigan State Foundation

Covers: Plants of the indigenous South American triploid cultivar Huayro (Solanum X chaucha, 2n = 3x = 36), in flower. 

W. J. Hooker 

All rights reserved. No part of this book may be reproduced in any form by photocopy, microfilm, 

retrieval system, or any other means, without written permission from the publishers. 

Copyright 1981, by 

The American Phytopathological Society 

ISBN: 0-89054-027-6 

Library of Congress Catalog Card Number: 80-85459 

The American Phytopathological Society 

3340 Pilot Knob Road, St. Paul, Minnesota 55121 

Printed in the United States of America 

ii

In memory ofimy respected colleague 

Joseph E. Huguelet 

1931-1977 

,.Ii

Preface 

This compendium, a compilation of information describing persons and organizations 

diseases 

has permitted 

and disorders 

inclusion 

of 


the 

pertinent 

potato, is intended to be applicable colored plates. 

throughout the world, including the tropics. 

For sorme time a need has existed 

The 

for 

continual 

a source of 

eizcouragement 

information and 

Associaticn 

cooperation 

of America 

of the 

and 

Potato 

concerning 

its members 

potato 

have been 

diseases 

most 

and 

grati 

production problems associated fying, encouraging, 

with disease 

and constructive. 

prevention. Because diseases frequently limit Without assistance 

successful 

from 

production, 

Michigan 

and 

State 

production 

University 

is an 

(MSU), 

expensive venture, 

concise, 

the International 

up-to-date 


informaticn 

Center, 

is 

and 

required. 

the Michigan Foundation, 

this work could not 

Accounts 

have been 


completed. 

diseases were 

All 

prepared 

have provided 

by individuals chosen for grants to enable manuscript 

theirexperience 

preparation. 

and knowledge 

The International 

of the subject. Literature on the Potato 

important 

Center 

diseases 

and 

is 

MSU 

extens;ve, 

have also 

and 

provided 

thorough 

re~earch 

understanding 

facilities. 

of Cooperaiion and professional 

a single major 

capabilities 

disease has 


involved 

library 

many 

staff 

investigations. Refer- and personnel of the Graphic Arts Center 

ences were 

(MSU) 

selected 

is greatly 

to provide recent information and access to 

previously 

appreciated. 

published literature. The continued 

The compendium 

enthusiastic cooperation 

results from 


the 

Dr. 

combined 

Teresa lcochea 

efforts of many in critically 

individuals 

reviewing 

and several 

this manuscript 

organizations. 

is sincerely 

Members 

appreciated. 

of the advisory The stenographic expertise, 

committee 

attention 

provided 

to 

guidance 

detail, and patience 

in coordination and initial of Suzanne J. Weise, Monica 

planning 

Stenning, 

as 

and 

well 

Elaine 

as in 

Creech 

critical 

in 

and constructive manuscript manuscript 

review. Many 

preparation 

others have 

have 

generously 

been invaluable. 

given their time in review To Frances, my 

of parts 

wife, 


for 

the 

her 

manuscript. 

patience, encouragement, and 

willingness to forego other interests 

Qualified 

so !hat 

persons 

this compendium 

prepared descriptions of individual might be completed, I am grateful. 

diseases. These and other persons and certain organizations 

have graciously loaned photographs. Financial assistance from 

W. J. Hooker 

DISCLAIMER 

Products and practices included in the control paragraph effectiveness of chemicals nor forauthorizing or recommending 

cf each disease are those reported to be effective. Permitted use use of chemicals or other preventive measures mentioned in this 

of c'icmicals varies among the nations producing and publication. Recommendatiotis for chemical selection, dosage, 

consuming potatoes. The international nature of this and method and time of application should be made only by 

public,;tion precludes limiting preventive measures to those authorized and informed personnel of the responsible 

accepted by particulargovermmental control agencies. Authors, governmental agency where potatoes are grown or marketed, 

sponsors. and organizations under whose auspices the and these instructions should be rigidly followed. 

compendium was prepared assume no responsibility for 

v

Acknowledgments 

Planning Committee 

W. J. Hooker, Coordinator, Michigan State University. East Lansing. 

Present address: International Potato Center, Lima, Peru 

Edward R. French, International Potato Center, Lima, Peru 

Robert W. Goth, USDA Plant Genetics and Germplasm Institute, 

Beltsville, MD 

Monty D. Harrison, Colorado State University, Fort Collins 

*J. E. Huguelet, North Dakota State University, Fargo 

Arthur Kelman, University of Wisconsin, Madison 

W. F. Mai, Cornell University. Ithaca, NY 

Frank Manzer, University of Maine, Orono 

James Munro, 561 Dickinson Ave., Ottawa, Ontario. Canada 

L. W. Nielsen, North Carolina State University, Raleigh 

Dick Peters, Agricultural University, Wageningen, The Netherlands 

*Otto E. Schultz. Cornell University. Ithaca, NY 

N. S. Wright, Canada Department of Agriculture Research Station, 

Vancouser. B.C. 

*Deceased 

Contributors of Manuscripts or Photographs 

Agrios, G. N., University of Massachusetts, Amherst 

ASARCO Inc., Department of Environmental Sciences, Salt Lake 

City, UT 

Bagnall, R. H., Agriculture Canada Research Station, Fredericton, 

N.1B. 

Beems'er, Wageningen, A. The B. R., Netherlands Research Institute for Plant Protection, 

Bennett, C. W., USDA, Salinas, CA 

Berger, K. C., Berger and Associates, Hartland, W! 

Bhattacharyya, S. K., Central Potato Research Institute, Simla 

(H.P.) IndSia 

Boawn, L. C., Washington State University, Pullman 

Booth, R., International Potato Center, Lima, Peru 

Boyle, J. S., Pennsylvania State University, University Park 

Brodie, B. B., Cornell University, Ithaca, NY 

Bryan, J., International Potato Center, Lima, Peru 

Burton, W. G., East Mailing Research Station, Maidstone, Kent, 

England 

Busch, L. V., University of Guelph, Guelph, Ont., Canada 

Butionitch, I. P.. lnstitiito Nacional de Technologia Agropecuaria, 

Balcarce, Argentina 

Caldcroni. A. V.. Instituto Nacional de Technologia Agropecuaria, 

Balcarce. Argentia 

Costa, A. S., rnstituto Agronomico de Estaoo de Sao Paulo, Sao 

Paulo, Brazil 

aln,, iter 

Darling, H., University of Wisconsin, Madison 

de Abad, G.., Internatir Il Potato Center. I.ima, Peru 

de Bx, G., Reerhnsti t PotaaCent or Proetim, Wa 

de Bokx, 

, 

J. A.. Research Instit; te for Plant Protection, Wageningen, 

The Netherlands 

de Icochea, T. A.. Universidad Nacional Agraria, Lima, Peru 

de Zoeten, G.. University of Wisconsin, Madison 

Dwivedi, R., Central Potato Research Institute, Simla (H.P.) India 

Dyson, P. W., Macaulay Institute of Soil Research, Craigiebuckler, 

Aberdeen, Scotlar.d 

Easton, G. D., Irrigated Agriculture Research and Extension Center, 

Prosser, WA 

Ellis, M. B., Commonwealth Mycological Institute, Kew, Surrey, 

England 

vii 

Ewing, E.E., Cornell University, Ithaca, NY 

Fernow, K. H., 1228 Ellis Hollow Road, Ithaca, NY 

Frank, J. A., Pennsylvania State University, University Park 

French, E. R., International Potato Center, Lima, Peru 

Frey, F., International Potato Center, Lima, Peru 

Fribourg, C. E., Universidad Nacional Agraria, Lima, Peru 

Gausman, H. W., U.S. Fruit and Vegetable Soil and Water Research, 

Weslaco, TX 

Genereux, H., Ministere de l'Agriculture de Canada, Sainte-Anne-dela-Pocatiere, 

Quebec, Canada 

Goth, R. W., USDA Plant Genetics and Germplasm Institute, 

Beltsville, MD 

Hampson, M. C., Agriculture Canada Research Station, St. John's, 

Newfoundland 

Harrison, B. 3., Scottish Horticultural Research Institute, 

Invergowrie, Dundee, Scotland 

Harrison, M. B., Cornell Nematology Laboratory, Farmingdale, NY 

Harrison, M. D., Colorado State University, Fort Collins 

Hide, G. A., Rothamsted Experiment Station, Harpenden, Herts, 

England 

Hiruki, C., University of Alberta, Edmonton 

Hooker, W. J., Michigan State University, E.Lansing 

Huguelet, J. E., North Dakota State University, Fargo 

Huttinga, H., Research Institute for Plant Protection, Wageningen, 

The Netherlands 

Interndtional Minerals and Chemical Corp., Libertyville, IL 

Iritani, W. M., Washington State University, Pullman 

Jatala, Jones, E. P., D., International Cornell University, Potato Center, Ithaca, Lima, NY Peru 

Jones, R. A. C., Internationa! Potato Center, Lima, Peru 

Keller, E. R., Institut fir Pflanzenbau der Eidgen6ssischen 

Technischen Hochschule, Z~irich, Switzerland 

Kelman, A., University of Wisconsin, Madison 

Kitajima, E. W., Instituto Agronomico de Estado de Sao Paulo, Sao 

Paulo, Brazil 

Larson, R. H., University of Wisconsin, Madison 

Laughlin, W. M., USDA, Palmer, AK 

Lawrence, C. H., Agriculture Canada Research Station, Fredericton, 

N.B. 

Leggett, S. E., Utah State University, Logan 

Lennard, J. H., Edinburgh School of Agriculture, Edinburgh, 

Scotland 

Letal, J. R., Regional Crops Laboratory, Olds, Alberta, Canada 

Logan, C., Department of Agriculture, Belfast, N. Ireland 

MacGillivray, M. E., Agriculture Canada Research Station, 

Fredericton, N.B. 

Mai, W. F., Cornell University, Ithaca, NY 

Manzer, F. E., University of Maine, Orono 

Martin, C., International Potato Center, Lima, Peru 

McIntyre, G. A., Colorado State University, Ft. Collins 

Kenzie, A. R., Agriculture Canada Research Station, Fredericton, 

N. B. 

n . , 

Munro. J., 561 ldickinson Ave.. Ottawa, Ontario, Canada 

Nelson. E., Colorado State University, Ft. Collins 

Nelson, P. E., Pennsylvania State University, University Park 

Nielsen, L..W., North Carolina State University, Raleigh 

Page, 0. T., International Potato Center. Lima, Peru 

Peters, D., Agricultural University, Wageningen, The Netherlands 

Raine. J., Canada Department of Agriculture, Research Station, 

Vancouver, B.C. 

Rich, A. E., University of New Hampshire, Durham

Rowe, R. C., Ohio Agricultural Research and Development Center, 

Wooster 

Salazar, L. F.,International Potato Center, L.ima, Peru 

Salzmann, R., Eidgcn6ssiechen Forschungsanstalt fUr landwirtschaftlichen 

Pflanzenbau, Ziirich-Reckenholz, Switzerland 

Schultz, 0. E., Cornell University, Ithaca, NY 

Sinden, S. .. , USDA Plant Genetics and Germplasin Institute, Beltsville, 

MD 

Singh. R. P.,Agriculture Canada Research Station. Fredericton, N.B. 

Slack. S. A., University of Wisconsin. Madison 

Sparks. W. C., Universitv of IJaho. Aberdeen 

Stace-Snith, R.. Agriculture Canada Research Station, Vancouver, B.C. 

Thurston, If. D., Cornell University, Ithaca, NY 

Torres, It., International Potato Center, lima, Peru 

Turkensteen, I...I., International Potato Center, Lima, Peru 

Ulrich, A.. University of California. Berkeley 

Untiveros, D., International Potato Center. Lima, Peru 

Valenta, V.. Slovak Academy of Sciences. Bratislava, Czechoslovakia 

Weingartner, D., University of Florida, Hastings 

Wright. N. S.. Agriculture Canada Research Station, Vancouver, B.C. 

Zachmann, R.. International Potato Center, lima, Peru 

Financial Sponsors 

Agan's Aviation, Inc.. Munger. MI 

American Hoechst Corp., Somerville, NJ 

BASF Aktiengese!lschaft, Ludwigshafen, Rhein, Germany 

British Columbia Coast Vegetable Co-operative Assoc., Richmond, 

B.C., Canada 

Blue Mountain Potato Growers Assoc., Hermiston, OR 

Brown, Miles, Elmira. MI 

Chevron Chemical Co., Ortho )ivision. San Francisco, CA 

Christensen, Ferris If., Edmore, MI 

CIBA-Geigy Corp., Greensboro, NC 

Diamond Shamrock Corp.. Cleveland. OHt 

E. I. du Pont de Nemours and Co., Wilmington, DE 

viii 

FMC Corp., Agricultural Chemical Group, Philadelphia, PA 

Fridell, E. W.. Plant Quarantine Division. Barrie, Ont., Canada 

Game;' Produce Co., Hereford, TX 

Great Lakes Chemical Corp., West lafayette, IN 

Greenberg Farms, Art. Grand Forks, NI) 

Growers Service Corp., lansing, MI 

Imperial Chemicals Industries United States, Inc., Wilmington, DE 

Idaho Crop Improvement Asvoc., Boise, ID 

Krueger. Paul, Jr.. Potato Seed. Hawks, MI 

Lamb-Weston, )ivision of AMFAC Foods, Inc., Portland, OR 

I.ennard, Wayne J., & Sons, Inc., Samaria, MI 

Malheur County Potato Growers Assoc., Ontario, OR 

Merck and Co., Inc., Agricultural Chemicals Development, Rahway, 

NJ 

Merck Sharp and Dohme International, Rahway, NJ 

Michigan Crop Improvement Assoc., l.ansing 

Michigan Potato Industry Commission, Lansing 

Mobay Chemical Corp., Chemagro Division, Kansas City, MO 

Montcalm County Board of Commissioners, Stanton, MI 

New York Seed Improvement Cooperatise. Inc.. Ithaca 

North Dakota Certified Seed Potato Growers Assoc., Inc., Fargo 

North Dakota State Seed Department. Fargo 

Olin Agricultural Products I)epartmcnt, Little Rock, AR 

Oregon Potato Commission, Salem 

Ore-Ida Foods, Inc.. Boise, I) 

Perham Ptato Farm, Fergus Falls, MN 

Richardson. Tuck, Lakeland Farm, Gilbert, MN 

Rohm and Haas Co., Philadelphia. PA 

Sackett Ranch, Stanton, MI 

Schalk, Allen and Paul, Rogers City, MI 

Schering AG,D-i000 Berlin 65. Germany 

Snake River Chemicals. Inc.. Caldwell, I) 

Stauffer Chemical Co.. Mountain View, CA 

Thompson-IHayward Chemical Co.. Kansas City, KS 

Union Carbide Corp.. Agricultural Products Division, Salinas, CA 

Velsicol Chemical Corp.. Chicago, I1 

Wisconsin Seed Improvement Assoc., Madison

Introduction 

1 Potato Disease 

1 The Potato 

1 Importance 

2 Cultivated Types 

2 The Plant 

5 Oxygen-Temperature Relationships 

Part I. Disease in the Absence 

of Infectious Pathogens 

7 Genetic Abnormalities 

8 Adverse Environment 

8 Oxygen Deficit 

8 Low Temperature Tuber Injury 

9 Low Temperature Foliage Injury 

10 Blackheart 

10 High Temperature Field Injury 

11 Internal Heat Necrosis 

12 Second Growth and Jelly End Rot 

13 Hollow Heart 

14 Surface Abrasions 

15 Blackspot 

16 Tuber Greening and Sunscald 

17 Internal Sprouting 

17 Secondary Tubers 

17 Coiled Sprout 

18 Hair Sprout 

18 Nonvirus Leafroll 

19 Hail Injury 

19 Wind Injury 

19 Lightning Injury 

20 Air Pollution: Photochemical Oxidants 

21 Air Pollution: Sulfur Oxides 

21 Chemical Injury 

22 Stem-End Browning 

22 Nutrient Imbalance 

22 Nitrogen 

23 Phosphorus 

23 Potassium 

23 Calcium 

24 Magnesium 

24 Sulfur 

24 Aluminum 

24 Boron 

25 Zinc 

26 Manganese 

Part II.Disease in the Presence 


27 

27 

29 

Bacteria 

Blackleg, Bacterial Soft Rot 

Brown Rot 

Contents 

ix 

31 Ring Rot 

32 Pink Eye 

33 Bacteria in Potatoes that Appear Healthy 

33 Common Scab 

35 Funq; 

35 36 

37 

Wart Powdery Scab 

Skin Spot 

38 Leak 

39 Pink Rct 

40 Late Blight 

42 

43 

Powdery Mildew 

Early Blight 

44 Alternaria alternata 

46 Pleospora herbarum 

46 Ulocladium Blight 

46 Stemphylium consortiale 

46 Septoria Leaf Spot 

47 Cercospora Leaf Blotches 

47 Phoma Leaf Spot 

48 Choanephora Blight 

48 Gray Mold 

48 White mold 

50 Stem Rot 

51 Rosellinia Black Rot 

52 Rhizopus Soft Rot 

52 Rhizoctonia Canker (Black Scurf) 

54 Violet Root Rot 

54 Silver Scurf 

55 Black Dot 

56 Charcoal Rot 

57 Gangrene 

58 Fusarium Dry Rots 

60 Fusarium Wilts 

62 Verticillium Wilt 

63 Thecaphora Smut 

65 Common Rust 

65 Deforming Rust 

66 Miscellaneous Diseases 

66 Mycorrhizal Fungi 

66 Principles of Foliage Fungicide Application 

67 Tuber Seed Treatment 

68 Viruses 

68 Potato Leafroll Virus 

70 Potato Virus Y 

71 Potato Virus A 

72 Potato Viru:; X 

74 Potato VirusM 

75 Potato Virus S 

77 

77 

78 

79 

79 

79 

Potato Virus T 

Andean 

Andean 

Potato Mottle Virus 

Potato Latent Virus 

Cucumber Mosaic Virus 

Tobacco Mosaic Virus 

Potato Mop-Top Virus

80 Tobacco Rattle Virus 93 Nematodes 

82 Potato Yellow Dwarf Virus 94 Potato Cyst Nematodes 

82 Alfalfa Mosaic Virus 97 Root-Knot Nematodes 

84 Potato Aucuba Mosaic Virus 98 False Root-Knot Nematodes 

84 Tobacco Ringspot Virus 99 Lesion Nematodes 

85 Tomato Black Ring Virus 100 Potato Rot Nematodes 

86 Potato Yellow Vein Virus 101 Stubby-Root Nematodes 

86 Tobacco Necrosis Virus 101 Nematicides 

87 Deforming Mosaic 101 Aphids 

87 Tomato Spotted Wilt Virus 103 Seed Potato Certification 

89 Potato Spindle Tuber Viroid 

90 Sugar Beet Curly Top Virus 

91 Mycoplasmas 107 Key to Disease 

92 Aster Yellows and Stolbur 111 Equivalent Names of Potato Diseases 

92 Witches' Broom Color Plates (following page 54) 

93 Insect Toxins 117 Glossary 

93 Psyllid Yellows 123 Index 

X

A potato disease is an interaction between a host (the potato) 

and a pathogen (bacterium, fungus, virus, mycoplasma, 

nematode, or adverse environment) that impairs productivity or 

usefulness of the crop. Frequently, adverse environmental 

effects are sufficient to initiate disease in the absence of an 

infectious entity. The host-pathogen interaction is influenced by 

environment acting on either the potato or the pathogen or on 

both and is determined by the genetic capabilities of I) the 

potato in being either susceptible or resistant and 2) the 

pathogen in being pathogenic (virulent) or nonpathogenic 

(avirulent). 

Furthermore, disease or adverse environment in one portion 

of the potato life cycle may severely limit effectiveness of 

production or quality at a later date. For example, field 

problems frequently become storage problems, which may later 

performance and, ultimately, 

h 

yielding ability. 

The value of any crop determines the extent to which control 

measures may be justified. Relatively speaking, the potato is a 

high-value crop with complex production, storage, and 

utili7ation problems, and therufore relatively elaborate 

prevention practices are appropriate. Correct diarnosis and 

identification of disease is of paramount :mntortance for initiation 

of appropriate control and prevention measures. 

General References 

BLODGETT, E. C., and A. E.RICH. 1949. Potato tube," diseases, 

Importance 

The potato is the most important dicotyledonous source of 

human food. It ranks as the fifth major food crop of the world, 

exceeded only by the grasses-wheat, rice, maize (corn), and 

barley. In North America, dry matter production of potatoes 

per unit ofland Lrea exceeds that ofwheat, barley, andmaizeby 

factors of 3.04, 2.68, and 1.12, respectively. Yields of protein per 

unit of land area exceed those of wheat, rice, and maize by 

factors of 2.02, 1.33, and 1.20, respectively. 

Pecause of increasing yields per unit area of land, total potato 

production has been increasing even though the area of land 

planted to potatoes isdecreasing. Yields in northern Europe and 

North America (1970-1973) generally ranged from 20 to over 

35 metric ton/ha (178-311 cwt/A) and were somewhat lower in 

the war mer areas of Europe. The percentage of arable land in 

potato production ranges from less than 1%in Canada and the 

Introduction 

Potato Disease 

defects, and insect injuries in the Facific Northwest. Wash. Agric. 

Exp. Stn. Pop. Bull. No. 195. 116 pp. 

CALDERONI, A. V. 1978. Enfermedades de lapapa y su control. 

Editorial Hemesferia Sur S. A., Buenos Aires. 143 pp. 

FRENCH, E. R., H. TORRES, T.A. de ICOCHEA, L. SALAZAR, 

C. FRIBOURG, E. N. FERNANDEZ, A. MARTINJ. FRANCO, 

M. M. de SCURRAH], 1.A. HERRERA, C. VISE, L. LAZO, and 

O.A. HIDALGO. 1972. Enfermedade.; de laPapa en el Peri6. Bol. 

Tecn. No. 77 Est. Exp. Agric. La Molina. 36 pp. 

HODGSON, W. A., D. D. PONDandJ. MUNRO. 1974. Diseasesand 

pests of potatoes. Canada Dept. Agric. Publ. 1492. 69 pp. 

KEI.L.ER. E. R., and A. ZAII. 1969. l)ictionarv of Iechnical Terms 

Relating to the Potato (in English. (erman. and French). Fur. 

Assoc. Iot. RCS..luris-I)ruck. Zurich. III pp. 

McKAY, R. 1955. Potato Diseases. Irish Potato Marketing Co., Ltd., 

Dublin. 126 pp. 

O'BRIEN, M.J.,and A. E. RICH. 1976. Potato Diseases. U.S. Dept. 

Agric., Agric. Res. Serv., Agriculture Handbook No. 474. 79 pp. 

SALZMANN, R.. and E. R. KEI.LER. 1969. Krankheiten und 

Schadlinge der Kartoffel. Verbandsdruckerei. AG, Bern. 150 pp. 

SCHICK, R., and M. KLINKOWSKI. 1961. Die Kartoffcl, ein Handbuch. 

Vol. I. 1,007 pp.; Vol. 11,2,112 pp. Veb Deutscher Landwirtschaftsverlag, 

Berlin. 

SMITH, W. L., Jr., and J. B. WILSON 1978. Market diseases of 

potatoes. U.S. Dept. Agric., Agric. Handbook No. 479. 99 pp. 

WHITEHEAD, W,.f. P. McINTOSH. and W. M. FINDLAY. 1953. 

The potato inhealth and disease, 3rd ed. Oliver and Boyd, London. 

774 pp. 

The Potato 

(Prepared by W. J. Hooker) 

United States to 18% or more in the Netherlands and Poland. 

The USSR, China, and Poland lead in area of land in potato 

production. 

In the tropics (between 300 north and south latitudes) yields 

are below 13 ton/ha (116 cwt/A), more commonly below 10 

tons (89cwt/A), and the percentage ofarable land in potatoes is 

low except in Peru (13%). However, potato production is 

increasing as measured by land area in potato production, yield 

per hectare, and total production. 

Most potatoes are used for human consumption. In the 

tropics potatoes are often available only in certain seasons 

because of storage problems. Approximately 50% of Europran 

potato production is used as stock feed, with perhaps 25% of 

table stock potatoes being diverted to stock feee because of 

defects. 

The potato is characteristically a crop of the cool, temperate 

reg.ins or of elevations of approximately 2,000 m (6,560 ft) or 

1

more in the tropics. It requires cool nights and well drained soil 

with adequate moisture and does not produce well in low 

altitude, warm, tropical environments. Certain types of South 

American potato have considerable tolerance to warm temperatures 

and to temperatures a few degrees below freezing; clones 

tolerant to both extremes are being sought. 

The potato is a native of the Andean highlands of South 

America, where it has served as a staple of the diet of Andeans 

for centuries or millennia. Widely diverse types have been 

selected. Dehydrated tubers have been preserved since antiquity 

as chuho, a product of various types obtained by freezing 

tubers, pressing liquid from them after thawing, and then 

freezingand drying them. Today tubers are boiled and dried for 

preservation. 

The potato was introduced into Spain sometime before 1573, 

when it was first mentioned as a food source. Its use in England 

was first reported in herbals in 1596. From northern Europe it 

was first reported in herbals in 1596. From northern Europe 

it was returned to North America in 1719 and grown in the 

colonies. 

Cultivated Types 

Cultivated potatoes, consisting of a number of species or 

species hybrids, belong to the Solanaceae, section Tuberarium, 

which contains approximately 150 tuber-bearing species. In the 

Andean highlands, the distinction between cultivated and wild 

varieties has little relevance to indigenous populations, 

The most common potato is the tetraploid (2n :=4x = 48 

chromosomes), Solanum tu/'erosum I..which may he divided 

into the completely cross-fertile subgroups Tuberosum and 

Andigena or into subspecies tuerosut and adigena.Survival 

of these in the wild occurs only in excep'ional cases. Their 

survivai and extensive dispersal have resulted from human 

selection. Andigena is the most widely grown in South America. 

It has deep eyes, is often pigmented. and produces tubers in 

days of short length. The Tuberosum type grown in northern 

Europe and North America tends to need a long day for effective 

tuberization. These two types are not completely distinct, and 

obtaining the Tuberosum type by selection from Andigena is 

possible. 

Another classification also places certain diploids and 

triploids within S. tuherostim. Diploid cultivated potatoes (2n = 

2x = 24) belong to two main groups, S. stenotomln, with a 

period of tuber dormancy, and S. phure/a, without a welldefined 

dormant period. S. stenotonmn is regarded as the 

ancestral type, giving rise to Andigena types through 

chromosome doubling. 

Cultivated triploids (2n = 3x = 36) in group S. X chaucha are 

possibly naturally occurring hybrids from crosses between 

Andigena and Stenotomum or Phureja. Another triploid 

species, S. X.juzepczukii, is highly frost tolerant and may have 

originated from natural hybridization between the wild species 

S. acaule (a tetraploid) and the diploid S. stenotomtm. 

A pentaploid, S. X curtilobun (2n = 5x = 60), believed to 

have originated from natural hybridization of S. acaule and S. 

and, gena, is grown in the high Andes because of its frost 

tolerance. It is bitter tasting but useful for making chuio. 

The hexaploid S. demisstm (2n = 6x = 72) has been used as a 

source for cultivars resistant to late blight, 

Perpetuation ofthe many geneticdifferences is attributable to 

asexual propagation through tubers. Variability existing within 

the potato groups is believed to have originated through: I) 

hybridization between diverse types, 2) chromosome doubling, 

3) mutations in germ plasm, and 4) nitatiori in vegetative 

tissue and perpetuation as chimaeras. Vegetatively propagated 

clone lines, assumed to be genetically stable, as are presently 

accepted cultivars, are capable of further variation and change 

through somatic mutation, 

The potato may be propagated from true seed, which is 

2 

common in genetic studies and in potato breeding programs. In 

certain parts of Ecuador and Colombia true seed is planted for 

commercial crop production. The Peoples Republic of China 

grows over 10,000 ha from true seed to avc,id virus spread and 

long distance transport of seed tubers. At the International 

Potato Center, transplants from true seed produce 

homogeneous families that yield an average of more than I kg 

per plant. These practices permit full use of tubers as food and 

avoid diseases carried through seed tubers. 

Commercial production of most potatoes is primarily through 

vegetative propagation by means of lateral buds formed on the 

tuber, a modified stem. Through such vegetative propagation, 

many diseases are transmitted from generation to generation. 

Although disease affects each of the types listed above, much 

of potato pathology has been done wth S. tuero.stim ssp. 

tuherostm in northern Europe and North America. Increased 

importance of the crop in the tropics and subtropics has 

occasioned unprecedented work during the past half century on 

tropical diseases and evaluation of wild and cultivated 

genotypes as sources of disease resistance. 

The Pjant 

The potato, S. tuberosun ssp. tuherosutn and ssp. andigena, 

is an annual, herbaceous dicotyledonous plant with potential 

perennial capacity because of reproduction through tubers. 

Flowers 

Flowers are five-parted of various colors with single style and 

stigma and two-loculed ovary. Pollen is typically windborne. 

Self-fertilization is natural; cross-fertilization is relatively rare, 

and when it occurs, insects are probably involved. Diploids are 

self-incompatible with very few exceptions. 

Fruits 

Fruits are round to oval (1-3 cm or more in diameter), green, 

yellowish green or brown, and red to violet when ripe. Fruits are 

two-celled, with up to 200-300seeds. Because of several sterility 

factors, seeds may be absent even though fruits are formed. 

Vegetative Structures 

Plants from true seed are typically seedling plants with 

primary tap root, hypocotyl, cotyledons, and epicotyl, from 

which a stem and foliage develop. In contrast, the commerical 

potato plant contains one or more lateral branches, each arising 

from a bud on the "seed tuher," and the roots are adventitious 

(Fig. I). The "seed" in commerical production is an asexual 

propagative organ and not comparable to the sexually derived 

true seed. 

Stems 

These are usually green, but can be red to purple, angular, and 

nonwoody. Late in the season the lower portions may be 

relatively woody, however. Leaves are pinnately compound, 

although early leaves of seedlings and the first leaves of plants 

grown from tubers may be simple. Leaf types differ widely 

among the many species and cultivars. Stomata are more 

numerous on the lower leaf surfaces, and hairs of various types 

are present on aboveground parts. Secondary branches are 

common, arising from axillary leaf buds. Leaves on the 

underground stem are small and scalelike, and stolons arise 

from these axillary buds. Stolons and tubers are modified 

adventitious stems. 

Roots and stolons develop from the underground stem 

between the seed tuber and the soil surface. Thus, the vegetative 

propagative unit (theseed tuber ora portion of it, theseed piece) 

should be planted sufficiently deep to permit adequate root and 

stolon formation.

Fig. 1.A, Lower portion of young potato plant showing: a, stem; b, stolons; c, roots; and d, seed tuber. B, Bud on stolon tip (bar represents 

100 ,m). C, Starch grains within cells of a potato tuber (bar represents 10pm), showing characteristic refraction patterns within the grain. 

Tubers 

The tuber (Fig. 2) is formed at the tip of the stolon (rhizome) 

as a lateral proliferation of storage tissue resulting from rapid 

cell division and enlargement. Enlargement approximates a 

64-fold cell volme increase. 

'Re stolon usually breaks offclose to the tuber during harvest 

or dies with the plant on maturity and is evident either as a short 

stub o r sm all scar .,E 

In stens, stolons, and tubers, vascular tissue initiallv forms as 

bikollateral bundles with groups of thin-walled phloem cells 

outside of'the xylem (outer phloem) and toward the center and 

inside the xyleml(inner phloem). As th' stolon enlarges to form 

the tuber. parenchyna developing within the bundles tends to 

split the separa it iroups. and the vascular ring becomes spread 

olt. New groups of phloem including sieve tubes, companion 

cells, and conducting parenchyma elements are formed as the 

tuber enlarges. Carbohydrates are stored within storage parenchyima 

ce',s of pith and cortex in the form of starch granules 

with characteristic markings. 

Tuber constitucnts vary with cultivar and growing conditions. 

E:stimated amounts of constituents may also reflect differences 

in methods ofchemical analysis. Ranges in the whole fresh tuber 

are: water, 63-87i: carbohydrates, 13-30("i (including a fiber 

content ofN. 17-3.48Ci ): protein, 0.7-4.61"; fat, 0.02-0.96(' ; and 

ash, 0.44-1.91". Additional constituents include sugars, notnstarchy 

polysaccharides, enzymes, ascorbic acid and other 

vitamins, phenolic substances, and nucleic acids, 

The tuber surface permits or excludes entrance of pathogens, 

regulates rate ofgas exchange or water loss, and protects against 

mechanical damage. The surface is not fixed and static but will 

maintain and regenerate itself through wound healing reactions 

which influence disease incidence and severity, preservation in 

storage, and seed germinability and performance, 

Tle epidermis exists for only a short time on tile youngest 

tubers of approximately I cm or less in diameter. Stomata are 

scattered ir the epidermis and permit gas exchange. A shortlived 

penuerm is derived from tile epidermis and is soon 

replaced by a more permanent periderm or cork layer arising 

from meristenatic cambium cells below the epidermis. This 

periderm in mature tubers is composed of 6-10 layers of bricklike, 

thin-wvalled cells, one on top of tie otiher, without 

intercellular spaces and with suberized cell walls. Periderm 

STEM ED J 

0 

\,\ 

. ". 

" APEX 

BUDEND 

NEEL E, ROSE END 

STOLO 

, 

R ID, ' A C A L U D 

ORSK-N ' OR'eye 

CORTEX' LATERAL UD 

VASCULAR RING LAOR EYE 

VASCULAR ITORASE BO OFEY 

ARENCHYA ! 

its Trts 

Fig. 2. The potato tuber and its parts. 

characteristics vary considerably with cultivar (Fig. 3). 

Wound healing (Fig. 3) develops under cut, bruised, or torn 

surfaces. Suberin forms within 3-5 days in walls of living cells 

under the wound. A cork cambium layer developing under the 

suberized cells gives rise to a wound periderm. The promptness 

with which wound healing develops is Jependent upon environment 

(temperature, humidity, and aeration) and the physiology 

of the tuber. 

Cut tuber surfaces exposed to dr. ing air may seem to have a 

tough, resistant covering. Drying kills living surface cells and 

interferes with normal wound-healing activity. Dried surfaces 

do not exclude pathogens nor prevent dehydration and should 

not be confused with wound healing. 

Rates of' wound healing, including both suberization and 

periderm development, increase approximately threefold 

between 5 and 10' C and again threefold between 10 and 200 C. 

Oxygen supply less than that of the atmosphere and carbon 

dioxide greater than that of tile atomosphere progressively 

inhibit wound healing. Wound healing is most rapid between 80 

and 100%rh: however, the presence of free water on the surface 

that excludes oxygen is detrimental. Wound healing is more 

rapid in stored, recently harvested tubers, and as the tubers age, 

ability to heal wounds gradually diminishes. Also, periderm 

development in the cortical areas is more rapid than in the 

medullary region. Irradiation by sunlight or by ionizinggamma 

3

- 

. .,Lenticels 

N", 

F r 

_. 

"break 

-.gas 

B. a r 

I Cbecomes 

rays impairs wound-healing processes. Certain pesticide 

chemicals on the cut tuber surface, such as some seed treatments, 

may impair the effectiveness of wound healing, 

certain 

whereas 

phenolic compounds enhance the wound-healing 

process and wound periderm formation. Under favorable environmental 

conditions, suberin is demonstrable within 24 hr 

S"and periderm within two to five days. Infection by some 

pathogens 

wound 

is greatly reduced by 

and 

the 

periderm 

rapid formation 

under 

ofsuberin 

wounds. 

-soils 

(Fig. 4) are formed under the stomata in the epidermis 

of stems as well as of tubers. A loose mass of thin-walled, 

relatively small, rounded cells initially forms under the periderm 

and eventually breaks through. Thus, the lenticel consists of a 

in the tuber surface underlaid 

walled 

with loosely 

cells. 

arranged, 

Lenticels 

thin 

(numbering l-/cm- of surface) permit 

exchange through the 

are 

relatively 

unfavorably 

impervious 

wet, 

periderm. 

lenticels 

When 

tubers become 

on 

enlarged 

underground 

(hypertrophied 

stems and 

or proliferated) and 

..." .. extrude beyond the surface as white tufts 

in 

approximately 

diameter. 

0.5 mm 

,- 'Lenticels provide infection sites for several pathogens, 

including those inciting bacterial soft rot and late blight. 

, - 

"-'''-' ""DEAN, 

Roots 

Plants from true seed produce a slender tap root that later 

fibrous. Plants grown from seed tubers have a fibrous 

system of lateral roots arising usually in groups of three at the 

nodes of the underground stem. Lateral roots originate in the 

pericycle regions of roots and in meristems of the subterranean 

stems close to the nodal piate. Cell divisinn in the pericycle gives 

rise to the root primordium, which pushes its way mechanically 

and possibly by enzymatic activity through the cortex. Sites of 

root emergence are essentially open wounds and provide 

infection courts for pathogens. 

Selected References 

ADAMS, M.J. 1975. Potato tuber lenticels: Susceptibility to infection 

by Erwinia carolooravar. airosepticaand Phvtophthorainfestans. 

Ann. AppI. Biol. 79:275-282. 

ARTSCHWAGER, E.1924. Studies on the potato tuber. J. Agric. Res. 

27:809-835. 

ARTSCHWAGER, E. 1927. Wound periderm formation in the potato 

as affected by temperature and humidity. J. Agric. Res. 

35:995-1000. 

BURTON, W. G. 1966. The Potato, 2nd ed. ff. Veenman and Zonen. 

Wageningen, B. B., P. Holland. E. KOLATITUKUDY, 382 pp. 

Chemical composition 

and R. W. DAVIS. 

and ultrastructure 

1977. 

of suberin from hollow 

heart tissue of potato tubers (Solanumn tuberosum). Plant Physiol. 

59:1008-1010. 

.DODDS, K. S. 1962. Classification of cultivated potatoes. Pages 517 

539 in: D. S. Correlled. The Potato and Its Wild Relatives. Section' 

Tuberarium of the Genus Solanum. Texas Res. Foundation, 

Renner, TX. 606 pp. 

HARRIS, P. M., ed. 1978. The Potato Crop: The Scientific Basis for 

Improvement. Chapman and Hall, London. 730 pp. 

HAYWARD, H. E. 1938. Solanum tuherosum. Pages 514-549 in: The 

Structure of Economic Plants. The Macmillan Co., New York. 

. .~i674 pp. 

HOWARD, H. W. 1970. Genetics of the Potato, Solanun tuberosum. 

Logos Press, Ltd., London. 126 pp. 

M1ZICKO, J., C. H. LIVINGSTON, and G. JOHNSON. 1974. The 

effects of dihydroquercetin on the cut surface of seed potatoes. Am. 

Potato J. 51:216-222. 

:i OCHOA. C. NI. 1962. los So,,um 'luheriteros Svlvestres del Peru 

(Sec. Tuterarium.Sub-scc. tly-prtasulrrn).Talleres (Grificos1P. 

L.Villanuesa S.A., Linua Peru. 297 pp. 

REEVE, 

commercial 

R. M. 1974. 

peeling 

Relevance 

losses. 

of immature 

Am. Po:ato 

tuber 

J. 

periderm 

51:254-262. 

to high 

SALAMAN, R.N. 1949. The Historyand Social Influence of the Potato. 

Cambridge University Press. London. 

Fig. 

685 

3. A, 

pp. 

Epidermis of stem. Tuber surfaces: B, immature SWAMINATHAN, 

periderm; 

M. 

C,slightly 

S., and H.W. 

more 

HOWARD. 

mature periderm; 

1953. The 

D,mature 

cytology 

periderm and genetics of the potato (Solanun? wtherosum)and 

of normal 

related 

tuber 

species. 

surface; E, well-developed wound healing pertderm 

on acut 

Bibliogr. 

surface. 

Genet. 

Bar 

16:1-192. 

represents 50 jum in all photographs. THOMPSON, N. R. 1978. Potatoes. Pages 485-501 in: M. Milner, N. 

4

+q I 

B 

Fig 4. Natural openings in a pota~o plant permitting entrance of pathogens: A, stor ate on leaf (bar represents 20 m): B, enlarged lenticels 

on tuber surface, usually inconspicuous bit enlarged when soil is wet: C, section through enlarged lenticel (bar represents 100pm); D, 

roots emerging through the surface of stems or other roots, producing open wounds (bar represents 100 pm). 

S Scrinisha%. and I). t. U. \W'ang, eds. Protein Resources and 

I clniology: Status and Rcscarch Needs. Avi Publishing Co., Inc.. 

Westport, Ct . 

VAN I)F R ZAAG. 1). L. 1976. Potato production and uoli/ation in the 

world. Potato Res. 19:37-72. 

Oxygen-Temperature Relationships 

Interrelationships between tuber respiration, gas exchange, 

and tuber temperature are operative in the field before, during, 

and after tuber enlargement. After harvest, they markedly 

influence storage life, seed performance, and market quality, 

[he potato tuber is capable of respiring both aerobically and, 

for a limited time, anaerobically. Because the natural periderm 

Of tihe tub( r is a harrier to gas diffusion, diffusion take:, place 

through the lcnticels. I)iffusion rates differ between individual 

lenticels. and diffusion is further dependent upon the exposed 

intercellular spaces of tile underly:ng tuber tissue. Within the 

tuber, gas difLusion takes place through the intercellular spaces, 

wkhich occupy close to II( of the internal tuber volume. 

Oxygen (():1 is present in the potlato tuber both in the atmosphere 

of the intercellular spaces and dissol~ed in the cell sap. 

Carbin dioxide WO()) diffuses through lenticels at a rate 

approxiniatelv 80( 1 of that for 0). )uring early and rnidseason 

stirage. CO: excess and () deficit %%ithinthe tuber are usually 

about equal. later in storage (0) evolution mav much exceed 

() absorption. 

I uber periderin permeability is highest thro iglh immature 

skins d uring growth of the crop, decreases du. ir', maturation of 

the vines, and reaches a low ic\el after deati of1vines. Permeability 

drops considerably during the first five weeks of storage 

and gradually rise!, to a level comparable to that of mature 

tub,'rs in the field. A thin film of water on the tuber surface 

virt dllV stops oxygen diffusion through the lenticels and can 

reduce the center of the tuber to anaerobic conditions within 6 

hr at 111VC and in 2 hrat 21CC. 

Respiration rates of small, medium, and large tubers are 

essentially similar per unit of volume tinder satisfactoryenvironmental 

condiion... However, the ratio of surface area to total 

volume is much higher in small tubers than in large tubers, 

Under conditions stimulating high respiration rates (high tem- 

WIG(N(IT N, M. .1. 1974. Effects of temperature, oxygen tension and 

relative humidity on the wound-healing process in the potato tuber. 

Potato Res. 17:200-214. 


perature) or reduced gas diffusion from tuber surfaces (surface 

water films), the smaller ratio of surface area to volume in large 

tubers may limit gas exchange and cause injury, whereas the 

larger ratio in small tubers may enable them to escape damage. 

Respiration rates ofimmature tubers are considerably higher 

than those of mature tubers early in storage but later become 

essentially similar. Respiration of mature tubers immediately 

after harvest is often three times that of the same tubers a week 

later. This increased respiration is in part associated with 

mechanical injury during harvest and storage. 

Respiration of potato tubers during storage (Fig. 5) is 

or 

12 

8, _ 

6 

4 

C 2 

0 

0 5 10 15 20 25 

Temperature *C 

Fig. 5. Respiration rates of potato tubers at various storage 

temperatures. (Redrawn from W. G. Burton 1966. By permission 

from the author and H. Veenman en Zonen B. V.). 

J 

5

elatively high at I and 2°C, drops to a low at 5 0 C, is slightly 

higher at 15 0 C, and then rapidly rises to 25' C and above. The 

relatively high respiration rates within a few degrees of freezing 

account for problems of suboxidation such as internal 

mahogany browning and blackheart. The increase in respiration 

rates at higher temperatures contributes to internal heat 

necrosis and also to blackheart. 

High respiration rates in freshly packaged tubers during 

transit deplete 02 and release CO, in sufficient quantities to 

predispose tubers to bacterial soft rot and cause severe losses. 

Increasing CO. concentration in storage causes increased cell 

membrane permeability, sucrose content, and decay. Oxygen 

levels of I% or lower at 14°C or higher temperatures severely 

impair wound healing reactions, stimulate anaerobic 

respiration, and increase surface mold growth, severity of decay, 

and blackheart. At lower temperatures these effects may not be 

so evident. 


BURTON, W. G. 1965. The permeability to oxygen of the periderm of 

the potato tuber. J. Exp. Bot. 16:16-23. 

BURTON, W.G,, and M.J. WIGGINTON. 1970. fheeffect ofa film of 

water up,n the oxygen status of a potato tuber. Potato Res. 

13:180-136. 

LIPTON, W. J. 1967. Some effects of low-oxygen atmospheres on 

potato tubers. Am. Potato J. 44:292-299. 

MEINL, Kartoffelknollen. G. 1967. Zur 

Eur. 

Bezugsgrbsse der Respirations 


Intensitait von 

NIELSEN, 

J. 

t.. W. 

10:249-256. 

1968. Accumulation of respiratory CO2 around 

potato tubers in relation to bacterial soft rot. Am. Potato J. 

45:174-181. 

WIGGINTON, M.J. 1973. Diffusion of oxygen through lenticels in 

potato tuber. Potato Res. 16:85-87. 

WORKMAN, M., E. KERSCHNER, and M. HARRISON. 1976. The 

effect of storage factors on membrane permeability and sugar 

content of potatoes and decay by Erwinia carotovora var. 

atrosepticaand Fusariumroseum var.sa9b34cinum. Am. Potato J. 

53:191-204. 

(Prepared by W. J. Hooker)

Part I. 

Disease in the Absence 


Somatic mutations arc of economic importance in clonally 

propagated potato because they may modify foliage type, tuber 

shape, or color of plant parts; delay maturity; and reduce crop 

yield. Whether yields and tuber shape are affected or not, 

variations are undesirable because foliage type and growth 

habits are principal features used to identify cultivars. A change 

as simple as an excess or loss of foliage vigor will cause doubt 

as to cultivar identity. 

Wildings 

These differ from normal plants by low growth, close bushy 

habit, numerous thin stems, reduced numbers of leaflets, large 

rounded terminal leaflets, almost complete absence of flowers, 

and increased numbers of stolons with numerous small tubers 

that produce many weak sprouts during storage. Yields are 

reduced severely by this abnormality. The small tubers may 

reduce the total weight of the crop by as much as 50%, but :ubers 

of table stock size are particularly affected and, in quantity, may 

reduce the weight by as much as 80-90%. 

Feathery Wildingr 

Feathery wildings bear no rese "blance to true wildings 

except that, compared to normal plat they produce more thin 

stems and many more small tubers. Plants closely resemble the 

normal, but the top leaflets are small, narrow, and pointed. In 

some cultivars, tubers have numerous eyes clustered at the 

apical i' d, producing many small, thin sprouts several weeks 

earlie? i an normal. Yield reductions from this disease are 

similar to those from the wilding abnormality. 

Giant Hill 

Plants (Plate I) have greater height and stronger, more 

vigorous vines, with leaflets smaller and often coarser and 

thicker than those of normal plants. Tubers sprout late and 

plants are late in maturing, which can result in reduced yields. 

They have flowers and fruits in profusion and large matted roots 

and numerous long stolons. When allowed to mature, they 

produce larger and coarser tubers than do normal plants. Giant 

hill plants survive late blight for three weeks longer than do 

normal plants. Because of its late maturity, this variant is most 

serious in crops of early cultivars. 

Although giant hill occurs in most commercial cultivars, it 

can be rogued with ease. However, the current practice of early 

foliage destruction of certified seed crops, before all giant hill 

plants are obvious, is probably responsible for their regular 

appearance in some stocks. 

Tall Types 

These are intermediate between giant hill and normal plants, 

Genetic Abnormalities 

being a little taller, more vigorous, and two or more weeks later 

in maturity. Like the giant hill, the tall type is not apparent until 

full vine growth and may affect up to 3% in certain cultivais. 

Giant hill and tall types are more frequent in the long days of 

higher latitudes than in lower latitude short days. Maximum 

yields are rarely obtained, however, because when the normal 

crop plants are ready to be harvested, giant hill and tall type 

plants are still immature. Given sufficient time for full maturity, 

giant hill plants may actually outyield normal plants. 

Other Variations 

Many other abnormal types of plants or plant parts too 

numerous to detail may occur in commercial crops. Examples 

are most russet-skinned variants (Fig. 6) and multiple-leaf, 

dahlia-leaf, raspberry-leaf, coarse-leaf, little-leaf, and stitchedend 

variants. 

Nature of Variations 

Most of the abnormalities described above are periclinal 

chimaeras caused by genetic changes, usually in the outer layers 

of tubers or stems. Normal plants may be recovered by excising 

tuber eyes and permitting growth to develop from the deeper 

t 

. 

a 

Fig. 6. Russet skin somatic mutation, in a white tuber, initiated 

near the stolon tip early in tuber enlargement, possibly a 

chimaera. 

7

tissues. Many different kinds of variants can be produced by 

developing adventitious growths from callouses on tubers where 

eyes have been removed. 


DEARBORN, C. H. 1963. "Stitched end," "giant hill." and fasciated 

stem of potatoes in Alaska. Am. Potato J. 40:357-360. 

HOWARD, H. W. 1967. The chimerical nature of a potato wilding. 

Oxygen Deficit 

Oxygen requirements of underground parts of the potato 

during plant development are high. When oxygen concentration 

is reduced, stolons are abnormal and tuber development is 

impaired and abnormal. The degree of abnormality depends 

upon the severity of oxygen deficit, 

Although soil compaction exerts various stresses upon 

underground parts of the plant, oxygen deficit may be one of the 

most important, resulting in delayed plant emergence, moderate 

to severe yield reductions, and frequently, but not always, 

abnormal tuber shapes. Oxygen levels within soil, root 

distribution, and yields are increased by cultural and tillage 

practices that favor improved soil porosity. 


BUSHNELL,J.1956. (;rowd,response from restricting the oxygen at 

roots of young potato plants. Am. Potato .1.33242-248. 

GRIMES, D. W., and J.C. BISHOP. 1971. The influence of some soil 

physical properties on potato yields and grade distribution. Am. 

Potato J.48:414-422. 

HARKETT, P. J.. and W. G. BURTON. 1975. The influence of low 

oxygen tension on tuberization in the potato plant. Potato Res. 

18:314-319. 

SOMMERFELDT, T.G.. and K. W. KNUTSON. 1968. Effects of soil 

conditions in the field on growth of Russet Burbank potatoes in 

southesastern Idaho. Am. Iotato .. 45:238-246. 


Low Temperature Tuber Injury 

Low temperature tuber injury may range from outright 

freezing and killing of some or all of the tuber to gradations of 

.A- B 

A 

Adverse Environment 

Plant Pathol. 16:89-92. 

HOWARD, H. W. 1969. The chimerical nature of a feathery wilding. 

Eur. Potato J. 12:67-69. 

HOWARD, H. W. 1970. Chimaeras. Pages 68-88 in: H. W. Howard, 

ed. Genetics of the Potato, Solaium tuherosum. Logos Press, Ltd., 

London. 126 pp. 

(Prepared by J. Munro) 

injury (chilling) following prolonged exposure to temperatures 

slightly above freezing. Tubers may be frozen in the ground 

before harvest or injured later by low storage temperatures. 

Tubers of many cultivars freeze at temperatures below - 1.7' C. 

Freezing results in formation of ice crystals within the tissue, 

followed by rapid death. Chilling results in eventual death of 

cells or tissues even though the tissies may not actually have 

been frozen. 

Symptoms 

The line of demarcation between frozen and unfrozen tissue is 

usually distinct. Upon thawing, tissue may change progressively 

from dull off-white to pink and red and eventually to brown, 

gray or black. Frozen tissue promptly breaks down in a soft, 

evaporates. watery rot or collapses, leaving a chalky residue as the water 

Low temperature surface injury occurs in diffuse patches as a 

brownish black metallic discoloration. Such tissue is 

predisposed to surface mold growth (Fig. 7A). 

Effects of low temperature storage are primarily inernal. 

Tuber tissue chilled to near freezing is typically adiffuse smoky 

gray to black and resembles certain aspects of Pythium leak. 

Chilling causes formation of reducing sugars in stored tubers, 

resulting in itsweet flavor when cooked. Development is most 

rapid at temperatures slightly above freezing (0-2.5oC), 

progressively less severe from 2.5 to 3.5O C, and usually absent at 

3.8-4.4C. Reducing sugars cause brown discoloration in 

french fries or chips. Tubers stored at low temperatures 

frequently turn gray to black when boiled. 

Chilling injury may also take the form of net necrosis, in 

which phloem tissue isselectively killed because it has greater 

sensitivity to cold than do the surrounding parenchyma storage 

cells (Fig. 7B). The necrotic phloem may be scattered 

throughout the tuber or on the chilled side or be concentrated 

f-. , / 

C D 

Fig. 7. Low temperature injury of tubers: A, surface injury of immature skin in low temperature storage; B, net necrosis resulting from 

selective killing of phloem tissue; C and D,tissue breakdown in the vascular area. 

8

more heavily in the vascular region. Cold-induced net necrosis is 

very similar in appearance to virus leafroll net necrosis. 

Following severe injury, blackish patches or blotches may 

develop near the vascular ring, which may also be partially or 

completely blackened (Fig. 7C and D). Injury is usually more 

severe near the stolon end. 

Internal mahogany browning (Plate 2) is a different low 

temperature response, in which diffuse brownish red to black 

discoloration ispresent, usually in the central part ofthe tuber. 

This disorder grades into blackheart. Shrinkage in affected 

tissue results in cavities. Blackheart and probably internal 

mahogany browning result primarily from asphyxiation of 

internal tuber tissue. 

Epidemiology 

Individual tubers from the same lot vary considerably in 

response to a given temperature. Immature tubers are 

frequently more severely injured. 

Biecaiuse of hardening or acclinmatizatior, tubers that have 

been drop stored in temperature 

at low temperatures are less 

than 

injured by a sudden 

are those stored at higher 

temperatures. 

.ow temperatures fra few hours or temperaturesjust below 

free/ing for a short freeingfor time tme call an shrt lower owerintrnalquaityshoten 

internal quality, shorten 

storage life, and impair storge suitability ifeuitailiy andimpir of' o the thetubr tuber for fr processing prcesing 

without leaving visible evidence. Tu,bers may be supercooled to 

approximately -3.0 C. and even to -6.5' C for a,few hours, 

without ice crystal formation and, if gradually warmed, do not 

havc evident injury. However, jolting or jarring supercooled 

tubers will cause intracellular ice crystals to form and cells to 

die. Storage at low temperatures, even in the absence of 

symptoms, impairs the tuber's ability to form wound barriers 

when returned to favorable temperatures. Injured seed tubers 

with or without symptoms sprout poorly and may fail to 

produce plants because of secondary seed piece rots. 

Alternating temperatures during the storage season avoids 

chilling injury and its associated problems. Tubers held 

alternately for three weeks at 0' C and one week at 16' C had a 

lowered content of reducing sugars (as well as of total sugars), 

reduced respiration rates, and no low temperature injury, 

whereas at constant O°C tuber injuries became progressively 

more severe after eight weeks in storage. 

Control 

I) Field-frosted tubers should not be moved into storage if at 

all possible. 

2) Hold storage temperatures at 3.5-4.51C, which is 

sufficiently high to prevent low temperature injury. 

3) Maintaia adequate air movement in stored potatoes to dry 

frost-injured tubers and provide adequate oxygen for 

respiration. 

4) Tubers injured by low temperatures or suboxidation 

should not be used for seed. 

5) Certain cultivars are more prone to mahogany browning 

than are others. Varietal differences with respect to other 

aspects of low temperature injury are not so pronounced. 


CUNNINGHAM. H1.IL.. M. V. ZAEH RINGER, G. BRAUSEN. and 

W. C. SPARKS. 1976. Internal quality' of Russet Burbank 

potatoes following chilling. Am. Potato .1.53:177-187. 

tR USCH KA, II. W.. W. I.. SM I If..r., and .1. E. BAKER. 1969. 

Reducing chilling injury of potatoes by intermittent warming. Am. 

Potato .1.46:38-53. 

.JONES. .. R., M. MII.L.ER. and 1. BAILEY. 1910. Frost necrosis of 

potato tubers. Wis. Agric. Exp. Sin. Res. Bull. 46. 46 pp. 

LINK. G. K. K.. and G. 1B.RAMSEY. 1932. Market diseases of fruits 

and vegetables. Potatoes. U.S. Dept. Agric. Misc. Publ. 98. 62 pp. 

RICHARDSON. L.T.,and W. R. PiIII.I.IPS. 1949. I.ow temperature 

breakdown of potatoes in storage. Sci. Agric. 29:149-166. 


Low Temperature Foliage Injury 

Certain symptoms of nonlethal low temperature foliage 

injury may be confused with virus symptoms or herbicide 

damage. Lethal freezing of leaves and stems isreadily identified. 

Symptoms 

Frozen leaves rapidly wilt, collapse. and when thawed, 

become water-soaked. They turn black when damp and brown 

when dried. Less severe low temperature injury, usually 

occurring in the early to middle part of the growing season, 

often produces a buff to light brown or yellow discoloration on 

the top of the plant and particularly at the bases of young 

leaflets. 

Temperatures at or near 0' C selectively injure leaf and stem 

primordia and possiblycell organelles. Symptoms ofthis injury 

become evident after leaflet expansion as unilateral leaflet 

development, irregular distortion of leaflets, or grayish 

transverse banding accompanied by restricted lateral expansion 

(Fig. 8). 

Chlorosis in diffused areas, in spots, or in portions of veins 

nay be seen and mottle patterns may be present with or without 

leaf Necrotic distortion specks following may develop nonlethal on young low leaves temperatures following (Plate -0.3° 3). C 

wet Nertcsckmadvlooiyunlaesflwng-.0 

bulb temperatures. Injury of this type appears after leaves 

from damaged primordia have expanded. Normal growth may 

precede and should follow these low-temperature effects, but 

symptoms on injured parts persist. 

Epidemiology 

Low temperature injury is usually most severe in low-lying 

areas of fields. At high elevations and latitudes, freezing may 

occur at any time in the growing season. 

Because leaf surfaces are frequently well hydrated and often 

wet with dew, wet bulb temperatures should be more reliable 

than dry bulb temperatures in determining critical temperatures 

for leaf injury. 

Plants on which some leaves have been frozen recover from 

injury slowly, suggesting more damage than that of the tissue 

actually destroyed. Growth retardation may be due to 

resorption of tissue degradation products. 

Solarim acauk,, its derivatives, and approximately 10 more 

wild potato species, as well as several cultivated clones 

Fig. 8. Leaf deformation following low temperature injury of leaf 

primordia. 

9

elonging to primitive species grown in the Andes. carry 

considerable frost tolerance, some to as much as -5°C . 

Control 

I) Potato crops seldom justify frost protection such as spray 

irrigation, mechanical air movement, or smoke application 

during low temperatures. 

2) Proper diagnosis of nonlethal injury is necessary in seed 

fields. 

3)Low temperature tolerance (approaching -6°C) of hybrids 

involving S. acau'le and other tuber-bearing Solanum species 

permits potato cultivation at high altitudes and possibly also at 

extreme latitudes. 


CHEN, P. M., M.,I. BURKEand P. IH.LI. 1976. -Thefrost hardinessof 

several Solanium species in relation to the free,,ing of water, melting 

point depression, and tissue water content. 3ot. (ia/. (Chicago) 

137:313-317. 

ESTRAI)A, R. N. 1978. Breeding frost-resistant potatoes for the 

tropical highlands. Pages 333-341 in: It. I'. l.i and A. Sakai. eds. 

Plant Cold Hardiness nd Freeing Stress. Academic Press. New 

HOOKER. W... 1968. Suhlethal chilling injury of potato leaves. m. 

Potato 45:250-254. v. 

Potao .1 45250-54.potatoes 

.I, P. H. 1977. Frost killing temperatures of60 tuber-hearing Solaium 

species. Am. Potato .1.54:452-456. 

McKAY, R.,and P. F.M. CI.INCH. 1945. Frost injurysitnulating virus 

disease symptoms on potato foliage. Nature 156:449-450. 

PAulA. .1.P.. and P. Ht.1.1.1979. Frost-hardiness in relation to leaf 

anatomy and natural distribution of several Solarum species. Crop. 

Sci. 19:656-670. 


Blackheart 

Blackheart results from inadequate oxygen supply for 

respiration (asphyxiation) of internal tuber tissue. Internal 

mahogany browning and internal heat necrosis grade into 

blackheart in severe instances and thus are, in different 

environments, symptoms of incipient to acute suboxidation. 

Blackheart was amajor problem when potatoes were shipped in 

Symptoms 

131ackheart symptoms consist of black to blue-black 

discoloration in irregular patterns in the central portion of the 

tuber (Fig. 9). With acute oxygen deficiency, the whole tuber 

may be discolored. Demarcation at the margins is usually 

definite, although the black discoloration may diffuse into 

relatively unaffected tissue. Discolored tissue is frequently firm 

but on exposure to room temperatures may become soft and 

inky. Individual tubers vary in their responses to conditions 

causing blackheart. 

Blackheart develops when oxygen isexcluded from orunable 

to reach internal tuber tissue. Longer times are required for 

blackheart development at lower temperatures. However, 

blackheart develops more rapidly between 0and 2.5°C than at 

51C. At extreme temperatures of 36-40'C or of 0 C or slightly 

below, blackheart may develop without oxygen exclusion 

because gas diffusion through the tissues is not sufficiently rapid. 

Tuber storage in closed bins or in deep piles without adequate 

aeration may result in blackheart development. 

Control 

I) Do not expose tubers to high temperatures no. to 

prolonged storage near 0C. 

2) Provide forced aeration of potatoes in closed bins. 


BENNETT, J. P..and E.T. BARTHOLOMEW. 1924. The respiration 

of potato tubers in relation to the occurrence of blackheart. Calif. 

Agric. Exp. Sin. Tech. Paper 14.41 pp. 

STEWART, F. C..and A. i. MIX. 1917. Blackheartand theaeration of 

436:321-362. in storage. N.Y. Agric. Exp. Sin., Geneva. tech. Bull. 


High Temperature Field Injury 

Stems may be injured at the soil line by high soil 

temperatures, particularly when plants are small and leaves are 

not large enough to shade the soil at the base of the plants. Stems 

typically are girdled and surfaces 

secondary 

are 

organisms 

tan to white, 

may 

although 

',ometimes discolor the tissue to a 

darker brown and, in severe cases, cause 

follow 

rotting. Injurycan 

defoliation 

also 

or vine displacement that suddenly 

lower 

exposes 

stems to intense sunlight. This results in a scalded 

apperance on the exposed side ofthestem or girdling at the soil 

line (Fig. 10). 

Tubers exposed 

may 

to 

be 

sunlight 

injured 

as they 

and 

lie 

thereby 

in the field 

predisposed 

after digging 

to rot in transit or 

storage without immediate external symptoms except possibly 

for watery exudates from lenticels. Intense exposure causes 

sunken scalded areas in a circular pattern. The threshhold of 

tuber flesh temperature predisposing tissue to soft rot is 

approximately 430C. Such internal temperatures may exceed 

Fig. 9. Blackheart at two cross sections of the same tuber. Fig. 10. Scald of stems following exposure to sun. 

10

the air temperature when tubers are in the soil within 2.5 cm of 

the surface, remain on the ground after digging, or are held in 

bags in the sun. (See also tuber greening.) 


NII'IS|-N. I.. WV. 1954. [he susceptibility of"seven potato varieties to 

bruising and bacterial soft rot. Phytopathology 44:30-35. 

(Prepared by W. .1.Hooker) 

Internal Heat Necrosis 

Considerable confusion exists both in symptom description 

and in terminologv for the causal factors of internal necrosis of 

tubers. The underlying cause of necrosis is believed to be 

suboxidation of rapidly respiring internal tissues during active 

tuber growth and high temperatures. (See also phosphorus 

deficiency, vello\k d\\art. mop-top, and stem mottle.) In recent 

literature, the name Eiserifleckigkeit refers specifically to 

internal heat necrosis, whercas l'ropfenbildtung and Spraing are 

used for stem mottle virus infections, 

Symptoms 

Syniplonis do not develop in vines. Affected tubers usually do 

not sho%%external syniptoims. Necrosis may be severe toward the 

center of larger tubers, appearing as light tal, dark yellowish to 

reddish bro, n. or rust-colored Ifccks that become, in extreme 

cases, dark brown or even black (Fig. II). 1n usually severe 

s. mptonis may be identical to blacklicart. Necrotic flecks are 

ustallyv clustered off-center in the pith towards the apical end. 

Necrotic flecks are firtii, do niot break do%%n or predispose to rot, 

and remain firm after cooking. Cortical tissues are seldom 

aft ected. .\ relat ionship exists bctx\ en Iisenfleckigkeit atid acid 

soils that ate Io\ iti calcium. (See also calciun deficiency.) 

losses can be se\ere because of buyer discrimination against 

internal discoloration. 

.\ sonlew\hal similar disorder. present in Israel, produces 

necrotic spots in the coritx near the vascular ring and maproduce 

interior cavities. I)amage is visible from the tuber 

sirft:ce. with h!:ckening of the eves at the apical end, sunken 

surface spots. and a silvery sheen. No true rot develops, but 

many affected tubers fail to sprout. Symptoms are believed to 

develop intstorage following high field temperature before 

har\est. 

Ifistopathology 

Suberin develops in walls of affected pith parenchyma cells. 

Cell walls first become dark at the corners. Protoplasm becomes 

granular and aggregates. Walls ofadjacent cells also darken and 

finally collapse at the corners. l.ayers of peridermlike cells may 

develop outside the necrotic tissue and may isolate it. Internal 

pressure from periderm formation may cause the collapse of 

necrotic cells, but cell lysogeny has not been observed. Starch 

grains are generally absent in affected cells. 

Epidemiology 

Internal necrosis becomes progressively more severe during 

the growing season and is most severe during hot, dry years in 

light soils of sand. gravel, muck, or peat. Lack of adequate soil 

moisture may be as influential as high temperature in 

predisposing to internal necrosis. Disease is most severe in 

tubers near the soil surface and progressively less frequent and 

severe with increasing tuber depth. Straw mulch reduces soil 

temperature and sexeritv of disease. Ini areas where the disease 

was formerly severe, maintenance of good vine coverage of the 

soil through adequate irrigation and good cultural practices has 

almost eliminated the problem. 

Discoloration does not increase and ma' decrease in storage 

if affected tubers are not predisposed to storage rots. 

Transmission through affected seed tubers has not been 

observed, although spindly sprouts have been reported from 

tubers exposed to 30-40°C. 

Control 

I) Cultivars differ in tolerance and sensitivity. 

2) Maintain vine growth adequate to shade the ground 

through the use of appropriate cultural practices (good fertility, 

Fig. 12. Second growth: A, dumbbell; B, pointed end; C, 

protruding eyes that later form knobs. Stoton end ineach case is 

Fig. 11. Internal heat necro'sis, at left. 

A 

rr.. 

V, 

11

?(1 

Fig. 13 Second growth as gemmation (left) and as a sprout (right) on an abnormally early tuber. (Left, courtesy W. M. Iritani) 

adequate irrigat on, and foliage protect ion by pesticides). 

3) )o not permit tubers to remain long in the soil alter vintes 

ha e died. 


IR .Al \. II )(', I ic I ieNtillcckitkcit dci Kait,,dlel . Ilannekr. 

Pllan/enchu. X542 541) 

I1RII )M.A\. It A 1955 .socialiron (i internal bro\t spot ofpolato 

tinher. \tlth hol. dr% \ cathl . Plant )is. Rep..39l37-44. 

IARSON. R If.. and \. R. \tlH1 R I. '145. 'h siolhogical internal 

if lot itt,, tiiCi, III ICOHiii s .1 A\arlr. RC, (Wlirihlngloir. 

1)() 71 4,7-505. 

/IM 1:RI \.(Vt I I S. S. 1964. Ilie occurrence ot potato healnecrosis 

,, inproms ini Israel and Ihe toe ofitfected tub.rs as seed. 

Fur. Po(tatio .1. 7:112-I 18. 

(Prepared by W. .1. [looker) 

Second Growth and Jelly End Rot 

Second growth may he of se\cral types: II deftorrmed tubers 

wit h protruding eves. lateral buds (knobby tubers), or apical 

buds (dumbbells or elongated tubers) ( Fig. 12); 2) 

gennimation sectondarv tubers on a1solon externsion of tire 

otriginal tuber (Fig. 13 lcft; or 31 recently f'ormed tubers that, 

before normal har\¢st. produC. either a sproultt or a leafy 

aho~egrtiun( plant (I-ig. 13 right), 

Second grolth is coiniiotinl attributed to high field 

tetmperatures aind drought. I nav.i hiwe\er, result from 

regeneration ftollo\wing ain\ condition causing irregular rates of 

12 

404 

tuber development, such as uneven availability of' nutrients or 

moisture. extrenies in temperat tire. or vine defoliation from hail 

or frost. Positive separation of heat effects from drought effects 

is difficult because high field iliperatures are ustiallv 

accompanied hy drought and i conconitant reduction or 

cessation of thuber gro\tII. When growing conditions improve. 

resumption ol tuber growth becoies evident as second growth. 

Second growth is usually' stimulated by soil temperatures of 

270C and above, although sonic develops at lower 

temperatures. IInder controlled condition.s subjecting plants to 

32'C tor seven days wIs sufficiCit to initiate second growth. 

Seerit\ \was greater \\ith longer periods of exposure and higher 

tenperat tires. Second growth %%'iws not initiated by varying tie 

water supply altmne. 

Second growth and jelly end rot are interrelated because jelly 

end rot is prevalent in abnormally shaped tubers, particularly 

those with second growth. felly end or glassy end rot is highly 

seasonal in occurrence, has been reported from many potato 

growing areas, and tnay involve 10-50"i or iiore of the crop. 

l.osses due to reduced tuber quality are high. 

"Iranslucent end" or "sugar end" refers to incipient 

svnptonis visible at harvcst or developing in storage. Tubers 

with such symptons frequently develop jelly end rot later. 

Reducing sugars in translucent end or sugar end tubers cause 

dark color in potato chips (Fig. 141)). 

Symptoms 

Stiloin etnds oftubers with.ielly end rot become translucent to 

glassy, lack normal starch content, have reduced specific 

gra\ity. slri\el. and collapse into a wet.jellylike substance (Fig. 

14A)..Iell\ end rot tissue dries down to a leathery layer in dry 

storage (IFig. 1411). )eiarcation between healthy and affected

iiO 

A B 'D C 

Fiq. 14 Second growth: A, knob and jelly end rot of stolon end of tuber (bottom); B, longitudinal section showing dried jelly end; C, 

starch-iodine stain test demonstrating starch depletion (white area) in tissue near the jelly end portion; D, sugar end (stolon end, at 

bottom) after deep fat frying with resulting discoloration due to reducing sugars. (D,Courtesy W. M. Iritani) 

ts~uc is distirrt. \\,ll hrakdl\\n sldoIt IxtrIdin ti into tile 

ietur \ S C1r. (ilass\ tissue rscthl,.is that o exhausted se d 

pieeC ,t,_et plnt dLse\.lopirnc.,t. 

Jell\ erd rot i , mor pr,'\alent in tubers Of Iong-tuhcrcd 

+.,hI1ap!.. 

thtais. pt paliiitt,. it 

.. 

u is.\ 

, 

t 

r 

hto,,,es e it ecttld t~ 

c 

th 

lh co 

suchl 

p. 

aispindle 

S I pe Mai 

po1) itt1 0 

grom 

dI i " o 

ll 

set r 

suchashndP 

duni bb1 el l shape -. 

ird,c 

0 s th e sto lori crid is 

rll. t..RtIinl-tithr.d ,ultli ars also dc\,.op .jilv nd rot but 

lil'l1t1 tish\ illittItiL'ld. 

\,) patho'rn hasN been co'n,sttIttl dctnostrflated in jelly etnd 

tiss11NIrt. ilthotmi piptulatinis til seclttdill\ organ1isms. 

i tILiiti Is\Al h . t ltn :. t u,talh high. 

I lie sllot -'ntd of the tIthet nt ittall\ has the Ieighest starch 

L.MI,.i I11SCLIIt l'ostlr . stlirCt depoisited in -oatIv tuher 

lhplo rnt.e!is tppale ill%h1hr(I[,.is'd and trattslo ilaled frum 

0ie i cut ciid.l tio the apicl lend (Iig . 14( I. 

\\heur,,uu t gI,\\1h L~k.s tihe 0u1nuellin;itli. ill 

tubers 

(pntt anll sll\ I tlid sar itsl ) d \Ite lip itI chaitns itlstolons. 

( , th , ih*%it .. s i, ti i s ,.a teld Ir u I Ilh e ptitn itrtv tith .e r into tle 

seitili, s titler. sIlch is oitolittal qtalit \.Internal qtality 

hin~i2 s in tie'lproit tither (glass \ teture rid lo\ specific 

etasits) hC1'line ;ipp eliit Altwr loliage Il the plant has died. 

IUettsh \ hot\ ni s\iipttuls. 'estertIih tlh titberscannt+t 

i..tl~. 

he 

tlet+lsepniiteit' 

!+hd '.'p d 

duinlge 

t! 11 

gradig 

!iiit)So 

ricrul c 

considerable t ns.' ide~ra b le: ss if) lo it 

tt1it\ iaid tuiket salue Ott tie rp. 

l.p~idemititii.\ ritirglg 

Ii t ,itt ,... ot ella end tilt is,st-, iilltuet ced hy seasonal 

tIlltilt l . hettil a se.\rc prlobI em in sole sears and not a 

pr ,ihlrl Itt(tlers. It is related to high field temperatures 

itt,+. Ip;iiiLd h\ dti010t frintslltiietnt irrigation it tihe carl. 

gt'r (MiIpet it.I t.lho st\d ha la\ trabe t nperatLre or sufficient 

\s;Ite ,tl ttinttt tither grl\tth V\hetr tube.'rs that are innature 

,ithnit lh5' et ce (lealsdrittght stress ire stored itmmrediaely 

AMler hrrt.st at hi l,t!rplure, (15.5 ('. the*\ are predispiosed 

tI 1111eael i!t..ICtIll .eIll traztshte etds. ,tt as cmtnpared to those 

red+t at hle 1t r t lll ititr+"(1) 

u; I1 . 

onrol 

III riLatC alcitiattlr to maintain unihorin growing 

condrtlitins, thstghot,ut tIre scastf, particularly during early 

ii her de\lhpment. 

2) As\+ list'ltisars akith second grottli characteristics. 


I-RII)MAN. It.... and I). 1-()t SOM. 1953. Poutt tuber glassy end 

and jell\ end rot ill the Noutheast in 1948 and 1952. Plant l)is. Rep. 

37:455-459. 

IRIIANI, W. 

traislh 

Mt.. and 

cnt ,nd 

I.. \\'!.I 

ti b,e 

FR. 

is n . aot t .1.51 

1973. 

:223 

lhe 

233. 

dclopnent ot 

I : . .. K. It.A. I NII IA NI)FR. and (G. i(ODL.IK. 1964. 

(bs.r\ations oilthe induction oli s, -td-prostlh in pottato tuhers. 

FLir. Potato .1 7:219- 227. 

\,I l'R P1Y.I' A. 936. Sonteellects ,t drought iltittttbers. Erp, 

I. t\11 .\grI. 4:230 2 46J. 

\IIH:SEN. I V.Wand W. C. 'S'PARKS.1953. lBottleneck tubers and 

Jell,..-end totin the Russel t turhank polato. Idaho Agric. lxp. Stn. 

Rcs. Bull. 23. 24 pp. 

(repares by V..1. Hooker) 

Hollow Heart 

llo' heart is associated vith exeessiv'elv rapid tuber 

enlargemetnt. It presentsi a serious problem because, lacking 

external sy'nptors. the detect usutally beetes apparent only 

w-i\hen the tihe cr iscot in halt. Iticideice t)f hollo\w heart i is highest 

in the largest tubers and incertain lots may alect rip to 40'; of 

lthe 

tubers h s,cight. 

,+'mptonis 

I !stall\ ot.e ca\it\ tortts near the center ofthe tuher. It matny 

c.-ultiCars a ties are lers or st r shape arnd aniular at the 

corners. l e\ appear as splitting within ietuher (Fig. I), 

and internal \salls tofthe -asities tre either s,tile or light tan to 

stra\ colr. I ttother ,ttltisars, but less cotmn tnly., ca\ities are 

rltlnd to irregular inshape. 

Bteotre h llo%\ hei.art dh\clips. central tissue may be watersolaikei 

or tratsltcent: Ibro\\n tecrotic patch appe'ars early in 

tuber fornation inlsome cultikars. Rolt seldotm starts at hollow 

lheart sites. atlttigh itt rlre instances mtold may he present. 

flistopatholog, 

lhte tpesof , origil arie described: I ),Inecrotic patch. tipto I 

cti in diairnter. ctmposed ut tman\'single cells or stuall groups 

13

of cells, becomes enclosed by periderm, then turns brown, 

shrinks, and collapses to produce a cavity: 2) necrotic starchfree 

cells differentiate, causing a brown spot approximately I 

mm in diameter, often in the center of very small tubers, and 

produce a cavity that enlarges with tuber growth and is 

surrounded by a partially suberized cambium layer: 3) internal 

tissue tensions cause splitting, which results in a lens-shaped 

cavity not preceded by cell necrosis. Translocation of substances 

from the central portion of the tuber and resorption in other 

parts of the plant may also be involved. 

Epidemiology 

Epideology hbefore 

Hollow heart is most severe during growing seasons or under 

cultural practices favoring rapid tuber enlargement. Rapidly 

growing tubers have a relatively higher incidence of hollow 

heart than do those that grow more slowly. Moisture stress 

(deficiency) followed by conditions favoring rapid growth 

predispose the uber to hollow heart, 

HJollo%%heart is lre(luc tis severe in fields with poor stands 

where plants are irregularly spaced. Practices that inhibit rapid 

tuber growth or that stimulate large numbers of small tubers, 

such as close spacing of plants, reduce incidence of hollow heart, 

Marginal potassium deficiency may be a factor in hollow heart 

predisposition, particularly in cultivars prone to the disorder, 

Increasing potassium fertility over that required for normal 

growth reduces hollow heart incidence. 

Identification for Marketing 

X-ray examination of whole tubers under water effectively 

identifies the condition without tuber destruction. Removal of 

large tubers and those with low specific gravity is only partially 

effective in eliminating hollow heart potatoes before marketing. 

Control 

I) Potato cultivars differ ii severity of incidence and in the 

type of internal cavity produced. 

2) Close and regular spacing of plants increases competition 

and prevents excessively rapid tuber enlargement, which usually 

reduces incidence of hollow heart. 

3) Avoid missing hills in planting, and use sound cultural 

practices to assure good stands. 

4) Maintain uniform soil moisutre levels to stimulate uniform 

tuber growth rates. 

5) Additional potassium fertiliation reduces incidence of 

hollow heart even though total yields may not be increased. 


CRUMBIL. I.I ). C. NELSON, and M. E. DUYSI-N. 1973. 

Relationships of hollow heart in Irish potatoes to carbohydrate 

reabsorption and growth rate of tubers. Am. Potato .1.50:266-274. 

FINNEY. E. R., Jr., and K. II. NORRIS. 1978. X-ray scans for 

detecting hollow heart in potatoes. Am. Potato . 55:95-105. 

NEI.SON, ). C. 1970. Effect of planting date. spacing, and potassium 

Fig. 15. Hollow heart, showing transverse and longitudinal 

splitting. 

14 

on hollow heart in Norgold Russet potatoes. Am. Potato J. 

47:130-135. 

VON WENZI,, H. 1965. Die histologische tnterscheidungdreier'lypen 

von Ilohlheriigkehbe Kairtoffelk nollen. Z. Pflan7enk1r. 

Pflanienschut,72:411-417. 

(Prepared by W..i. Hooker) 

Surface Abrasions 

Immature tubers that are mechanically injured during harvest 

the periderm is mature exhibit feathering, i.e., shreds of 

loose skin exposing underlying flesh (Fig. 16). The wound may 

heal under optimum conditions but frequently dehydrates, 

becomes somewhat sunken, and turns dark brown with a sticky 

surface due to bacterial growth. Such tuers do not store well. 

Mature tubers mav be skinned by rough handling during 

harvesting and grading operations, thus providing infection 

courts for wound pathogens. Sunken scald spot develops when 

fresh wounds are dehydrated, especially after tubers are allowed 

to stand for some time in direct sunlight or desiccating ind 

before storage. Surface discoloration of wounds, with 

associated rot problems, also follows low emperature storage 

before wound healing is complete. Such tubers may become 

flaccid from dehydration. 

Control 

I) Avoid mechanical damage at every stage of the digging, 

harvesting, and grading operatiots. 

2) Protect tubers from sunlight and heat;avoid excessive 

dehydration before storage. 

31 Provide optimum storage conditions until wounds are 

completely healed. 


SMITH. W. ... Ir. 1952. Effect of storage temperatures, injury, and 

exposure on weight loss and surface discoloration of new potatoes. 

Am. Potato .1.29:55-61. 

WHITEMAN, T. M., and .1.1M.L.UTZ. 1954. Sunken scald spot field 

injury evident in stored potatoes. Am. Potato .1 31:43-49. 


Tuber Cracks 

Tuber cracking is of four types: I) growth cracks from 

internal pressure, 2) growth cracks from virus infection, 3) 

mechanically produced cracks, and 4) harvest cracks. 

Growth cracking (bursting) usually follows the long axis of 

the tuber and results from internal pressure exceeding the tensile 

strength of surface tissues during tuber enlargement. High 

internal turgor pressure develops from tissue expansion during 

rapid tuber growth. Fertilizer placed so that growth is 

excessively rapid increases growth cracking. Growth cracks in 

'' 

Fig. 16. Immature tuber surfaces, skinned and abraded.

identifying tissue bruised by black spot without rupture of the 

surface, nor is the reaction obtained after wounded tissue has 

hea led. 

Corntrol 

I) Little can be done to avoid cracking during the growing 

period except by judicious irrigation, fertilizer application, 

plant spacing, and cultivar selection. 

2) Delay harvest until vines have been dead for some time and 

tuber periderm has matured. Avoid harvesting from cold soil. 

3) Avoid sudden impact on tubers, and protect them from 

rapid drying after digging and during transit from field to 

storage. 

Fig. 17. Cracking: A,crack caused by impaction of turgid tuber 

during digging; B, growth crack that healed over before digging. 

- . •. 


IRIIANI. W. M. 1968. [he use of catechol for enhancing bruise 

detection. Am. Potato J. 45:312. 

PAINTER. C.G..and .. AUiUS I N. 1976. the effect of soil moisture 

and nitrogen on yield and quality of the Russet Burbank potato. 

. ' ,: L ', jP 

., 

Am. Potato .1.53:275-284. 

SM IT I.E., 1). A., R. E. TIIORNION. C. IL.PETERSON, and B. B. 

IFAN. 1974. ltarscsting potatoes with minimum damage. Am. 

Potato .1.51:152-164 

WER NER. II.0.. and .1.0. I)FT T. 1941. Reduction of cracking of late 

crop potatoes at harvest time b\- root cutting or vine killing. Am. 

ota t o .1. 18: 189- 208. 

(Prepared by W. .1. Hooker) 

Blackspot 

Fig. 18. Harvest or thumbnail cracks following mild bruising and 

surface drying. (Courtesy W. C. Sparks) Blackspot is alays caused by bruising injury. either from 

ctied bfotr hirvcst o requetit wound heal aid. as tubers 

impact during harvest, handling, and grading, or from pressure 

during storage. File 

and 

disorder 

northern Europe 

is well known 

and has 

in 

become 

North America 

atn increasingly serious 

consttl to groi. becotie relanets shallow a nd of little problem in most potato-growing areas that have adopttd 

contisequtenice (Fg. 17131. Wound-healed cracks seldom become mechanical harvesting and handling techniques. 

infected. Potato culti\ars differ in susceptibility to injury. 

(Itorwth cracks may also develop in tubers of plants with tile Symptoms 

yello\\ dwarf \irus. potato mop-top virus, or certain strains of Blue-gray to black discolored areas develop just beneath 

the 

the 

spindle tuber viroid. tuber skin (Fig. 19). Internal symptoms do not appear 

Mecha nical cracking during harvesting may follow sudden immediately after brusing but develop to full intensity 

impacts 

over 

(Fig. 

a 

17A). Cracking is dependent upon varietal period of 1-3 days as flattened, spheroidal blue-gray patches 

response. tuber maturity, internal tuber turgor, and degree of centering in the vascular region. Margins are diffuse and grade 

mechanical cmnpressiin during Iaiest and iovetntient into into the unaffectcd tissue. Blackspot is usually 

storage. 

more 

Imutture 

noticuablc 

tubers and large tubers are most easily at the stolon end of the tuber than at the apical 

inilured. 

end. Tubers 

Severit\ 

with 

is greatest when tuber temperatures are low internal blackspot frequtentilv show no external sylmptols. 

and tissue is turgid. Iu bers s\ith high internal turgor are easily Melanin is present on intracellular 

cracked 

protoplast 

to a depth 

surfaces 

of 5 

and 

min or 

on 

more. Extreme turgidity results inner wall surfaces of affected cells. The absence of wound 

\when soil moistuire le\cls are hlgh :atd tuts contitnue to function periderm in lesions is characteristic of blackspot 

after 

and helps 

\ines 

to 

hase been suddenly killed by frost, by herbicides, or differentiate this disorder from other internal defects such 

b\ harvesting 

as 

tubers when vines are green. Root pruning. internal brown spot, heat necrosis, and certain internal lesions 

undercutting, or prc-har\est vine killing reduces incidence of caused by pathogens. 

cracking. I)eiayingdigging fora few htlrsCarhlin thledaV until 

the soil is %\ar ied may also reduce cracking considerabyh. Histopathology 

Seserel\ cracked tubers are of little %,alue because wound Bruising injury initiates a series of biochemical oxidations 

healing 

in 

is incon,pletc, deh.ydration is rapid. and incidence of damaged cells. Phenyl substrates such as tyrosine are oxidized 

tuber rot may be high. Paradoxically. shatter bruising becomes to conjugated quinones by polyphenol oxidases. The 

no10 

quinones 

se crc \kith high tuber turgor and black spilt intensifies polymerize to produce the black pigment. Oxidation reactions 

%%11 lth Io tuber turuor. 

are usually completed within 24 hr of bruising. and spots neither 

Ilaivest cracks are crescent shaped. resembling cracks made enlarge nor disappear during subsequent storage. 

with a 0humbriail. lhrev are usually shallow, 1-2 Inm deep. aInd 

result rom ough handling and drying of the tuber surface Epidemiology 

tissue after digging. particularly when tubers are turgid (Fig. Severity if' blackspot is determined by both the number of 

18). Severity 10 injury depends on intensity of bruising and damaged 

rapidity 

cellsand 

ol deh.dration. 

the amount 

Direct 

of melanin 

harvesting 

produced 

by iachinery 

in each one. 

often An impact will damage more cells in susceptible tubers 

reduces 

than 

incidence 

it 

of harvest cracks as compared to harvesting will in resistant ones, and larger, deeper spots will form. Tuber 

by lifting tubers to the soil surface and gathering them later, susceptibility is influenced 

[Hie 

by a 

catechol 

number of 

test 

factors. 

(I- 1.5"1 practical grade) reveals areas of Tubers with low turgor pressure arc more likely 

injury 

to 

by 

have 

turii ig 

severe 

them dark red to purplish within 3-5 min of blackspot. Iherclore, blackspot is usually nmore serious 

treatment. 

after 

Catcchol, 

a 

a polyphenol, is oxidized by phenolase, dry growing season in nonirrigated growing areas. Conditions 

which isreleased from recently broken cells. It is net effective in such as low soil moisture, poor root development, or hot dry 

15

ATuber 

Fig. 19. Blackspot internal bruising. (Courtesy S.L.Sinden and R. 

W.Goth) 

days before harvest tend to predispose to bruising injury, 

Hecause oftuber hydration differences, tubers with high specific 

gravity are usually more susceptible to bruising than are tubers 

with low specific gravity from the same lot. Susceptibility can 

increase du ring storage because of physiological aging and 

dehydration, 

Mature tubers are more susceptible than immature tubers, 

altdi the stolon end is more susceptible than tile apical end. 

" emperature of' tile tubers at the time of bruising influences 

ses erit v. lit bers br tirsed at 20-.30 C*are less aIf ected b lilac kspot 

than are those brui:--d at temperatures below 10°C. 

Because of differences in both mechanical strength and solids 

content, cultivars differ significantlv in susceptibility to bruising 

and blackspot de elopient. 

Tubers harvested from soils deficient in potassium tend to be 

i1re susceptible to Ilrisinug arid blackspot deelopnerit. I.o\ 

potiassium content ill tubers is associated with high phenolic 

content and low tuber hydration. High phenolic content and 

active oxidase systems in damaged cells result in abundant 

produ ction of melanin. 

Nitrogen fertili/ation. ethylene concentrations, and soil 

carbon dioxide lesels Itrse been reptorted to affect blackspot 

susceptibility in some growing areas. The specific effect of any 

oi ens ironimental factor on susceptibility of tubers to blackspot 

depends on the cultivar, the cultural conditions, and tile 

interaction with other environmental factors. 

Control 

I) Reduction of bruising is most important for control of 

blackspot. Use Cltiplllclll Ion harvesting. trainsporting. 

grading, and handling tubers that is well designed and carefully 

adjusted to minimize impact forces. 

2) Use sound cultural management practices, including 

adequate 

I pIOAPST. 

potash fertilization, especially on heavy soiils that are 

likely to be deficient in potassium. Irrigate ars long as vines are 

green. 

3) Warm tubers in storage to 200 C before grading and other 

handling operations. Using sprout inhibitors and adding 

16 

moisture to the storage atmosphere will help prevent 

dehydration and bruise damage in tubers taken out of storage. 

4) Use resistant cultivars. 


")WI .lI, . It. B..(. I. SI \1.1 KNI- II I R.IE. V cl)( l.l. aid .1..1. 

)PAVI-K. Effects of soil potash treatnent aid storage temperature on 

blaekspot bruise development iii tihers off our Sohonuor ruhr'routot 

ctiltixars. Amf Potato .1.54:137 146. 

KUNKEI., R.. M. I.. WEAVER, and N. M. lIOISVAI). 1970. 

Blackspot of Russet Burbank potatoes and the carbon dioxide 

content of soil and tubers. Am. Potato .1.47:105-fl 7, 

SCIII PIERS. P. A. 1971. Measurement of black spot susceptibility of 

potatoes. Am. Potato .1.48:7 1-81. 

SMft III0. I''X. Internal black spot olpotatoes. Pages 303-307 in: O. 

Smith. cd. Potatoes: PIrductior. Storing. Processing. A\i 

Publishing (o.. Iic.. Westport. C 1.642 pp. 

IIM M, II.. M.YAMAGI ('III. l).I.llt'(illl!S. arf M. I. WEAVER. 

1976. Influence of ethylene oil black spor of potato tubers. Am. 


(Prepared by S. L. Sinden and R. W. Goth) 

Greening and Sunscald 

When tubers are exposed for some time to light in the field or 

after harvest, chlorophyll forms in the leucoplasts and tuber 

tissue turns green. Stiln green. somieties less correctly called siriscald, 

develops in tubers not covered by soil in the field and 

therefore exposed to intense sunlight. 

Green tissue may extend 2 cm or more into the tuber and is 

often accompanied by purple pigmentation. Such tissue is high 

in solanine, bitter in flavor, and believed to be toxic to hurnaits 

when ingested. The processes of greening and solanine 

production are independent. Affected tubers are not marketable. 

and losses may be high. 

Srnnscald iniur\ de\clops in tubers exposed ftrintenrise 

sunlight as restricted areas with ahiost-white skin. often 

covering a sunken necrotic area. (See high temperature field 

i ni ry.) 

Certain potato cultivars have atendency to set tubers near the 

soil surface. Throwing soil toward tie planats during ct,ltivatiens 

often effectively covers tubers and redces greening. However. 

tubers may be exposed later by soil erosion or by cracks formed 

is soil dries or tubers enlarge. Ordinarily, severely greened 

tubers ire not predisposed to rot unless sunlight and heat have 

been intense. 

Table stock potatoes should be stored in the (lark. 

Fluorescent or natural lighting in market displays causes 

superficial and, occasionally, deeper lavers of the tuber to turn 

green. Color is persistent it.is not removed by placing tubers in 

the dark. Greening develops more rapidly at room temperature 

than in cold storage. Potato cultivars show differences in 

intensity of greening and the depth to which it develops. Tuber 

rinses with surfactants. used experimentally, show promise of 

reducing the intensity of greening. 


AKEIFY. R. V., i. V. C. ItOUGII.ANI, and A. E. SIIARK. 1962. 

Genetic differences in potato-tuber greening. Am. Potato .1. 

39:419-417. 

G I1.1.. 1).D.. and . M. ISENItER(. 1960. Chlorophyll and solanine 

content and distribution in foul varieties of potato tuber. Proc. Am. 

Soc. Ilorlic. Sci. 75:545-556. 

I'. A.. I. PRICE. arid F.R.FORSY III. 1978. Controlling 

post storage greening it table stock potatoes with ethoxylated 

mono-and diglyceride surfactants and i,adjuvant. Am.Potato J. 

55:35-42. 

(Prepared by W. .1.Hooker)

Internal Sprouting multiple sprouts also cause internal sprouting. 

Sprouts that develop during storage may become ingrown by 

penetrating into the tuber. Internal sprouts frequently are in 

eyes with tightly clustered multiple "rosette" sprouts, which may 

be unbranched or. more frequently, nranched (Fig. 20). Sprouts 

may penctratCtile tuber directly above. or sprouts from an eye 

on the bottom of the tuber may grow up through the same tuber. 

Sprouts from tubers ssith deep eyes may penetrate into tile side 

of the eve depression. 

The disorder has been kno\n for oser a century. It is more 

frequent in old tubers and in those stored at 12-15 ° C. Pressure 

on tubers within the storage pile restricts sprout growth and 

induces sprout penetration of tuber tissue. In old tubers, sprouts 

often tuberi/e within the parent tuber, splitting it open. 

Internal sprouting was recently associated with sprout 

inhibitors used in concentrations below those required for 

complete sprout inhibition. Concentrations that completely 

inhibit all external sprouts also inhibit internal sprouts, but 

insufficient concentrations actually stimulate internal sprouts. 

Isopropyl-nm-chlorocarbanilate (CI PC) stimulates internal 

sprouting to agreaterextent than does pressure on tubers under 

a deep pile. Other chemicals stimulating tightly clustered, 

r t 

" 

Fig. 20. Internal sprouting, showing rosette of sprouts on the 

underside, small tubers on internal sprouts, and necrosis under 

or at the sprout apices. The last resembles calcium deficiency. 

(Courtesy E. E.Ewing) 

r 

-'"Coiling 

Fig. 21. Secondary tubers formed directly on sprouts from 

physiologically old tubers. 

Necrosis at or slightly below the sprout apex is common on 

the external sprouts of tubers containing internal sprouts, and 

apicies of internal sprouts become similarly necrotic when they 

emerge from the tuber. (See Ca deficiency.) 


EWING. E. E...1. W. LAYER. .1.C. IIOHN, and 1). J. I.ISK. 1968. 

Effects of chemical sprout inhibitors and storage conditions on 

WIEN, internal II.C.and sprouting 0. SMITH. in potatoes. 1969. Am. Influenceof Potato .1.45:56-71. sprout tip necrosisand 

rosette sprout formation on internal sprouting of potatoes. Am. 



Secondary Tubers 

Tubers sprout either in storage or in the field, producing tiew 

tubers directly without forming a normal plant. Secondary 

tubers form on sprouts from physiologically old tubers after 

completion of the rest period when carbohydrate reserves are 

low (Fig. 21). The disorder is associated with warm (200C) 

storage followed by low temperature after planting or by 

transfer of sprouted tubers from warm to cold storage. Even at 

low temperatures, however, physiologically overmature tubers 

held past normal usage form secondary tubers. Usually the 

problem is of minor importance, although poor field stands with 

missing hills result. (See also calcium deficiency.) 


BURTON, W.G.1972. The response of the potato plant and tuber to 

temperature. Pages 217 -223 in: A. R. Rees. K. F. Cockshull. I). W. 

Hand, and R. G. [lurd. cos. Crop Processes in Controlled 

Environinents. Academic Press. Ness York. 391. pp. 

DAVIDSON, T. M. 1958. t)ormancy in the potato tuber and the effects 

of storage conditions on initial sprouting and on subsequent sprout 

growth. Am. Potato J. 35:451-465. 

VAN SCHREVEN, I). A. 1956. On the physiology of tuber formation 

in potatoes. 1. Premature tuber formation. Plant Soil 8:49-55. 

(Prepared by W..1. Hooker) 

Coiled Sprout 

The disease has been reported primarily from the British Isles, 

where up to 26% of plants in certain fields are affected, but it 

probably exists elsewhere. 

Symptoms 

Underground sprouts lose their normal negative geotropic 

habit and coil. sometimes rather tightly, with the curved portion 

of the stem often swollen and sometimes fasciated or split (Fig. 

22). Light brown lesions with transverse or longitudinal cracks 

may be present on the stem inside the coil. Delay in emergence of 

coiled sprouts results in uneven stands. Affected plants may 

produce more stems than normal, and tubers may form 

unusually early and mature slowly. 

Causal Factors 

is believed to be the result of overmature seed, soils 

resistant to sprout penetration and emergence, or infection by a 

fungus. Verticillium nuhilunt Pethybridge has been isolated 

from affected stems. This pathogen has caused superficial 

browning and russeting of some stem bases, accompanied by 

shallow cortical invasion underlaid by suberin. In some 

instances, inoculation with the pathogen has caused coiled 

sprout, but IVnubihmn is not the sole cause of the disease. 

Low soil temperatures. presprouting in light, long sprouts at 

17

Wk,- 

Fig. 22. Coiled sprout. (Courtesy M.A. Alli, J.H. Lennard, and A. 

E. W. Boyd) 

the time of planting, overmature seed tubers with long sprouts 

that may form tubers before sprouts emerge from the soil, and 

deep planting in compacted soil have been associated with the 

disorder. Ethylene in low concentrations as produced by sprouts 

induces coiled sprout characteristics. 

Control 

I) Avoid planting seed tubers with long sprouts. 

2) Avoid planting in compacted soil resistant to sprout 

penetration. 


AI.l.M.A.. J. I. LENNARD. and A. . W. BOYD. 1970. Potato 

coiled sprout in relation to seed tuber storage treatment and to 

infection by 1I'rticillium nubihon Pethybr. Ann. Appl. fliol. 

66:407-415. 

CAT(CffPOf,- A. i1., and .I. R. fIl1I IMAN. 1975. Studies of the coiled 

sprout disorder of the potato. Parts 2and 3. Potato Res. 18:539-545 

and 597-607. 

COX, A. E. 1970. Early tuberisation associated with coiled sprout in 

Craigs Royal potatoes. Pliant Pattiol. 19 :49)-50. 

TIMM. I.., .1.C. BIS HOP. I. W. PERI)UE. I). W. GiRIMIES. R. E. 

VOSS. and 1), N. WRIGIII1. 1971. Soil crusting on potato plant 

emergence aid gros tli. Calif. Agric. 25(August):5-7. 

(Prepared by W. .1. Hooker) 

Hair Sprout 

Tubers with hair (or spindle) sprout germinate early, 

sometimes even before harvest, producing thin sprouts as small 

as 2 mm in diameter. A single produce 

tuber may normal 

18 

sprouts and hair sprouts fron d ifferent eves. Hot. dry 

conditiot.s in the late growing season, particularly during tuber 

development, favor hair sprout lormation. flair sprout has been 

induced in tubers of certain. but not all, culti\ars by warmrl water 

treatment for 2 fir at 45C. 

Virus infection has not been consistently associated with 

spindle sprouts. Early maturity foilowing attack by 

Colleiotrichum atramentarium may predispose to spindle 

sprout. Certain mvcoplasma (liseases (aster vellows) and pysllid 

yellows are also known to cause hair sprout. (See also genetic 

abnormalities -wildings and feathery wildings and internal 

heat necrosis.) 


ORAD. : 

A. G., and 1. P. SAN ROMAN. 1955. Conditions which 

dIetermine 

Stretntgers. spindling A. Ii. R. spotli licet'tistcr, of potto 1). Noo'daiun. in Spain. anidt .1. 1 ) . Lages 160 

11. \Van dlr 

171 in. :. 

\Want. eds. Proc. Second (onl. Potato Virus f)is.. lissc-Wagcningen, 

June 1954, II. Veenmnan an(f Zonen. Wageningcn. 193 pp. 

SNYDER. W. C., H., . I IIMAS, and S. J. I-AIRCIIl.tD 

Spindling 

1946. 

or hair sprout of potato. Phytopathologv 36:897-904. 

STEINI-CK, 0. 1955. ntersuchungen und Bleohachtungen diber die 

Fadenkeimnigkeit %on 

24:195-210. 

Kartoffelknollen. Phltopalhol. Z. 

SWENZI.. II. 1966. Fadenkeitnigkeit und Kallose-bildung durch 

Varnm\a .schearidundhg \on Kartolfelknolh.n. Re. Rourn. hiol. 

Ser. Ilot. 1:271-276. 

(prepared by W. .1. H,oker) 

Nonvirus Leafroll 

Leafrolling is a symptom with several unrelated causes. When 

carbohydrate translocation from the foliage is impaired, starch 

accumulates in the leaves, causing them to become leathery and 

roll upward (Fig. 23) in a way similar to that of virus lea froll. 

Leafroll-like symptoms, with or without chlorosis and 

pigmentation, 

red 

may accompany Rhiioctonia, Fusarium wilts. 

and other diseases; injury by mycoplasitas. and mechanical 

injury of stems. 

Leafrolling may also be genetic. Although genetic nonvirus 

leafroll has symptoms similar to those of' virus leafroll. its 

nonvirus origin was established by I'ailure of graft 

infect 

transfers 

suitable 

to 

indicator hosts. The recessive mutant gene (I r) 

causes starch accumulation in leaves, but anatomically defective 

phloem is not detectable. 

Certain nutritional soil conditions. such as nitrogen toxicity. 

also cause nonvirus leafroll. Rolling of leaves is uniformly 

intense from plant to plant. In contrast, leaf'roll severity in virus 

leafroll usually differs 

differ in 

considerably 

degree of response. 

between plants. 

Correction 

Cultivars 

of unsatisfactory soil 

- 

A4 B 

Fig. 23. Nonvirus leafroll: A, plant grown in calcareous muck; B, 

apparently normal plant grown in similar soil supplemented with 

sulfur. (Courtesy W.J. Hooker and G. C. Kent) 

:

conditions permits normal leaf development. 

Toproll affects the plant's apical leaves. Its symptoms are 

similar to those of virus leafroll, but toproll results from feeding 

by the potato aphid lfacrosiphum euphorhiacin the absence of 

thle leafroll vrus. When aphid feeding is discontinued, new 

growth is normal. Plants grown from progeny tubers are free 

from toproll and give normal yield. 


I)ZIEWONSKA. M. A.. and R. K. McKEE. 1965. Apparent virus 

infection in hcalthy potatoes. lotato Ies. 8:52. 

(0IBSON. R W. 11I75. Potato sced tubcrsdo not transmit lop-roll. Plant 

Pathol. 24:107-108. 

HOOKER. W. .1..and G. C. KENT. 1950. Sulfur and certain soil 

amendments for potato scab control in the peat soils of northern 

lossa. A\n. Potato .1.27:343-365. 

L.eCI1R(i, 1. I.. 1944. Non-s irus leafroll of Irish potatoes. Am. Potato 

.1.21:5-13. 

REESIMAN, A. l. 1973. Some observations on "toprol" in the 

Netherlands. Proc. Irienn, Conf.. Fur Assoc. Potato Res. 5:184. 

SIN NIMONIS, N. V. 1965. Mlutant expression in diploid potatoes, 

Ann. An'pl. Biol. 20:65-72. 

VOL K. G. M.. and N. (GAMMON. .r. 1954. Potato production in 

Florida as influenced by soil acidity and nitrogen sources. Am. 

Potato 1.31:83-92. 


Hail Injury 

Hail tears and often perforate, leaves (Plate 4). Although the 

potato plant has a remarkable ability to recover from foliage 

damage, hail may caust defoliation sufficiently severe to impair 

y'ields. On stems. injury is localized at the point of impact; 

epidermal tissue turns gray with a paperlike sheen. 

Yield reduction varies with severity of injury, time of injury, 

and cultivar. (ireatest losses result from vine damage within 2-3 

weeks after blossom set. Marketable yields are adversely 

affected through the relative increase in small tubers or in offshaped 

tubers. Specific gravity may be reduced when hail 

damages mature vines. Hail injury seldom predisposes foliage to 

infection except for the Ulocladium disease in the tropics. 

Selected Reference 

IBER .SFOR1).I.C. 1967. Effect of simulated hail damage on yield and 

quali.v of poiatoes. Am. Potato .. 44:347-354. 


Wind Injury 

Wind injury is evident on upper surfaces of leaves that, 

through wind movement, have been rubbed by other leaves, 

usually those directly above the affected area. Discolorid tissue 

is brown when dry, varies in size, has a glistening or oily 

appearance (Plate 5). and sometimes extends through the leaf. 

following severe high winds, leaves may be tattered at the edges 

and the plant may appear hard (non succulent). Verycold winds 

lasting for some time cause undersurfaces of leaves, particularly 

those turned over by the wind, to be brown, sometimes with a 

silvery or glassy 

leaf 

sheen. 

injur ay be more severe at the edges of the field. 

D uring harvest. tubers Lcafinjry e moein 

y rvin, 

sver 

harvest, 

sacks ay in attheedge 

tubrsi 

tile fied 

sacks 

m oftil av be 

ince 

fild.Am. damagedA 

fedtae damage 

by drying wind. Injury may become evident later during storage 

as sunken spots underlying the skinned portions of tubers. The 

surfaces may be overgrown with bacterial slime, causing decay 

in storage. Damage is greater with immature than with n,,tture 

tubers and with open mesh sacks than with tightly woven ones. 


GRACE,.. 1977. Plant Response to wind. Academic Press, New York. 

204 pp. 

WHITEMAN, T. M.. and .1.M. LUTZ. 1954. Sunken scald spot field 

injury evident in stored potatoes. Am. Potato J. 31:43-49. 


Light Injur 

Liggtuin 

Lightnir,- injury frequently accompanies severe 

thunderstornis, ';everity is influenced by field and plant 

hydration. Diagnosis of injured plants without information 

about the distribution of plant injury in the field is hazardous 

because plant symptoms may resemble those of blackleg or 

Rhizoctonia injury, and tuber symptoms may closely resemble 

those of ring rot. Bleached stems at soil line often resemble those 

injured by high temperatures. 

Symptoms 

Within a few minutes to a few hours following lightning, 

stems collapse and tops of plants irreversibly wilt. Leaves may 

remaiti green and turgid even though stems collapse. In most 

cases, injury extends 5-10 cm or more above the soil line; it 

rarely proceeds from the top downward. Affected portions are 

soft, water-soaked, and discolored black to brown. Tissues soon 

dry and become chocolate brown to tan, with the surfac= layer 

light tan to almost white. Pith collapse results in flattened, 

ribbed, or angular stems with longitudinal depressions of the 

surface. Collapsed pith forms horizontal plates, and when the 

stem is split longitudinally the pith pnears crosshatched or 

ladderlike (Fig. 24A). 

Leaf petioles in contact with soil are often collapsed. 

Belowground portions of stems and roots frequently escape 

injury. Water transport is often sufficient to maintain green, 

turgid tops, which may survive despite collapse of 

parenchymatous stem tissue. 

Injured tubers have brown to black skin necrosis with some 

cracking. Surfaces may be injured on opposite sides of the tuber, 

with intermediate cortex and pith becoming soft and remaining 

relatively normal in color for ashort time. Later, decay extends 

completely through the tuber, leaving a hole. Unaffected 

portions of tubers often remain solid. In some, the cortex is 

intact even though the pith iscompletely collapsed and watery. 

Tubers may resemble those affected by other diseases such as 

Pythium leak or bacterial ring rot (Fig. 24B). 

Epidemiology 

A field may show various patterns of injury: I ) areas in which 

all plants are killed adjacent to ciearly defined areas of healthy 

plants, 2) areas with dead plants at the center and progressively 

reduced injury toward the periphery, 3)poor defined arias with 

no focus of injury, in which plants with varying degrees of injury 

are scattered among dead plants and unaffected ones (Fig. 25), 

and 4) a number of scattered, relatively small foci containing 

seseral plants in various stages of injury. 

These variations result from differences in intensity of 

electrical discharge and from variations in soil hydration. 

Electrostatic discharge and conduction along irrigation pipes is 

related to field distribution of injured plants. 


HOOKER. W.J. 1973. Unusual aspects of lightning injury in potato. 

m Potato Poa oJ 

SAM J.50:258-269. 

50 5 -69 

)EL, G. 1940. Lightning injury to potato tubers. Ann. Appl. Biol. 

27:196-198. 

WEBER. G. F. 1931. Lightning injury of potatoes. Phytopathology 

21:213-218. 


19

IAA 

94 / 

I Am 

/N 

F. n iFig. 26. Photochemical oxidant injury, first evident as collapse of 

Fig. 25. Lightning damage, showing irregularly affected area. palisade mesophyll. Bar represents 50 pm. 

Air Pollution: Photochemical Oxidants progresses upwards. Later, plants become generally chlorotic, 

with premature leaf death progressing usually from the bottom 

upward. 


Leaves eventually 

injury by photochemical 

drop but do not 

oxidants 

abscise rapidly. 

such as ozone, Lower leaf surfaces may be light in color occasionally with a 

probably peroxyacetyl nitrate, and related compounds has glazed or silvery sheen. 

recently been recognized. Symptom differences in the field Except for severe reduction in yield associated 

between 

with 

the 

veryearly 

several photochemical oxidants have not yet been senescence, tuber symptoms have not been reported. 

determined. Losses in sensitive cultivars may be severe Symptoms become evident within 24 hr following 

following 

heavy 

exposure early in the season, exposure, but symptoms of advanced necrosis and chlorsis may 

require 10-14 days. 

Symptoms 

Histopathology 

Upper leaf surfaces are stippled by darkly pigmented spots, Palisade mesophyll cells are first affected (Fig. 26), becoming 

sometimes with chlorosis and often with a bronzed appearance water-soaked and later necrotic. The spongy mesophyll and 

(Plate 6). Injury is most severe on the lower, older leaves and epidermis collapse later. 

20

Epidemiology 

Oxidant injury is present in North America along the Atlantic 

coast, in the Great Lakes region, the southeastern states, and the 

Pacific southwest. 

Photoche-:cal oxidants accumulate under two conditions: 

when relati, - large areas of high atmospheric pressure are 

present or wl.en air masses stagnate under a layer of warm air 

over cool land surfaces. Episodes in which normal dispersion of 

air pollutants is prevented may occur infrequently during the 

growing season. Extent of injury is influenced by the 

concentration of oxidants, length and frequency of exposure, 

plant genotypc, and stage of plant growth. 

Field exposures of approximately 0.15 ppm ozone for a day 

or two are usually sufficient to injure xposed foliage. The 

amount ofdaniage islargely influenced by density of the foliage 

mass. If the foliage mass is sufficiently large, a "sink" effect is 

produced, by which air pollutants are absorbed or adsorbed by 

leaf surfaces and removed from the immediate environment, 

thereby protecting nearby foliage. Thus, exposed leaves above 

the foliage canopy may he severely damaged and leaves within 

the canopy escape injury. Injury may be more severe at field 

margins than in the center. If plants are small, leaf and stem 

exposure is complete and the sink effect is negligible; thus plant 

injury may be severe following an earl) season episode. 

Ozone injury can predispose potato leaves to Boir tiscinerea 

infection and may increase susceptibility to other pathogens. 

Control 

Wide varietal differences in tolerance exist. 

Cultural practices stimulating vigorous early season vine 

growth may hasten plants past the susceptible, small vine stage. 

Maintenance of a heavy foliage canopy until the tuber crop is 

assured may lessen or avoid midseason injury, 

Selectd References 

BRASIIER, E.P.,I). J. FIELI)HOUSE, and M. SASSER. 1973. 

(/one injury in potato variety trials. Plant l)is. Rep. 57:542-544. 

HEGGESTAD, H. E. 1973. Photochemical air pollution injury to 

potatoes in the Atlantic Coastal States. Am. Potato J. 50: 315-328. 

HOOKER. W.., T. C. YANG, and H. S. POTTER. 1973. Air 

pollution injurv of potato in Michigan. Am. Potato J. 50:151-161. 

MANNING, W. J..W. A. FEDER. 1.PERKINS, and M. 

GLICK MAN. 1969. Oione injury and infection of potato leaves by 

Botrviis ciwerea. Plant Dis. Rep. 53:691-693. 

MOSI.tY. A. R., R. C. ROWE, and T.C. WEIDENSAUL. 1978. 

Relationship of foliar ozone injury to maturity classification and 

yield of potatoes. Am. Potato .1.55:147-153. 


Air Pollution: Sulfur Oxides 

Although potato leaves are relatively resistant to injury by 

sulfur oxides, they re-pond with iaiterveinal necrotic areas that 

are light tan to white (Plate 7), and yields may be reduced. Injury 

should be anticipated in areas with air flow drainage patterns 

downwind from power plants and smelters. If sulfur oxides a-r 

injuring potatoes, symptoms on nearby sensitive plants (alfalfa, 

bean, soybean, beet. /1maranthus spp., bindweed, morning 

glory, lettuce, curly dock, plantain, ragweed, or sunflower) 

should confirm the diagnosis. 


JONES, H. C.. 1). WEBER, and 1). BALSILI.IE. 1974. Acceptable 

limits for air pollution dosages and vegetation effects: Sulfur 

dioxide. Paper No. 74-225. Air Pollution Control Assoc. 67th 

Annual Meeting, )enver. 

THOMAS, M. I)., and R. H. HENDRICKS. 1956. Effect of air 

pollution on plants. Section 9. pages 1-44 in: P. I.. Magill, F. R. 

Holden. and C.Ackley. eds. Air Pollution Handbook. McGraw- 

Hill. New York. 


Chemical Injury 

A wide range of chemicals accidentally or improperly applied 

can cause divergent symptoms on foliage and in tubers, with 

severity depending upon the nature of the chemical, its dosage, 

environmental factors, and plant maturity and variety. Vinekilling 

preharvest defoliants frequently cause necrosis at the 

stolon attachment and vascular discoloration of the stem end, 

resembling symptoms of stem-end browning or Verticillium 

wilt. Interveinal leaf tissues may be burned. Moisture stress 

increases symptom severity. 

Growth-regulating herbicides for weed control in potatoes or 

herbicide-s airborne from nearby areas may cause leaf distortion 

superficially suggesting virus infection (Fig. 27A and B). Tuber 

skin color may be affected. Some ( 2 ,4,5-trichlorophenoxyacetates) 

cause necrosis not unlike that from severe deep 

scab and also tuber deformation (Figs. 27C and D). 

In storage, netting of tuber surfaces and dehydration have 

followed foliage application of maleic hydrazide; abnormal 

sprouting has been associated with other compounds. (See 

internal sprouting.) 

Improper application of fertilizer to foliage or application 

too close to the seed piece in the soil causes foliage or seed tuber 

necrosis, followed by decay, poor stands, and low plant vigor. 


FRYER, J. D., and R.J. MAKEPEACE, eds. 1972. Weed Control 

Handbook. Vol. 2. Recommendations Including Plant Growth 

Regulations, 7th ed. Blackwell Scientific Publications, London. 424 

HOOKER, W. J., and A. F. SHERF. 1951. Scab susceptibility and 

injury of potato tubers by 2 ,4,5-trichlorophenoxyacetates. Am. 


MUNSTER, J.,and P. CORNU. 1971. D~gts interne3 causes aux 

tubercules de pommes de terre par lasfcheresse ou par I'application 

de reglone. Rev. Suisse Agric. 3:55-59. 

MURPHY, H. J. 1968. Potato vine killing. Am. Potato J. 45:472-478. 

POABST, P. A., and C. GENIER. 1970. A storage disorder in 

D 

Fig. 27. Chemical injury: A, burn of interveinal leaf tissue; B, Leaf 

deformation by growth-regulating herbicide; C and D, tuber 

injury from foliaga application of 2,4,5-trichlorophenoxyacetate. 

(C and D,Courtesy W.J. Hooker and A. F. Sherf) 

21

Kennebec potatoes caused by high concentrations of maleic 

hydrazide. Can. .1.Plant Sci. 50:591-593. 

STEPHENS, H.J. 1 9 65. The place of herbicides in the potatocrop. Eur. 

PotatonJ. 8:33-51. 


Stem-End Browning 

Stem-end browning describes an internal, brown 

discoloration of tuber tissue near the stem end or stolon 

attachment. In its broadest sense, the term is applied to a 

shallow discoloration with one or more unknown causes. These 

may include chemical injury, sudden death of the vines, or 

infection from pathogens, including viruses. Usually it does not 

show up at harvest but develops during the first one to three 

months in storage. It is often confined to the 12-mm section at 

the stolon end of the tuber and is more frequent in smaller 

tubers. If penetration is deeper, the brown strands are confined 

to the xylem of the vascular ring. 

The disorder may b" :onfused with virus leafroll net necrosis 

(Fig. 28A). However. the latter penetrates deeper into the tuber, 

and its brown necrotic strands involve the phloem either inside 

S-. 

A B 

"' -z--. 

-. ,. 

Fig. 28. A, Stem-end browning; B, virus leafroll net necrosis. 

(Courtesy Main Life Sciences and Agricultural Experiment 

Station) 

Nutrient deficiencies or excesses are frequently difficult to 

diagnose without analysis of the plant and may beconft sed with 

other environmental stresses. )eficiency or exce.;s of a 

particular nutrient may be influenced by its availability, its 

balant e with other nutrients, soil pH. ion-exchange hivels, and 

other factors. Because potatoes are grown unjer widely 

different conditions of altitude, day length, light inensities, soil 

types, temperatures, and soluble salts, general symptoms 

described for nutrient disorders are often based upon controlled 

sand culture trials rather than on field conditions. 

Potatoes grow well in soils above pH 5.0. In more acid 

conditions, Ca atd Mg deficiency, phosphate fixation, and 

ammonium, Mn. and Al toxicity may occur, and leaching of 

some nutrients (e.g.. Mg) is increased. Conversely, highly 

calcareous or overlimed soils crL.Ite unfavorable alkaline 

reactions that reduce availability of Mn, Fe, B, and Zn. 


CHAPMAN, H. D.. ed. 1966. Diagnostic Criteria for Plantsand Soils. 

University of California. I)ivision of Agricultural Science. 793 pp. 

22 

Nutrient Imbalance 

or outside of the xylem. It is more prevalent in larger tubers, and 

affected tubers always produce leafroll-infected plants. 

Recently, stem-end browning has been associated with early 

season leafroll virus infection, in which a limited amount of 

tissue is affected and the virus does not always establish 

infection. Thus affected tubers ma: not produce leafrol plants. 

Stem-end browning may also come from another virus, as yet 

unidentified. The virus isapparently graff-transmitted and is 

more prevalent in certain clone lines: its characteristics have not 

been further clarified. 

Stem-end browning has noapparent effect on yield, although 

affected tissue is believed to he sterile. Stem-end browning is 

distinguished from Fusarium or Verticillium wilts by culture 

techniques and from Verticillium infection or defoliants by 

darker color and coarser strands. Other tuber discolorations 

often confused with stem-end browning include those due to 

rapid vine killing (by chemicals or flame) or to frost or frost 

necrosis. 

Control 

Cultivars differ in resistance. 

Avoid excessive applications of phosphorus, potassium, or 

chlorine in the fertilizer. 


FOLSON, D., and A. E. RICH. 1940. Potato tuber net-necrosis and 

stem-end browning studies in Maine. Phytopathology 30:313-322. 

MANZER. F. E.. I). C. MERRIAM. and R. Hf. STORCH. 1977. 

Effects of time of inoculation with PIRV on internal tuber necrosis. 

Am. Potato J. 54:476 (Abstr.). 

RICH. A. E.1950. '1hle effect of various defoliants on potato vines and 

tubers in Washingion. Am. Potato .. 27:87-92. 

RICH, A. F. 1951. Phlocm necrosis of Irish potatoes in Washington. 

Wash. Agric. Exp. Sin. Bull. 528. 

ROSS, A. F. 1946. Susceptibility of Green Mountain and Irish Cobbler 

commercial strains to stem-end browning. Am. Potato J. 

23:219-234. 

ROSS. A. F. 1946. Studies on the cause of stem-end browning in Green 

Mountain potatoes. Phytopathology 36:925-936. 

ROSS, A. F., J. A. CHUCKA, and A. HAWKINS. 1947. The effect of 

fertilizer practice including the use of minor elements on stem-end 

browning, net necrosis, and spread of leafroll virus in the Green 

Mountain variety of potato. Maine Agric. Exp. Sin. Bull. 

447:96-142. 

(Prepared by A. E. Rich) 

HOUGHIAND. G. V. C. 1964. Nutrient deficiencies in the potato. 

In: Sprague. II. B.. ed. 1964. Ilunger Signs in Crops. 3rd ed. David 

McKay Co., Inc.. New York. 461 pp. 

WAlLACE. T. 1961. The I)iagnosis of Mineral )eficiencies in Plants 

by Visual Symptoms, a Colour Atlas and Guide, 3rd ed. Chemical 

Publishing Co.. Inc.. New York. 125 pp. with 312 color plates. 

Nitrogen 

Adequate N in the presence of sufficient P and K stimulates 

apical and lateral meristems and thus increases leaf 

development. Adequate N should be available during rapid 

plant growth and tuberization. N requirements increase rapidly 

with plant growth, as N is translocated from lower to upper 

leaves and much of it eventually to the tubers. 

Deficient plants are generally chlorotic, slow growing, erect, 

and have small, erect, pale green leaves (Plate 8). Lower leaves 

are most severely affected. Veins stay green somewhat longer 

than does interveinal tissue. The extent ofdeficiency determines

sevritof stnting, chiorosis. loss of' lower leaves, and vied 

reduction, 

Speckle leaf'. brown to black spots about I mm in diameter 

that may coalesce on lower leaves of some early cultivars. is 

particularly severe ollos ing heavy rainfall or irrigation and is 

alleviated by nitrogen side dress. 

When N toxicity occrs.iCiclds arc reduced: root de\ehlptiicnt C' 

is poor: and lea\es may roll upward or be deforned as "mouse 

ear.- N toxicity can result from the forn of N available to the 

plant. Alnmonil illd or nitrites formed Iromii urea and 

dianmroniuni phosphates are toxic. Incertain soil conditions, 

principally \,er acid soils. conversion of amlnoniuni nitrogen to 

nitrate nitrogen is i paired. In nutritional leafroll, nitrate 

nitrogen is insufficient to balance ainotherwise normal amount Fig. 29. Potassium deficiency symptoms on tubers. 

ot annioniur 

Note corky 

nitrogen a\ailable to tie plant, sunken areas at stolon end. (Courtesy W. M.Laughlin) 

Surf'ace applications of urea. esrecially when banded tihigh 

rates. can cause damage from ammonia \olatiliiation. 1Burning 

of leaves and stem lesions de\elopi ng near urea pellets are due to green spots (approximately I mm in diameter) appear between 

am monia \olatili/ation and not to an osmotic or salt effect, veins of larger leaflets, resembling mild mosiac. When K is in 

relatively short supply, older leaves first become bronzed, then 

Selected References necrotic (Plate 9). and senesce early. Leaflet margins from the 

middle to the top of the plant roll 

NIItN(iIR.I 

upward. l.eaflets are small, 

1). R. IOt'll)l Nand E. I). JONES. 1978. Potato cupped, crowded together, 

ield 

crinkled, 

reductions 

and 

associated 

bronzed on 

\%ith 

the 

certain 

upper 

fertiliier mixtures. Am. surface. The overall bronzed 

Ilotarn 

effect 

.I. 55:227-234. 

of the foliage is 

predominant, leaves frequently 

VI ;OSL 

have dark 

I. I... 

brown 

and 

specks 

R. W.('IIASE. 

on the 

atfected by fr tier and ,sater manuagement. 

1973. Speckle leaf 

A m. 



potato as 

.I. 

lower 

S m 

surface, 

t m 

which 

a' 

may 

d v. 

coalesce 

rr 

and 

i 

cause 

l 'i'' 

marginal necrosis. 

. ' 

50:311-314. 

Phosphorus 

Symptoms 

bright weather 

may develop rapidly 

following 

within four days during 

cloudy, sunny, 

rainy periods. Necrosis is 

severe and may superficially resemble early blight. Stalks may 

be slender with short internodes. When K is acutely deficient, 

P1is essential early in plant growth and later in tuberization. 

Early season deficiency retards growth of terminals, and plants 

are small, spindly, and somewhat rigid. l.eaflets fail to expand 

nornially. are crinkled or cup-shaped (Plate 8), darker than 

normal. lusterless, and may be scorched at the margins. L.ower 

leaves may drop. ILeaflets are not bronzed, leaf petioles are 

More erect than normal. Maturity may be delayed. 

Roots and stolons are reduced inboth number and length. 

lhibers lack external syniptoms. but internal rusty' brown 

necrotic flecks or spots are scattered throughout the flesh in 

sometimes radial patterns. (See also internal heat necrosis and 

calcium deficiency.) 

l)eficicncy occurs on a \wide range of' soil types: calcareous 

Soils. pear or rmuck. light soils with low initial P content, and 

heavy soils in sshich P is lixed. Muclh of the P is translocated 

frorn vines to tubers, and the crop rerioves a considerable 

ariount if ' froi the soil. Banding of P lateral to the seed piece 

decreases P)fixation and improves P uptake over that from 

broadcast application. little can be done to alleviate P- 

deficiency symptoms during the growing season, although 

foliage a pplicatiorns with neutral ammonium phosphate or 

polyphosphate 

p herevplea are archeful. hielpf'ul, h , e ln ie 

Where P levels are vry ig. especially in alkaline soils, the 

uptake and or utilization of' Zn or Fe may be reduced. 

the growing point is affected and general dieback develops. 

Plants become short and squatty with shiortened internodes. 

They' appear droopy because of downward leaf curling. 

Roots are poorly developed and stolons ate short. Tuber size 

and yield are reduced. Necrotic, brown, sunken lesions develop 

at stolon ends of tubers of plants with necrotic foliage. Later, the 

affected tissue dries out, Iortiiing a hollow spot. 2mm or more in 

diameter. surrounded by corky tissue (Fig. 29). 

K deficiency predisposes to black spot. During early storage, 

K-deficient tubers frequently develop brown to black enzymatic 

discoloration (f raw cut surfaces on exposure to air. 

Discoloration is frequently more severe at the stolon end of the 

tuber. Tuber flesh also becomes dark after cooking. 

K deficiency is most common on light, easily leached, sand, 

muck, or peat soils. Exchangeable K should exceed 200 kg/ ha 

(178 l b A) in the upper 20 cm of soil. 


BAER UG,R., and R. EN(E. 1974. Influence of potassium supply and 

s:orage conditions on the discoloration of raw and cooked potato 

tubers of cv. Pimpernell. Potato Res. 17:271-282. 

FONG, K. It. and A. I.RICl-. 1969. Growing potato plants by the 

L.AUGHl.IN, ater culture W. technique. M. 1966. Am.Potato Effect of soil .1.46:269-272. 

applications of potassium, 

nagnesium sulfate and niagnesi unl sulfate spray on potato yield. 

composition and nutrient uptake. Am. Potato J. 43:403-411. 


L.AUGH I.IN, W. M., and C. I. )EARIBORN. 1960. Correction of leaf 

necrosis ofpotatoes Nitlh foliar and soil applications of potassium. 

IIA-Rt'(i. R.. and K. SI ENIIERG. 1971. Influence of placement 

method and vater supply on the uptake of phosphorus by earl' 

poratoes. Potato Res. 14:282-291. 

llt)t'(ilI NI). . '. U. 1960. [he influence of phosphorus on the 

gros, rh and physiology of the potato plant. Am. Potato .1. 

37:127-138. 

Am.Potato .1.37:1-12. 

MUL.) R, . G . 1949. Mineral nutrition in relation to the 

biocliemistry and phvsiology of potatoes. Plant and Soil 2:59-121. 

Calcium 

Potassium Ca-deficient plants are spindly, with small, upward rolling, 

crinkled leaflets having chlorotic margins that later become 

necrotic (Plate 9). In severe deficiency, leaves are wrinkled and 

K is essential ftornormal growth and is highly mobile within stem tips cease to funitii. giving a rosette appearance. Root 

tIre plant. meristems cease to grew. 

Early appearance of unusually dark green, bluish green, or Tubers on Ca-deficient plantsdevelop diffuse brown necrosis 

glossy foliage is a dependable symptom of K deficiency. I.ight in the vascular ring near stolor attachnments, and later similar 

23

Fig. 30. Calcium deficiency on potato sprouts: A, healthy sprout; 

B, sprout treated with calcium sulfate; Cand 0, calcium-deficient 

sprouts. Note necrosis of tips and tendency for lateral branching. 

(Courtesy P.W. Dyson and J.Digby, and copyright permission of 

Macaul,y Institute for Soil Research) 

flecks form in the pith. Tubers may be extremely small. Internal 

rust spot is more severe on dry soils with low Ca, a tendency 

towards acidity, and amoderate to low base-exchange capacity. 

(See also internal heat necrosis and phosphorus deficiency.) 

Seed tubers in Ca-deficient soil remain hard and produce 

relatively normal roots. Sprouts become necrotic immediately 

behind the tip and fail to grow (Fig. 30). In storage, sprouts 

become necrotic 3-5 mm below the tip due to collapse of outer 

cortex and inner pith and, later, of vascular tissue. Multiple 

lateral branches form below the sprout tips, and, with certain 

cultivars, small tubers known as "little potato" form 

prematurely before the development of aboveground sprouts. 

Ca deficiency and internal sprouting show certain relationships. 

Symptoms are most severe on sandy soils below pH 5.0, 

where symptoms of Mn or Al toxicity may also be present. 

Calcium treatment of sprouts reduces incidence of necrosis 

below the tip. liming the soil above pH 5.2 should be avoided 

because of potential Tranferof problems ld lave Ca with fom toyoun common levesand scab. romthe 

Transfer of ('a from old leaves to young leaves and from the 

top of the plant to the tubers is limited. Ca must therefore be 

available during the entire growing period, particularly during 

tuberization. 


BRAUN, H., and I). E. WILCKE. 1967. lodenprofile und ihre 

Beziehungen zum standortbedingten Auftreten der Eisenfleckigkeit 

bei Kartoffeln. Phytopathol. Z. 59:305-336. 

DeKOCK, P. C., P. W. DYSON. A. HALL, and F.B.GRABOWSKA. 

1975. Metabolic changes associated with calcium deficiency in 

potato sprouts. Potato Res 18'57-5 I. 

WALI.ACET.,and E.J.HEWITT. 1948. Effects of calciumdeficiency 

on potato sets in acid soils. Nature 161:28. 

Magnesium 

Mg deficiency is one of the most commonly encountered 

nutritional problems. Because Mg is highly mobile within the 

plant, new growth appears essentially normal and symptoms 

develop on older leaves. A pale, light green color--later, amore 

definite necrosis begins at the leaf tips and margins and 

24 

progresses between the veins, becoming most severe toward the 

center of the leaf. l.eaves are usually thick and brittle and roll 

upward, with tissue raised between tile veins (Plate 10). Necrotic 

leaves either hang on the plant or abscise. Roots are stunted, 

reducing the ability of the plant to absorb Mg. 

Mg deficiency usually occurs on sandy acid soils that are 

readily leached. but may occur on heavier soils. High rates of K 

fertilizer or high K levels in soil accentuate Mg deficiency. 

Solubility of Mg is increased b. acid-forming fertilizer. 

Sym ptomis freq uenti'follow leaching after periods of heavy rain. 

Exchangeable Mg should exceed 50 ppm for mineral soils and 

higher (100 ppm) for muck soil. 

Mg may be supplied as MgSO 4 in fertilizer or dolomitic 

limestone or as a 2'i MgSO 4 foliage spray. Higher 

concentrations usually may be applied to foliage without injury. 


BONI)E, R. 1934. Potato spraying -- lhe value of late applications and 

magnesium-bordeaux. Am. Potato .1.11:152-156. 

CH UCKA, J.A., and B.E.BROWN. 1938. Magnesium studies with the 

potato. Am. Potato .. 38:301-312. 

SAWYER. R.L.,and S.L.I)AI.t.YN. 1966. Magnesium fertiliation of 

potatoes on Long Island. Am. Potato J. 43:249-252. 

Sulfur 

S deficiency, as reported in several locations in Wisconsin on 

Planefield loamy sand, is a generai yellowing with a slight 

upward rolling of leaflets. Symptoms vary from slight to 

marked chlorosis over the entire plant. Beneficial responses 

have been obtained with sulfur soil applications or with 

fei ,;,'izers containing sulfur. 

Aluminum 

A Itoxicity causes roots to become short and stubby with few 

branches. Leaves remain normal in color although plants are 

small and spindly, with branches rising at acute angles. Potato;, 

relatively tolerant to Al toxicity. 

Al solubility is often high in soils below pH 5.0. Soil 

conditions may be corrected by adding superphosphate 

fertilizers, increasing soil pli to 5.5 or above with lime, or 

increasing the organic content of the soil. 


BROWN, B.A.. A. H AWKINS, F.. J. RI)BI3NS. A. V. KING.and R.I. 

MUNSEI.LI. 1950. Causes of very poor growth of crops on a 

formerly productive soil. Soil Sci. Soc. Am. Proc. 15:240-243. 

HAWKINS, A.. B.A. BROWN, and E..1. RUIBINS. 1951. Extreme 

case of soi toxicity to potatoes on a forme rlyproductive soil. Am. 


Boron 

In plants with B deficiency, growing points die; lateral buds 

become active: internodes are shortened: leaves thicken and roll 

upward: and tileplant assumes aI bushy appearance. Starch 

accumulation in leaves is pronounced and may resemble virus 

leafroll. Roots are short, thick, and stunted. Tubers are small. 

showing surface cracking particularly at the stolon end and 

localized brown areas under the skin near the stolon end or 

brown vascular discoloration. 

Some sandy soils, peat soils, and overlimed, acid, upland, 

podzolized soils are inherently low in B or apparently fix B so 

that it becomes unavailable to plants. 

Applications of B should be made cautiously because B is 

toxic to potatoes in relatively small amounts and deficiency is 

rare.

Selected Reference brown to bronze areas, later becoming necrotic, may develop on 

leaves near the middle of the plant and later involve all leaves. 

MIIGI.EY. A. R., and 1). F. I)IINKII. 1940. Ihe cause and nature Brownish spots may develop on petioles and stems. 

of oserliming injury. VI Agric. Exp. Stin. Bull. 460. 22 pp. Zn deficieney in recently developed land. alkaline soils, or 

soils with excessivcly high1P results in severe stunting, leaf 

Zinc malformation, and indistinct bron/ing or yellowi ng around leaf 

margins. The "fern leaf" sympton (Fig. 31 ) is present when the 

youngest leaves are cupped upwards and rolled, becoming thick, 

Zn deficiency causes stunting of plants and upward rolling of brittle and puckered from expansion of intercostal tissue and 

young. chlorotic leaves suggestive of early virus leafroll apparent lack of expansion of leaf margins. Severely affected 

symptoms, with terminal leaves being somewhat vertical. Gray plants die early. 

Foliage applications of ZnC I : or ZnS0 4 alleviate deficiency 

symptoms. In some cases without recogni/able Zn deficiency. 

yield increases have been obtained when Zn salts were applied to 

foliage as fungicides or used as soil treatments. Excessive liming 

or application of 1)enhlnces symptoms of Zn deficiency. 

Speckle bottom (small to large necrotic spotting and chlorosis 

of basal leaves, which progress upward) has responded to 

applications of zinc. 

In laboratory studies, Zn toxicity develops as general 

stunting, with a slight chlorosis at tips and margins of upper 

leaves and purple coloration on the undersides of lower leaves. 


HOAWN, I.. C., and (i. lECGE'. 1963. Zinc deficiency of the 

Russet Burbank potato. Soil Sci. 95:137-141. 

CIPAR. M.S., D. E. ItUN IR. W. W. WE1IR. R. MII.1.ER.and P. 

PORIER. 1974. Soil fumigation and /inc stattus of soils in 

relationship to potato speckle-hottom disease de\elopment and 

control. Potato Res. 17:30'/-319. 

HOYMAN. W. G. 1948. Potato-lungicide experiments in 1948. N.D. 

Agric. Exp. Stn. IBimonthly Bull. 11:32-35. 

Fig. 31. "Fern leaf" symptom of zinc deficiency. (Courtesy L. C. I.ANGII.E, A. I.. and R. I. IATlEESE, Jr. 1974. Influence of inc 

Bowan and G. E. Leggett) concentration in nutrient solution on growth and elemental content 

• | 

.., 

' 4l' 

Fig. 32. Manganese toxicity: A, early symptoms on stems; later symptoms of manganese toxicity within (B) and on (C) stems. (A, Courtesy 

H. W. Gausman; B and C, courtesy K. C. Darger) 

25

26 

of the "Katahdin" potato plant. Am. Potato J. 51:345-354. 

SOI.TANPOUR. P.N.,J.O. REUSS, J. G.WAIKER, R. D. 1EIL. .. 

W. IlNDSAY. J. C. HANSEN. and A. .1.REIYEA. 1970. Zinc 

experiments on potatoes in the San L.uis Valley of Colorado. Am. 


Manganese 

Deficiency symptoms develop on the upper parts of the plant 

as loss in luster. Light green interveinal chlorotic tissue later 

becomes yellow to white (Plate 10). lower leaves are least 

affected, but leaves nearshoot tips often roll upward. When the 

deficiency issevere, brown necrotic spots develop along the vcins 

of younger leaves. 

Mn deficiency is possibly the most common micronutrient 

problem for potatoes grown on muck, sandy muck, or 

depressional soils in central and eastern coastal areas of the 

United States. It is reported on calcareous or excessively limed 

soils of high pH. Mn should be applied when leaf tissue tests 

show less than 25 ppm Mn. Manganese sulfate applied to foliage 

at the rate of 1.1-2.2 kg of Mn per hectare ( - 2 !b A)is useful to 

correct the deficiency. Certain fungicides containing Mn also 

alleviate the condition. 

Mn toxicity, to which the potato is especially, sensitive, has 

been called stem streak, stem streal necrosis, land streak, or 

stem break. Cultivars differ in sensitivity or tolerance. Early 

season Mn toxicity develops slowly: initial symptoms are 

necrotic flecking of stem and petioles (Fig. 32A). Sometimes leaf 

flecks develop into elongate, dark brown pitted streaks. This 

occurs first at the lower stem and progresses upward, being most 

severe at petiole bases and developing on the petioles (Fig. 

32Band C). Necrosis becomesevident at400 ppm in lowerleaves, 

It appears first on the epidermis and later extends deep into 

the cortex, ray tissue, and pith. The Mn content in leaf 

tissue and the symptom severity increase rapidly after the 

blossom stage. Affected parts become necrotic and dark brown 

and are extremely brittle. The terminal bud may eventually die. 

The plant remains stunted and may die early. In solution 

culture, 25 ppm Mn reduces growth. 

Leaves lose their typical bright green color and show a pale, 

yellow-green interveinal chlorosis that becomes progressively 

severe, often with marginal necrosis. Eventually the leaves dry, 

hang down, and break off as the petiole becomes brittle. 

Inverveinal necrosis may precede leaf death. 

Symptoms have not been described in tubers except that yield 

may be severely impaired. 

Neither pH alone, Ca deficiency, Mg deficiency, nor Al 

toxicity cause stem streak necrosis. Stem necrosis by rugose 

mosaic virus may be superficially somewhat similar. 

Symptoms of Verticillium wilt are enhanced in pot culture in 

soil with a high level of Mn. 

Mn icre:!es in soluHlity as the soil becomes more acid; 

toxicity occurs on light acid soils at pH 5.0 and below. Additions 

of lime to raise soil above pH 5.0 are usually effective in avoiding 

injury. Both symptom severity and Mn content of leaves are 

reduced with Ca lime soil treatment and increased with chloride 

or sulfate fertilizers. 


BERGER, K. C., and G.C. GERLOFF. 1947. Stem streak necrosis of 

potatoes in relation to soil acidity. Am. Potato J. 24:156-162. 

CHENG. B.T.. and G.J.OUEILETTE. 1968. Effect of variousanions 

on manganese toxicity in Solaoun: tuberosum. Can. J. Soil Sci. 

48:109-115. 

I.ANGILI.E. A. R.. and R. 1. BATTEESE, Jr. 1974. Influence of 

manganese concentration 

elemental 

in nutrient 

content 

solution 

of the "Katahdin" 

on the growth 

potato 

and 

plant. Can. 

54:375-381. 

J.Plant Sci. 

ROBINSON, D. B.. G. D. EASTONand R. H. IARSON. 1960. Some 

common stem streaks of potato. Am. Potato J. 37:67-72. 

WHITE, R. P.. E. C.DOLL, and J. R. MELTON. 1970. Growth and 

manganese uptake by potatoes as related to liming and acidity of 

fertilizer bands. Soil Sci. Soc. Am. Proc. 34:268-271. 

WHITE. R. P., A. R.SIETING. and E. C. DOLL. 1972. Manganese 

fertilization of potatoes in Presque Isle County. Mich. State Univ. 

Agric. Exp. Stn. Res. Rep. 179. 2 pp. 

(Prepared b' W. J. Hooker with assistance from L. M. 

Walsh on nitrogen and sulfur sections and from R. E. 

Lucas on magnesium and manganese sections)

Part II. 

Disease in the Presence 


Blackleg, Bacterial Soft Rot 

Blackleg affects stems and may produce soft rot in tubers. 

Blackleg and bacterial soft rot are principally caused by two 

varieties of the same species of bacterium, Erwinia carotolora. 

They are found wherever potatoes are grown. Bacterial soft rot 

also affects the fleshy and leafy organs of a wide range of other 

plants and E. cuarolovora var. atroMsetlica has been reported on 

sunflowers in Mexico and sugar beets in the United States. 

Symptoms 

Blakeg.Symptoms occur at any stage of plant development, 

Stems of infected plants typically exhibit an inky black decay, 

which usually begins at the decaying seed piece and may extend 

u; the stem only a few millimeters or for its entire length (Fig. 

33A. Plate I1). Stem pith is often decaved above the black 

discoloration, and vascular tissues in the stem are often discolored. 

Infected plants are commonly stunted and have a stiff, 

erect growth habit, particularly early in the season. Foliage 

becomes chlo-otic, and leaflets tend to roll upward at the 

margins. L.eaflets and, later, entire plants may wilt, slowly 

Bacteria 

*,. e,2" . 

,,,:,, 4,, 

decline, and eventually die. Young shoots may be invaded and 

killed before emergence. 

Stems, petioles, and leaves may also become infected through 

wounds such as petiole scars, hail, or wind damage. Infection 

may progress up or down the stems or petioles, thus producing 

typical blackleg symptoms on plants that do not show infection 

from infected seed pieces. In wet weather, decay is soft and slimy 

and may spr-ad to most of the plant. Under dry conditions, 

infected tissues become dry and shriveled and are often 

restricted to the underground portion of the stem. 

Tubers produced by infected plants may show symptoms 

ranging from slight vascular discoloration at the stolon end to 

soft rot of the entire tuber. Typically, infected tubers have soft 

rot in the pith or medullary region of the tuber only, extending 

into the tuber from the stolon end (Fig. 33B and C). 

Soli Rot. Tubers can also be affected with soft rot while in 

storage or in the soil before harvest, and seed tubers decay after 

planting. Infection occurs through lenticels and wounds or 

through the stolon end of the tuber via the infected mother 

plant, Lesions associated with lenticels appear as slightly 

sunken, tan to brown, circular water-soaked areas, approxi 

!° 

..... ? 

A BC 

Fig. 33. Blackleg: A,Erwinia carotovora var. atroseptica infection progressing up stems from decayed seed piece; B and C,tuber infection 

through stolon from plant infected with blackleg. 

27

mately 0.3-0.6 cm in diameter (Plate 12). In dry environments 

they may become sunken, hard, and dry. Sometimes 

infection is arrested, and the diseased area dries, leaving a 

sunken area filled with a mass of hard, black, dead material, 

Lesions associated with injuries are irregular in shape, sunken, 

and usually dark brown. 

Soft rotted tissues are wet, cream to tan, with a soft, slightly 

granular consistency (Plate 13). Infected tissues are sharply 

delineated from healthy ones and are easily washed away. 

Brown to black pigments often develop near the margins of 

lesions. Rotting tissue is usually odorless in the early stages of 

decay but develops a foul odor and a slimy or ropy consistency 

as secondary organisms invade infected tissue, 

Causal Organisms 

Blackleg. I. ,arotevora var. atroseptica (Van Hall) Dye and 

sometimes E. (arotovora var. e'arotovora (.Jones) l)ve cause 

blackleg. tE. 

has 

chrysanthemi 

recently 

Burkholder, 

been isolated 

McFadden, 

from 

&Dimock 

infected potato plants with 

blackleg symptoms in Peru. 

.So/' Rbt. E. arotovora var. aro ovura (.Jones) Dyc and 

c'arouovora 

. 

var. atros.eptica (Wan IHall) l)yc are the most 

common causes of soft rot. Sorie pectolytic PCo'Idonloaas spp., 

Bacillhus spp.. (/lo1tridiu,, spp.. and Ilavothacteriunm 

pectinocvortnt have also been found associated with soft rot 

infections. 

L. carotovora is easily cultured and produces deep pits, or 

craters, on selective media that contain polypectate, such as 

Stewarts MacConkey-pectate medium or the Cuppels and 

Kelman crystal violet-pectate medium (CVP). Some 

P.'etidonronasspp. and . pctiovorumcan also be cultured on 

these media but produce only very shallow pits. Bacillus spp. 

cannot be cultured on the CVP medium. 

I:. carotooravar. alr) tla and E'. 'arlovoravar. 'arotovora 

are rod-shaped, (ram-negative bacteria, approximately 

0.7 × 1.5 pim in si/c. and have peritrichous flagella. They are 

Tionspore-forming and are facultativelv anaerobic. 

. carolovoravar. atlro. ep a forms acid frotn maltose and 

at-methylglucoside, produccs reducing substances from sucrose, 

atnd does not grow above 36°C on nutrient agar or in nutrient 

broth. 

Typical strains of' . caro ovora var. carolovora do not form 

acid from e-methiylglucoside nor reducing substances from 

sucrose and will not grow above 360 C on nutrient agar or in 

nutrient broth. Most strains do not produce acid from maltose, 

although strains that do so are sometimes encountered, 

IHistopathology 

Bacteria invade intercellular spaces, where they multiply and 

produce pectolytic enzymes, including pectin methyl esterase, 

depolymerase, and pectin lyase. These macerate the tissues by 

breaking down the middle lamella. Cellulolytic enzymes, produced 

in much smaller amounts, partially soften the cellulose in 

the cell walls. Water diffuses from the cell into the intercellular 

.7naces, and the cells collapse and die. Starch is not destroyed 

except in the later stages of decay. 

Disease Cycle 

Blackleg. The primary blackleg inoculum is borne on or in 

seed tubers. After being planted, seed pieces decay at varying 

times throughout the growing season, releasing large numbers 

of bacteria into the soil, and sometimes infecting the stem of the 

host plant (Plate 13). Bacteria may multiply and persist during 

the growing season in the rhizosphere of the host and, possibly. 

in the rhizospheres of certain weeds. They may survive the 

winter in infected stems or tubers. Bacteria will survive in soil for 

at least ashort time. Survival is longer in cool, moist conditions 

than in warm. dry conditions. The presence of infected plant 

debris or tubers extends survival of bacteria, 

Bacteria may move for sonic distance in the soil water and 

contaminate developing daughter tubers ofadjacent plants. The 

amount of contamination of daughter tubers may vary greatly 

28 

from season to season depending upon environmental 

conditions. Bacteria enter lenticels, growth cracks, or injuries at 

harvest time and can survive in contaminated tubers during the 

entire storage period. They are readily spread during seed 

cutting and handling operations. 

Soft Rot. Soft rot has asimilar disease cycle. Bacteria are also 

efficiently spread in water used to wash tubers. 

Epidemiology 

Blackleg. Contamination of seed tubers by Erwiniais favored 

by moist soil and relatively cool temperatures (generally lower 

than 18-19'C) and is generally more frequent in northern 

production areas. 

Erwinia cells released into the soil from decaying seed pieces 

survive for varying periods of time, depending upon soil 

temperature and, to a lesser extent, soil moisture. They may 

survive for 80-110 days at 2'C but for shorter times at higher 

temperatures. Some studies have indicated 

Erwinia 

that the half 

cells 

life 

in 


soil is approximately 0.8 days 

° 

at -290C, 7.8 

days at 0 C, 5.6 days at 70 C, J. I days at 130 C, 0.8 days at 180 C, 

and 0.6 days at 240C. 

Tubers produced under warm (23-25' C or higher), dryconditions 

are less likely to be contaminated because the pathogens 

are less likely to survive, and they spread through the soil for 

shorter distances than when the soil is cool and moist. Tubers 

harvested from crops grown under dry soil conditions and high 

soil temperatures may be essentially (or completely) free from 

Erwinia contamination even though they were produced by 

plants grown from Erwinia-contaminated seed tubers. 

Cool wet soilsat planting time followed by high temperatures 

after plant emergence favor postenergence blackleg expressionhigher 

soil temperatures favor seed piece decay and preemergence 

death of shoots. Greater total blackleg losses occur in 

warm areas than in cool ones. 1. caroiovoravar. carolovora 

may cause typical blackleg infection ifsoil temperatures are very 

high (30-35 0 C). 

Invasion of seed pieces by Fusarium spp. may predispose 

tissues to soft rot and favor blackleg development. High 

nitrogen fertilization may retard blacklegexpressioi iii die field. 

Several species of insects disseminate bacteria from potato 

cull piles or infected plants to seed pieces or stems of healthy 

growing plants. Erwinia aerosols generated by rain or overhead 

sprinkler irrigation or those generated by mechanical vine 

destruction may also aid in spreading disease. Mechanical seed 

piece cutters are responsible for widespread contamination of 

seed pieces by Frwvinia spp. 

Soli Rot. Soft rot in tubers is favored 

wounding, 

by immaturity, 

solar irradiation, invasion by other pathogens, warm 

temperatures, high moisture, and lack of oxygen. Tubers harvested 

at soil temperatures above 20-25' C are highly susceptible. 

Decay isfavored by temperatures above 100 C and retarded 

by lower temperatures. The optitnim temperature for decay by 

Erwiniais above 25-30' C, which isalso the optimum range for 

growth of the pathogens in vitro. 

Soft rot caused by species of Psetudonronas, Bacillus, and 

Chostrid/ium is favored by temperatures of 30' C or higher. 

Anaerobic conditions resulting from poor aeration, flooding 

of soil, or the presence of I water film on tubers after washing 

favor disease development. High nitrogen fertilization also 

increases susceptibility. 

Control 

Blackleg. 

I) Plant seed tubers and, especially, cut seed tubers in welldrained 

soil. 

2) Avoid excessive irrigation to prevent anaerobic soil conditions 

that favor seed piece decay and subsequent stem invasion. 

3) Treat seed tubers with approved fungicides or suberize 

them well before planting to reduce infection by Fusarium spp. 

and other pathogens that predispose to bacterial invasion. 

4) The use of seed tubers derived from stem cuttings may 

greatly reduce losses cauised by blackleg and soft rot. Such seed

should be planted on land with at least two to three years 

between potato crops, longer if volunteer potatoes are a problem. 

Lri'inia-free stocks may be rapidly rccontaminated. especially 

by L. caroto\vora var. carotovora under some conditions. 

5) Remove potato cull piles, discarded vegetables, and plant 

refuse to avoid inoculum sources from which insects transmit 

:rivinia spp. 

6) Frequently clean and disinfect seed cutting and hanaling 

equipment as well as planters, harvesters, and conveyers to 

eliminate contamination. This should be done at least between 

different seed lots. 

7) Avoid washing seed potatoes unless absolutely necessary, 

and exercise care 

to 

during 

seed tubers.Br 

handling operations to reduce damage 

t) Fertilie adequately with nitrogen. 

9) To reduce spread of bacteria to healthy plants, remove 

infected plants as soon as they appear. 

iectdt lati 

i Aoid eand 

lenticel infection, 

2) lilarvst tubers only when mature and only when soil- 

2) n~v 1laresttubrs henmatre nd n~v hensui tell- 

peratures are less than 20' C. Minimize mechanical damage to 

tubers during harvesting and handling. 

desiccation. 3) Protect harvested tubers from solar irradiation and 

4) Cool tubers to 10 ° C or lower as soon as possible after 

h4rest Cool tstoor atltomp t r as oo as possible ftery 

arvest and store at temperatures as low as possible (preferably 

.- 4.50 C). Good ventilation to keep tubers cool and to prevent 

accumulation of CO: and moisture films isespecially important. 

5) Avoid water films on tuber surfaces, eg, condensation that 

results from placing tubers with low pulp temperatures into 

storage with relative humidity above 90('. 

6) IDo not wash tubers before storage, and when washing 

them 

package 

before 

them 

marketing, 

in well-aerated 

dry 

containers, 

them as soon as possible and 

7) pse only clean water to wash potatoes. Contaminated 

holding tanks used for soaking potatoes almost assure soft rot 

hdinction sed frshowater potato ing almose ue 

infection. 

ast 

Treat 

ont 

wash water with chlorine to reduce the amount 


BUCIIANAN. R.[-..and N.E.GIBBONS, eds. 1974. Bergey's Manual 

of )e:erminative Bacteriology.8thed. Pages337-338. Williamsand 

Wilkins. Baltimore, M). 1,268 pp. 

('IPITI.S. I)..and A. KEIMAN. 1974. Evaluation of selective media 

for isolation of soft rot bacteria from soil and plant tissue. Phytopathology 

64:468-475. 

I)elOIR. S.II.. and A. KF I.MAN. 1975. F.valuation of procedures for 

detection of pectolytic Erwinia spp. on potato tubers. Am. Potato J. 

52:117- 123. 

)el.INI)O, I... F.R. FRE-NCII,and A.KEIMAN. 1978. Erwiniaspp. 

pathogenic to potatoes in Peri. Am. Potato .1.55:383 (Abstr.). 

GRAHAM, I). C., and .1. . IIARI)IE. 1971. Prospects for control of 

potato blackleg disease by the use of stem cuttings. Proc. Br. 

Insectic. Fungic. Conf.. 6th. pp. 219-224. 

IARRI SON. M. I).. C. E. QUINN. I. A. SE.L.S, and 1). C. 

(iGRAlAM. 1977. Waste potato dumps as sources of insects contaminated 

with soft rot coliform bacteria in relation to 

recontamintion of pathogen-free potato stocks. p'otato Res. 

20:37--52. 

I.NI), B. M., and G;.M. WYATT. 1972. The effect of oxygen and 

carbon dioxide concentrations on bacterial soft rot of potatoes. I. 

King Edward potatoes inoculated with Eroinia carotovora var. 

ltro ep tima . P o ta to R e s . 15 :17 4- 17 9 . 

MOIINA. ... , and M. I). IHARRISON. 198. The role of Erwinia 

rarotovora in the epidemiology of potato blackleg. II. The effect of 

soil temperature on disease severity. Am. Potato .1.57:351-369. 

NII-IS-N, I.. W. 1946. Solar heat in relation to bacterial soft rot of 

early Irish potatoes. Am. Potato .1.23:41-57. 

NIEIlSEN. ILW. 1949. Ftu.oaritom seedpiece decay of potatoes in Idaho 

and its relation ti blackleg. Idaho Agric. Exp. Stn. Res. Bull. 15. 

31 pp. 

NIEI.SIEN, I. W. 1978. Eritiniaspecies in the lenticels of certified seed 

potatoes. Am. Potato .1.55:671-676. 

O'NEI I,., R., and C. LOG AN. 1975. A comiparison of various selective 

media for their efficiency in the diagnosis and enumeration of soft 

rot coliform bacteria J. Appl. Bacteriol. 39:139-146. 

PEROMBELON, M. C. M. 1974. The role of the seed tuber in the 

contamination potato Res. 17:187-199. by Erwinia carotovora of potato crops in Scotland. 

STEWART., D.J. 1962. A selective-diagnostic medium forthe isolation 

of pectinolytic organismts in the Enterobacteriaceac. Nature 

195:1023. 

(Prepared by M. D. Harrison and L. W. Nielsen)- 

Brown Rot 

Brown rot, also known as bacterial wilt or southern bacterial 

w roas kn w asb ceilw tors uh nb cera 

wilt, affects potatoes in almost every region in the warmtemperate, 

semitropical, and tropical zones of the world and has 

been reported from relatively cool climates. It limits growing of 

potatoes and other susceptible crops in parts of Asia, Africa, 

South and Central America. In the United States the disease 

occurs in the Southeast from Maryland to Florida. It has rarely 

occurred in the Southwest or Midwest and has not been confirmed 

west of the Rocky Mountains. 

Symptoms 

Field symptoms are wilting, stunting, and yellowing of the 

foliage. These may appear at any stage in the potato's growth. 

Wilting of leaves and collapse of stems may be severe in young, 

succulent plants of highly susceptible varieties. Initially, only 

one branch in a hill may show wilting. If disease development is 

rapid, all leaves of plants in a hill may wilt quickly without much 

change in color. Wilted leaves may fade to a pale green and 

finally turn brown without rolling ofthe leaflet edges as they dry 

(Plate 14). In young potato stems, dark narrow streaks, 

corresponding to infected vascular strands, become visible 

through the epidermis. 

Brown rot and ring rot have similar but distinguishable 

symptoms ('Fable 1). A valuable diagnostic sign of brown rot is 

glistening beads of a gray to brown slimy ooze on the infected 

xylem in stem cross sections. If the cut surfaces of a sectioned 

infected stem are placed in contact and then drawn apart slowly, 

fine strands of bacterial slime become visible and stretch ashort 

distance before breaking. 

To demonstrate bacteria in vascular tissue, a longitudinal 

section from a diseased stem can be placed s, that surface 

tension holds it to the side of a beaker of water and a short 

segment of the tissue projects below the water surface. Fine 

milky white strands, composed of masses of bacteria in extracellular 

slime, stream down from the cut ends of xylem vessels 

Table I. Differences Between Brown Rot 

and Ring Rot 

Characteristic Brown Rot Ring Rot 

Gram GrOham stain staearnn 

Bacterial exudate 

Conditions 

seodoaoorws L oneln t 

Negative Positive sie onict m 

Abundant droplets From vascular tissue, 

from vascular tissue, usually with 

usuallywithout squeezing 

u squeezing 

Color 

Symptoms 

Vines 

V i n e s 

Grayish hite Milky white 

Wilting by rapid Wilting usually with 

g r e e n w ilt i u s u a ll owi 

collapse; green wilt 

free from 

chlorosis 

chlorosis or yellowing; 

later, necrosis between 

veins of leaves 

Vascular 

tissue 

Tubers 

Eyes 

uistinct brovning 

usually evident in 

stems 

Surfaces usially not 

cracked 

Eixudate causes soil 

to adh,:re 

Discoloration in 

stems, often 

indistinct 

Cracks, when present, 

distributed randomly 

Free from adhering 

soil 

29

(Fig. 34B). Bacterial streaming can also be seen rnicroscopically 

in thin sections of infected tissue mounted in water under a cover 

slip. This bacterial exudate, combined with wilting and related 

symptoms, distinguishes this wilt from fungous wilts, 

Underground stems, stolons, and roots of plants with initial 

foliage symptoms show few advanced symptoms of infection, 

Grayish brown discoloration, usually evident through the tuber 

periderm, indicates well-established infection. Tubers from 

infected plants may or may not show symptoms: cross sections 

usually show distinct, grayish brown vasculardiscoloration that 

may extend into the pith or cortex from the xylem tissue, 

However, certain strains from Portugal and Kenya produce no 

browning of the vascular ring. 

When tubers are cut in half and light pressure is applied, 

grayish white droplets of bacterial slime ooze out of the vascular 

ring (Fig. 34A). The eves. often at the bud orapical end, become 

grayish brown, and a sticky exudate may form on them or at the 

stolon connection (Plate 15). The bacterial ooze mixes with the 

soil, causing soil particles to adhere to the tuber surface. An 

infected tuber left in the ground continues to decay; secondary 

organisms convert it to a slimy mass surrounded by a thin laver 

of cortex and periderm. 

Causal Organism 

Pseutdomonas solanacearum F3. F. Smith is a nonsporeforming, 

noncapsulate, Gram-negative, nitrate-reducing, 

ammonia-forming aerobic, rod-shaped bacterium. In liquid 

media, the wild-type bacterium is usually nonmotile and does 

Fig. 34. Brown rot: A, bacterial exudate from vascular ring of 

tuber; B, streaming of bacteria from infected stem in water; C, 

cells of Pseudomonas solanacearum (electron micrograph) of 

avirulent type with wavy flagellum; D,virulent form (flagellum is 

atypical). (A,Courtesy L.W. Nielsen; B,courtesy C.Martin; C and 

D, courtesy A. Kelman) 

30 

not form a polar flagellum. Avirulent variants that develop in 

culture are actively motile (Fig. 34C and D). 

Starch is not hydrolyzed by this bacterium, and gelatin is 

liquefied slowly or not at all. . solanacearuniis sensitive to 

desiccation and is inhibited by relatively low concentrations of 

salt in broth cultures. Optimal growth of most strains occurs at 

30-32' C,although some strains from Colombia grow relatively 

well at lower temperatures. 

Strains differing in biochemical characteristics and host range 

have been described. A strain pathogenic to potatoes is weakly 

virulent on tobacco but avirulent on banana; the banana strain 

is avirulent on potato; in contrast, tobacco and tomato strains 

are usuall \iitnllI potato. Somic strains of P..hnacearinm 

from Portugal and ..*;iya do not forl the typical lyrosinase 

reaction in cult ure tiedia. 

Cultures of . o/tltlcealIII)rlll aintinied io unicratcd liquid 

ilcdia rapidly lose kirulcnce and \iahilit and shilt tron the 

Iltuidal (11oni6otilC) \\ill-tvp'C to a\ irulnt. highl\ Motile 

variants. Colonies of virulent wild-types are irregularly round 

and are white with pink centers; colonies of avirulent variants 

aic uiiifolumly round, butyrous, and deep red. Colony characteristics 

are best observed when cell suspensions are streaked on 

plates of peptone casamino acid glucose agarcontaining 2,3,5triphenyltetrazolium 

chloride and examined in obliquely 

transmitted light after incubation at 32'C for 36-48 hr. 

Epidemiology 

In tropical and semitropical regions (southeastern Asia, 

Central and South America, and parts of Africa and Australia) 

the pathogen can be borne by tubers; quarantines exist against 

importation of seed potatoes in sonie areas. Infected seed 

potatoes are an important factor in the distribution and 

increasing severity of the disease in tropical countries such as 

Peru, where latent infections can occur in seed grown at high 

elevations. 

Temperature plays an important role in the geographic 

distribution of the organism, which is rare where mean soil 

temperaturesare below 15' C. In North America, seed potatoes 

are grown in the temperate regions where P. solanaearumdoes 

not occur, and tuber transmission is not a problem. tligh temperatures 

favor growth of the pathogen in vitro and 

development of the disease in the field. Recently, however,/: 

solanacearutn was reported in Sweden and at high altitudes in 

Costa Rica, Colombia, Peru, and Sri l.anka. Thus, the 

bacterium can possibly survive and infect potato crops at 

relatively low temperatures. 

The disease occurs in soil types ranging from sandy to heavy 

clay and over a wide range of soil pH. Disease usually develops 

in localized areas often associated with poor drainage. On newly 

cleared forest land, bacterial wilt may be severe if a susceptible 

crop is planted. 

Other Hosts 

Important economic hosts of P. solanacearum include 

tobacco, tomato, pepper, eggplant, peanut, banana, and a 

number of ornamentals and weeds. Although species in over 33 

different plant families may be attacked, most susceptible hosts 

are in the Solanaceae. 

Resistance 

At least three dominant and independent genes control 

resistance in potato to certain strains of bacterial wilt. 

Resistance is relatively sensitive to changes in environment; 

increased temperatures and decreased light intensity enhance 

susceptibility to wilt. 

Immunity or high levels of resistance have not been identified 

in clones of S. ttu/erosum. Colombian clones of S. phure/aJuz. 

& Buk. with resistance to bacterial wilt have been crossed with 

haploid lines of S. tuberosuim. Strains of P. solanaceartan 

differing in virulence have complicated breeding for wilt resistance, 

but two resistant varieties, Caxamarca and Molinera, have 

been released in Peru.

Control 

I) Use disease-free tubers and disinfect the cutting knife. 

2) Soil treatment chemicals such as sulfur are not widely 

accepted because of the low level of control and the high cost. 

3) P.solanaceartni survives for extended periods in some 

soils. In others it may not survive 1-6 months of fallow, 

4) Some crop rotation sequences reduce disease severity; they 

may act indirectly by reducing populations of root-knot 

nematodes that enhance bacterial wilt disease infection in 

potato. 


fllI)DEN IIAGI-N, I..and A. KELMA\ 1964. tiologicil and physiological 

aspects of bacteiial v%!t causcd by I.%edO mtontals 

sola m)ceartom . A nnu. Rev. PhIytopathol. 2:203-231. 

F ))INS. A. If. 1936. Irowvn rot of Irish potatoes and its control. Fl. 

Agric. F-xp. Sin. Bull. 299,.44 pp. 

FII.I)MESSER, .1.,and R. W. (Ill. 1970. Association of root knot 

with bacterial wilt of potato. Phytopathology 60:1014 (Abstr.). 

IIAY\WARI). A. C. 1964. Characteristics of Aseudonoas 

khn'aocarum.I.1. Appl. Itacteriol. 27:265-277. 


Cor' neacteritm sepedonictn (Spieck. & Kott.) Skapt. & 

Burkh. I is a (ram-positive nonmotile bacterium. Cells are 

KIFtM AN.A. 1953. fhe bacterial wil ca used by P'odomonal .vohaa 

('varulrm. N.C. Agric. F\p. Sin. fcch. Bull. 99. 194 pp. 

KIlIMAN. A. 1954. The relationship of pathogenicity in Pveudomo as 'ram stain (Reeds rapid) for bacterial smears: Stains 

vola'a'curon 

are Gram 

to colony appearance on a tetra/olium medium, positive bacterial cells blue and Gram-negative cells pink. Mix 

Phyt opathologv 

in equal 

44:093- 695. 

parts: I) crystal or gentian violet 0.251" aqueous 

KII.MAN. 

with 2)NaIICO 

A., and .1. IIRtSCII .KA. 1973. The role of motility and 

1.25(7 alqneous. Hood fot 1(lsee and drain. Mix 201i iodine 

aerotaxis 

in If 

in the selective increase of avirulent bacteria in still broth NaOII and dilute 1:10 in watcr. Flood for 10sec and wyash. 

C l t -resof Pwvd1 Ilotoo Iolata caru mt. . Ge. M cr0 il. 

acetone 

Mix I part 

svashes from 

and 

sicar. 

3 parts 

Flood 

957 

with 

ethyl 

watr. 

alcohol. 

I)ilute 

Rinse 

basic 

until 

76:177-1818. 

fuchsin 

no 

saturated 

more color 

in 

ethyl alcohol I: 10 in water. Stain not ,\er 2 sec. rinse thoroughlv, 

LOZANO. 

and 

.1.C.. ard I.. S OI lR.,'.. 197). )ifferentiation ofraces of dry. (Front Glick. 1).P.,1). A. Ark, and It. N. Racciot. 1944. Am. 

Po\'l' by a leaf infiltration technique. Phyto- Potato J. 21:311-314.) 

~toloill.I .;/apla~uvarm 

pathology 60:833-838. 

NIFI.SFN. I.. W., and F. I. IIAYNES. .Ir. 1957. Control of southern 

bacterial \kilt. Potato tHandbook Vol. 2. Am.Potato Assoc., New 

Itrunsssick. N.I. pp. 47-51. 

NIIlSEN, L. V..and F. I.. IIAYN-S, Ir. 1960. Resistance inSola,,tn 

t/'troulll tI P''tdowtoIaI .\oNl'anac'rumI..Atn. Potato .1. 

37:200- 207. 

ROIlNSON, R. A. 1968. the concept oIf vertical and hori/ontal 

resistance as illustrated bv bacterial wilt of potatoes. Phlvopathol. 

Paper No. Ill Cottntonsn. Mvcol. Inst.. Kew, Surrev. England. 37 

ROWE,1. R.. and I.. SEQUI£1RA. 1970. Inheritance of resistance to 

I.tml"ola(w(1l armin in Soh/11 (l IIrc0. Ph t tIth 

61:1499-1501. 

SfAIP, C. 1965. Die bakteriellc Schleitifliule und ihr Erreger 

'oIlIeodImoia .11solancearumi. Zentralb. flakteriol. Parasitenkd. 

Itfektionskr. Ilyg, Aht. 2 119:166-190. 

I'ItI, fON,II. I).. and .1.C. LOZANO. 1968. Resistance to bacterial 

s iltof potatoes in(o1hmbian clones of SI(anui ptureia. Am. 


(Pr1,epred by A. Kelman) 

Ring Rot 

Ring rot, or bacterial ring rot, was first recorded in Germany 

in 1906 and has since been found in man),other areas. Despite 

the lack of documentation in a few countries, ring rot has 

probably occurred wherever potatoes are grown. Through seed 

certification programs, many countries have successfully 

eradicated the disease. 

Symptoms 

Plant symptoms begin with wilting of leaves and stems after 

midseason. L.ower leaves, slightly rolled at the margins and pale 

green. are usually the first to wilt (Plate 16). As wilting progresses, 

pale yellowish areas develop between veins. Often only 

one or two stems of an infected hill develop symptoms. Two 

important diagnostic features are the wilting of stems and leaves 

and a milky white exudate that can be squeezed from the 

vascular ring of tubers (Fig. 35) and of stems when crosssectioned 

at their base. A dwarf-rosette type of symptom has 

been described in the Russet Burbank cultivar in the western 

United States (Fig. 36). 

This disease derives its name from the characteristic internal 

breakdown in the vascular ring of an infected tuber crosssectioned 

at the stem end. Squee/ing the tubers, particularly 

those fror.1 storage, expels creamy, cheeselike ribbons of 

odorless bacterial ooze, which leaves a distinct separation of 

tissues adjacent to the ring. Secondary invaders (usually soft rot 

bacteria) cause further tissue breakdown in advanced disease 

stages, obscuring ring rot symptoms. Pressure developed by this 

breakdown can cause external swelling, ragged cracks, and 

reddish brown discoloration, especially near the eyes (Plate 17). 

Although typical tuber symptoms are invariably apparent in 

badly infected lots at harvest, some infected tubers may remain 

symptomless for man weeks in cold storage. Occasionally, 

sym ptoms ay n bond ste n d 

typical internal symptoms may not he apparent at the stem end 

of the tuber but may be found near the apical or rose end. 

- • 

. " 1 

" " 

4,t " I 

"ology 

Fig. 35. Bacterial ring rot: A, surface cracking from Corynebacterium 

sepedonicum infection; B, cheesy breakdown of tuber 

vascular tissue. 

Fig. 36. Dwarf rosette symptom of ring rot. (Courtesy J. R. Letal) 

31

0.4-0.6 X 0.8-1.2 Mm and predominantly wedge-shaped, 

although curved and straight rods are also present. Single cells 

are most abundant, but V and Y configurations are often 

observed. Growth on all media is slow, and colonies rarely 

exceed I mnn in diameter after five days on nutrient glucose 

agar. 

Disease Cycle 

The organism overwinters primarily in infected tubers, either 

those in storage or those that survive the winter in tire field, It 

apparently cannot survive it unsterilized field soil, although it 

remains viable for nine months or more in dried shime on bags, 

crates, etc., in storage and in unprotected sites. Infection occurs 

through tuber wounds, especially from contaninated 

machinery and containers. Contaminated seed-cutting knives 

and picker planters are excellent disseminators. Invasion also 

occurs through wounds in stetns, roots, stolons, or other plant 

parts, and transmission has been experimentally obtained 

through tomato seed. Root inoculation is highly efficient and 

hastens syrnlitor development. Bacteria become established 

in large vessels and later invade xylem parenchyma and adjacent 

tissue and cause separation at tile vascular ring. Certain sticking 

insects transmnit tihe disease from diseased to healthy plants. 

Epidemiology 

Conditions for dissemination of the pathogen are most favorable 

itt the spring when infected seed tubers are warmed before 

planting, thus increasing bacterial activity. Surfaces of freshly 

cut seed provide ideal infection courts. Disease develops most 

rapidly at 18-22' C soil temperatures, but higher temperatures 

decrease infection from seed piece inoculation. In general, 

warm, dry weather hastens sympton development. but temperitures 

above optimum delay symptom expression. 

I)isease-resistant cultivars have been developed, but 

immunity isas yet unknown. No resistant cultivar has achieved 

economic prominence, and such cultivars may still serve as 

carriers. 

Other Hosts 

Only S. tulerurtom is affected naturally, although 28 

Solunnmt spp. and two L.r'colwrsicon spp. have been demonstrated 

experimentally to be symptom-producing hosts. 

Inoculation assays with young eggplants or tomato plants 

demonstrate the presence of ring rot bacteria in suspected 

potato plants. 

('ontrol 

Use of disease-free seed accompanied by strict sanitation 

procedures is the only method of control. 

I) Dispose of all potatoes from the farm when the disease is 

found. 

2) Thoroughly disinfect warehouses, crates, and handling, 

planting, harvesting, i.nd grading machinery. 

3) Use new bags for clean seed because disinfection of bags is 

not effective. 

4) Plant seed that is free of ring rot. Seed certification 

programs regularly reject stocks in which any ring rot is found. 

5) Do not plant disease-free seed in a field with volunteer 

plants from a previously infected crop. 


BONDE, R., and M. COVEIt.. 1950. Effect of host variety and other 

factors on pathogenicity ot potato ring-rot bacteria. Phytopathology 

41:161-172. 

CI.AFLIN. .. E.,and .. F.SIIEI'ARI). 1977. Anttgglutination test for 

the serodiagnosis (if ('orrthartgrioor .oepedoi r.n.notal r.. 

54:331-338. 

DeBOER, S. I1., and R .1.COPENIAN. 1974. Endophytic bacteria] 

flora in Solantui tuherosntt and its significance inbacterial ring rot 

diagnosis. Can. .1.Plant Sci. 54:115-122. 

DUNCAN, .I., and II. GENERE:UX. 1960. La trarsmrission par les 

insectes de (orr-nbac'eriom .%edothim (Spieck. and Kott.) 

32 

Skapason and IBurkholder. Can. .1.Plant Sci. 40:110-116. 

GUTI RIF. .1.W. 1959. hliearly, dwarf symplon of bacterial ring rot 

of potato in Idaho. I'hytopathology 49:453-454. 

KNOR Ani.R, Polatlo I. . .1. 1948. 25:361-37 Stiscept 1. range of the potato ring rot bacterium. 

tI..IOTT, R. A.. and 1. W. SF1.I.AR. 1976. the detection of latent 

ring rot (Corrneba'leritn.wpedotfictn (Spieck. et Kotth.) Skapt. 

et lurkh.) in potato stocks. For, and Mediterr. Plant Prot. Org. 

(F-1111O) full. 6:101-106. 

PAQUIN. R.. and II. GENEREI . 1976. Effet du clirnat stir la 

lietrissure bacterienne de la poninie de terre et relation avec le 

contenu en sucres des tiges. Can. .1. Plant Sci. 56:549-554. 

REIP()RT 10 (ER Ii FICA IION C(OMMII IF FlOFI I .11 P(OIAT 

AS"()(IA I ON 01" AM FRICA. 1957. Iow cal we interpret the 

zero tolerance for hactlial ring rot in certified seed potatoes'.' All. 

SLACK. S. A.. I. A. SANFORD) and F. F. MANZER. 1979. [Ie 

latex agglutination test as a rapid seriological assay for 

'orrnehacierihrm .upedonic on. Arn. Potato .1.56:44 1-446. 

(Prepared by F. Manzer and I1. Genereux) 

Pink Eye 

The disease is of minor importance, and little isknown about 

factors influencing tuber infection and disease development. It 

is not a problem with certain cultivars, but in susceptible 

cultivars incidence may be high. Pink eye isfrequent in tubers of 

plants infected with Verticillium wilt. 

Symptoms 

Pink areas around tile eye later turn brown. Discolored areas 

are particularly abundant at the apex of the tuber and are 

usually superficial but may extend into the tuber 8mm or more. 

Internal discoloration may result in cavities. 

Symptoms are most conspicuous at harvest, particularly 

following high soil moisture levels during tuber formation 

(Plate 18). In dry storage, tissue superficially affected with pink 

eye soon dries out, becoming scalelike and inconspicuous. In 

storage at high relative humidity, especially at high temperatures, 

rot may follow pink eye (Plate 19). Infection follows 

bruising and is involved in seed tuber decay. 

Although thedisease isassociated with Verticillium wilt, both 

diseases occur independcntly. Infection has also been linked to 

Rhi:octonia and to the wet rot phase of late blight infection. The 

color of affected tissue is very similar to that from late blight. 

The red xylem symptom follows infection of tile stolon end, 

c-using a scar at the stolon attachment or reddish brown 

vascular discoloration. 


The pathogen was identified in early in vestigat ioils as 

Pscudomonas./luorescensMigi:la Gram-negative rods, 0.3-0.; X 

1.0-1.3 pu in size, occurring both singly and in pairs. Cei;s are 

tsuallly motile and possess apolar fIlagellum but are occaslonally 

nonniotile. I'ectolytic enzymes are apparently active in pathogenesis. 

This identification of th causal bacterium is presently 

in considerable doubt. Mrich more infornation is needed on 

types of bacteria present in tuber lesions, pathogenicity of 

isolates to potato tutbers, and identification of the pathogen or 

pathogens involved. 

Control 

Store tubers under cool dry conditions to dry out affected 

tissue and to prevent disease progression in storage. 


('tPPFI.S. 1). A.. and A. KIIMAN. 1980. Isolation of pectolytic 

fltorescent pseuhmornads frot soil all potatoes. Phyt opt iItology 

70:111 (Ilt- 15. 

DOWSON. W.aJ.,nd I). R.JONES. 1951. Bacterial wet rot of potato 

tubers following Piot/thlwra ib-istans. Ann. Appl. Biol. 

38:231-230.

FOI-SO M. D, and I. A. FRIEDMAN. )959. I'.,,o,,ona. 

fluore.mens in relation to certain diseases of potato tubers in Maine. 

A mn. Potato .1.36:90-97. 

FRANK, J. A., R. E. WEBB. and I). R. WILSON. 1973. The 

relationship between Vcrticillium wilt and the pinkeye disease of 

potatoes. Am. Potato .1.50:431-438. 

SANDS, 1). C.. and I. IiANKIN. 1975. Ecology and physiology of 

fluorescent pectolvtic pseudomonads. Phytopathology 65:921-924. 


Bacteria in Potatoes 

That Appear Healthy 

Bacterial populations of various types are frequently present 

in stems and tubers of apparently healthy plants. Bacillus 

negaterium de Barv is comnon. as are somc apparently nonpathogentc 

(iram-positive bacteria and strains of .%licrococcU.. 

Psetdomonas, \atlhontmiop, .lgrobacterium, and "lavoha 

terium. Populations are high in vascular tissue, possibly 

resulting from root invasion, and are present in higher numbers 

in plants front cut seed than in those from whole seed. The role 

of these apparently nonpathogenic organisms is unknown, 

Frequency of reports and differences in types of organisms 

observed suggest that considerable variation exists. 


CIAMII, I_, R., 11..1.DtUBIN, and C. JOFRE. 1976. La flora bacteriana 

vascular en tubrculos de papa en cl sur de Chile. Fitopatologia 

11:57-61, 

t)eBOER. S. If., and R. 1. COPEMAN. 1974. Endophvtic bacterial 

flora in .'olaum tu/'ero.iim and its significance in bacterial ring rot 

diagnosis. Can. .1.Plant Sci. 54:115-122. 

413I.,It-. 1. 1951. Bacteria in healthypotatotissue. Phytopathology 

41:350-366. 

(Prepared by W. .J.Hooker) 

~J 

VV 

. . 

Common Scab 

This disease, present to some extent in most areas where 

potatoes are grown, isa major production problem that affects 

grade quality ana has only asmall effect on total yield or storing 

ability. 

Symptoms 

Tuber lesions are usually circular, 5-8 (seldom exceeding 10) 

mm in diameter, but they may be irregular in shape and larger 

when infections coalesce. Affecter' tissues vary from light tan to 

brown. They may consist of asuperficial corklike layer (russet 

scab), an erumpent or cushionlike scab (raised scab) 1-2 mm 

high, or an extension into the tuber (pitted scab) of various 

depths to 7 mm (Plate 20). Pitted lesions are dark brown or 

almost black (Plate 21). Tissue under the lesion is straw color 

and somewhat translucent: under russet scab such tissue tnav 

not be evident. 

Brown to tan stem and stolon lesions originate at lenticels as 

elongate lens-shaped lesions or at other natural wounds 

(emergence points of roots or split portions of stems) as 

approximately circular lesions. 

Naturally occurring aboveground symptoms have not been 

reported, but leaves of potato and other plants have been 

infected experimentally. 


Sireptomyces scahie.s (Thaxter) Waksman & Henrici (syn. 

Actinom'cts scabies (Thaxter) Gfissow) has barrel-shaped 

conidia 0.8-1.7 X 0.5-0.8 jum. Conidiophores are branched, 

having sepia, of the "attenuated isthmus" type with long, 

spirally coiled, terminal branches (Fig. 37). Other Sireptomrces 

spp. of lower virulence have been described as pathogenic, but 

more work is needed to properly evaluate differences in 

pathogenicity among species. An acid-tolerant pathogenic 

species distinct from S. scabies and as yet unnamed can survive 

in soils with pH below 5.2. 

Streptomycetes are classified with bacteria because they are 

Fig. 37. Streptomyces scabies: A,vegetative filaments within tuber tissue infected with common scab; B,coils of spores and vegetative 

filaments within cells near surface (bar represents 10 jim); C, spores photographed by scanning electron microscope (X10,000). (C, 

Courtesy G. A. McIntyre) 

q.t".

akaryotic and have cell wall biochemical characteristics more 

closely resembling those of bacteria than of fungi. [hey do 

resemble fungi in their filamentous morphology but differ 

notably in the small (approximately I-,m) diameter of their 

vegetative filaments, 

S. scabies. is aerobic. It produces colorless vegetative 

filaments and pale, mouse-gray acrial mycclia on a number of 

media, often with mclanin pigmentation of the medium 

surrounding the colony. Sporulation is good on potato agar 

media with low sucrose (0.5(' ) levels and issparse to lacking on 

media rich in peptone. S. scahie. can usually be successfully 

isolated from the straw-colored translucent tissue immediately 

below the lesion by dilution plating with soil-water agar or low 

(0. 1-0.5Ci ) sucrose potato agar. l.ight reflectance from 

Strepiortf'e.s colonies is distinct from that of typical bacterial 

colonies because of the radiating Strepi~omntyes filaments. 

Growth in culture ranges ( from ' ; 

5 to 40.5 optimum 

temperature is 25-30 ' C. 

Other Hosts 

The organism causes scab on the fleshy roots of other plants 

such as beets (red and sugar), radish, rutabaga, turnip, carrot, 

and parsnip. In these, it is seldom of economic importance. 

Fibrous roots of potato and other plants are also susceptible. 

Ilistopathology 

Actively growing tubers are infected through young lenticels 

and probably also through stomata of the epidermis before the 

periderni differentiates. Portiois of tubers protected by welldeveloped 

pcridern arc not susceptible. Wounds also serve as 

infection sites. Insect larval feeding aids initial penetration and 

progression through wound periderm layers. Filaments are 

small and difficult to detect in tissue. They are believed to be 

initiallv intercellular and t) become intracellular as tissue involvernent 

progresses. 

Scab lesions may be deep or shallow. The type of lesion is 

frequently determined genetically by potato resistance or sinsceptibility. 

Resistance is apparently associated with the 

effectiveness of the peridcrm, which underlies iesions and walls 

them off from the tuber. In susceptible cultivars with deep scab 

lesions, successive periderm layers form as penetration progresses. 

In resistant cultivars, lesions are shallow and a single 

peridcrm Lver seems to prevent further infection. l)iffercnt 

lesion types may occur on the same tuber, which may reflect 

differences in pathogenicity between infection propagules or in 

naturitv of the tuber surface at the time of infection. 

Epidemiology 

S. scabih's has been introduced into virtually all potato soils by 

infected potato seed. Evidence exists, however, that pathogenic 

st reptomnivcctes were present in native -.oils before potatoes were 

introduced. The organism isessentiallya low-grade saprophytic 

pathogen that survives for long per!ods on decaying plant parts 

in the soil or possibly on roots of living plants, in old feed lots, or 

in fields heavily manured with animal wastes. 

Physiological specialization of parasite subculture isolates to 

different potato genotypes have been demonstrated in greenhouse 

trials. In the field, however, selective pathogenicity by 

biotypes is usually of minor importance because the resistance 

or susceptibility of potato cultivars remains relatively constant 

over a wide range of natural soil populations. 

Continuous crops of potatoes generally increase severity of 

scab. In contrast, as time between successive crops is increased, 

scab severity decreases to a relatively constant level. 

Maintaining adequate soil moisture during tuber set and 

enlargement is critical in controlling the extent of scab. Field 

irrigation after tuber set and during enlargement reduces scab 

appreciably. Optimum levels of soil moisture are those at field 

capacity, which favor optimum potato growth. Permitting 

tubers to develop in infested dry soil increases incidence of scab 

34 

in susceptible genotypes. 

Sulfu, has been applied to reduce soil p1t. However, 

reduction of scab cannot regularly be explained as an effect of 

soil p1l alone. Manganase applications have reduced scab, and 

the reduction of the calcium-phosphorus ratio of the soil has 

reduced scab severity. 

Chemical treatment of soil depends on the proper 

incorporation of chemicals into the soil and should be 

coordinated with other prevention methods. Ideally, chemical 

treatments should be effective in subsequent years and increased 

crop value should justify costs. Pentachloronitrobenzene has 

been widely tested. When it is properly mixed into the soil, 

results are generally beneficial the first year; residual effects are 

less or nonexistent in following years. Repeated application 

may be necessary and treatment costs may be high. Band 

application is more economical than broadcast, and small yield 

increases are possible. Urea formaldehyde liquid as a furrow 

application has been successful in certain trials. 

Control 

Prevention depends on acombination of practices. 

I) Avoid planting scabby seed tubers. 

2) Increase time between successive potato crops. This 

reduces scab incidence to a relatively constant level but seldom 

completely eliminates soil populations. 

3) Varietal resistance or susceptibility determines incidence 

and lesion type. Cultivars with low levels of resistance nevertheless 

often produce amarketable crop in the presence of scab. 

4) Maintain high soil tio0isture levels durirg and after tuber 

set for 4-9 weeks as determined by cultivar, growing practices, 

and climate. 

5) Avoid overliming of soil, which increases soil pH and 

lowers soil Ca-P ratio. 

6) Soil treatments include: sulfur and acid-forming fertilizers 

to increase soil acidity, pentachloronitrobenezene, urea 

formaldehyde, and other soil fumigants. 

7) Seed treatments with organic mercury avoid introducing 

inoculum to new areas but are not permitted in certain 

countries. Effectiveness of other treatments in destroying 

tuberborne inoculum has not been established. 

8) Mancozeb (8%) dust as a tuber seed treatment effectively 

controls acid scab. 


DAVIS. .1. R.. G. M. MMASIERS, R. II. CA.I.IHAN, F. I. 

NISSI.EY, and .1.J. PAVEK. 1976. Influence of soil moisture and 

fungicide treatnments on common scab and mineral content of 

potatoes. IPhvtopathoh)gy 66:228-233. 

DAVIS.J. R.. R.E.McI)OL.E. and R. It CAI.l.I HAN. 1976. Fertilier 

effects on common scab of potato and the relation of calcium and 

phosphate-phosphorus. IPhytopathology 66:1236-1241. 

IJOFFMAN. G. M. 1959. tlntersuchungen zur physiologischen 

speiialisierung yon Strelnomoce. .vcabie. ('ha xt.) Waksman et 

Ilenrici. Zentralhl. Bakieriol. Parasitenkd. Infectionskr. Ilyg. Abt. 

1100K 2. FR, :9. W. J.. and 0. 1. PAGE. 1960I. Relation of potato tuber 

growth and skin riaturitv to inlection by common scab, Streiomrc.%.wahie.. 

Am. Potato .1.37:414 -423. 

JONES, A. P. 1965. The streproniycetes ;ssociated with common scab 

of tie potato. Plant IPathol. 14:8(r-88. 

I.APWOO), 1). II. I.. W.WEItINGS, and .1.II. HAWKINS. 1973. 

Irrigation as a practical nicans to control potato common scab 

(Strepnomi*'cm .cahh'): Final experiment and conclusions. Plant 

Pathol. 22:35-41. 

MANZER. I-. IL. i. A. McINTYRE. and I). C. MFIRRIAM. 1977. A 

new potato scab problem in Maine. Maine Agric. Exp. Sm. 

Bull. 

Tech. 

85. 24 pp. 

SIAIIP. C. 1956. Streptomkosc der Kartoffeltn (Kartoffelschorf). 

Pages 494-534 in: 0. Appel and II. Richter, eds. Baklericlle 

Krankheiten. Ilandh. lflan.cnkr. 2. Paul Varey: Berlin-Ilamburg. 

(Prepared by W. .1.Ilooker)

Fungi 

Powdery Scab liberating powdery masses of cystosori into the soil. Galls 

superficially resemble those of wart, except that S. 

Although powdery scab develops best under cool, moist endohioticumn does not attack roots. 

conditions, it is found in practically every potato-producing 

area in the world from latitudes 65" N to 530 S and at higher Causal 

altitudes 

Organism 

in the tropics. 

Spongospora subuerranea (Wallr.) lagerh. f. sp.suhierranlea 

Tomlinson is a member 

Symptoms 

of the Plasmodiophorales. Cystosori 

are ovoid, irregular, 

Tuber 

or elongate, 

infection 

19-85 

in lenticels, 

Mm in diam.ter, 

wounds, and 

and 

(less frequently) in consist of an aggregate of closely associated resting spores 

(cysts). Each spore 

diameter, 

is polyhedral, 

extending 

3.5-4.5 

laterally 

pm in 

under 

diameter, 

the periderin 

with 

and forming a smooth, thin, yellow-brown 

raised or 

walls. 

pimplelike 

Primary 

lesion. 

and 

Enlargement 

secondary 

and division of host zoospores are uninucleate, 

cells force 

ovoid 

the periderm 

to spherical, 

to rupture, 

2.5-4.6 Pim 

resulting 

in 

in white, wartlike diameter, with two flagella of unequal length (e.g., 13.7 

outgrowths 

and 4.35 

(Plate 22). p m). 

Wound periderm forms beneath the lesion, which gradually Disease Cycle 

darkens and decays, leaving a shallow depression filled with 

powdery 

a 

mass 

The 


f yc 

dark 

e 

brown spore balls (cystosori) (Fig. 38, The fungus survives in soil 

Plate 

in the 

22). 

form 

The 

ofcystosori 

lesion is usually 

made up 

surrounded 


hv the raised, torn resting spores. Stimulated by the presence of roots 

edges 

from 

ofthe 

suscep 

burst periderm. If, in very wet soil,'wound periderm tible plants, resting spores germinate 

does 

to produce 

not 

primary 

develop, the lesion expands in depth and width, zoospores. These penetrate epidermal cells of roots and 

forming 

stolons 

hollowed-out areas or very large warts. This is the 

cankerous 

or root hairs, 

form 

ultimately 

of powdery 

producing multinucleate 

scab. 

fungus masses 

(sporangial plasmodia), 

In 

which 

storage. 

yield secondary 

powdery scab 

zoospores 

may lead 

that 

warts or cankers. If infected 

to a dry rot 

tissue 

or to more 

has not 

further 

burst 

spread 

through 

infection to 

the 

roots and tubers. Invasion by 

pcrid errs. infeettion 

secondary 

ad necrosis 

zoospores 

may spread 

stimulates 

latera lly, 

the 

and 

host 

more 

cells 

numerous, 

to become 

and gallsare 

larger 

periern,ndinecton n.er.osisma 

produced. Within 

sprad 

these 

lterlly 

galls, 

producing one or two necrotic 

balls 

rings surrounding 

of resting 

the 

spores 

original 

are ultimately formed (Fig. 39). 

infection. Under humid conditions, after the periderm has 

ruptured, warts may become somewhat larger and secondary 

warts 

Epidemiology 

may develop beside the primary warts with little or no Inoculum is spread 

necrosis 

by 

beneath 

soil and 

the 

by 

skin. 

tuberborne resting spores. 

Tuber and root 

lPowderv 

infection 

scab lesions 

is favored 

may 

by 

serve 

cool, 

as infection 

moist soil 

courts for late conditions in the 

blight 

earlier 

and 

stages 

a number 

of infection 

of wound 

and 

pathogens. 

later by gradual 

drying of the soil. Cysts may persist 

Infection 

in the soil 

on roots 

for up 

and 

to six 

stolons 

years. 

parallels that on tubers, with The 

small 

time 

necrotic 

from tuber 

spots 

and 

developing 

root infection 

into milky 

to gall 

white 

formation 

galls varying 

;s 

in less than three weeks at a 

diameter 

temperature 

from 


I to 10 

16-20' 

mm 

C. 

or 

Powdery 

more. Galls on roots may become scab occurs 

so 

in field 

severe 

soils 

that 

ranging 

young 

from 

plants wilt 

pH 4.7 

and 

to 

die. 

7.6. 

As galls mature, they Fertilization experiments 

turn dark 

with 

brown 

N, P, K, 

(Plate 

ammonium 

23) and 

sulfate, 

gradually break down, calcium nitrate, and minor elements have shown generally that 

nutrition of the soil has little or no effect on incidence of 

powdery scab. However, sulphur added to the soil can decrease 

the intensity of scabbing. 

incorporated Recent studies indicate 

intp 

that zinc 

soil 

oxide 

reduces the amount of scab. 

-The effect of liming is not clear. In some areas, liming of the 

soil has resulted in an increase of powdery scab, whereas in 

others, liming has decreased or had no effect on incidence of the 

disease. 

Spores survive passage through the digestive tracts of 

animals. 

S. subterranea is a vector for potato mop-top virus. 

'" 

-infect 

root 

7opofZZosyo 

Zooreoo 

([I)Resting 

4.I/ 

hosmodim Zoosticcongi -, 

porongium~m 

4 Zygote 

smoe Ro atRo 

( Restng sOOwes 

Root l RoofJqX~ infection / 

"re T" infection 

Fig. 38. Powdery scab: A, lesions breaking tuber periderm; B, 0 l Scab -"o" i cell 

spore balls of Spongospora subterranea within lesion. (A, ..In scobs on tuber 

Courtesy R. Salzmann and E. R. Keller; B, courtesy C. H. 

Lawrence) 

Fig. 39. Disease cycle of powdery scab caused by Spongospora 

subterranea. (Courtesy G. N.Agrios) 

35

Therefore, control can concomitantly diminish incidence of 

mop-top. 

Other Hosts 

The fungus infects and completes its life cycle on other tuberbearing 

Solt/um spp. and on roots of nontuber-bearing S. 

nigrm L. and Nicotianarustica L. Other hosts that are infected 

without formation of resting spores include dicotyledons, 

monocotyledons, and a gymnosperm. 

Control 

1) No completely adequate measures have been developed. 

Resistant cultivars are recommended, but no immune varieties 

are known, r ot 

2) Crop rotations of three to 10 ,ears have been 

recommended, depending on climate and soil conditions. 

3) Plant disease-free seed. 

4) Crop in porous and well-drained soils, and avoid planting 

on hmnd known to be contaminated. 

5) )o not use manure from animals fed infected tubers. 

6) Fertilizers and other chemical soil treatment.s are generally 

not effective. Sulphur has given beneficial result!, bilt its use is 

limited because soil may be made too acid for optimum potato 

growth. 

7) Soaking infected seed tubers in solutions of formaldehyde 

or mercuric chloride reduces seedborne inoculum. 


C(OOPER..1. I.,R.A.C..(ON.S, and B.I). HARRISON. 1976. Field 

and glasshouse experiments on the control of potato mop-top virus. 

Ann. Appl. Biol. 83:215-231). 

I IMS. I..I.. and I. F. PR lI('F.1975..lgo .lUhtrrranca.No. 

477 in: Descriptions of Pathogenic Fungi and Bacteria. Commonw. 

Mycol. Inst.. Kew. Surrey, England. 2 pp. 

KAR .IN(..I.S. 1968. 1)nwderyv Scab of I')ot itoL5eand Crook Root of 

Watercress. Pages 180-192 in: .1.S.Karling, ed. The Plasmodiophorales. 

Ilafner Pub. Co., New York and London. 

KOILIE, A. P. 1954. A contribution to the knowledge of Spongospora 

.tllerra'a (Wallr.) L.angerh.., the cause of powdery scab of 

polatoes. lijdschr. Ilantcn/icktcn 60:1 05. 

KOIE. A. P.. and A. .. GIEIINK. 1963. The significance of the 

Moosporangial stag-_-in the life cycle of the Plasmodiophorales. Neth. 

.. Plant Pathol. 69:258-262. 

WENZI., If. 1)75. l)ie Bekiimpfung des Kartoffelschorfes durch Kulturmassnahmen. 

Z. Pflanzenkr. Pflanienschut7 82:410-440. 

(Prepared by C. H. Lawrence and A. R. McKenzie) 

Wart 

Wart has been recorded in Africa. Asia, Europe, and North 

and South America. In certain areas, disease spread has been 

contained through strict quarantine. 

Symptoms 

Warty outgrowths or tumorous galls, pea-sized to the size ofa 

man's fist, develop at the base of the stem. Aboveground galls 

are green to brown, becoming black at maturity and later 

decaying. Occasionally galls form on the upper stem, leaf, or 

Ilow~r. Belowground galls appearat stem bases, stolon tips, and 

tuber eyes (Plate 24). Tubers may be disfigured or completely 

replaced by galls (Plate 25). Subterranean galls are white to 

brown, becoming black through decay. Roots are not known to 

be attacked. 


.Sivfchittrimu endlohioticuint (Schilb.) Pere. does not produce 

hyphae but enters the host epidermis as a zoospore, swells to a 

prosorus, and develops into a sorus. Haploid sori form inside 

the cells, each sorus containing 1-9 sporangia. Resting or winter 

sporangia are golden brown, spheroidal, measuring 35-80pm in 

diameter. The thick sporangium wall is prominently ridged, 

36 

generally with three ridges confluent at two sides of the 

sporangium. Zoospores measure 1.5-2.2 /m in diameter, are 

pear-shaped, and are motile by a single posterior flagellum. 

The fungus exists in a number of physiologic races, making 

evaluation of resistance difficult. 

Zomsore 

reochesebd " 

Zo-,or 

penclrot1- Ecess,ve Grmlnoling 

potolocell celld ion p r O s o 0uS 

. .. . - 

zoo,e n 

cell / enlargement Sorus of 

,... P ro 

7 

'Germmuhmg 

-es 

'-" 0zoSI,e emtCts 

,,ln9 se tube, Sporongurm 

Molure Zyqole 

,reoflanq siy3mPsckonrl ,ellc S 

pututo tuber 

"Zgoe 

'.,lmrooot mq 

Zoospores 

Fig. 40. Disease cycle of black wart caused by Synchytrium 

endobioticum. (Reprinted, by special permission, from Plant 

Pathology, 2nd ed., by G. N.Agrios. c,1978 The Academic Press, 

New York) 

. 

A 

. 

• W 

0 

0 

N 

. 

n . 

Fig. 41. Synchytrium endobioticum winter sporangia (A, resting; 

B, germinating) range in diameter from 35 to 80 pm. (A,Courtesy 

M. E. Hampson; B, courtesy F. Frey) 

"


Sort of sporangia develop in epidermal cells of meristematic 

tissues of growing points, buds, stolon tips, or young leaf 

primordia. Invaded and surrounding cells enlarge. Rapid cell 

division following infection from either zygotes or haploid zoospores 

causes an increase in meristematic tissue, providing 

additional infection courts. The gall is a malformed branch 

system largely composed of thin-walled parenchyma. In nearimmune 

cultivars, the warts remain superficial and scablike, 

whereas, in resistant cultivars, tilezoospore dies soon after 

invasion by necrotic abortion (hypersensitive reaction) of the 

infected tissute. 

Disease Cycle 

From the initial infection, summer sporangia form as membranous 

sacs, producing motile zoospores (Fig. 40). Zoospores 

encyst and penetrate epidermal cells of susceptible tissue 

approximately 2 hr after formation. After a developmental 

period, ioospores are released outside tileplant. These may 

reinfect surrounding meristematic tissue in a secondary cycle, or 

they may conjugate fortning a zygote that reinfects several cells 

deep, giving rise to the resting or winter sporangium (Fig. 41). 

Resting sporangia are released from galls through decay of host 

tissue. The fungus can survive in soil as resting sporangia for as 

long as 38 years, even through adverse conditions. Spread of 

inoculum is through soil-infested tubers, implements, 

containers, etc. Resting sporangia germinate erratically, 

producing zoospores. 

Epidemiology 

The fungus is most active where susceptible tissue is present in 

growing sprouts, stolons. buds, and eyes. Water is required for 

germination of winter and summer sporangia and for zoospore 

distribution. Cool summers with average temperature of 18' C 

or less, winters of approximately I60days of 5'C or less, and an 

annual precipitation of 70 cm are necessary for disease 

development, and disease is limited to such environments. Soil 

reaction is of less importance, with disease occurring in soil with 

pH from 3.9 to 9.5. Temperatures of' 12-24'C favor infection. 

S. endobioticum is reported to serve as vector for potato virus 

X. 

Other Hosts 

Potato isthe principal [lost, although S.enelohioticn has 

been experimentally transferred to a number of the Solanaceae. 

Roots and leaves are attacked, with resting sporangia 

developing sparsely. Tomato cultivars are particularly susceptible 

Plants other than potato are not believed to be of importance 

in 

specie 

the disease 

s show 

cycle. 

resistance 

Some 

to a 

South 

var iahle 

American 

extent. 

wild potato 

Control 

I) Worldwide control of spread is being attempted through 

quarantine legislation, 

2) Resistant cultivars have been developed in Europe and 

North America. 

3) No chemical control is known that is not also injurious to 

soil and crops. 

4) [ie herbicide dinoseb ( 2 -sec-butyl-4,6-dinitrophenol) 

reduces infection to some extent. 


BRAUN. II. 1959. Rassenhildung der Kartoffelkrebs (Si'nch'triun 

'ndoioticun).Kartoffelhau 10:234-237. 

CURTIS, K. M. 1921. The life-history and cytology of Sinchyitrium 

endoioticuni (Schilb.) Per., the cause of wart disease in potato. 

Philos. Trans. R. Soc. London Ser. 1 210:409-478. 

I1AM ISON, M. C.. and K. ;. PROII)FOOTl. 1974. Potato wart 

disease, its introduction to North America, distribution and control 

problems in Newfoundland. [AO Plant Prot. Bull. 22:53-64. 

KARIING, .1.S. 1964. Svnchytrium. Academic Press. New York. 470 

PP. 

NOBLE, M., and M. D.GI.YNNE. 1970. Wart )isease of Potatoes. 

FAO Plant Prot. Bull. 18:125-135. 

(Prepared by M. C. Hampson) 

Skin Spot 

The disease is common in northern Europe and also occurs in 

North America and Australasia. 

Symptoms 

Following infection, roots, stolons, and stems belowground 

develop discrete, light brown lesions that enlarge, darken, and 

crack transversely. Cortical tissues may become detached. !n 

storage, purplish-black, slightly raised spots up to 2 mm in 

diameter form on tubers singly or in groups, either at random 

over the surface or aggregated arourd eyes, stolon scars, or 

damaged skin (Fig. 42A). Sometimes larger necrotic areas form 

over the tuber surface. Brown lesions may occur on sprouts of 

tubers stored in humid conditions (Fig. 42B). Irregular stands 

and delayed plant emergence frequently follow severe infection 

of seed tubers. 


Po/y sc*talum pustulans (Owen & Wakef.) M. B. Ellis (syn. 

Oospora pustulans Owen & Wakef.) has erect, branched 

conidiophores up to 140pm long, the lower part pale brown and 

sometimes swollen at the base (Fig. 42C). Conidia are dry, 

cylindrical, mostly unicellular but occasionally l-septate, 

measuring 6-18 X 2-3 pm. They develop in chains that fragment 

readily. In culture, colonies are gray and powdery. Sclerotia up 

to I mm in diamneter may form in aging cultures. 


Conidia germinate and infect tubers through lenticels, eyes, 

and skin abrasions. The fungus penetrates tuber tissue to a 

depth of about 12 cells and within two weeks is checked by 

formation of a cork cambium; after two months, infected 

tissues degenerate and spots become visible. If formation of a 

cambium is delayed or prevented, e.g., by treatment with certain 

sprout inhibitors, the fungus can penetrate deeper into tuber 

tissue, subsequently causing larger spots to develop. Toward the 

end of the growing season, sclerotia form within cells of 

decaying cortical tissues of stems and tubers. 

Disease Cycle 

First infections originate from inoculum on seed tubers. 

Brown lesions develop initially on stems near the attachment to 

the 

h 

seed 

e dt 

tuber 

b 

and 

r f n 

later 

a e 

a 

i 

nodes. 

o es 

Stolons 

t h s 

are 

a e 

often 

ot n 

first 

f rti 

infected 

at the apex, 

f c e 

and the fungus infects buds and bud scales of tuber 

eyes as they form. Further irfection of underground parts 

before harvest and of tubers during harvest and in storage 

originates from conidia produced abundantly on infected 

tissues. Infected tubers usually appear symptomless when harvested; 

skin spots and necrotic buds in eyes develop about two 

months later and increase in storage. 

Epidemiology 

The disease, spev,du(&iciI cool wet seasons and is more severe 

in crops grown on heavy clay loam than in those grown on sandy 

or organic soils. Skin spot is common in crops lifted moist and 

stored cool (40 C), and conidia produced on the spots spread 

infection in storage. Cultivars with thick tuber skin develop few 

skin spots. Cultivars susceptible to skin infection are usually 

also susceptible at tuber eyes. Most inoculum originates from 

infected seed tubers, but sclerotia of P. pustulans in decaying 

stems can remain viable in soil for at least eight years. 

Other Hosts 

Skin spot develops only on potatoes, but brown lesions can 

develop on roots of other Solanaceae (Solanum spp., 

lcopersicon escuilentuni, Nicotiana spp., and Datura spp.). 

37

l, 

I 

Fig. 42. Skin spot: A, on potato tuber; B, on stem and roots; C, Oolyscytalum pustulans(Oosporapustulans).Bar represents 25 jum. (A, 

Copyright National Institute of Agricultural Botany, Cambridge, England; B, courtesy Rothamsted Experimental Station, Harpenden, 

Herts, England; C, reprinted, by special permission, from More Dematiaceous Hypomycetes, by M. B. Ellis. 1976 Commonwealth 

Mycological Institute, Kew, Surrey, England) 

Control 

If)Skin spots aInd damnage to tuber eyes can be prevented by 

Leak 

stongueris diarl75in th) indethm.1'C) lhog h 

fungsn threain inectins.wherever viale 

2) lDisinfection of'seed tubers soon after harvest w/ith fungi 

Leak, also called watery wound rot, may occur sporadically 

potatoes are grown. 

cides, including organomercurials and 2-aminobutane, is S m t m 

effective in preventing disease during storage. 

Sym p t ubs 

3) Betnomyl and thiabendozole applied at harvest also appea brsarn 

decrease the disease. Because these materials persist inth tu ethe tuber appears 

r af e t d A di c l e .w t r-o k r a 

bie f ct on thdis n.ore d ieatrsae d e as 

to b ie solle au ndthe skin is mis t.sInternally 

skin;In prventspoulaionof P 17sitlan on eedtubrs, 

they greatly reduce subsequent infection of' plants and progeny 

tubers. 

diseased flesh is clearly demarcated from healthy tissue by a 

dark boundary line. Rotted tissue is spongy, wet, I.nd may have 

4) Ther 1 fre putulns frin cn b prouce by 

4) can 

propagating plants 

cr fretssvel.. 

from stem cuttings, although, to maintain 

tile health of' stocks, treatment with fungicide is needed to 

cavities. Oil cutting and exposure to air it changes color 

toogray 

pogsieytgrbowadfnlamstlakoc 

brownan. fialy almoste blcy 

sionally with it pink tinge. Affected tissue has the smoky gray 

prevent reinfection during their commercial multiplication. color of frosted tissue. After infection, at tuber may become so 

completely rotted (Plate 26) within ;I few days that even a slight 

Selected References, 

pressure causes the skin to rupture and large quantities of liquid 

to exude. In the storage pile, all that remains of infected tubers 

B()NA), A. F. W. 1972. IVotmo, storage dise~ases. Re~v. plant Patho)l. 

5 1:297-32 1. 

BOYD,. A. E. W.. and .1. If. I.ENNARI). 1962. Se~asonal fluctuation in 

potato skin spot. Plant Pathol. I: 16 1-1 6. 

GRAIIAM, 1). C., G;.A. [JAMI1.T1ON, C'.F-.QUI NN. ad A. It.ittfi D 

R t I IV- E\ :N. 19 73. 1lfst If2-a in nobutane is a fuminiga nt for c trol 

of gangrene. skin spot and silver scurf diseases (it potato tube~rs. 

are the tuber shells with thin papery skins (Fig. 43A). Cut seed 

tubers may also be rotted. 

C u a r a i m 

!.'lit tli 

i 

to 

m 

r 

r 

v 

w,/ 

,I.r 

lb 

'~ rla 

r a 

tt 

umH 

tI e se s ,a Idp d p s sil i l 

other P'thittm spp. cause the disease. Oospores, which are 

Potato Res. 16:1019-125. 

11II)W. G. A.. ,1. M. IIIRS 1. and F. .1. MUIND)Y. 1969. The phonology 

fskin spot I0Or.spralpti~tulan.Ovn and Waktf.)and othr fungal 

diseass f potato tubers. Ann. Appl. Biol. 64:266-279. 

II. .A . M.IfIRS ,,and O.1I STIF MAN. 1973. Efftcts olskin 

sp t WOr sporal i.vtuha ) on potatoe~s An . Appl. Biol. 73:151-162. 

IIIRST,...M.. G;. A. IDE, R. L_CRI|:FIN, aInd 0. .. ";TEl)MAN. 

1970. Improving the health of seecd potatoes. .1.Agric. Soc. E'ngl. 

smooth, thick-walled, and spherical, measure 14.2-19.5 um and 

are terminal on branched coenocytic hyphae. Sporangia (Fig. 

43B and C) are spherical, 12-29 mam,when produced terminally 

and barrel-shaped, 17-27 X 14-24 mm, when intercalary. Sporangia 

of A.uhinum do not produce zoospores. The myceliumn 

is often difficult to isolate from diseased potato tissue. 

131:87-106. 

l-RS'I, .1.M., and G. A. SAI.T. 1959. OosporaIp.tulan Owe~n and 

Wakefield it. ;Ipara,ite of potato ro)ot systems. Trans. H~r.Mycol. 

Soc. 42:59-66. 

K HtARAKOVA. A. 11 1961. On the biology of the causal agent f 

Disease Cycle 

The fungus lives in the soil and can enter tubers only through 

wounds. Infection, therefore, usually occurs at harvesting, 

grading, or less frequently at planting. Cut seed tubers are 

predisposed to infection fter planting its soil temperatures 

Mycpool.s 40:558. uan OenIdWaeild 

Myco. 40558.immature 

(Prepared by G. A. Hide) 

e. pl begin to rise. Serious crop loss does take place in bruised, 

tubers harvested during hot, dry weather. The rot that 

develops is gretly aggravated by relatively high temperatures 

38

any time but generally occurs late in the season. Leaves become 

chlorotic, vilt. dry up, and abscise, starting at the stem base, 

Aerial tubers may form. Infection occurs in the roots, and all 

root, stolon, and stem tissues are killed as lesions develop. Stem 

lesions may extend up to the basal leaves, with water-soaking 

and light brown vascular discoloration at theadvancing margin. 

Necrotic stems and roots are brown to black and may be 

confused with blackleg. 

Tubers generally become infected (Plate 27) through diseased 

stolons, but some infections appear to occur at buds or lenticels. 

Rot proceeds uniformly through the tuber, with the advancing 

margin usually delimited by a dark line visible through the skin. 

Periderm over rotted portions is brownish-cream in white 

cultivars; tissues beneath lenticels are dark brown to black. 

• . Rotted tissues remain intact but are spongy. When recently or 

partially rotted tubers are cut, internal tissues are cream color, 

odorless, and rubbery or spongy in texture; if the cut tuber i, 

squeezed, aclear liquid appears. On exposure to air, the color of 

infected tissues progressively changes to salmon pink (in 20-30 

4 rmin) brown, and black (in about I hr). Internal tissues of tubers 

71 d rotted for somec time are black. 

" 3 Causal Orgarnism 

Pin, rot is most commonly caused by Phytophihora 

ert'throseptica Pethybr. Sporangia are nonpapillate, highly 

B C .. variable in shape, ellipsoid or obpyriform, and 43 X 26 mm. 

Oogonia, 30-35 mm in diameter, have smooth walls I pm thick 

Fig. 43. Leak: A, typical tuber shell rot. Pythium sp. from rotted and may turn faintly yellow with age. Antheridia are 

tuber: B, resting sporangium; C, spore with germ tube (bar amphigynous, ellipsoid orangular, and 14-16X 13pm. Oospores 

represents 20 pm). (Fig. 44) have walls 2.5 pm thick and nearly fill the oogonia. 

The fungus grows on several media but not on dilute malachite 

green. Optimum and maximum growth temperatures are 

and poor ventilation but may be completely arrested under cool 24-280 C and 340 C, respectively. Asexual structures form in 

conditions. mycelial mats when transferred successively to mineral solution 

and water or when grown in water culture with boiled hemp 

Other Hosts seeds. Sexual organs form abundantly in agar media. 

Both species of Pithium are pathogenic on an extremely wide P. cryp)togea Pethyb., P. drechseri'Fucker, P. megasp(erma 

range of hosts, including many market-garden crops, causing Drechsler, and P. parasitica Dastur also infect potatoes and 

damping-off, root rot, or soft rot disease, induce plant and or tuber symptoms similar to those caused by 

P. erthrosepica. Single strains of P. cr'vptogea form sexual 

Control organs only sparingly after a few weeks in culture but promptly 

I) losses can be minimized by delay in lifting the crop so that when grown with complementary strains of'. cr'tnamomi. The 

tuber skins may mature. dimensions of reproductive structures of P. rt*plogea are 

2) Avoid mechanical injury to tubers by taking all possible similar to those of P. drechsleri,but its optimal growth temcare 

in harvesting. peratures (22-25 0 are lower than those (28-31"C) for P. 

3) 1f rotting begins in storage, increase air movement, and drechseri.P. megaslwrma has paragynous antheridia, in concool 

and dry the crop as quickly as possible. trast to amphigynous antheridia in the other species, and it has 

larger oospores (an average of 41 pm vs. about 24-25 Pm). 

Selected References Sporangia of P. parasiticaare papillate, and those of the other 

species are nonpapillate. 

It I I.R,. I'.. and S. (i. .lt)NTS. 1949. IPlant Pathology. Macmillan 

and Co.. ltd.. London. 979 pp. 

MIITI)I.E-ON, .1. I. 1943. The taxonomy. host range and geographic r . " 

distribution ol the genus I'vthion. Wein. Torrey Iot. Cluh . i. . . 

20:1-171. 

I)MPKINS. C. M. 1975. World literaturc on I'r'hitimand Rhi:octwi'n, 

Species and the IDisease% Ihey ('ause. (ontrib. No. 24. Reed 

lerbarium. Baltimore, 10 I). 

WIllIE ItAt). J.. J. I'. MINIOSII. and W. NI. FINI)LAY. 1953. 

The Polato ill Ilcalth and l)iscase. 3rd ed. Oliverand Boyd. London. 

744 pp. 

(Prepared by A. R. McKenzie and C. HI.l.awrence) 

Pink Rot 

Pink rot has been reported from nine states in the United 

States and from II other countries in North and South America, 

Europe the Middle and Far East. and Australia. 

Symptoms Fig. 44. Pink rot. Meture oospore of Phytophthora erythroseptica 

Wi Iting. which issonilt imes t lie initial symptom. may occur at (bar represents 10 pm). (Courtesy R.C. Rowe and W.J. Hooker) 

39

Disease Cycle 

P. er t/lro.sptica is soilhorne and endemic in many soils, 

Zoospores, sporangia, or oospores may serve as inoculum, but 

oospores are probably the significant propagule in pathogen 

dissemination and survival in soil. Plants of all ages are susceptible, 

but the disease is most frequently observed in mature 

plants approaching harvest, 

Epidemiology 

Disease develops in soils approaching saturation from poor 

drainage or excessive precipitation or irrigation. l.arge amounts 

ofdecomposing plant residues in soil enhance waterabsorption, 

retention, and disease incidence In wet soil, the disease develops 

overa wide range oftemperatures but is most severe between 20 

and 30' C. 

Other Hosts 

Although I'. erth'irosepti'ahas been reported as a pathogen 

only on potatoes and tulips, it has been recovered from the roots 

of 17 nonsolanaceous plants, including wheat and rye. 

Control 

I) Plant seed tubers in soils with good drainage, 

2) Avoid excessive irrigation late in the growing season. 


GOSS. R. W. 1949. i Inyk rot of poaioes caused by Hll.1i.tfora 

£'rtroWIi- 1thN . Neh. Agric. T Fxp. Sin. Re. Bull. 160. 27 

ROWE, E.C.. and A.F.SCHlMIlTlHlNNlER. 1977. Potato pink rot in 

Ohio caused hy /'htropilthora ertihro. i/c'T 1(In I'. rrptogea. 

plant Dis. Rep. 61:80t7-81t0. 

STAMPS, 1).J. 1978. 'hoitop/hihoraerrth-.7pti(a. No. 593 in: t)escriptions 

of IPaihogenic hungi and Bacteria. C'mmonw. Mycol. 

Inst.. Kew. Surrey, l-ngland. 2 pp. 

VARGAS, I.. A.. and .. W. NIELSEN. 1972. I'hvtoph/hora 

rithro.T'apOtt. ini'Peru: Its identilication and pathogenesis. Am. 

WAtI.R IOUSE. . 1963. Key to the species of I'hthra Ie 

WarS. No. 92 in: M'co. Kipers ommo,,. Mycol. Inst.. Kew. 

Surre ' Eingland. 22 pp. 

(Prepared by R. C. Rowe and L. W. Nielsen) 

Late Blight 

Late blight is probably the single most important disease of 

potatoes worldwide. It is destructive wherever potatoes are 

grown without fungicides, except in hot, dry, irrigated areas. 

The Irish potato famine" of the 1840s was caused by PIeqopititorainfisians, 

the fungus that causes late blight. Immense 

quantities of fungicides are applied to potatoes throughout the 

world for protection against P. inf'sian. 

Symptoms 

moisture, Leaf lesions light are intensity, highly and variable, host cultivar. depending Initial on smptomsare temperature, 

typically small, pale to dark green, irregularly shaped spots. 

Under favorable environmental conditions they rapidly grow to 

large, brown to purplish black, necrotic lesions that -ay kill 

entire leaflets and spread via petioles to the stem, ev, .itually 

killing the entire plant. A pale green to yel!ow halo is often 

present outside the area of leaf necrosis (Plate 28). Under moist 

conditions, a white downy mildew of sporangia and 

sporangiophores appears at the edge of lesions, mostly on the 

underside of the leaves (Plate 29). 

In the field, plants severely affected with late blight give offa 

distinctive odor. This odor actually results from rapid breakdown 

of potato leaf tissue and also follows chemical vine killing, 

frosts, etc. 

Positive identification of late blight requires confirmation of 

sporangia and sporangiophores either on lesions in the field 

40 

under moist conditions or on leaf or tuber lesions incubated in a 

moist chamber. 

On susceptible cultivars, exteriors of infected tubers show 

irregular, small to large, slightly depressed areas of brown to 

purplish skin (Plate 30). A tan-brown, dry granular rot 

characteristically extends into the tuber approximately 1.5 cm, 

the depth varying according to length of time after infection, 

cultivar, and temperature. The boundary between diseased and 

healthy tissue is not clearly defined; delicate, brown, peglike 

extensions penetrate to variable depths. Under cool, dry storage 

conditions, tuber lesions develop slowly and may become 

slightly sunken after several months. Secondary organisms 

(bacteria and fungi) often follow infection by '. it/i,stans, 

resulting in partial or complete breakdown of tubers and 

complicating diagnosis. 


Phytoplithora infi 'sans(Mont.) de lary has sporangia (conidia) 

that are hyaline, lemon-shaped, thin-walled, and 21-38 X 

12-23 mm in size. Each has an apical papillum (Fig. 45C). 

Sporangia of P. infestan.s are borne on the tip of a sporangiophore 

branch (Fig. 45A); as it elongates, the sporangiophore 

swells slightly and turns the attached sporangium to the side. 

The sporangiopore is thus characterized by periodic swellings 

(Fig. 4513) at points where sporangia were produced. 

Sporangia may germinate by means of a germ tube (Fig. 45E), 

but most commonly they form about eight biciliate zoospores 

(Fig. 45D) that swim freely in waterand encyst on solid surfaces. 

i'ncysted zoospores can germinate by germ tubes that enter 

thhotvalfsomabtualyanpreoiu isomd 

the host via leaf stomata, but usuallyanappressoriumisformed 

and penetration hyphae enter directly through the cuticle. Once 

inside the plant, the nonseptate mycelium is intercellular and 

intracellular by means of haustoria (Fig. 45G) that extend into 

cells. 

Sexual reproduction resultsin oospores(Fig. 45F) formed by 

the union of oogonia and antheridia. Oospores within oogonia 

are 24 -46 pm in diameter and germinate via a germ tube with a 

terminal sporangium, which, in turn, either liberates zoospores 

or forms another germ tube. 

Disease Cycle 

Oospores in nature have been found only in Mexico, where 

both mating types (A 1 and A.) occur. Leaves touching the soil 

are often infected first, suggesting that oospores probably playa 

role in the survival of P.itnrestarisunder adverse conditions. 

In tropical areas where the crop is grown all year, overwintering 

of R itirestars is not an important consideration. 

However, where distinct seasons occur, P. ittf'stans overwinters 

as on mycelium farms or in near unharvested commercial tubers, storages, tubers 

or 

dumped 

tubers 

in 

stored 

cull piles 

saved for seed. After plant emergence, the fungus 

and 

invades a few 

of the growing sprouts and sporulates under moist conditions, 

producing primary inoculum. Once primary infection has occured, 

further spread of P. inl.san. takes place by airborne or 

waterborne sporangia (Fig. 46). 

of Tubers succulent on tissue cull piles that frequently are easily infected sprout and by form 

. it/.Vllns dense masses 

frotm diseased tubers. 

spores 

Spoi ulation within the foliage mass 

produces pr digious numbers f sp res to infect nearby fields. 

Epidemiology 

Tubers, particularly those inadequately covered by soil, may 

be infected in the field by spores that have been washed from 

infected leaves into the soil by rain or irrigation. Rapid tuber 

growth frequently causes soil to crack, exposing tubers to 

infection. Tuber infection may also occur during wet harvest 

conditions via contact between ttibers and sporangia on vines or 

via airborne sporangia. Little, if any, spread of P itiA,stans 

occurs under optimum conditions in storage. 

Field infection is most successful under cool, moist 

conditions. lowever, infections take place over a range of 

environmental conditions, and high temperature strains of the

'40 

ff .. . 

'1 f . ."L', . 

'1 .,. " . 

.. ;, B C 

.. :-,I 

-, 

.141 

Fig. 45. Late blight. Phytophthora Infostans: A, sporangiophore; B, sporangiophore branch showing swellings at successive sites of 

sporangium formation; C, sporangia, germinating by zoospores (D) and germ tube (E=);F, oospore with antheridium; G, haustoria within 

tuber cells Bar in A represents 50 pm. hars in D. E. and G represent 10 pm. (F. Courtesy of Plant Pathology Section, West Virginia 

University) 

41

fungus have been reported. Sporangial production is most rapid 

and prolific at l0o( rh and at 21' C. Sporangia are sensitive to 

desiccation and, after dispersal by wind or splashing water, 

require free water forgermination. The optimal temperature for 

indirect germination via zoospores is 12' C, whereas that for 

direct germination of sporangia via gern tubes is 240 C. Both 

types of germination occur at overlapping temperatures, 

however. Zoospores, although quickly killed by drying. produce 

germ tubes and appressoria in the presence of free water. 

Penetration occursat temperatures between lOand 29' C. Once 

penetration has occurred, infection and subsequent development 

of disease is most rapid at 21' C. 

Systems for forcasting late blight and for timing fungicide 

applications rely on records of temperature and rainfall (tlyre) 

or temperature and relative humidity (Wallin) and predict the 

probability of late blight development, assuming the presence of 

inoculum. .\ forecasting system combining bot hthese systems is 

"Blitecast" (Krause et al), which is used in the northeastern 

United States for timing fungicide applications. Where rainfall 

and relative humidityare closely related, fungicides are applied 

after rainfall accumulated to 1.27 cm has theoretically washed 

previously applied fungicide from the foliage (Barriga et al). 

on several continents are directed toward obtaining cultivars 

with high levels of generalized resistance that can be used with 

reduced amounts of fungicide oreven without fungicide in drier 

areas. 

Control 

I) Avoid development of early season (primary) inoculum by 

the use of blight-free seed and destruction of potential inoculum 

sources such as cull piles, volunteer plants, etc. 

2) Apply protectant fungicides as recommended by a fore 

casting service or (if such service is not availahle) as early as late 

blight is present in the area. Apply fungicides regularly as new 

vine growth develops and regularly after vines overgrowing the 

rows have caused high relative humidity within the canopy. Be 

sure that coverage of vines and leaves is thorough and uniform. 

3) Prevent tuber infection by maintaining good soil coverage 

of tubers through adequate hilling. (Exceptionally large hills are 

commonly made in the Andes, resulting in relatively rare tuber 

infection.) Maintain adequate foliage protection to reduce 

inocnlum production on leaves. Kill vines two weeks before 

harvest so that sporangia on leaves dry out and die and infected 

tubers rot, thus permitting identification and removal before tite 

Other Hosts 

L.ate blight often severely affects tomatoes and occasionally 

affects eggplant and many other members of the Solanaceae. 

crop is placed in storage. 

4) Prevent rot in storage by removing infected tubers before 

storage and maintaining adequate air circulation and 

temperature as cool as is compatible with other considerations. 

Resistance 

Two types of resistance to A inbr.taii. in potatoes are recognized: 

1)specific resistance (also called race specific, vertical, 

oligogenic, or monogenic resistance) and 2)general resistance 

(also called field, race nonspecific, horizontal, or polygenic 

resistance). Before the discovery of specific resistance, fairly 

high levels of gencial resistance were obtained. For several 

decades after discovery of specific resistance in Solanum 

hentissum, breeders incorporated one or a few S. demissin 

genes into each new variety. Because /A.itn'eistans is highly 

variable, the pathogen rapidly overcame such resistance; use of 

specific resistance has therefore contributed little to controlling 

late blight. All potato cultivars and all tuber-bearing Solnutnti 

species are susceptible to late blight in the Toluca Valley of 

Mexico, where (lie sexual stage of P in~fistans occurs; thtus the 

probability of obtaining lasting specific resistance is very low. 

No cultivars in Furope or North American allow commercial 

cultivation of potatoes without fungicide protection. Some 

comenrcial cultivars, such as Sebago, have a tmoderate level 

of general resistance and are protected by lower amounts of 

5) Use resistant cultivars where possible. 


IIARRIGA, R., 11. ). IIJRSTON, and .. E. llEIDRICK. 1961. 

Ciclos de aspersion para el control de li"gota" de lapapa. Agric. 

CROSIER, W. 1934. Studies in the biology of I'hrfopht/ora ifi-sOanx 

(Mont.) IC flary. N. Y.Agric. lxp. Stn.. Cornell. Mci. 155. 40 pp. 

GAL.L.EGILY, M. E. 1968. Genetics of pathogenicity of lv/ytoplithora 

ifi,.tans.. Ann. Rev. Phytopathol. 6:375-396. 

GAI.L.EGL.Y, M. E. and .1.S. NIEI)ER'IIAUSER. 1959. Genetic 

controls of host-parasite interactions in the Phytophthora late blight 

disease. Pages 168-182 in: C. S. Ilolon. (i. W. Fischer. R. W. 

Flton. II. Hart. and S. F.A. Mc(allan. eds. Plant Patlhology 

Problems and Progress,. 1980-1958. Univ. Wis. Press,. 

IIYRE, 588 pp. 

Madison. 

R. A. 1954. Progress in forecasting late blight of tomato and 

potato. Plant Dis. Rep. 38:245-253. 

KRAUSE, R.A., I.. B.MASSIE, and R.A. IIYRE. 1975. Blitecast: A 

computeri/ed forecast of potato late blight. Plant Dis. Rep. 

59:95-98. 

L.ARGE, E. C. 1962. The Advance of tile Fungi. t)over IPubl., New 

fungicide than are required by other cultivars. Breeding efforts York. 488 pp. 

S A 

V " ' " ' I 

WAI.I.IN. J. R. 1962. Summary of recent progess inpredicting late 

blight epidemics in the United States and Canada. Am. Potato .1. 

39:306-312. 

(Prepared by H. 1). Thurston and 0. Schultz) 

,-;P- /Powdery Mildew 

, ~ J'~iPowdery mildew can be an important foliage disease in arid 

',,, \ 

\ 

LTh 

SUnited 

"',. 

7j, 

-Washington 

or semiarid climates. 

Mexico, New 

It has 

Zealand, 

been reported 

Europe, and 

from 

thf: 

Chile, 

Middle 

Peru, 

States it is of economic 

East. 

importance 

In the 

only in the state of 

under row irrigation, although it has been reported 

K in Ohio and Utah. 

Symptoms 

Elongated, light brown stipples, 0.5-2 mm in length, may 

appear on stems and petioles of infected plants. These often 

coalesce to form larger, water-soaked, blackened areas on the 

Fig. 46. Disease cycle of late blight caused by Phytophthora petioles. Infections 

infestans. 

are initially 

(Reprinted, 

powdery 

by 

white 

special 

(Fig. 47A, 

permission, 

Plate 

from Plant 31) and later 

Pathology, 

tan. Sporulation 

2nd ed., by 

on 

G. 

both 

N.Agrios. 

leaf surfaces 

1 1978 Academic 

appears as 

Press, New dusty, grayish-brown 

York) 

deposits that superficially resemble soil or 

spray residue. Severe infections may superficially resemble late 

42

A 

\, 

2) Powdery mildew is rarely a problem on potatoes grown 

under sprinkler irrigation. A heavy rain will also stop progress 

of the disease. 


DUTT, B. L., R. P. RAI, and i1. KISHORE. 1973. Evaluation of 

reaction of potato to powdery-mildew. Indian J. Agric. Sci. 

43:1063-1066. 

ROWE, R. C. 1975. Powdery mildew of potatoes in Ohio. Plant Dis. 

Rep. 59:330-33 1. 

(Prepared by R. C. Rowe and G. D. Easton) 

Early Blight 

This disease is found worldwide wherever potatoes are grown. 

Symptoms 

Initial infection is most frequent on lower, older leaves. 

Lesions first appear as small (1-2 mm) spots, dry and papery in 

texture, later becoming brown-black and circular-ovoid as they 

expand. Advanced lesions often have angular margins because 

of limitation by leaf veins. Concentric rings of raised and 

depressed necrotic tissue usually, but not always, give lesions a 

characteristic "target board" or "bullseye" appearance (Fig. 

48A). Leaf tissue often becomes chlorotic around and among 

lesions. As new lesions develop and older ones expand, the 

entire leaf becomes chlorotic, later necrotic, and desiccates but 

"j usually does not abscise (Plate 33). Damage to leaves is 

/ /"considerably in excess of tissue actually destroyed by lesions, 

suggesting that toxins cause leaf death some distance from the 

site of infection. Advanced vine symptoms intergrade with those 

-of Verticillium wilt and leaf scald associated with moisture stress 

in irrigated potatoes. 

" Tuber lesions are dark, sunken, circular to irregular in shape, 

and often surrounded by a raised border of purplish to gun 

metal color (Fig. 48B). The underlying flesh is dry, leathery to 

k, "corky, and usually brown. Tissue in advarced decay is often 

water-soaked and yellow to greenish yellow. Lesions can 

increase in size during storage, and tubers can become shriveled 

, ,._ in advanced cases. Early blight tuber lesions are not as prone to 

invasion by secondary organisms as are many other tuber rots. 

' 

,-. . . :. - C Causal Organism 

Ahernariasolani Sorauer (syn. Macrosporium solani Ellis & 

Fig. 47. Powdery mildew: A, early symptoms; B, Erysiphe Martin) has conidia 15-19 X 150-300 pm with 9-11 transverse 

cichoracearum conidiophore; C, mature conidia. septa and few, if any, longitudinal septa. Spores are usually 

borne singly but may be catenulate. They are straight or slightly 

bent, the body being ellipsoid to oblong and tapering gradually 

blight, with leaves becoming almost black (Plate 32), necrotic to a long beak (Fig. 48C and D). Color varies from pale to light 

and abscising, leaving a rosette of upper foliage. Eventually, tan to olive-brown. The beak is flexuous, pale, occasionally 

general infection can occur and the entire plant may collapse branched, and 2.5-5.0 pm wide. Conidiophores occur singly or 

and die. in small groups and are straight or flexuous, pale to olivebrown, 

6-10 pm in diameter and up to 100 pm long. 

Causal Organism Cultural characteristics vary widely. Most isolates grow well 

Conidia of Erysiphe cichoracearum DC. ex Merat form in on artificial media; however, they sporulate sparingly unless the 

chains on unbranched conidiophores, 7-13 X 36-50 pm (Fig. mycelium is wounded or irradiated or theyare cultured on a low 

4713). Mature conidia (Fig. 47C) are oval to ellipsoid with nutrient medium. Colonies are spreading, hairy, and grayflattened 

ends. 13-16 X 20-30 pm, and lack well-developed brown to black. Some isolates produce a yellowish red pigment 

fibrosin bodies when mounted in water or 10,7 KOH. in nutrient media. 

Cleistothecia have simple appendages and contain several asci, 

each usually containing two ascospores. Cleistothecia 135-165 Disease Cycle 

/1i1 in diameter with indeterminate appendages and 5-10 asci Depending upon the location, A. solani persists in crop 

are very rare, having been reported only on field-grown potatoes debris, soil, infected tubers, or other solanaceous hosts. The 

from the western United States. fungus penetrates the leaves directly through the epidermis. 

Differences in iesistance exist among tuber-bearing Solantm Primary infection can occuron older foliage early in the season. 

spp. and within S. tuheroxtn. However, actively growing young tissue and plants heavily 

fertilized with nitrogen do not exhibit symptoms, and most 

Control secondary spread occurs as plants age, especially after bios- 

I) )ust or spray foliage with elemental sulfur at intervals of soming, when secondary inoculutn levels are higher. In many 

one to two weeks. locations, early blight is principally a disease of senescing plants. 

43

Immature tuber surfaces are easily infected, whereas those of 

mature tubers are much more resistant. Wounds are generally 

necessary for infection through mature tuber skins. A period of 

3-4 days or more between vine killing and digging considerablv 

increases tuber resistance. 

Epidemiology 

Maximum mycelial growth of*A.so/ani in pure culture occurs 

at 280C, whereas optimum temperature for formation of 

conidiophores and conidia is 19-23'C. Conidiophore 

formation is inhibited, but not irreversibly, at temperatures 

greater than 320 C. Temperatures above 270 ( stop conidia 

formation. Conidiophores develop in light, whereas light 

inhibits conidia formation at temperatures above 150C. 

Maximum spore production in the field occurs between 3:00 

1.O , 

' 

' !41 

I 

/1 

H °A 

C I D 

Fig. 48. Early blight: A, leaf lesions with concentric targetlike 

markings, somewhat limited by the larger veins; B,tuber lesions; 

C, dormant spores of Alternaria solani with short-beaked A. 

alternata type near top (bar represents 50 pm); D, germinating 

spore. 

44 

a.m. and 9:00 p.m. Spores in water germinate within 35-45 min 

at the optimum temperature (24-30' C) and within 1-2 hr at 

6-34' C. Optimum temperature for tuber infection is 12-16' C 

but varies with cultivar. 

Most rapid progress of the disease occurs during periods of 

alternating wet and dry weather. Early blight can be severe in 

irrigated desert regions because of prolonged periods of dew. 

The disease is often more severe when the host has been 

predisposed by injury, poor nutrition, or other type of stress. 

Field resistance to foliage infection is associated with plant 

maturity. Late maturing varieties are usually more resistant. 

liarly blight does not red uce yields when inlection occurs late in 

lhe season. 

Other Hosts 

The fungus is pathogenic on tomato and other solanaceous 

crops and has been reported on other genera such as Brassica 

spp. 

Control 

I) Cultivars with levels of field resistance are available, but no 

cutivars are immune. 

2) Protectant fungicides such as the dithiocarbamates, fentin 

hydroxide, and chlorothalonil effectively control early blight on 

loliage. 

31) Fungicide applications scheduled by spore trapping or 

other methods so as to coincide with secondary spread of the 

disease are most effective. Early season applications of 

.fgicides before secondary inoculum is produced often have 

little or no effect on the spread 

permit tubers 


to inature 

disease. 

in the ground before digging, and 

avoid bruising in handling. 

5) Avoid disturbing seed tubers until ready to plant. 


)OUGLAS, 1). R., and M. I). GROSKOIPIP. 1974. Control of c:arlv 

blight ineastern and soutlicentral Idaho. Am. Potat .I.51:361-368. 

I)OtJGL.AS. I I). R., andt i. .t. FPAVE K. 1972. Screening potatoes for field 

EI.IIS, resistance M. .B., to and early I. A, blight. S. GIBSON, Am. Potato 1975. .1.49:1-6. .lhernariasolani. No. 475 

in: Descriptions of Pathogenic Fungi and Bacteria. Comnmonw. 

Mycol. Inst.. Kcn. Sorrey. Ingland. 2 pp. 

IIARRISON, M. )., C. II. LIVINGSIION. and N. OSFIIMA. 1965. 

Control of potato carly blight in Colorado. I. Fungicidal spray 

schedules in relation to the epidemiology of the disease. Am. Potato 

J. 42:319-327. 

IIARRISON, M. I)., C. If. 1IVINGSTON, and N.OSIIIMA. 1965. 

Control of potatocarly blight in Colorado. 1I.Spore traps asa guide 

for initiating application%ol 

VFNETTE, 

hngicidcs. 

.1.R., 

Am. 

and 


M. 

,I.42:333-340. 

1). IIARRISON. 1973. Factors affecting 

infection of potato tubers by .lhernariasolani in Colorado. Am. 


WAGGONER, P. E.. and J. G. IIORSFAI.L.. 

simulator 

1969. Epiden. 

of plant 

A 

disease written fora computer. Conn. Agric. Exp. 

Stn. [lull. 698. 811pp. 

(Prepared by D. P. Weingartner) 

lternaria alternata 

Alernaria ahernata (Fries.) Keissler (syn. A. tenuis Nees.) 

infects potato and other solanaceous crops, forming lesions on 

potato leaves similar to those of early blight. Spores 

x 

(20-63 

9- 18 Mpn) are snialler than those of' . solani,are formed in 

chains, and lack the typical long beak (Fig. 49A). Their sizeand 

shape may vary considerably. The fungus is often associated 

with considered other diseases 

a 

and 

weak 

isfrequently 

parasite, 

isolated. It isgenerally 

which attacks plants weakened by 

viruses, deficiencies, stress, or senescence. 


EIIIS. M.B. 1971. Dernatiaceous Ilyphomycetes. Commonw. Mycol.

R., 

Inst.. Kew. Surrey. ngland. 609 pp. RAMACIIANI)RA 

.".\I. 

RAO. 

NI 

1973. A virulent 

,\\ and I:. R. 

strain 

K II 


1R 

Ahernaria 

, . Kriinkheitcn ill d alternatacausing leaf and fruit spot of chilli. Indian Phytopathol. 

Schiid linge der Kartoffel. L.andwirtschaltliche I chrmittelentrale 26:6(-603. 

Zollikofen. 1501 pp. 

SREFKANIAII. K. R.. K. S. NAGARAJA RAO. and I. N. (Prepared by L. J. Turkensteen) 

AMAr 

GE 

a., 

G H Ij 

Fig. 49. Representative st! uctures for identification of: A,Alternaria alternata, conidia; B, Pleospora herbarum (Stemphylium botryosum), 

conidia and (C) ascospores in ascus; D, Ulocladhum atrum (Stemphylium atrum), conidia; E,Septoria lycopersici,conidia; F,Phoma andina, 

spores from plate culture; G-J, Choanephora cucurbitarum, sporanglophores and conidia of two distinct types. Bars represent 20 Mm. 

(B and C. Courtesy Research Institute for Plant Protection, Wagen rugen; A and D-J, courtesy L. J. Turkensteen and W. J. Hooker) 

N.2 

45

Pleospora herbarum 

Pleosporaherbarum (Pers. ex Fr.) Rabenh. and its imperfect 

stage, Stemphyilium hotr'osuin Wallr., are often found 

associated with potato plants poorly adapted to warm 

conditions or to other environmental stresses. Round, rapidly 

enlarging, light colored leaf lesions develop, affected tissues 

appear as thin paper (Plate 34). The same fungus is commonly 

isolated from dead and dried materials and wood, but is also 

known as a pathogen for several crops. 

Conidia are olive to brown and oblong, with three transverse 

septa and 1-3 longitudinal septa The spores are 19.5 X 28.5 mm, 

with asingle basal pore 8 um in diameter (Fig. 49B). Ascospores 

are dark, yellow-brown, ellipsoid to clavate, muriform, and 

26-50 X 10-20 ym (Fig. 49C). Transmission is by airborne 

ascospores or conidia, and penetration is through stomata. 


BOOTH, C., and K.A. PIROZYNSKI. 1967. Ph'osporaherharum.No. 

150 in: Descriptions of pathogenic Fungi and Bacteria. Commonw. 

Mycol. Inst., Kew, Surrey, England. 

ELLIS, M.B. 

2 pp. 

1971. Dematiaceous 

Inst., Ke w , 

Hyphomycetes. 

S u rrey. E n gla n d . 

Commonw. 

6 0 8 p . 

Mycol. 

(Prepared by L. J. Turkensteen) 

Ulocladium Blight 

Ulocladium atrum Preuss (syn. Stemphylium atrum (Preuss) 

Sacc.) is a weakly pathogenic organism (Fig. 49D). In the high 

(over 3,500 m) Andean region around I.ake Titicaca, it causes 

a potato foliage blight that is associated with damage from 

insects and, especially, from hail. Damage caused by the 

frequent hail storms is increased considerably as torn edges of 

leaves turn dark to black. When heavily attacked by U.atrum, 

the whole foliage turns blackish and becomes necrotic. Also, 

tiny, dark colored lesions up to 3 mm in diameter with irregular 

margins are formed on healthy lcaves, apparently without 

previous wounding. Peruvian natives call the disease kasahui. 


FRENCH, E.R., H.TORREST.A.de ICOCIEA, I.. SAI.AZAR, C. 

FRIBOURG, E.N.FERNANDEZ, A. MARTIN.J. FRANCO, M. 

M.de SCURRAH, I.A.HERRERA, C.VISE, .. .AZO, and O.A. 

HIDALGO. 1972. Enfermedades de lapapa in el Peri6. Bol. Teen. 

No. 77. Est. Exp. Agric. La Molina. 36 pp. 

ELLIS. M. B. 1976. More )ernatiaceous |lyphomycctes. Commonw. 

Mycol. Inst., Kew, Surrey, England. 507 pp. 

(Prepared by .. J. Turkensteen) 

, • 

Lv~~ ~ -_.. 

Fig. 50. Leaf spot lesions of Septoria lycopersici.(Courtesy E. R. 

French) 

46 

* 

Stemphylium consortiale 

Sternphvliuni consortiale (Thiim.) Groves & Skolko (syn. 

Ulocladium consortiale (Thiim.) Simmons) causes lesions 

occurring with and superficially resembling those caused by 

Alternaria solani, except that lesions lack the concentric 

markings of early blight and are lighter brown. Lesions develop 

three to fourdaysafter inoculation and cause defoliation similar 

to that of early blight. 


EI.l.lS, M. B. 1976. More t)ematiaceous Hyphomycetes. Commonw. 


WRIGIHT, N.S. 1947. A stemphylium leaf spot on potatoes in British 

Columbia. Sci. Agric. 27:130-135. 


Septoria Leaf Spot 

Thedisease ispresent in Centraland South America. It occurs 

T e d s a e i r s n n C n r l a d S u h A e i a t o c r 

in cultivated potatoes at elevations that differ considerably from 

one region toanother, e.g., at 1, 6 00-2,500 m in Venezuela and at 

3,800-4,200 m in Peru. It occurs in wild potato at a wider range 

of elevations. 

Symptoms 

Lesions on leaves are round to oval (Fig. 50) and have concentric 

rings of raised tissue when viewed from the upper surface. 

Rings are similar to those of early blight or Phoma leaf spot. 

Septoria leaf spot can be distinguished with the help ofa good 

hand magnifier by the presence of one or more relatively large, 

erumpent pycnidia ( 9 0-230,um) in older lesions. Leaves in alate 

stage of attack become bri'tle, deformed, and susceptible to 

wind damage. In advanced stages, leaves become necrotic and 

may drop from the plant. Yield reductions are considerable. 


Septoria l.vcopersici Speg. is similar on tomato and potato 

plants but exhibits differences when isolates from the two hosts 

are grown on artificial media. Dampened pycnidia release 

masses of hairlike spores (1.8-2.4 X 25-135 pm or longer) with 

three or four, sometimes up to seven, cross walls (Fig. 49E). On 

artificial media, lead gray colonies expand very slowly, and 

oatmeal agar becomes brown below the colony. 

Epidemiology 

The disease is present in regions characterized by cool, moist 

weather during the growing season. Inoculum is transported by 

rain splash and probably carries over on plant debris in soil. 

Long moist periods during which leaves stay wet are thought to 

be necessary for infection. 

Other Hosts 

Tomato is the principal other host. 

Cntrol 

I) Nonsystemic fungicides capable of controlling late blight 

are effective agaist Septoria. Treatment should be started at an 

early stage of infection because lesions, once present, form a 

continuous source of inoculum. 

2) Differences in susceptibility have been observed. 


PIGLIONICA. V., G. MAI.AGUTI. A. CICCARONE, and G. H. 

BOEREMA. 1979. L.a Septoriosi della patata. Phytopathol. 

Mcditerr. 17:81-89. 

JIMENEZ, A. T., and E. R. FRENCH. 1972. Mancha anular foliar 

(Septoria lycopersicisubgrupoA)de lapapa. Fitopatologia 5:15-20.

TORRES, H.. E. R. FRENCH, and I.. W. NIELSEN. 1970. Potato Control 

diseases in Peru, 1965-1968. Plant Dis. Rep. 54:315-318. Foliage sprays used for other leaf pathogens are apparently 

effective. 


Cercospora Leaf Blotches 

The disease is reportcd from cool and temperate climates of 

Europe and Russia and from the eastern part of the United 

States, where it isnot considered an important disease. It is also 

reported from restricted areas in Africa and Asia and from 

India, where it occurs with early and late blights. 

Symptoms 

First symptoms on lower leaves are small yellow to purplish 

lesions that increase from 0.2 to I cm in size. On the underside of 

the lesions, a dense, plush, gray layer of conidiophores and 

conidia is formed. Later, lesions are separated from 

surrounding tissues by a dark line. When lesions become 

necrotic, tissue may drop out, leaving only holes. Necrotic 

lesions are distinguished from those of Ahernariasolani by the 

lack ofconcentric rings. The disease becomes apparent at about 

the same time as late blight. The leaf may be killed; stem lesions 

become dark; and the entire plant may die. Symptoms on tubers 

have not been described. 


ifYcoVs'llosiela ((erco,jpora)conlcors (Casp.) Deighton has 

dark spores formed on densely branched sporophores that 

emerge through stomata. The straight or slightly bent, dark 

spores are variable in length (14-57 X 3.5-6 pm) and may have 

up to six septa or none (Fig. 51). 

An additional Cercospora species can attack potato. This 

larger spored form, C. solani-tuherosi Thirumalachar, with 

conidia 4I- 120 X 3.3 pm (1-12 septate), is described from India. 

-/ 

_! 

' B 

'The 

r '' , 

~to 

/// ~'Other 

/m 

U"in 

Fig. 51. Cercospora leaf blotch. Conidia and conidiophores of 

Mycovellosiella (Cercospora) concors. Bar represents 25 pm. 

(Reprinted, by special pirmission, from More Dematiaceous 

Hyphomycetes, by M. B. Ellis. 1976 Commonwealth 

Mycological Institute, Kew, Surrey, England) 


ELLIS, M.B.1976. More l)emaiiaccous ltyphomycetes. Commonw. 


NAGAICH, B.B., G.S.SHEKHAWAT, S. M. KHURANA,and S.K. 

BHATTACHARYA. 1974. Pathological problems of the potato 

cultivation in India. J. India Potato Assoc. 1:32-44. 

SALZMANN, R.. and E. R. KELLER. 1969. Krankheiten und 

Sch'idlinge der Kartoffel. Landwirtschaftliche Lehrmittelzentrale 

Zollikofen. 150 pp. 

THIRUMAI.ACHAR, M. J. 1953. Cercospora leaf spot and stem 

canker disease of potato. Am. Potato J. 30:94-9"'. 


Phoma Leaf Spot 

Yield losses up to 80% have occurred from Phoma leaf spot in 

the Andes of Peru and Boliva at altitudes of 2,000-3,500 m. 

Symptoms 

Small leaf spots, up to I cm but mostly less than 2.5 mm in 

diameter, have concentric rings and are similar to early blight 

lesions except that the lesions are not depressed into the leaf 

tissue (Plate 35). At first a few lesions form on the lower leaves; 

gradually infection spreads to the whole plant. Primary lesions 

continue to expand, and secondary infections give rise to many 

smaller lesions. which may coalesce. Foliage becomes blackish 

and when it dies remains attached to the stem fora time before it 

drops. On stems and petioles, elongate lesions develop. 


Ploioa anfl(ila Turkensteen ha:. light-colored pycnidia, 

125-200 pm in diameter (on artificial media) containing a 

distinct ostiole surrounded by 2-3 rows of brown cells. In leaf 

lesions, many submerged pycnidia are present at the upper side 

only. From the same pycnidium, two types of spores are formed: 

I) hyaline, one-celled infective spores, 14-22 X 5-7 pm, shaped 

like two-seeded peanut pods (Fig. 49F), and 2)small sporelike 

bodies, 5.8-7.8 X 2.0-2.6 um, which do not germinate on 

artificial media nor infect plants. On artificial media, single, 

hyaline chlamydospores develop in series, but complex 

chlamydospores are also formed. In rare cases, spores in old 

cultures may be two-celled and considerably larger. 

colony is light colored on artificial media. It is relatively 

slow growing, and on acid (pH 4.5) media its growth is strongly 

inhibited. On potato-dextrose agar and oatmeal agar the 

medium turns yellow-green and yellow, respectively, within two 

three weeks. When grown on slightly acid agar for one week, 

the medium turns yellow when a drop of IN NaOH is added to 

the surface. 

Hosts 

Cultivated and wild species of potato are as yet the only 

known hosts. 

Control 

I) Applications of fungicides are effective when started early 

the season before lesions are abundant. 

2) Resistance is known. 


TORRES, H,, E. R. FRENCH, and L. W. NEILSEN. 1970. Potato 

diseases in Peru, 1965-1968. Plant Dis. Rep. 54:315-318. 

A7

ITURKENSTFEN. L... 1978. Tiion foliar de lapapa enelIPer: I. 

Especies de Phorna asociadas. Fitopatologia 13:67-69. 

(Prepared by L. .1. Turkensteen) 

Choanephora Blight 

Choanephora blight, caused by ('lhoinelhoracueurliturun 

(Berk. & Rav.) Thaxter is only known so far in hot, moist, 

tropical sites in Peru wh'-ere potato has recently been introduced. 

It is marked by long (4-5 mm). spiny spora ngiophores (Fig. 

49G-.J) on initially water-so- '.ed. hut later necrotic, lesions 

(Fig. 52). Affected plants i. die rapidl3y or slowly. 


TURKENSITEN L..I1. 1979. Choanepliora blight of potatoes and 

other crops grown tinder tropical conditions in Peru. Neth. J. Plant 

Paihol. 85:85-86. 

(Prepared by 1..J.Turkensteen) 

Gray Mold 

The fungus is found on a wide range of plants throughout the 

world but in potato the disease is usually considered of minor 

economic importance. 

Symptoms 

Syvmptonls become apparent on foliage towsard the end of the 

growing season. Lesions on upper leaves are rare, developing 

Only during periods of cool weather. Lesions ate usually oi the 

Margins or tips of' leaves. typically wedge-shaped. often 

bordered by ma }jerveins,. ;ld have wide concentric /oiation. 

lleev may sitperficiallv resenle late blight lesions. When 

infected flower parts fallon leaves. the fungus may grow from 

the dcaying part and produce a sonewhat circular lesion (Fig. 

53 B). 

I.\eer lea\es t liat have become chlorolic from shading break 

dos itwith ill ,iiv rot. Rot spreads fro infected leascs through 

the petiole aid into the cortex of the stei (F1ig. 53A). 

BOt rvtis fruits profcusely oiiaffected tissue, producing it lcu1//y 

appea ra ice. Spece masses and aerial mycelia wit h gray liltl)( are 

relati\elycleise and tff-white or gray to tiatn in contrast to those 

\\ith late blight. \\Iich ilresparse and white. 

1Ocber inlection, which is uncommon, is not apparent at 

digging bit de\clops during storage and may become severe. 

lie surface ,olinfected tissue is wrinkled. Underlying tissue is 

flabby. temporarily darkened, and later becomes semiwatery 

w'ith browndecay. Tufts Ofthie fungus may emerge from wounds 

and eyes (Fig. 53C and )). A dry type of rot also develops, 

Fig. 52. Choanephora cucurbitarum infection on potato leaves, 

(Courtesy L. J. Turkensteen) 

48 

-usually 

appearing as sunken. pitted, discolored areas penetrating 

usuall\. less than I rin. 


Bolrvti. cin'rea 'ers. produces conidia in a grapelike cluster. 

conidia are ellipsoid to ovoid, one-celled, 9--15'X 6.5-jIp in,and 

borne on the tips of condiophores (Fig. 531-(i). 1otrytis fruits 

on decaying petioles, stems, flowcrs, and tuber parts, and on 

sclerotia. Sclcrotia are hard, black. irregularly shaped, 1~15 im 

long, and firmly attached to the substrate. 

The perfect stage. Scle'roiniia iwc'liane (de Bary) Fuckel 

(syi. Botr.,otiia liwkelilnu (dc Bar3,) Whet/.) is relatively rare, 

viih apothecia 1.5-7.0 nin in diameter and 3-15 mm high. 

Epidemiology 

Infection, sometimes initially latent, becomes apparent on 

senescent plant parts under stress from shading or excessive 

humidity. Spores are spread by wind and rain, and lesion 

development is limited by dry sunny conditions. Leaf infection 

requires high humidity and relatively cool temperatures. 

Pnoculum is apparently ubiquitous. 

High levels of K and N fertility reduce tle percentage of tuber 

infection. Relative maturity of tubers has little influence on 

incidence of infection. Tuber decay may be severe when tubers 

are placed immediately into storage at moderately low 

temperatures and high humidity without previous wound 

healing. 

Control 

I) Foliage protectant sprays may be useful if foliage is not 

severely shaded. 

2) Permit tubers to wound heal before placing them in low 

temperature storage. 


Et.IJS, M. B., and .1. M. WAL.L.ER. 1974. Sc'rolinia fuckeliana 

(conidial state: Botrrtiscinerea). No. 431 in: Descriptions of Pathogenie 

Fungi and Bacteria. Comnonw. Mycol. Inst.. Kew, Surrey, 

England. 2 pp. 

HARPER, P. C., and II. WII... 1968. A response of grey mold of 

potatoes to fertilizer treatment. Eur. Potato .1. I11:134-136. 

HOLI.IOMON, I). W. 1967. Observations on the phylloplane flora of 

potatoes. Fur. Potato .1. 1):53-61. 

RAMSEY, G. B. 1941. Botri.s and Schrotinia as potato tuber pathogens. 

Phytopathology 31:439-448. 


White Mold 

White mold is a cool temperature disease occurring in the 

Andes and in temperate zones nearly everywhere that potatoes 

are grown. 

Symptoms 

Water-soaked lesions covered by a cottony mycelial mat and 

sclerotia are most frequent on the main stem at the soil line or on 

lateral branches in contact with the soil. They may appear, 

however, in the angles ift secondary branches, leaves, petioles, 

and flower peduncles. Leaf lesions, irregularly shaped, are 

at the base of leaflets. First symptoms are small areas of 

discolored tissue that turn gray and look wet. In severely 

affected plants, the stem is girdled and plants die (Plate 36). 

Infected sterns often with zonate lesions (Fig. 54A) have mycelia 

and sclerotia in the pith (Fig. 5413). 

Tubers near the soil surface may be infected, beginning with 

small depressed areas sometimes located near the eyes and 

having a distinct demarcation between affected and healthy 

tissues. As lesions enlarge, flesh shrinks and becomes 

superficially blackened and spongy (Plate 37). Rot is wateryand 

soft, becoming leaky under pressure. It is whiter than normal 

and, even in advanced stages, discolors the tuber only slightly

d 

AC D 

A 0 

Fig 53 Gray mold. A, Botrytis sporulating on stem lesion and dead petiole: B, leaf lesion; C and D, Botrytis tuber infection with feltlike 

mass of mycelium at arrow: E and F,Botrytis cinerea conidia on conidiophore; G, conidia. Bar in E represents rnl 

50pm; bar in F represents 10 

and gives no odor. Infected tissues later develop internal cavilies 

Ildled %kithII iceliirIr and selerotia. 

 

Ca~usal Organi~ss* 

Ni+h'riuloiz liuirriri (IIih.I de lirrv (svNr. IfI i:'hnia 'I 

%cI'roiorum(Fib.) Korl. & D)rniont ) and also S. mior lagger 

~ 

ani .5 um1'rI,'dia Rarin sev ar. Ceauisal agents. Sclerotia (Fig. 

54(*);are hard. lenticular or irregular in shacpe, and varied in si/c. 

[he iaV he nmirlitetor .vhe over i cerntinetei- in diameter. 

ouuli ., s',l'ri al i;i \ hla k c ci'nr gs arid \ hite interiu s: liter 

thei MIrri1 li h~CO InL' bl;I~k ;1rid 1i1i11. [I i s elCCirirnI is rite1 

and 

1 

flu Is. MIinute. ghhose spermatia (2-3 mill)develop infre- 

qtmently inrinvelial mats at the base o the plant or in drying 

cultures. lheir role in pathogenicity is unkrnowvn. Apothecia 

(Fig. 55 top) orned at tlie soil surface may' he funnel-shaped to 

flat. Iheircolors include pale orange, pink, light tan. and white. 

Apothecia can he 1.5 cm, r nmre in diameter., and ore or several 

ma erI.iwrge frrrm a single scleroliuni. Asci are eight-spored, 

hyaline. cylindroclavate. 84-2510 X 4-23 pm. Ascospores 

unicellular, 

are 

6-2X8 2--15.2 in, ovoid, hvaline, narrow at the 

base, and slightly inflated at the apex. IParaphyses are filiform 

and hyalirne (Fig. 55 bottono). 

" 

" 

.. 

B 

C 

Fig. 54. White mold: A, zonate lesions on stem; B, stem interior 

showing cavity containing Sclerotinia sclerotiorum mycelium 

and a sclerotium; C, sclerotia. 

4P

Disease Cycle 

Soilborne sclerotia near the surfacegerminate, forming either 

an apothecium or, if enough moisture and organic matter are 

available, a mycelial mat. The mycelium penetrates stems at the 

soil line and forms a white, fluffy mat on the stem and, frequently, 

also oil adjacent soil. The fungus invades plant tissues 

rapidly, entering the inner stem tissues and pith, where sclerotia 

are formed. Apothecia forcefully eject numerous ascospores at 

maturity. Ascospores may spread aconsiderable distance from 

tile source, settle on lateral br-.iches or leaf surfaces, germinate, 

infect, and cause lesions. -the fungus overwinters as sclerotia in 

the soil and in crop residues. 

Epidemiology 

Cool temperatures (16-220 C) and high relative humidity 

(95-100(' ) favor disease development. Sclerotia are killed 

within 3-6 weeks in flooded fields. Older tissue appears to be 

more susceptible than young tissue because the disease spreads 

METRIC 1W 

411111 11 1111 IHIISe 

P2 

• .,of 

""N 

Fig. 55. Top, Sclerotinia sclerotiorum apothecia attached to 

sclerotia. Bottom, Hymenial layer of ascus: a,ascus with spores; 

b, paraphyses; c, an ascospore. Scale at top is in centimeters; 

bar represents 20 m. (A,Courtesy T. A. de Icochea) 

50 

:: 

r 

iF 

' 

more rapidly after plants are flowering and forming tubers. 

Heavy rainfall or irrigation induces apothecia production from 

sclerotia. Ejected ascospores are more effective in disease dissemination 

than is mycelium from sclerotia. 

Other Hosts 

S. sclerotiorutn has awide host range, attacking many dicotyledonous 

crops and weeds. Among solanaceous plants, potato, 

tomato, pepper, tobacco, and eggplant are severely attacked. 

Control 

I) Crop rotation with gram'naceous crops for four or more 

years reduces disease incidence. 

2) Fungicide application, especially with systemics, has been 

reported to give good control. 

3) Flooding fields between crops may destroy sclerotia. 


BUSTAMENTE, E.R.. and 11.t). Ill tIRSTON. 1965. Pudrici6ndura 

del tubi~rculo de la papa. Agric. Trop. 21:113-121. 

EDDINS, A. I. 1937. Sclerotinia rot of Irish potatoes. Phytopathology 

27:100-I 013. 

MOORE, W.t). 1949. Flooding as a means of destroying the sclerotia 

Scr(inia .wh,,tioruo.Phytopathology 39:920-927. 

some chemicals on Scerotinia sclcrotiorun in laboratory and 

potato field. Phylopathology 52:766-770. 

PU R L)Y. I.. II. 1955. A broader concept of Scierotinia sclhrotiorun 

based on variability. lPhytopathology 45:421-427. 

RAMSEY, G. B. 1941. Thotrvtisand Sch,rotiniaas potato tuber pathogens. 


(Prepared by T. A. de lcocheca) 

Stem Rot 

o 

Stem rot affects potatoes in the tropical and subtropical 

regions. It isalso reported from some countries with temperate 

climates: New Zealand, Denmark, The Netherlands, Argentina, 

Chile, the United States, and Russia. 

Symptoms 

Plant stems are infected at or below the soil surface (Plate 38). 

The plants wilt and lower leaves become chlorotic. An 

appressed, white, fanlike mycelial growth radiates over the soil 

surface, and numerous round, tan sclerotia form in the older 

mycelia at the stem base and soil surface. Lesions usually grow 

up and down the stem, and all living tissues are killed. Initially, 

infected tissues are soft, depressed, and brownish. As the dead 

cortical stem tissues dry out, xylem remains as fibrous strands. 

Tubers become infected through the stolons of diseased 

plants and through lenticels from mycelia growing over tuber 

surfaces. The fungus radiates, forming symmetrical circles 

around the lenticels. Fresh lenticel lesions are moist, semifirm, 

and cheesy. They are easily dislodged and leave a cavity. After 

drying, the circular lesions become white and chalky (Fig. 56B). 

Multiple lesions may form on the tubers, destroying them before 

harvest. Secondary invaders, Ern'iniaspp., enter through these 

lesions and accelerate tuber decay. Infections incipient at 

harvest continue rotting during transit and storage, and often 

white superficial, closely appressed, mycelial strands radiate 

from the infection site (Fig. 56A). 

Natural infection of seed tubers in the field occasionally 

causes seed decay and reduced stands. 

Dead or dying plants devoid of fungus signs can often be 

diagnosed by placing them in a moist chamber for a few days; 

abundant mycelia grow from them. 


The mycelium of Schrouiumrol4fii Sacc. iswhite when young, 

becoming tan as it gets older. It is 6-9,pm in diameter and has 

thick clamp connections (Fig. 56C). Older mycelia usually form

strands of pigmented hyphae. Sclerotia are numerous, round, 

0.4-2.0 mm in diameter, white when young, then tan, and dark 

brown when old. [he hasidial stage. I'elliculariarolfvii (Sacc.) 

West, is uncommon, with basidiospores approximately 3.5-5 X 

6-7 j.m, elliptical to obovate, rounded above and either rounded 

or pointed at the base. Basidiospores do not seem to be 

important in the disease cycle, 


Hlyphae are both intracellular and intercellular and are constricted 

at the point of penetration of the cell wall. Host cells are 

killed well in advance of fungus hyphae. The hyphae produce 

oxalic acid in considerable quantities and also the enzymes 

polygalacturanase and cellulase, which hydrolyze and disrupt 

cell walls. 

Disease Cycle 

The fungus is soilborne as selerotia or mycelia on decay'ing 

vegetable 

vgtae ungusaistsoibor matter. Scle rotia nclerotia permit mitorlong-term y survival vival d5) but 

contain relatively low energy reserves. They produce short-lived 

mycelia unless a suitable living or dead plant part is available. 

Mvcelia infect seed tubers, sprouts, grown plants at any stage, 

and tubers. As an energy supply is exhausted, the mycelia 

aggregate, and sclerotia are formed. Disease spread in the field is 

by mycelial growth or by dispersal of mycelial fragments and 

sclerotia in debris or infested soil. Spread is therefore slow. 

Disease incidence within a field is often erratic, with infected 

plants 

plant 

as foci. Long 

parts 

distance 

containing 

spread 

hyphae 

is by 

or 

transfer 

sclerotia, 

of infected 

by movement of 

sclerotia by wind or surface water, or by mechanical means. 

Epidemiology 

Germination of sclerotia and mycelial growth are favored by 

aerobic conditions, high temperatures (28-30'C), and high 

relative humidity. Vegetative survival is in the upper few 

:'"';,: ' 

,. .. ..4 

*fruiting 

Fig. 56. Stem rot. Symptoms on tuber: A, radiating white 

mycelium; B, later stage with sclerotia. C,Clamp connections in 

hyphae of Sclerotium rollsii. (A, Courtesy L. W. Nielsen; B, 

courtesy T. A. de Icochea; C, courtesy T. A. de lcochea and L.J. 

Turkensteen) 

centimeters of the soil but may be deeper if the soil is dry and 

well aerated. Cool climates (elevations above 1,000 m in the 

tropics) are not favorable for disease development. 

Other Hosts 

S. rol'ii infects cultivated and noncultivated plants such as 

ferns, certain mosses, gymnosperms, grasses, cereals, banana, 

and many dicotyledonous plants including certain woody trees. 

It also grows on plant residues, including wood, in appropriate 

temperature and relative humidity. 

Control 

I) Use pentachloronitrobenzene as tuber seed treatment. 

2) Fumigate soil with 3M%sodium N-monomethyldithiocarbamate 

dihydrate. 

3) Bury plant debris by deep plowing. 

4) Avoid throwing sod or organic material (weeds) onto 

lower stems of potato plants during cultivation. 

lae Control nsi defoliating ufcs diseases to prevent accumulation of 


AYCOCK, R. 1966. Stem rot and other diseases caused by Scerotium 

ro~llfii. N. C. Agric. Exp. Sin. [ech. Bull. 174. 202 pp. 

AYCOCK. R.. chairman. 1961. Symposiumn on Schrotiuo rollii. 


ED)INS, A. H., and F..WEST. 1946. Sclerotium rot of potato seed 

pieces. Phytopathology 

FRENCH, 

36:239-240. 

FRIBOURG, 1. R., F.N.FERNANDEZ, 11. TORRES, T.A.de 

A. 

ICOCIIEA, 

MARTIN.J. I.. SAt.AZAR, 

FRANCO, 

C. 

M. 

M.de SCURRAtt, I.A. HERRERA, C. VISE, L.L.AZOand 0. A. 

HIDAI.GO. 1972. Enfermedades de ]a Papa en el PeriL Bol. recn. 

No. 77. Est. Exp. Agric. La Molina, 36 pp. 

(Prepared by T. A. de lcochea) 

Rosellinia Black Rot 

The disease is prevalent in the tropics, where temperate and 

moist climates are found during the growing season. Especially 

heavy yield losses, rivaling those of late blight, are reported from 

Costa Rica and Ecuador. The disease has also been reported 

from Bolivia, Colombia, Peru, and Chile. 

Symptoms 

Plants become stunted and wilted. Leaves yellow, and plants 

slowly die. Stems may be cankered, Roots and stolons may be 

partially or completely destroyed, dark colored, and covered by 

a mat of rough, loose, fast growing strands of a grayish white 

mycelium (Fig. 57A). Affected tubers are partially or completely 

covered by the loose fungus strands at harvest (Plate 39). A 

hard, dark brown carbonaceous mass soon forms in affected 

tissue under the white mycelium. When cut, tubers often show a 

band of striate projections growing inward from the tuber surface 

(Fig. 57C). Single plants or groups of plants may be 

attacked in,the field. Infection expands from affected phmts in 

the fungus are found to extend from one plant to another. 

'ubers frequently rot before harvest. 


Morphology of the mycelium 

istic swellings 

and, especially, 

of the hyphae 

the character 

above the septa (Fig. 57B) are 

characteristic of the genus Rosellinia, which produces no known 

bodies and should be considered a member of the 

Mycelia sterilia. 

Rosellinia black rot can be distinguished from stem rot 

because the fungal strands from Rosellinia may be present on all 

parts below soil level, whereas Sclerotium rolfiiaffects only the 

parts close to the soil surface. Rosellinia does not form round 

sclerotia. It also differs from the perfect stage of Rhizocionia 

51

solani (Thanatelphorus 'uco,ris),which forms a velvety white ROI)RIGIUEZ, R. A. 1958. "Torbo," a tropical disease of potatoes. 

sheet in close contact with plant parts touching the soil. Plant Dis. Rep. 42:972-980. 

Epidemiology (Prepared by L.i. Turkenstcen) 

The disease occurs in level or moderately sloping fields where 

water accumulates. The fungus develops in warn soils rich in 

organic matter at lower elevations, frequently on recently Rhizopus Soft Rot 

cleared land that has been forested or planted with pasture. It 

bectones a problem when potatoes are not rotated. 

This fungus occurs throughout the world, but the disease is 

Other IHosts important chiefly in the tropics. Tuber losses under high tem 

'[he fungus affects carrots, beets, and members of the peratures may he high. 

Brassicac and of the genera ' maranthus. Runie.v, and 

Polh'gontnt. Symptoms 

Water-soaked lesions on skin, initially small, enlarge rapidly 

('ontrol and become a soft, watery rot extending into the flesh. Rotted 

I) Remove all debris from freshly cleared land. tissue later becomes brown to chocolate brown. Mycelium in 

2) Keep the land free of weeds, which may maintain the tissue is at first white and later dark. Grayish, later dark, sporfungus. 

angiophores develop on the surface. Rotted tissue develops 

3) Rotate potatoes with nonsusceptible crops. zonate markings and at low relative humidity becomes adry rot. 

4) Soil treatments (iletani-sodium pentachloronitrobenzene) 

have reduced the disease to some extent. Causal Organisms 

Rhizopus stohmniter (Fr.) lind., R. arrhizus, and other 

Rhizopusspp.are typically saprophytes but may also be wound 

Selected References parasites on a wide range of fleshy storage organs of fruits and 

()RII.I.ANA, If. A. 978. studio de la enfermedad "l.anosa" de Ii vegetables. Invasion is characterized by dissolution of the cell 

papa en Fcuador. [itopatologia 13:61-66. wall middle lanella. (ierminating spores and mycclitim growth 

arc markedly inhibited by low temperature. The disease is most 

° 

severe at temperatures of 2 0 - 4 0 C. 

Control 

I) Chilling tubers just after harvest to 2.50C or below inactivates 

spore germination and mycelial growth. 

2) Tuber treatment with disinfectants has been successful. 

3) Avoid wounding tubers. 


MATSUMATO, T. T., and .1.F. SOMMER. 1967. Sensitivity of 

Rhizopu.s siolohifr to chilling. Phytopathology 57:881-884. 

lINK, G. K. K., and G. B.RAMSEY. 1932. Market diseases of fruits 

- • and vegetables. Potatoes. U.S. Dept. Agric. Misc. Publ. 98. 62 pp. 

THAKUR, 1). P.,and V. V. CIIENIJI.UJ. 1974. Chemicalcontrol ofsoft 

rot of potato tubers caused by Rhliopus arrhizus. Indian Phytopathol. 

27:375-378. 

,". (Prepared by S. K. Blhattacharyya and R. 1)wivedi) 

Rhizoctonia Canker (Black Scurf) 

Rhizoctonia canker, commonly called black scurf, is present 

in all potato-growing areas. 

Symptoms 

Black or dark brown sclerotia develop on surfaces of mature 

tubers (Plate 40). Sclerotia may be flat and superficial or large, 

irregular lumps resembling soil that will not wash off.The tuber 

periderm under such sclerotia is usually unaffected. Other tuber 

symptoms include cracking, malformation, pitting, and stem 

• ' ,,end necrosis. 

Plants are most severely damaged in the spring short, after 

planting; killing of underground sprouts delays emergence, 

especially in cold, wet soils. This results in poor, uneven stands 

of weak plants and subsequent yield reduction. Emerging 

potato sprouts may also be infected with cankers on the developing 

stem, often causing girdling and stem collapse (Fig. 58). 

Partial or complete girdling may promote a variety of plant 

Fig. 57. Rosellinia black rot: A, infection of underground parts; B, symptoms, including stunting and rosetting of plant tops, corcharacteristic 

swellings of mature hyphae (bar represents 20pm); tical necrosis of woody stems, purple pigmentation of leaves, 

C, tuber rot with characteristic black lines projecting into tuber. aerial tubers, upward leafroll, and often chlorosis, most severe 

(A, Courtesy E. R. French; B, courtesy G. deAbad and W. J. at the top of the platt. 

Hooker) Reddish brown lesions on stolons cause stolon pruning or 

52

tuber malformation. Roots are also pruned, resulting in a sparse 

root svsten. 

The sexual (perfect) stage of the pathogen occurs on stems 

just above the soil line as a whitish gia. mat on which 

basidiospores are formed, giving the surface a powdery 

appearance (Fig. 59A). [hc mat is easily rubbed off, and the 

stem tissue below the mat is healthy. These mats are often 

located above a lesion on the belowground portion ofthe stem 

(Plate 41). 

A type of uber malformation (Fig. 60), incompletely 

understood and not directly linked to Rhi:ocotniainfection, is 

frequent when Rhi:ocioniais severe on tubers. The condition is 

believed to follow raycelial infection of' the tip of very young 

tubers. (rowth is retarded under the area of infection, and the 

tuber is deforned, often with superficial scalelike discolored 

tissue. 


Ihe pathogen in its imperfect stage is Ihow,nia .solani 

Kiihn and in its perfect stage (Fig. 59 C and )) uanateplhorws; 

cticu,wris Frank.) )onk. (svn. (orticium vagunt Berk. & Curt., 

I'cllih'aria.ilaniento.,a(Iat.) Rogers, and lIpoi/ntis .s. ani 

stomosis lPtill. & IDclicr. (hyphal ). I fusion), lie Rhiz'oioom and isolates hvphac have aire capable been of further anaclassified 

according to anastomosis groups. Isolates pathogenic 

to potato are generally placed in group A(i-3 (Parameter et al). 

I he myceliun is generally tan to dark brown and hyphae are 

hvphae 

rather large 

have 

(generally 

multinucleate 

8-I0 m 

cells 

in diameter). 

and branch 

Young, 

near 

'cgetative 

the distal 

septun ol'a cell. Right-angle branching, constriction of branch 

hvphae at the poinor of' origin, formation of' a septum in 

branch 

tire 

near the origin (Fig. 59B). and a prominent septal pore 

apparattus are all characteristics of IR. .ol n.i 

Rhi-o ctojnia produces a growth-regulating toxin that m y e 

partially responsible for tuber malformation. 

Disease (ycle 

The pathogen overwinters as sclerotia on tubers, in soil, oras 

m'nceliurm on plant debris in the soil. In the spring, when 

conditions are generally favorable, sclerotia germinate and 

invade potato stems or emerging sprouts, especially through 

wounds. Roots arid stolons are invaded as they develop 

throughout the growing season. Sclerotial formation on new 

tubers is initiated at on 

ainy time, depending environmental 

conditions. however, maximum development occurs as tubers 

remain in the soil after death of vines. 

Epidemiology 

Rhi:octoniapopulations may increase in soils where little or 

no rotation is practiced. Planting seed tubers that arc heavily 

infested with sclerotia also favors inoculum buildup in soils. 

Environmental conditions favoring the pathogen are low soil 

temperatures and high moisture levels. rhe optimum soil temperature 

for disease development is 180 C and disease 

i 4 | 

,/ 

Fig. 58. Rhizoctona cankers on young stems, sprout girdling and 

death, and lateral sprouts forming from nodes below lesion. 

(Courtesy R. C. Rowe) 

400 

Fig. 59, Rhizoctonia solani (Thanatephorus cucumeris): A, perfect stage on potato stem; B, mycelial branching from such superficial 

mycelium on stem surface; C,basidiospores; D,basidium from potato stem surface near the soil line. Bar represents 10pm and applies to 

B-D. 

,\

development decreases with increasing temperatures. Iiigh 

moisture levels in soils, especially those poorly drained, also 

tend to increase severity of sclerotial formatior. on new tuber.i. 

Tuberborne sclerotia range in pathogenicity to stems and 

stolons from avirulence through moderate to high virulence. 

The influence of tuberborne sclerotia on the health of the 

following crop is not consistent and varies from essentially no 

deleterious effect to a measurable increase in sprout-pruning, 

stem cankers, and yield reduction. 

IHigh resistance within potato has not yet been identified. 

Other Hosts 

R. solani is a pathogen of numerous crops and weed hosts 

throughout the world. Its selective pathogenicity depends on the 

strain present. 

Control 

I) Seed treatment isnot effective in heavily infested soils. Use 

disease-free seed combined with seed treatments such as the 

systemic fungicides (benoyivl, thiabendazole, or carboxin) or, 

where acceptable, organic mercury. 

2) Soil treatments of benomyl or pentachloronitrobenzene 

reduce soilborne inoculum, but the returns may not justify the 

Cost. 


1IEl1N, W.I.. 1969. Evaluation of seed and soil treatments forcontrol 

of Rhitoctonia scurfand Verticillium wilt of potato. Plant Dis. Rep. 

53:425-427. 

I-RANK.A..and S. K. FRANCI.S. 1970. Ihecllect of a Rhi.:,loia 

.olani phytotoxin ol potatoes. can. .1.Bot. 54:2536-2540. 

IlIDI. (i. A., .1.M. III RSI. and 0. .1.STIEI)MAN. 1973. Effects of 

black scurf (Rhizocionia solani) on potatoes. Ann. App!. 1iol. 

74:139- 148. 

.AMES. W.C.,and A. R. McKENZIE. 1972. The elect of tuber borne 

sclerotia of Rhi:octonia .olami Kiihn on tile potato crop. A;ii. 

Potato .J.49:296-31)!. 

PAR M IT R.J.IR., ed. 1970. Rhioi tonia. odani:Biologyand Pathology. 

Unik. of Calif. Press, llerkeley. 255 pp. 

PARNI-EER. 1. R., Jr., R. I. SIEI!RWOOI), and W. I). PI.ATT. 

1969. A nast omosis grouping anmong isolates of hanatelphorus 

c'ucuniri.%. Phytopathology 59:1270-1278. 

SAN E(1)R I). Ii. I. 1956. Factors influencing formation of sclerotia by 

Rhi.:otomia.%ortai. lPhytopathology 46:281-284. 

VAN EMI)IN, .1.If., 1958. Control of Rlhi:octonia ..ohmi Kiihn in 

potatoes by disinlection ol seed tubersand by chemical treatment of 

the soil. Eur. Polato .t. 1:52-64. 

VAN F.MI)I'N..I. I1., R.E. I.ABIJRYERF,and (. M. IICIIEL.AAR. 

1966. On thecontrol of Rii:o'tonias.olaniin seed potato cultivation 

M.puriureum. 

Fig. 60. Injury at tuber apex, common under certain conditions 

when Rhizoctonia is present. (Courtesy H. Torres) 

54 

in the Netherlands. Instituut voor Plantenziektenkundig 

Onder/oek. Mededeling 412. 42 pp. 

WENIIAM,. I., If. I.. MacKINTOSII. and If. A. BOIKAN. 1976. 

Evaluation of fungicides for control offpotato black !eurf diseam, 

N.Z. J. Exp. Agric. 4:97-101. 

(Prepared by .1.A. Frank) 

Violet Root Rot 

Although infrequent, violet root rot has been reported from 

most of the major potato-growing areas of the world. 

Symptoms 

Aboveground symptoms are not distinctive. The foliage may 

become chlorotic, and plants may wilt and die suddenly in 

localized areas in the field. Belowground plant parts are often 

covered only with a reddish-purple mycelial network on the 

uninjured skin. Under the mycelial mats, tubers may have dark 

gray, somewhat sunken spots covered with purplish lack 

sclerotia. The fungus tends to be limited to the cells near the 

periderm of the tuber. Wet rot of tubers may develop under 

mycelial mats. 


Ih,licobasidiutm purpure'n (Tul.) Pat. (syn. Rhizoctonia 

'rocortam(Pers.) iDC) has young hyphae that are light violet, 

becoming more intensely violet with age. IHyphal branches arise 

at right angles close to a septum. The mycelium is branched, 

septate, and distributed evenly over tile host surface. On occasion, 

strands are clearly visible. l)ark brown to purplish black 

r funga 

sclerotia form on the al mats. Sclerotia are essentially 

round, covered with a thick velvety felt, and vary in diameter 

from a few millimeters to several centimeters. The basidial stage 

is present infrequently on the base of potato stems near the soil 

surface as awhite, superficial growth similar to that of R. solani. 

The b:tsidium is hyaline, with two to four cells, each bearing a 

sterigma (0-35 pm in length) that produces a basidiospore 

(I0-12x 6-7/pm). 

Disease Cycle 

The fungus overwinters in the soil as sclerotia. These 

germinate in the spring and infect the crop. Basidiospores may 

spread the disease. 

Other Hosts 

The fungus parasitizes a wide range of hosts, the most important 

being carrot, lucerne (alfalfa), asparagus, and sugar 

beet. 

Control 

Rotation may be useful. Avoid rotation with other hosts. 


BUDI)IN, W.,and E.M. WAKEFIEI.). 1927. Studies on Rhizovionia 

ocrgoorionflPers.) D)C. and llelicollavidium,ipuriiurewn (Tul.) Pat. 

Trans. [r. Mycol. Soc. 12:116-140. 

DBUDIN, W., and E. M. WAKEFI1:I.I). 1929. Further notes on the 

connection between Rhizoiontia (rocortom and Ilclicohasidium 

Trans. Br. Mycol. Soc. 14:97-99. 

KOTTE, W. 1930. Beobachtungen iber den Parasitismus von 

Rhizoctoia violacea HlI. auf der Kartoffel. Bar. l)tsch. Bot. Ges. 

48:43-51 

(Prepared by L. V. Busch) 

Silver Scurf 

Silver scurf is probably present in all of the major potato 

growing areas.

1. Giant-hill plants, taller than normal plants. 2. Mahogany browning in low temperature storage. 

5. Wind injury. 

3. Low temperature leaf injury from 4. Hail injury. 

temperatures above those freezing tissue. 

6. Photochemical oxidant air pollution injury. 

COLOR PLATES '

* Y 

7. Air pollution injury from suilfur oxide (Courtesy AS,'RCO 8. Nitrogen (left) and phosphorus (right) deficiencies. 

Inc., Department of Environmental Sciences, Salt Lake City, UT) (Courtesy Department of Soils and Plant Nutrition, University of 

California. Berkeley) 

9. Potassium (left) and calcium (right) deficiencies. (Courtesy 10. Early sumptoms of magnesium deficiency (left) and 

Department of Soils and Plant Nutrition. University of manganese deficiency (right) (Left, Courtesy Department of 

California, Berkeley) Soils and Plant Nutrition, University of California, Berkeley; 

right, courtesy International Minerals and Chemicals Corp., 

Libertyville, IL) 

t; v 

.C '* . t V 

11. Blackleg, Erwinia carotovora var. atrosepfica infection in 12. Bacterial soft rol. Erwinia carotovora lenticel infection of 

the field. (Courtesy M D. Harrison) tubers. 

COLOR PLATES 

13. Bacterial soft rot. Erwinia carotovora infection of tuber. 14. Brown rot, Plant infected with Pseudomonassolanacearum. 

(Courtesy J. E. Huguelet) 

(Courtesy E. R. French) 

15. Brown rot. Tubers infected with Pseudomonas solanacearum 

exhibiting discolored eyesand vascular breakdown. 

? " 

" 16. Ring rot. Interveinal chlorosis and 

upward curling of leaf margins. (Courtesy 

R. H. Larson) 

17. Bacterial ring rot. Tuber infected with Corynebacterium t 

sepedonicum. (Courtesy J. E. Huguelet) 

18. Pink eye. Infection at the tuber apex. 

COLOR PLATES

19 Pink eye. Tuber rot from severe pink eye infection. 20. Common scab. Streptomyces scabies infection of tubers 

ranging from surface russeting to deep lesions. 

21. Deep common scab. Streptomyces scabies infection with 

sparse gray sporulation on the lesion surface. (Courtesy J. E. 

Huguelet) 

COLOR PLATES 

23. Powdery scab. Spongospora 

subtorranea infection of potato roots. 


IN 

/ 22. Powdery scab. Early and late infection of tuber. (Courtesy C. 

9H. Lawrence and A. R. McKenzie)

24. Wart. Synchytrium endobioticum infection of meristems 

of stems, stolons, and tubers. (Courtesy R. Zachmann) 

27. Pink rot. Tubers infected with Phytophthora erythroseptica. 

(Courtesy R. C. Rowe) 

,~ 

25. Wart. Syncnytrium endobioticum 

infection of tuber. (Courtesy M. C. 

Hampson) 

26. Leak. Tuber infected 

Huguelet) 

with Pythium sp. (Courtesy J. E. 

28. Late blight. Rapidly expanding lesions with pronounced 

chlorotic border. (Courtesy D. P. Weingartner) 

COLOR PLATES

29. Late blight. Leaves and slems infected "!lh Phytophthora 30. Late blight. Exterior and interior discoloration of tubers 

infestans. Note sporulation on leaf surface. (Courtesy R. infected with Phytophthora infestans 

Zachmann) 

COLOR PLATES 

31. Powdery mildew. Recent infection of young leaves 

by Erysiphe cichoracearum. (Courtesy R. Zachmann) 

32. Powdery mildew. Advanced stages 

of infection by Erysiphe cichoracearum. 

(Courtesy R C Rowe) 

33. Early blight, Alfernaria soiani infection of leaves. 

(Courtesy L. J. Turkensteen)

34. Pleospora herbarum (Stemphylium botryosum). Infected 35. Phoma andina. Infected leaves. (Courtesy L. J. 

leaves. (Courtesy L. J. Turkensteen) Turkensteen) 

36. White mold. Sclerotinia sclerotiorum 

infection of stem. (Courtesy R. Zachmann) 

38. Stem rot. Sclerotium rolfsii stem infection at the soil line. 


37. White mold. Sclerotinia sclerotiorum infection of tuber. 

(Courtesy T. de lcochea) 

39. Rosellinia black rot. Infection of 

tubers, with white mycelium on the tuber 

surface and soil. (Courtesy J. Bryan) 

COLOR PLATES (!

40. Rhizoctonia black scurf. Sclerotia of R. solani on 41. Rhizoctonia canker. R. solani infection of 

tuber surface. underground stems, sclerotia on seed tuber, and 

aboveground perfect stage (white area) on larger central 

stem. (Courtesy R. Zachmann) 

42. Silver scurf. Helminthospsorium solani infection of tuber. 


COLOR PLATES 

43. Black dot. Colletotrichum atramentarium 

on stem. (Courtesy E. R. 

French)

44. Charcoal rot. Macrophomina phaseol infection of tuber. 45. Gangrene. Phoma exigua var. foveata infection of tubers. 


(Courtesy R. Booth) 

46. Fusarium dry rot infection of tuber (exterior view). (Courtesy 47. Fusarium dry rot infection of tuber (interior sections). 

J. E. H'jguelet) 


48. Fusarlum dry rot. Cultural differences between F. roseum (fast 49. Fusarium wilt. Vine symptoms of F. eumartii infection. 

growing pink) and F. solani (slow growing purple). (Courtesy L. 

W. Nielsen) 

COLOR PLATES

50. Verticillium wilt of plant. (Courtesy R. Zachmann) 

' 1 

51. Verticillium wilt. Vascular discoloration in tubers. 

52. Thecaphora smut. Infected tumors. (Courtesy J. Bryan) 53. Common rust. Puccinia pittieriana infection of leaves. 


COLOR PLATES 

54. Deforming rust. Aecidium cantense infection of leaves and 

petioles. (Courtesy E. R. French)

55. Leafroll virus. Current season (primary) symptoms. 56. Leafroll virus. Secondary symptoms from tuberborne 

(Courtesy R. Salzmann and E. R. Keller) Infection. (Courtesy E. R. French) 

57.Leafroll virus symptoms. Marginal and interveinal chlorisis, 58. Rugose mosaic. Veinal necrosis and necrotic spotting of 

in andigena type potato. (Courtesy R. A. C. Jones) leaves. 

59. Rugose mosaic. Mosaic mottle. 

60. Rugose mosaic. Leaf drop and rugosity. 

(Courtesy J. Bryan) 

4, 

COLOR PLATES

61. Potato virus X. Mosaic mottle of this type is 

indistinguishable from that of other viruses such as PVY, 

PVM, PVS, etc. (Courtesy C. Fribourg) 

63. Potato virus M. Early symptoms. 

62. Potato virus X. Ring spot symptoms on Havana tobacco. 

64. Andean potato mottle virus. Secondary symptoms of 

severe patchy mottle and leaf deformation in the Peruvian 

cultivar, Revolucion. (Courtesy C. E. Fribourg) 

65. Andean potato latent virus. Symptoms in Peruvian cultivar, 66. Mop-top virus. Secondary leaf 

Ml Peru. (Courtesy C. E. Fribourg) symptoms. (Courtesy L. Salazar) 

COLOR PLATES

67. Mop-top virus. Primary tuber 68. Mop-top virus. Secondary tuber symptoms (left) and 

symptoms. (Courtesy R.A. C.Jones) healthy tuber (right). (Courtesy R. A. C. Jones) 

69. Tobacco rattle virus. Symptoms in leaves. (Courtesy D. P. 

Weingartner) 

71. Potato yellow dwarf virus. (Courtesy S. Slack) 

70. Tobacco rattle virus. Symptoms on tuber. (Courtesy D. P. 

Weingartner) 

COLOR PLATES

72. Alfalfa mosaic virus. (Courtesy I. Butzonitch) 73. Tobacco ringspot virus, (Andean potato calico). Early 

symptoms in Peruvian cultivar, Tichahuasi. (Courtesy C. E. 

Fribourg) 

COLOR PLATES 

74. Andean potato calico. Advanced 

symptoms. (Courtesy C. E. Fribourg) 

75. Potato yellow vein virus. (Courtesy J. Bryan) 

76. Tomato spotted wilt virus. Symptoms in potato leaves. 

(Courtesy E. R. French)

77. Aster yellows mycoplasma symptoms. Rolling and 78. Aerial tuber iii aiils of 

pigmentation in upper leaves. leaves of plant with aster 

yellows mycoplasma symptoms. 

(Courtesy International 

Potato Center) 

-,VFW",,, 

79. Hair sprouts from tuber infected with aster yellows 80. Psyllid yellows. Result from toxins introduced during 

mycoplasma (left) and sprouts from healthy tuber (right). feeding by nymphs of the potato psyllid. (Courtesy E. Nelson) 


81. Cysts of the golden nematode, 82. Cysts of the nematode, Globodera 

Globodera rostochiensis, golden pallida, white or cream colored before 

yellow before turning brown. (Courtesy turning brown. (Courtesy International 

International Potato Center) Potato Center) 

COLOR PLATFR

83. Lesion nematode (Pratylenchus penetrans). Damage on 84. Buckthorn aphid (Aphis nasturtii). (Courtesy M. E. 

tubers of Katahdin variety. (Courtesy W. F.Mai, B. B. Brodic, M. MacGillivray) 

B. Harrison. and P. Jatala) 

85. Common potato aphid (Macrosiphum ouphorbiae). 86. Foxglove aphid (Aulacorthum solani). (Courtesy M. E. 

(Courtesy M. E. MacGillivray) MacGillivray) 

87. Green peach aphid (Myzus persicae). (Courtesy M. E. 

MacGillivray) 

COLOR PLATES V)

Symptoms 

Small, localized, light brown, circular spots with indistinct 

borders frequently enlarge to cover a considerable area of the 

tuber. Affected areas have a distinct silvery sheen, particularly if 

the surface is wet (Plate 42). The color may deepen with age. Ifa 

large percentage of the surface is affected, tubers may shrivel 

during storage from excessive moisture loss. Red skinned varieties 

may lose their color. 

tuber Black surface dot and and silver may occur scurf 

together. 

produce similar blemishes on the 

Margins of soung silver 

r s c nExp. 

scurf lesions are more definite and frequently have a sooty 

appearance ca used by conidiophores and conidia. Silver scurf 

lesions do not have sclerotia. 


Ih'inithosporium.volani l)ur. & Mont. (syn. SpldV(/hoclauitmn 

atroviren. lilar,.) has a hyialine mycelium that is 

septate, branched, and turns brown with age. Unbranched 

conidiophorcs are septate, with the conidia borne in whorls 

from the distal ends of the cells (Fig. 61). Sporesare 7-8 X 18-64 

pim, have up to eight septa, and are dark brown, rounded at the 

base, and pointed at the ends. 

disease Cce 

lransmission of the fungus is largely from infected seed 

pieces; soil transmission may also occur to a lesser extent. 

Infection takes place through the lenticels and periderm before 

tubers are dug, with intercellul:ir and intracellular mycelium 

developing only in the periderm layer. 

Epidemiology 

Itigh humidity is necessary for disease development. The 

longer mature tubers remain in the soil, the more severe the 

problem becomes. Minimum conditions for infection are 3°C 

and 90'i rh. I)isease continues to increase in storage, and 

fLurther infection may develop if the tubers are kept at high 

relative humidity and temperature. Sporulation is more abundant 

on young lesions than on old ones. 

Some vartieties may be more susceptible than others. 

Other Hosts 

II. *slni has never been found on any other host and only 

infects the tubers of potatoes. 

Control 

I) Use disease-free seed. Treat seed with benomyl. 

! .t 

+ ° " 

S 

Send, 

*: 1Z 

Fig. 61. Helminthosporium soan A,conidiophores and conidia; 

B, conidia from tubers infected with silver scurf. Bar represents 

20pm.(A,Drawing from Taubenhaus, J.J. 1916. Acontribution to 

our knowledgeof silver scurf (Spondylocladium atrovirens Harz) 

of the potato. New York Bat. Gard. Memoirs 6:549-560.) 

2) Harvest the tubers as soon as they are mature. 

3) Ventilate storage area with warm air for drying, and store 

tubers at a low temperature consistent with wound healing and 

avoidance of other storage diseases. 


BOY). A. E. W. 1972. Potato storage diseases. Rev. Plant Pathol. 

51:297-321. 

BURKE, 0. 1). 1938. The silver-scurf disease of potatoes. N.Y. Agric. 

Sin., 

JE.l.IS. 

Cornell. 

I., and i. 

Bull. 

S. 1AYI.OR. 

692. 30 pp. 

1974. The relative importance of 

silver scurf and black dot: Two disfiguring diseases of potato tubers. 

Agric. t)ev. Advis. Serv. Q. Rev. (london) 14:53-61. 

JOUAN, B...1 M.L.eMAIRE. P. PERENNEC, and M.SAII.t.Y. 1974. 

Etudes sur lagale argent e de lapomme de terre, Ih'hinitho.sporium 

.olani Dur. et Mont. Ann. Phytopathol. 6:407-423. 

SCUII.TZ, 1. S.1916. Silver-scurf of the Irish potato caused by 

Sl(nthjli atroiren....Agric. Res. 6:339-35. 

(prepared by L.V. Busch) 

Black Dot 

The pathogen is common in many areas of the world, but the 

relative importance of the disease has not been well 

documented. 

Symptoms 

Black dot describes abundant, dotlike, black sclerotia on 

tubers, stolons, roots, and stems above and below ground (Fig. 

62A, Plate 43). Symptoms vary from belowground rot of roots, 

stems, and stolons to aboveground yellowing and wilting of 

foliage. Foliage symptoms, which first occurat plant apices and 

later at mid and basal regions, may be confused with those of 

other wilt pathogens (e.g., 1e'rtivillium and Fusarium spp.). 

Lesions on belowground stems and stolons may also resemble 

Rhizoctonia disease of potato. Severe invasion of cortical tissue 

causes sloughing of the periderm. Following removal from the 

soil, roots may have a "stringy" appearance from decortication. 

As stems dry, cortical tissue is easily scaled away, an amethyst 

color is common inside the vasuclar cylinder, and sclerotia on 

stems develop abundantly externally and internally. With high 

relative humidity, the development of setae is inhibited. 

Severe rotting of belowground plant parts and early death of 

the plant cause reduction in tuber size. At digging, pieces of 

dried stolons, with or without sclerotia, frequently adhere to the 

tubers. Stolons may be severed at any stage of tuber development. 

with the lesion usually 15-45 mm from the tuber. Sclerotia 

may develop on the upper surface of tubers and, in storage, 

grayish areas oti tubers may closely resemble silver scurf. 


Colhtotrichum atramentarium (Berk. & Br.) Taub. (syn. C. 

cocco(es (Wallr.) Hughes) appears on a variety of media, 

including potato-dextrose agar, as a white, superficial 

mycelium. Sclerotia, 100 pum to 0.5 mm in diameter, are 

arranged in concentric rings and have acervuli that produce 

numerous spores and setae (Fig. 46B-D). Setac vary in length 

from 80 to 350 pm, are septate, and are pointed at the tip. 

Conidiophores develop free or in palisade layers and are subhyaline, 

10-30 um long, cylindrical, and tapering to slightly 

chavate. Spores en masse appear yellow to pink depending on 

media pH, are hyaline, 1-3 guttulate, attenuated at the basal 

round at the apical end, and 17.5-22 X 3.0-7.5 pm in size. 


Mycelium and sclerotia are commonly associated with cortical 

and vascular tissue below the ground and at the base of the 

aboveground stem within several centimeters of the soil line. In 

certain instances, however, mycelium grows rapidly up the 

vascular cylinder of stems into leaves, even invading trichomes. 

55

S. ~active 

Epidemiology 

Overwintering is by sclerotia on thc surface of tubers or in 

plant debris in the field. T he pathogen does not appear to bean 

soil inhabitant, but it may survive in soil for long periods. 

C. atrameniariumn, generally regarded as a low grade pathogen 

,,I " 

k ._ 'i.+ i,!temperatures, 

that attacks under conditions of stress, commonly acts in comrelative 

bination 

importance 

with one or 

difficult 

more additional 

to determine. pathogens, 

Black dot making is most its 

frequently associated with light sandy soils, low nitrogen, high 

and poor soil drainage. 

tl Because C. atranwntariumis elusive and lack ofrecognition is 

frequent, very little work on disease control has been done. 

Other Hosts 

AIn additional to potato, the fungus occurs on tomato and 

other plants in the Solanaceae (eggplant, pepper, tomato), on 

weed hosts such as Physalis peruiviana, and, with inoculum 

increase, on lDandra .stranonium. a common weed. 

Control 

I) Clean seed, crop rotation, adequate fertility, and good 

irrigation management are commonly recommended. 

2) No known potato cultivar offers resistance. 

SSelected References 

~~DA V I S, . R., and M. N. 1-1OWA RD.1976. Presece cof Colh'totri(-hum 

atramentariumn in Idaho and relation to Verticillium wilt 

(V'erticillium dahliae). Am. Potato J. 53:397-398. 

DICKSON, B. T. 1926. The "black dot" disease of potato. Phytopathology 

16:23-41. 

HARRISON, D. E.1963. Black dot disease of potato. J. Agric. Victoria 

61:573-576. 

McINTYRE, G.A.,and C. RUSANOWSKI. 1975. Scanning electron 

microscope observations of the development of sporophores of 

Colletotricu/n atramentarium(B. etBr.) Taub. on infected potato 

periderm. Am. Potato J. 52:269-275. 

STEVENSON, W. R., R.J. GREEN, and G.B. BERGESON. 1976. 

Occurrence and control of potato black dot root rot in Indiana. 

Plant Dis. Rep. 60:248-251. 

THIRtJMALACHAR, M. J. 1967. Pathogenicity of Colleotrichun 

atranwntarium on some potato varieties. Am. Potato J.44:241-244. 

(Prepared by J. R. Davis) 

.-.+/i , '. , 

. . " .Charcoal Rot 

- " .The fungus is worldwide but economically important only in 

warra regions where soil temperatures exceed 281C. 

T , Symptoms 

Under hot conditions, the pathogen can attack potato stems 

'" , 

and cause a sudden wilt and yellowing. Stem infection is not 

usually important. More important is tuber attack, which may 

occur before harvest and in storage, causing loss of the entire 

crop. Early symptoms develop around the eyes, near lenticels 

(particularly those that have enlarged), and frequently at the 

stolon attachment. The skin appears unaffected at first, with 

underlying tissue, usually that within I cm of the surface, 

becoming slightly water-soaked and light gray. Cavities filled 

with black mycelium and sclerotia form later. Rapidly invaded 

tubers, when cut, exhibit semiwatery, flabby breakdown, with 

color changing from yellowish (Plate 44) to pinkish to brown 

and finally to black. Wet rot may later develop from secondary 

invaders. 

9Causal Organism 

D The pathogen isMacropltoninaphaseoli (Maubl.) Ashby 

Fig. 62. Black dot: A, on potato root; B, portion of typical (syn. Al.phase'olina(Tassi)Goid., Sc h'rotiumbataticolaTaub.). 

Colletotrichum atramentarium colony growing on nutrient Na- Sclerotia within roots, stems, leaves, or fruits are black, smooth, 

polygalacturonic acid medium; C, cross section of acervulus hard, and 0.1-1 mm in diameter. They are smaller in culture. 

showing setae and conidia arising from acervulus; D, spores Pycnidia, dark brown on leaves and stems, are 100-200 pm in 

approximately 3.8 x 17.5 um. (Courtesy J. R. Davis) diameter. Single-celled conidia are hyaline, ellipsoid to 

56

obovoid, and 14-30 X 5-10 pm. Pycnidia production in culture 

is rare except on propylenc oxide sterilized leaf tissue in agar. 

Epidemiology 

The fungus maiatains itself saprophytically on unthrifty or 

senescent plant partsand survives unfavorable periodsas microsclerotia. 

Pycnidiospores are relatively short-lived. Tubers are 

infected through wounds, eyes, enlarged lenticels, and the 

stolon. 

Tubers are predisposed to infection at temperatures of 320 C 

or higher. Rot development is restricted at low temperatures, 

slow at 20-25'C, and most rapid at 36'C and above. No 

secondary spread is apparent during storage, but infected tubers 

rot in warm storage. Rot stops in refrigerated storage, but when 

tubers are returned to warm temperature, the rot continues. 

Thus, seed from cold storage should be warmed before being 

planted so that infected tubers may be removed. 

Most commercial cultivars are equally susceptible. Resistance 

exists in certain Solanum chacoense clones, in some of its 

hybrids, and in hybrids of the series Commersoniana. 

Other Hosts 

The fungus has been found on underground parts of an 

extremely wide range of plants, both cultivated and wild. 

Control 

I) Harvest early, before soil temperatures become high. 

2) Avoid bruising and wounding of tubers in harvest and 

postharvest handling. 

3) Field irrigation may be useful to prevent excessive soil 

temperature. 

4) Do not leave tubers in soil after plants have matured. 

5) Do not harvest during periods in which soil temperatures 

exceed 28' C. 

6) Do not store tubers at high temperatures, 

7) Do not use seed originating from areas where the disease is 

frequent. 


IIJARGAVA, S. N. 1965. Studies on charcoal rot of potato. 

Phvtopathol. Z. 53:35-44. 

GOTII, R. W., and S.A. OSTAZESKI. 1965. Sporulation of Macroplominaiphaseolionpropylene 

oxide-sterilized leaf tissues. Phytopathology 

55:1156. 

IOI.LIDAY, P., and E. PUNITIIAI.INGAM. 1970. ,tfacrophonina 

phaseolina. No. 275 in: Descriptions of Pathogenic Fungi and 

Bacteria. Cornnionw. Mycol. Inst., Kew, Surrey, England. 2 pp. 

I1tSlKARNATIIi. 1976. Potato in Sub-Tropics. Orient L.ongman, 

SAIIAI, ).eB. DJI, and K. D. PAIIARIA. 197t). Reaction of 

sonic wild and cultivated potato varieties to charcoal rot. Am. 

potato J.47:427-429. 

TIIIRUMAI.ACIIAR, M.J. 1955. Incidence of charcoal rot of potato 

in Bihar (India) in relation to cultural conditions. Phytopathology 

45:91-93. 

von AMANN. Ni. 1960. Untersuchungen Uber einen sklerotienhildenden 

Pil an Kartoffeln. vermutlich Sclerottiuo hataticola 

(Taub.), synonyn Macrophotina phaseoli tMaubl.) Ashby. Z. 

Plianienkr. Pflanzenschutz 67:655-662. 

(Prepared by L. J. Turkensteen and W. J. Hooker) 

Gangrene 

The pathogen Phoma exigua var.foveata was first described 

in 1940 and is now prevalent in most northern European 

countries and parts of Australia. P. e'xigua var. exiguaoccurs in 

most European countries, Russia, the United States, Canada, 

and Australasia. 

Symptoms 

Small dark depressions develop in the tuber skin, usually at 

wounds, eyes, or lenticels, and may enlarge to form "thumbmark" 

or larger, irregularly shaped, sharp-edged lesions, the 

surface area of which isoften unrelated to rot depth. Internally, 

diseased tissue is well defined. Rots caused by Phoma exigua 

var..ioveata are usually extensive and dark brown or purplish 

(Plate 45), with variously shaped cavities; those caused by P. 

evigta var. cxiguaaresmaller, become restricted, and are usually 

black with small cavities. Pycnidia may form singly or in clusters 

on lesions or in the mycelium that lines cavities. Infrequently, 

lesions may be only of skin thickness, becoming extensive, dark, 

and irregularly shaped; this condition is termed skin necrosis. 


Either of two varieties of Phoma exigua Desm. may cause 

gangrene. rheprincipalcauseis P. t'xiguavar./o'eata(Foister) 

Boerema (syn. P. foveata Foister; P. solanicola f. foveata 

(Foister) Malcolmson; P. exigua Desm. f. sp.foveata (Foister) 

Malcoimson & Gray). The more ubiquitous but weaker parasite 

is P. exigua Desm. var. exigua (syn. P. solanicola Prillieux & 

Delacroix; P tuherosa Melhus, Rosenbaum, and Schultz; P. 

exigua Desm. f. sp. exigua Malcolmson and Gray). 

The two fungi have similar morphological characteristics. 

Pycnidia are usually globoid (90-200 pm) and dark brown to 

black. Initially subepidermal, they become erumpent and 

extrude hyaline, nonseptate, cylindrical pycnidiospores (4-5 

X 2-3 pm). In culture on 2% malt agar, P. exigua var.foveata 

(having nonzonate colonies) is readily distinguished from P. 

exigua var. exigua (having zonate colonies) (Fig. 63) by its 

production of anthraquinone pigments that turn red within 

seconds on exposure to ammonia vapor. 

Disease Cycle 

Infected orcont;ninated seed tubers produce diseased stems, 

in which infection remains latent during the growing season 

unless the stems become moribund. Pycnidia appear in sporadic 

groups, usually associated with nodes, as stems begin to senesce 

either naturally or through chemical desiccation. Raindrops 

wash pycnidiospores into the soil and spread inoculum to 

neighboring plants. Rots in mother tubers usually continue 

active in the soil, produce pycnidia, and constitute another 

important source of inoculum for tubers at harvest. Before 

harvest, tuber infection may occur through eyes and 

proliferated lenticels, usually when soil moisture is high. Most 

gangrene, however, develops after harvest through damage to 

the tuber skin. Wounding introduces infection from contaminated 

soil on the tuber surface or stimulates development of the 

fungus already latent in the periderm. Wound infection may 

occur at lifting, grading, or at any time during handling. 

A B 

Fig. 63. Gangrene. Distinguishing characteristics: A, Phoma 

exigua var. exigua, zonate culture; B, Phoma exigua var. foveata, 

nonzonate culture, on malt agar. (Courtesy C. Logan; photographs 

by G. Little) 

57

Epidemiology 

In the United Kingdom, higher than average soil temperatures 

(20-24' C) during crop growth keep '. e.vi gi var. /iolait 

inoculum levels low. However, wet soil conditions, night frosts, 

or low day temperatures (less than 12' C) around harvest time 

and low storage temperatures (2-00C) following lifting, 

grading, or handling all increase gangrene incidence. laty in Is II 

haulm destruction of seed crops or in harvest of both seed aind 

market crops encourage soilo inthe a inoculum otat bsece hot. buildup i 'xgiw in the soil. ar.periderm In field 

soils intle absence of a potato host, n .isoua var. li,\a[ 

usually becomes undetectable by present isolation or baiting 

techniqles after 1s moths. whereas !'e.iguu var. i,,U is 

(letectable in most soils. 

Otier losts 

1'.vx.iua var. exi,u occurs oil various parts ofa wide range 

ofiplants. I.e.xIi,ua var./0 'eaia occurs mostly on potato but has 

occasionally been found on weed species growing in potato 

lields. 

Control 

I)Avoid highly susceptible cultivars, damage to the tuber 

skin, and exposure to low temperattires, especially after 

damage. 

2) Burn vines and harvest tubers as soon as practical. Hold 

tubers at 18-20' C for one week to permit wound healing. 

3) Disinfect tubers with organic mercury dips (where permitted), 

by fumigation with 2-aninobutane, or by mist sprays of 

thiabendatole within three weeks of harvest. 


BOI'REMA. G. II. 1976. the Phonia species studied in culture by I)r. 

R. W. G. )ennis. Itr.Mycol. Soc. Trans. 67:289-319. 

BOYI) A. E.W. 1972. Poiato storage diseases. Rev. Plant Pathol. 

51:297-321. 

LOGAN, C.. R. It. COPEIANI), and G. I..ITE. 1975. Potato 

gangrene control by ilt ra low volurme sprays of thia bendaole. Ann. 

AppI. Biol. 81):199-20)4. 

AB 

(Prepared by C. Logan) 

t 4• 

Fusarium Dry Rots 

Fusarium dry rots are found on potatoes worldwide. 

Symptoms 

After This disease about one affects month tubers of storage, in storage tuber and lesions planted at seed wounds tubers. are 

visible as small brown areas. Infection slowly enlarges, and 

visibeam over the rowareaion lesion sinks and s wrinkles. lowlyoenires sometimies in nd concentric 

rings, as the dead tissues dr' out Wig. 64). Fungus 

pustules containing mycelia and spores may emerge from the 

dead periderm. Rotted tubers shrivel and become mummified 

(Plate 46). 

Internal necrotic areas are shades of brown from fawn to dark 

chocolate. with the advancing margin faint for lighter shade!, 

and distinct for darker shades. Older dead tissues assume it 

variety ofcolors, develop .:'v.ities lined with mycelia and spores, 

and are dry and punky in texture (Pltte 47). 

When relative humidity in storage is saturated or 

approaching saturation, I:ruiniaspp. are frequently secondary 

Fig. 64. Fusarium dry rot wound infection from storage. Note 

periderm wrinkling over rotted tissue and internal cavity. 

(Courtesy L. W. Nielsen) 

Fig. 65. A,Fusarium seed piece decay after two weeks at 13'C, showing pits on cut surfaces and mycelium growing in pits. B, Periderm 

removed from surfaces exposes rot from several infections. Comparative plant growth from healthy seed piece (C)and Fusarium decayed 

seed pieces (D and E). (Courtesy L. W. Nielsen) 

58 

.

invaders through the IFusarium lesions and rapidly rot the reinainder 

of the tuber. Suspended bacteria and juices exuded 

from the soft rot endanger surrounding tubers. 

Whole-tuber seed becomes infected through wounds during 

storage or preparation for planting. The cut surfaces of large 

seed tubers are major infection courts. In stored seed tubers, 

brown to black flecks appear on the cut surface in about one 

week and depressions or pits form in two weeks (Fig. 65A and B). 

Mycelia often grow on the depressed surfaces, and undet humid 

conditions, depressions may become slimy and black from 

bacterial growth. Soft rotting bacteria may also invade through 

the IFttsarium lesions and accelerate decay. With numerous 

cut-surfacc infections, lesions coalesce: the seed piece rots from 

the surface inward: and buds (eyes) are destroved as decay 

progresses. 

In the field, the shriveling of infected seed tubeis and pitting 

of infected pieces may not he evident. The surface over the 

lesions is brown, and the underlying necrotic tissues have fewer 

cavities. Necrotic tissue may attract soil insects and larvae such 

as the seed-corn maggot, which is avector of Erwiniaspecies. In 

wet soils, these species often enter as secondary pathogens. 

Fusarin spp. alone or in conjunction with Erwinia spp. 

partially or completely destroy the seed piece, resulting in 

extreme variability in plant size and manl, missing plants (Fig. 

651) and E). Often single ;prots emerge: these are small, grow 

slowly, produce few marketable tubers, and have a high 

incidence of blackleg. 


1usariun solani (Mart.) App. & Wr. emend Snyd. & Hans. 

'Coeruleum and 1.ro'seum (l.k.) Snyd. & Hans. 'Sambucinum' 

are most frequently implicated in seed piece decay. In sonic 

regions one species is dominant over the other, nut both are 

often associated with a seed stock. I. solani is most frequently 

encountered and is the more aggressive pathogen. Both grow 

and are maintained ott potato-dextrose agar, and the acidified 

medium facilitates their isolation when bacteria are present. F 

roseu'um grows more rapidly, forming athin, white mycelial mat 

and abundant pink to salmon spores. The slower growing . 

soani forms a denser, white mycelial mat that exhibits a purple 

pigment with age (Plate 48). F.slthnisporulates in culture more 

sparsely than does I-'. rosetun (Fig. 66). The optimum temperature 

for growth in culture is 20-25°C and for infection, 

10-20" . 

1:.roseum 'Avenaceum' also causes adry rot of potatoes, but 

less frequently than the other species do. 


Fusariumn spp. cannot infect intact tuber periderni or 

lenticels. Cuts and periderm-breaking wounds incident to harvesting, 

storage, grading, and transport are the major infection 

courts. Wounds from insect and rodent feeding and frost are 

sometimes infected. The Fusaria can also invade surface lesions 

of powdery scab, late blight, mop top virus, and possibly other 

di:,eases. 

Hlyphae are at first intercellular becoming intracellular in 

dead cells. In spreading lesions, hyphae may be sparse in intercellular 

spaces, with host cells :',owing little reaction to the 

fungus. Toward the center of the lesion, less 

intercelluar 

starch 

spaces 

is 

by 

present, 

suberin audnt deposited abe inhostcellwalsaandnt 

nfetoh 

and the myceliuni. usually abundant, may be confined to the 

intercellular spaces. In susceptible tissue, starch hydrolysis and 

suberin deposition are lacking. Small lesions restricted near the 

site of infection may be underlaid by a continuous layer of 

wound meristem cells with suberin deposition. With other 

isolates, hyphae kill and penetrate cells within two cells of 

normal-appearing tissue. Details of the reaction depend on the 

pathogen, the resistance of the tuber, and the part of the lesion 

examined. 

Disease Cycle 

Fusariumspp. can survive for several years in field soil, but 

the primary inoculum is generally borne on seed tuber surfaces. 

Surfaceborne propagules contaminate containers and equipment 

used in handling or storing potatoes and enter wounds 

incident to handling seed tubers. Infected seed tubersand pieces 

decayand infest the soil that adheres to the surfaces of harvested 

tubers. 

Epidemiology 

Tubers of potato cultivars differ in susceptibility to F. solani 

and F roseum, but none tested was immune to either pathogen. 

Certain cultivars are tolerant to both. 

Tubers are tolerant to infection when harvested. 

Susceptibility increases during storage and ,:aches its maximumin 

early spring about planting time. 

Wound healing can reduce infection. Deposition ofsuberin in 

the cell walls does not prevent infection, but wound periderm 

does. Wound periderm forms in three to four days at approximately 

21°C with adequate aeration and humidity but more 

slowly at lower temperatures. At 15'C, near optimum for 

infection, a period of approximately eight days is required to 

form periderm; wound healing is not effective at this cr lower 

temperatures. 

Dry rot develops most rapidlyin high relative humidityand at 

15-20' C. Relative humidities about 70% do not alter rot development, 

but lower iiumidities retard infection and disease 

development. Disease development continues at the coldest 

temperatures safe for potatoes. 

If the soil temperature and moisture are suitable for rapid 

sprout growth and emergence, seed tuber or piece decay after 

planting maybeoflittle consequence. Conditioning seed tubers 

from cold storage at 20-25' C for one week before cutting pieces 

reduces decay and accelerates sprout growth. Holding contaminated 

cut seed several days or weeks before planting or planting 

in soils too cold or dry for prompt sprout emergence and plant 

growth will accentuate losses. Excessively wet soils after 

planting increase secondary infection by Erwinia spp. 

Other Hosts 

F. solani isolates from Colocasia corms can infect potato 

tubers. Generally, tuber-rotting Fusaria do not infect other 

plants or plant organs. 

Resistance 

Differences in resistance exist among potato cultivars. Relative 

ranking of resistance isinfluenced by the Fusarium sp. used 

for inoculation. Seed lots infected with potato virus X are 

relatively more resistant than those free from the virus when 

harvested within three weeks of top kill. 

Control 

1ontrm 

I) For storage and seed purposes, harvest tubers from dead 

vine 

2) Use all precautions with machinery and equipment to 

171V' I, 

. __ 

V.. 

" 

,,00 , 

.)'. . 

- 

Fig. 66. Fusarium solani from culture with many macroconidia 

and a single microconidium in center. (x950) (Courtesy P. E. 

Nelson) 

59

prevent wounding during harvest and storage. 

3) Provide high humidity and good ventilation early in 

storage to facilitate wound healing, and prc vide aeration during 

storage. 

4) Seed tubers may be treated with a fungicide, dust, or liquid 

spray before storage. 

5) Do not move stored tubers until they are ready for 

planting. 

6) Warm seed tubers from cold storage to 20-25' C fora Wes'K 

before planting or cutting pieces. 

7) Plant seed immediately after cutting in soils sufficiently 

warm and moist to promote prompt sprout growth and good 

wound healing. 

8) Spray or dip seed tubers with fungicide suspensions or 

treat pieces with 7-8% fungicidal dusts. 

9) Handle treated seed with noncontaminated containers and 

equipment. 


BOY), A. E.W. 1952. Dry-rot disease of the potato. Ann. Appl. Biol. 

39:) 22."-''.'.purpling 

CUNNINGHAM, H. S.,and 0. A. REINKING. 1946. Fusarium 

seedpiece dOcay of potato on t.ong ls!and and its control. N.Y. 

Agric. Exp. Stn., Geneva, Bull. 721.32 pp. 

JON"2S, . D., nd IJ. M. MttULEN. 2 

1974. Thecff, . ;otato virus X 

on susceptihility of potato tubers to Fusuritt ro.v ta WAvenaccum.' 

Am. Potato .1.5':209-215. 

LEACI, S. S.,and I.. W. NIEI.SEN. 1975. Elimination of fusarial 

contamination on seed potatoes. Am. Potato J. 52:211-218. 

McK EF,R. K. 1954. l)r)-rot disease of the potato. VIII. Astudy of the 

pnthogenicity of Fusaritom caeruh'un (Lib.) Sacc. and Fusarium 

avenacewo (Fr.) Sacc. Ann. Appl. Biol. 41:,':17-434. 

NIELSEN, .. W. 1949. Fu,;:arium seedpiece decay of potatoes in Idaho 

and its relation to blackleg. Idaho Aric. Exp. Stn. Res. Bull. 1. 

31 pp. 

NIELSEN, L. W., and J. 1. JOHNSON. 1972. Seed potato 

contamination with Fusarial propagules and their removal by 

washing. Am. Potato J. 49:391-396 

SMALL, T. 1944. Dry rc- of potato (Fusariun,caeruhl, (Lib.) Sacc.). 

Investigation on the sources and time of infection. Ann. Appl. Biol. 

31:290-295. 

(Prepared by L. W. Nielsen) 

Fusarium Wilts 

These diseases are widespread and most severe where 

potatoes are grown at relatively high temperatures or when 

seasons are hot and dry. 

Symptoms 

Several Fusariun pathogens cause essentially similar symptoms. 

Tubers exhibit surface blemishes and decay, including 

stem end browning and decay at the stolon attachment, and 

internal vascular discoloration that severely impairs market 

quality because such tubers cannot be removed during grading. 

On vines, symptoms include cortical decay of roots and lower 

stems; vascular discoloration or rot in the lower stem; wilting; 

chlorosis, yellowing, or bronzing of foliage; rosetting and 

of aerial parts; aerial tubers in leaf axils; and premature 

death of the plant. Additional symptoms vary with the pathogen 

involved and the environment. 

invol andt enrn ment 

EutartiiWilt. Generally the most important and severe, this 

wilt becomes apparent toward the end of the growing season, 

The first symptom is yellowing between the veins of the youngest 

leaves, producing islands of green against a chlorotic background 

(Plate 49). Chlorotic areas later become necrotic. Affected 

leaves become yellowish bronze, wilt, dry, and hang on 

the stem, which eventually dies. Rolling and rosetting occur 

under moist conditions. Leaf discoloration and death may be 

most severe on one sde of the stem or on stems on one side of the 

plant. Internally, the pith is often discolored at the nodes (Fig. 

67A), even in those near the stem tip. Vascular tissues of the 

stem and leaf petioles are deep brown. The underground stem 

does not rot until later stages of disease. 

Tubers are sunken at the stolon attachment, with brown 

C D 

A I 

A E F G 

Fig. 67. Fusarium eumartii: A, pith necrosis (arrow) in stem; B and D,necrosis at stolon attachment; C,discoloration at eyes; E and F, 

internal vascular discoloration; G, water-soaked and firm vascular tissue. 

60

necrosis extending into the tuber to various depths (Fig. 

67B-G). Firm, brown circular lesions (up to 2.5 cm in diameter) 

may be present elsewhere on the tuber surface. In transverse 

section at the stem end, slight to severe vascular browning is 

evident, and the vascular ring may have a few thick, black 

strands (up to I mm in diameter) or more numerous, smaller 

brown to tan, netlike strands in the vascular ring. Highly 

diagnostic, but not present in every tuber, is a water-soaked, 

firm, light brown to tan discoloration extending 3-5 mm on 

either side of the vascular ring. This discolored area isfirm, does 

not produce exudate as in bacterial ring rot or brown rot, and 

usually shows little tendency to break down with secondary rots. 

Vascular necrosis extending into the eyes may cause eyes to be 

brown and necrotic, 

Oxvsporum Wi/. Usually milder than eumartii wilt, this 

disease is a typical vascular wilt in contrast to the other 

Fusarium wilts described here, which are more nearly cortical 

rots. Symptoms appear during the middle of the growing 

season, wilt is rapid, giving the impression that the lower stem 

has been cut off- and the plant is prematurely killed. Yellowing 

begins at the lower leaves and progresses up the plant. Vascular 

discoloration of the stem is confined to portions below or 

slightly above the soil line. Tubers generally show discoloration 

of the vascular strands and usually no stem end rot. 

Tuber infection through wounds or possibly lenticels causes 

circular lesions and a di y rot in storage. This condition has been 

associated with high humidity and temperature. 

Av'enacutn Wilt. This disease is comparable in severity to 

oxysporum wilt and generally less severe than eumartii wilt. It 

develops from mid to late season. Symptoms may be more 

severe on one side of the plant. Wilting and rapid collapse of the 

plant are common in hot, dry weather. A different response, 

possibly when growing conditions are more favorable, consists 

of chlorosis at bases of apical leaves, followed by general 

bunching of leaflets, chlorosis of the plant beginning at the base, 

shortening of internodes, carbohydrate accumulation in 

aboveground portions of the plant, red or purple pigmentation, 

and aerial tubers in leafaxils. The plant resembles those affected 

by mycoplasma or psyllid yellows. However, vascular 

discoloration may be seen in the lower portion of the stem up to 

six inches above the soil. Tip burn and loss of lower leaves is 

common. Early season infection produces severely dwarfed 

plants similar to those with yellow dwarf disease. 

Tubers show dry stem end rot and vascular tissue that is 

discolored brown, lacks the water-soaked border of eumartii 

but is characteristically dry, and may be gray to pink. 

/-. solani Wilt. This wilt is distinct from eumartii wilt. It is 

characterized by rotting of the root system, the stem pith, and 

the lower and underuround stem, with dry shredding of the 

strands ofwoody tissue, and wilting and yellowing of foliage. In 

moist conditions rosetting of tops and aerial tubers appear. 

Tuber infection follows wound infection and differs from 

other wilts in lacking typical vascular discoloration. Neither 

stolons nor tubers are directly infected from the parent plant. 


Taxonomy of genus Fusarium is complex. Species designations 

used here are those used in disease discriptions. Designation 

of species by the system of Sryder and Hansen is given in 

synonyms. 

The four pathogens associated with the Fusarium wilts are: F. 

eumnartii Carp. (syn. F. solani f. sp. eumartii (Carp.) Snyd. & 

Hans.): F. oxisporuw Schl. (syn. F. o.ry'sporum Schl. f. sp. 

tuherosi (Wr.) Snyd. & Hans.); F avenaceun (Fr.) Sacc. (syn. 

F. roseum (Lk.) Snyd. & Hans.); and F.solani (Mart.) App. & 

Wr. (syn. F. solani f. sp. eumartii (Carp.) Snyd. & Hans.). 

Descriptions on the basis of spore characteristics will not be 

attempted because of the well known variability of Fusariumas 

influenced by environmental factors. 

Isolations of F.eumartiiare readily obtained from roots and 

less readily from stems. Discolored tissue from upper stems and 

tuber apices is sterile. Isolation from stored tubers is difficult, 

Tissue discoloration develops in advance of the fungus and is 

apparently associated with toxic substances. 

F. o.x.spforun is easily isolated from roots and lower stems 

and, with difficulty, from stored tubers. Wilting is, in part, due 

to toxins. 

F. avenaceum is successfully isolated from vascular 

discolored stem tissue below or close to the soil line and from 

discolored vascular tuber tissue. 

F. solani is readily isolated from discolored stem tissue. 


Diseases caused by the four wilt fungi are essentially similar. 

Root tips, following infection from the soil, become watersoaked. 

Epidermal cells of young roots are invaded. Cell walls 

become sc lened and swollen, and cortical necrosis follows. 

Xylem of roots and stems is invaded; vessels become plugged 

with granular material; and surrounding cells of outer phloem 

and cortex break down in ways varying with the particular 

pathogen involved. 

Disease Cycle 

Fusarium wilts are typically soilborne, and the disease is 

transmitted with varying degrees of effectiveness from inoculum 

within and on seed tubers. 

F. eumaruii survives in field soil for long periods without 

noticeable reduction in pathogenicity when potatoes are again 

planted in the field. Because of this disease, many fields have 

been abandoned for potato production. The other wilt 

organisms may be shorter-lived in the absence of potatoes, but 

evidence is lacking. 

Planting potatoes in artificially infested soil or placing 

inoculum on freshly cut seed efficiently establishes the disease. 

Infection isthrough roots into the stem and, except for F.solani, 

from the stem through the stolon into the developing tubers. 

Infected seed pieces with stem end rot transmit disease to the 

new plant, more efficiently with eumartii than with oxysporum. 

Inoculum is introduced into new fields primarily through the 

planting of infected seed tubers. Contintal potato production, 

particularly replanting infected tubers, accelerates inoculum 

buildup. Inoculum is dispersed from infested fields by surface 

drainage water, windblown soil, soil carried on implements, etc. 

Epidemiology 

Wilts are most severe at high temperatures and particularly 

when plants are under stress in dry, hot growing conditions. 

Although evidence is lacking, the rosette symptom with aerial 

tubers probably follows increased availability of water and 

somewhat cooler temperatures. 

F.eumartii is capable of infection at lower soil temperatures 

(20 and 24 C), whereas F. oxy'sporum and F. avenaceum are 

more pathogenic at 280 C. F.solani in culture can grow at 350 C 

but grows most rapidly at 300 C. 

Other Hosts 

The cultivated potato is the only known natural host for the 

several Fusarium spp. causing wilt of the crop. Morphologically 

similar pathogens attack plants of widely divergent types. 

Species differentiation has been based on pathogenicity specific 

to a particular plant species. Several Solanum spp. related to 

potato have been experimentally infected with F. eumartii. 

Resistance 

Minor differences in resistance within S. tuberosum are 

known, but identified resistance is not sufficiently high to be of 

general use. S. spegazzinii, S. acaule, and S. kurizianum seedlings 

carry considerable resistance to root infection by F. 

eumarhii in infested soil. 

Control 

I) Grow potatoes in land free from wilt fungi. 

2) Tubers infected with Fusarium wilt should not be used for 

seed. 

Al

3) Avoid contamination of clean fields by inoculum transfer Verticillium Wilt 

through infested soil or diseased tubers and plant refuse. 

The disease apparently occurs wherever potatoes are grown, 

Selected References although it may be confused with other diseases that cause early 

maturity. 

GOSS, R.W. 1923. Relation of environment and other Iactors to potato 

wilt caused by I..oarint oxi.vorinn. Neb. Agric. Exp. in. Res. Symptoms 

Bull. 23. 84 pp. 

Verticillium wilt causes early senescence of plants. Leaves, 

GOSS, R. W. 1924. Potato wilt and stem-end rot caused by I usariumn which become pale green or yellow and die prematurely, are 

eumartii Neb. Agric. Exp. Sin. Res. Bull. 27. 83 pp. 

described as "early dying" or having "early maturity." 

GOSS, R. W. 1940. A dry rot of potato steins caused by Ihusariwn l)uring the ,,rowing season, plants may lose their turgor and 

solani. Phytopathology 30:160-165. 

wilt, especially on hot, sunny days (Plate 50). Single stems or 

Mcl.EAN. J. G., and .1.C. WAI.KER. 1941. A comparison of Fusarito, leaves on one ide ofthe stem may wilt first. Vascular tissue of 

avenaceawn. ' oxirsporui,and 1. ,olani var. e'u artiiinrelation to 

s 

potato wilt in Wisconsin. I. Agric. Res. 63:495-525. 

stems becomes a light brown, best observed if the stem issevered 

RADTKE. W., and A. ESCANI)E. 1975. Verglcichendc Unter- at about ground level with a long slanting cut. Externally visible 

suchungen Uiber verschiedene Methoden tur Inokulation von Kar- necrotic stem streaking occurs in certain cultivars when soil 

toffelsiimlingen mit I.uvariun solani (Mart.) Sace. f. sp. cnm' ariii moisture and fertility are high. 

(Carp.) Snyder et Hansen. Potato Res. 18:243-255. 

Tubers from infected plants, but not necessarily all tubers, 

SNYDER, W. C., and I|. N. HANSEN. 1941). 1941, 1945. The species usually develop a light brown discoloration in the vascular ring 

concept in Flsarium.Am .J. Bot. 27:64-67; 28:738-742; 32:657-666. (Plate 5I, Fig. 68A); severe vascular discoloration may extend 

UPSIONE, caused by M. IPusariumo.i-sporuni. E. 1970. A corky rot plant of ,Jersey Pathol. Royal 19:165-167.ovrhlwytouhheue.Caiesmydeopnie 

potato tubers ay through the tuber. Cavities may develop inside 

severely affected tubers. Pinkish or tan discoloration (see pink 

(Prepared by J. E. Huguelet and W. J. Hooker) 

bA 

eye) may develop around the eyes oras irregular blotches on the 

surface of affected tubers. This may be confused with mild late 

blight infection. 


V'erlicillium alho-airum Reinke & Berth. develops septate, 

resting dark mycelium on stems in the field and also in culture, 

in contrast to 1'. dahliae Kleb., which forms dark mycelial 

strands with black, thick-walled pseudosclerotia (Fig. 69), also 

called microsclerotia, 30-60(lm in diameter. Vegetative hyphac 

of both are similar (2-4 pm in dia meter and colorless). Conidiophores 

are septate with side branches (Fig. 6813), swollen at the 

base, and arranged in a whorl. First-formed conidia of I'.alhoairtim 

;,re (T-12 X 2.5-3 p in. Those of 1'. dlalijot are 3-5.5 X 

1.5-2 pin. Conidia produced later, particularly those in culture, 

may be considerably smaller, 3--6 x 2-3 pm. Conidia arc usually 

single celled but may he one-septate (Fig. 68C and )). 

Both types may be present within a single potato plant. 

Disease Cycle 

Infection is through root hairs, wounds (including those at 

points of emergence of adventitious roots), and through sprout 

and leaf surfaces. Hyphae progress intracellularly and 

intercellularly to the xylem (Fig. 68D). Transport of conidia 

within vessels of potato is probable. Conidia are short-lived and 

Fig. 68. A, Verticillium vascular discoloration in tuber. B, 

Verticillium albo-atrumin culture: a, "ater droplets surrounding Fig. 69. Verticillium isolates from potato. A,Dark mycelial type in 

conidia on tips of conidiophores; b, a single conidium (bar one-month culture, at X100 and X375 approximately. B, Pseudorepresents 

50 mm). C, Conidia from culture; D, fungus mycelium sclerotial isolate in cne-month culture, x175 and x200. (Courtesy 

in discolored xylem of tuber tissue (bar represents 10 pm). D. B. Robinson et a. 1957) 

62

do not survive drying. 

Both species are poor competitors and survive poorly in soil 

in the absence of suitable hosts. Infectious propagules of dark 

mycelium and pseudosclerotia are usually relatively short-lived, 

but survival time isinfluenced by soil type and is severely limited 

by anaerobic soil conditions. Infectious propagules germinate 

and produce conidia within hours. 

Epidemiology 

V allo-airwtnigenerallyappers to be more pathogenic than I. 

(Iahliae. Warm soil temperatures (22-27' C) favor growth of v 

daliae. tempeatures. I" a/bo-atrun 

itsrnge 

is 

is 

relatively more pathogenic 

reltivlC.moepratoenicatsl 

at lower 

r 

temperatures; its range is 16-27'C. Crop rotation 

buildup 

affects 

of soil inoculum, 

th 

and three-year rotations have effectively 

reduced soilborne inoculum. Inoculum is reduced when 

cereals, grasses, and legumes are included in the rotation. When 

potatoes are grown several years in succession or in rotation 

with susceptible crops, inoculum increases in the soil. Other 

factors that favor incidence and severity of Verticillium wilt 

include disconuatinion planting 


highly 

the 

susceptiblc 

practice 

cultivars such 


as Kennebec, 

burning potato tops, and 

red 

a 

u ation the f practice of chemical 

reuction in the formerly common practice of chemical 

treatment of seed potatoes. 

Inoculum in field soil or in soil adhering to the surface of 

potato tubers is more important in initiating wilt symptoms 

than is inoculum from seed tubers with vascular discoloration. 

Paradoxically, seed tubers with vascular discoloration often 

produce plants as wilt-free and as vigorous as those from 

comparable seed tubers free from vascular discoloration. 

hnoculum can he distributed long distances by contaminated 

soil adhering to seed surfaces and from field to field by 

contaminated equipment or irrigation water. Inoculum may 

also be airborne or spread from phint to phint by root contact, 

Other Hosts 

Isolations of 1'. albo-atruni, which may have also included 

I. (/ahlia , havc been made from a very wide range of dicotvle- 

dotis planits, both wvoody anrd herbaceous. Man of t hese Were 

sy symtmlss. iptomlcss. I. 

1as 

dahia, 

athe 

infects oiver 50 species if 

nfecort50speesofanhts 

plants in 23 

i 2h 

families. (rasses aid (ither minocits are nonosts (if both 

species. Numerous common weeds are suscepts, including 

('henopodoMin albiumi, (apsela bIur.sa-iastoris, Tara.'aculn 

spp., and I:qui.etttn arvcn.e. 

Resistance 

Varieties carrying different levels of resistance have been 

identified within S. tuertostim ssp. titherostim. Certain cultivars 

etdifferently tc 

react to varying conditions, including geographic 

location, abundance of inoculum, and type or strain of the 

fungus involved, suggesting that pathogenic strains of the causal 

agent exist. Even highest known levels of resistance break down 

with high inocultm density in the soil. . lulerostin, ssp. 

atdigena is reported to have wilt resistance. 

Control 

I) Seed tubers contaminated with infested soil should be 

disinfested before being planted. Liquid seed treatments are 

more effective than dusts. Organic mercuries are very effective, 

but their use is generally prohibited. 

2) Rotate potatoes with cereals, grasses, or legumes. Avoid 

rotation with highly susceptible solanaceous crops such as 

eggplant and most tomato cultivars. 

3) Do not plant susceptible cultivars. 

4) Control weed suscepts. 

5) Systemic fungicides (benomyl or thiophanate-methyl) and 

nonsysternics (mancozeb, captan, or metiram) applied to seed 

tubers are reported effective. 

6) Several soil treatments show promise; sodium methyldithiocarbamatc, 

benomyl, and systemic insecticides (aldicarb, 

acephate) have delayed symptoms and increased some yields, 

7) Several nematodes increase incidence and severity of 

Verticillium wilt. Soil fumigation with nenaticides alone (tri- 

chloronitromethane or 1,3-dichloropropene and related compounds) 

or with chemicals that control both fungi and 

nematodes is effective. 


AYERS, G. W. 1974. Potato seed treatment for the control of verticillium 

wilt and Fusarium seed piece decay. Can. Plant Dis. Surv. 

54:74-76. 

BIEHN, W. L. 1970. Control of Verticillium wilt of potato by soil 

treatment with benomyl. Plant Dis. Rep. 54:171-173. 

BUSCH, I.. V. 1966. Susceptibility'of pcotato\arieti,:sto Ontario isolates 

of Verticilliumalto-atruni. Am. Potato J. 43:439-442. 

EASTON, G. D., M. E. NAGI., and D. 

effect 

I.. BAII.EY. 

of soil fumigation 

1975. 

with 

Residual 

vine bt ning on control of Verticillium 

wilt of potato. Phytopathology 65:1419-1422. 

ENGEI.HARD, A. W. 1957. Host index of Verticillium alho-atrun? 

Reinkeand Berth. (including I'erticillium dahliae Kleh.). Plant t)is. 

Rep. Suppl. 244:23-49. 

FRANK, .. A., R. E.WEBB, and I). R.WILSON. 1975. The effect of 

inoculum levels on field evaluations of potatoes for Verticillium wilt 

resistance. Phytopathology 65:225-228. 

I).G. A.. and 1). C. M. CORItArI. 1973. Controlling 

potatoes caused 

early death 

by Ilhterodera 


rostochiensis and I'erticillium 

dahliae.Ann. Appl. Biol. 75:461-462. 

HOYMAN, W.G. 1974. Consequence of'planting Norgold Russet seed 

infected with Verticillium a bo-atrioo. Am. Potato J. 51:22-25. 

KHEW, K. .., and .. V. BUSCH. 1968. Soil temperature affects 

infection of potato and tomato by mixtures of DM and MS strains 

of 1'erti'illitot al'o-atruti. Ant. Potato .1.45:419-413. 

KRAUSE, R. A...1. P).HUETIIER, P. SATIROPOULOS, and L. E. 

ADAMS. Verticillium 1975. wilt. Systemic 

Plant 

insecticide control 

Dis. 

of aphids and potato 

Rep. 

MORSINK, 

59:159-163. 

F., and A. E. RICH. 1968. Interactions between Vertiillium 

albo-airtm oand I'rat hInchus /lnetrans in the Verticillium 

wilt of potatoes. phytopathology 58:401 (Abstr.). 

POWEI.SON. R. I., and G. E. CARTER. 1973. Efficacy of soil 

fumigants for control of Verticillium wilt of potatoes. Am. Potato J. 

50:162-167. 

RICHl, 

Potatoes: 

A. F. 1968. 

Production. 


Storing, 

diseases. Pages 

Processing. 

397-437 

Avi 

in: 

Publ. 

0. Smith, 

Co., Inc., 

ed. 

Westport, CT. 

ROBINSON, 1). B., and G. W. AYERS. 1953. The 

cillium 

control 

wilt of potatoes 

of Verti 

by seed treatment. Can. J. Agric. Sci. 

33:147-152. 

ROBINSON. 1). B.. R. H. LARSON, and J. C. WALKER. 1957. 

Verticillium wilt of potato in relation to symptoms, epidemiology, 

and variability ofthe pathogen. Wis. Agric. Exp. Sin. Res. Bull. 202. 

49 pp. 

SMITH, H. C. 1965. The morphology of Verticilliun albo-atrum, V' 

dahliae, and I. tri.orl.%. N.Z. .. Agric. 

TIANASSOIJI.OPOULI.OS, 

Res. 8:450-487. 

C. C., and W. J. 

and 

HOOKER. 

sprout infection 

1970. Leaf 

of potato by i'erticillium alho-atrua. Phytopathology 

60:196-2(13. 

WOOI..IAMS, G. E. 1966. Host range and symptomatology of Verticillim 

dahliac in economic, weed, and native plants in interior 

British Columbia. Can .1.Plant Sci. 46:661-669. 

(Prepared by A. E. Rich) 

Thecaphora Smut 

Thecaphora smut is found in northern Central America 

(Mexico) and the northern regions of South America (Bolivia, 

Chile, Colombia, Ecuador, Peru, and Venezuela). Loss up to 

80% is known. 

Symptoms 

Usually no aboveground symptoms are found. Affected 

tubers have wartyswellings on the surface (Fig. 70A) and, when 

sectioned, reveal dark brown, !ocular sori pervading the interior 

(Fig. 71 A and B, Plate 52). Galls resembling deformed tubers 

form directly from infections on the sprouts, stems (Fig. 70B), or 

stolons and, less frequently, on the tubers. Rootsare not known 

to become infected. 

63


Angiosortis solani (Barrus) Thirum. & O'Brien (syn. 

Thecaphora solani Barrus) has locular sort, 1-1.2 mm in 

diameter, that are surrounded by a periderm six to eight cells 

deep and contain globose-ovoid spore balls 15-50 X 1 2 -401m in 

diameter (Fig. 71C). Each spore ball has two to eightrust- brown, subglobose 

easilyseparablc 

to angular 

into 

spores. 

freesporcs 

7.5-20X 

when teased. 

8-18 

Spore 

Mm that 

ballsdevcltp 

are 

fromasofepro frehe thapore wheteased. Spore hals d p 

frot sporiferous hphae that form the focules and are pushed 

outward to fill the cavitY, 


Tumor growth, caused by hypertrophy of the outer phloem 

and parenchyma of the stem and stolon, consists largely of 

enlarged parenchymatous cells. The fungus is intercellular, 1.8 

Mm in diameter, producing clamp connections and thick 

branches. In the cambium, the fungus mycelium stimulates cell 

proliferation. 

Disease Cycle 

Dt .:Is are unknown. Spore germination has not been observed. 

Smut is introduced by planting infected seed tubers; it 

may also be carried in irrigation water and infected soil. 

Epidemiology 

Smut is favored by high soil moisture and possibly high soil 

salinity. The planting of potatoes year after year increases 

disease when the pathogen is present. 

Spores are believed to be long-lived in the soil. Although the 

disease was originally considered to be restricted to the Andes at 

elevations of 2,500-3,000 m, it is now known to persist and to be 

extremely serious in irrigated, sea-level desert terrain with high 

temperatures. Once introduced, the fungus would probably 

persist well in other potato-growing areas of the world. 

Other Hosts 

Infection develops on S. ittherosu'n ssp. tuherostum and ssp. 

andigena, S.stf:)lomferutn, and I)attura strunonium. 

Control 

I) The most effective control is to use cultivars with known 

resistance. 

2) Planting smut-free seed isessential where the fungus is not 

present. 

3) L.ong rotations reduce buildup of inoculum. 

4) I)atura stramoniumn becomes infected and should be 

eliminated in fields used for potatoes. 

5) Removal of all smutted galls from an infested field reduces 

buildup of inoculum. 

6) Strict quarantine, particularly of seed stock, should be 

exercised to avoid introduction into other potato-growing 

areas. 


BARRUS, M. F., and A. S. MULLER. 1943. An Andean disease of 

BAZAN 

potato tubers. 

l)eSEGURA, 

Phytopathology 

C. 1960. The 

33:1086-1089. 

gangrena 

Peru. 

disease 

Plant 

of potato 

Dis. Rep. 

in 

44:257. 

O'BRIEN, M. J., and M... THIRtJMALACHAR. 1972. The identity 

of the potato smut. Sydowia Ann. Mycol. Ser. 2.26:199-203. 

UNTIVEROS, D. 1978. El carbon de lapapa (Thecaphora .solani 

Barrus), algunos aspectos de su sintomatologia y biologia del agente 

Fig. 70. Thecaphora smut: A,early infections on tuber; B,section Fig. 71. Thecaphora smut infections: exterior, Interior, and spore 

through gall on stem. (Courtesy D.Untiveros) balls. (Courtesy R.Zachmann) 

64

cauisal. Tesis Magister Scientiae en Fitopatologia. Universidad 

Nacional Agraria iaMolina, Peru. 61 pp. 

ZACHMANN, R., and 1). BAUMANN. 

potatoes 

1975. "lhwcaphorasolani 

in Peru: 

on 

Dis. Rep. 59:928-931. Present distribution and varietal resistance. Plant 

(Prepared by 0. T. Page) 

Common Rust 

The disease occurs inrestricted mountain valleys of the cool 

highlands of Mexico, Costa Rica, Venezuela, Colombia, 

Ecuador, and Peru, and possibly in Bolivia and Brazil. In Peru, 

it is usually on the eastern watershed of the Andes. Only in 

Ecuador is it of economic importance. The disease is most 

common at elevations of 3,000-4,300 m. alth-ugh it occurs in a 

lower, warmer valley in Peru at an elevation of 2,700 m. 

Symptoms 

Round and occasionally elongate lesions usually develop on 

the underside of leaves as minute greenish white spots, 3-4 mm 

in diameter, although the longer axis of some oval lesions may 

reach 8mm (Plate 53). Lesions later become cream with reddish 

centers, then tomato red, and finally rusty red to coffee brown 

(Fig. 72A). Achlorotic-necrotic halo maysurround the lesions, 

Pustules protrude 1-3 mm and are matched by corresponding 

depressions on the upper side of the leaf. Defoliation results 

when hundreds of pustules form on a leaf. 

Elongated and irregular lesions also occur on petioles and 

stems. Fruit and flowers are also affected. 


Puccinia pittieriana P. Henn., a short cycle (microcylic) rust, 

produces teliospores and sporidia (Fig. 72B). Sor are 

hvpophyllous and gregarious. Teliospores are smooth, orange 

to brown, two-celled, broadly ellipsoid, slightly constricted at 

the septum, and 16-25 X 20-35 Mm. The pedicel is 60 X 6 pm, 

and the hyaline sporidia are 8-18 X 11-25 Mm. 

Disease Cycle 

Initial inoculum, probably from wild hosts, is windborne. In 

vitro, teliospores germinate in I hr to produce a promycelium, 

which, at temperatures above 15 C, usually continues to grow 

vegetatively. Below 15' C, most promycelia (basidia) give rise to 

four sporidia (basidiospores) in 3-24 hr. When detached, 

sporidia germinate immediately. First symptoms appear in 

14-16 days on potato at temperatures of 16' C or below. Lesions 

are fully grown in 20-25 days. Teliospores mature 30-40 days 

after inoculation. 

Epidemiology 

Average temperatures around 10'C with 10-12 hr of free 

moisture on lea ,cs are necessary for development and spread. 

The appearance of two distinct lesion sizes (2-4 mm and 4-8 mm 

in diameter) on a given variety and on different varieties suggests 

the existence c- two races and two levels of susceptibility. 

Lesion size may vary with Solanum spp. Epidemic development 

may result in death of most plants and severe yield depression. 

Other Hosts 

Solantun denissutm in Mexico is heavily infected. Tomato, 

the only other naturally infected host, is apparently more 

susceptible than potato. In greenhouse tests, S. caripense and 

.. gru'n-americanum are susceptible. 

Control 

Several carbamate fungicide sprays are effective when applied 

five times during the growing season at 14-day intervals at rates. 

recommended for other foliage fungi. 

(See Selected Rclereiincs following next section.) 

Deforming Rust 

This disease has been reported primarily from Peru, on the 

Pacific watershed range and at altitudes (2,378-3,172 m) over 

lapping thv,.ci ommon rust but generally somewhat lower. 

Symptom. 

Symptom.. usually develop in mid to late growing season. 

Aecia initials first appear on leaves as smooth swellings that 

enlarge and rupture through the epidermis to form cups with an 

crose or lacerate peridial margin, which finally become saucershaped 

(Plate 54). The rim is yellowish and the center, a darker 

orange. 

Rust pustules, consisting of crowded groups ofaecia up to 100 

mm across, are circular on the underside of leaf lamina and 

elongated along veins, petioles, and stems. They also affect 

flowers and fruit. The initial color, orange-red, turns at maturity 

to rusty brown. Lesions are largest on veins, petioles, and stems, 

causing pronounced enlargements and deformations such as 

thick curved leaves, stems swollen to double their size, and 

stems doubling over to the point of snapping. Defoliation and 

death of plants occasionally occur. 


Aecidium cantensis Arthur produces aecia, crowded in 

circular groups 5-10 mm across, on the underside of leaves. 

1 1E 

! p" 

. 

Fig. 72. Common rust: A, mature red to brown colored son; B, 

spores of Puccinia pittieriana. (A, Courtesy E. R. French) 

a 

65

Each ae--ium is cupulate. 0.3-0.5 mm in diameter, with a 

colorless periderin. Aeciospores are angularly globoid or ellipsoid, 

I(r-21 X 20-23 , in. 

Epidemiology 

The source of inoculum is probably cultivated potato, which 

is grown under irrigation in the drier season. Because this 

disease occurs below the elevation of severe frosts, tile causal 

fungus may survive year around in plants and 'or debris, but no 

research has been done on the overwintering of the pathogen. 

Other Hosts 

Potato is the only well verified host. 

Control 

Although Peruvian rust can be very damaging and recurs 

every rainy season in some localities, it is not widespread and 

thus not considered an important disease. No research on its 

control has been underta ken. 


ABBOTT, F. V. 1931. Further notes on plant diseases in Peru. Phytopathology 

21:1)61-11)71. 

ARTII IR, ,. C. 1929. las royas de los vegetales (Uredinales) del Peril. 

Est. Exp. Agric. Soc. Nac. Agrar. Lima. Peru. Bol. 2. 14 pp. 

BIIRI ICWA. I'.. and .1. OR.I I-IA. 1968. Estudios fisiol6gicos (Ie 

I'td(ina pi/iteria a Ilenn. ca usta lt d Ii ioa v de IaIpapa (Solattiom 

ttheroom, I..) Fitotecnia Lahinoamericana 5:81-88. 

I)IAZ, .1. R., and .1. CIII-VERRIA. 1963. Chemical control of 

l'o icia pitieriana on 

47:800--801. 

polatoes in Ecuador. Plant Dis. Rep. 

FR ENCI. F. R.. II. TOR RES. I. A.de IC()CFII A, . SAILAZAR, C. 

FRIBOtRG. F.N.FERNANI)EZ. A. MARTIN,.J. FRANCO. M. 

M. (l(eSCUIRRAII. I. A. IIERRERA. C. VISF., I.. l.AZOand 0. A. 

I DAl) l. O. 1972. EnfernedLades de Ia Papa en el Perti. Bol. Tecn. 

77. Est. Exp. Agr'.. l.a Molina. 36 p 

lIEN NIN(iS. I'. I9d4. Linige neue pil/c aus (ostarica utid Paraguay. 

Iledwigia 43:147-149. 

IIIURSION. II. 1). 1973. Threatening plant dise,.es. Ann. Rev. 

IPhytopathol. 11:27-52, 

66 

(P~repared by I'. R. French) 

sintuhaneousl present in leaf spots, severely defoliating potatoes 

in Peru. 

C(haetomiwnu spp. leaf spot, superficially resembling early 

blight but without the targetlike markings, is reported in South 

Dakota. Necrosis and chlorosis develop around points of 

mechanical injury. 


COOK, A. A. 1954. A foliage diseaseof potato induced by Chaetoioiunt 

species. Plant Dis. Rep. 38:403-404. 

FABRICATORE, .. 1953. Volanon tuherosun, ospite casuale di un 

Ietero.,wrihon. Rev. Appl. Mycol. 1953:504. 

JONES, W.. and if. S. MacL.EOl). 1937. Armillaria dry rot of potato 

tubers in British Columbia. Am. Potato .1.14:215-217. 

KUIFUSS, K. II. 1957. (Ionostachys arau'ariae Corda var. rosea 

Preuss an faulenden Kartoffelknollen. Nachrichtenbl. Pflan 

/enschutz. 1). I). R. 11:144-146. 

NYAK. M. L..1964. A new organism causing dry rot of potatoes. Sci. 

Cult. 30:143-144. 

PF1T1NA RI. C. 1949. A/ione patogena della ('lowsoach'r.s ara'ariae 

Corda var. ro.wa Preuss su tuberi di Solanwm uberostui. Ann. 

Sper. Agriar. 3:665-672. 

RIEHI.E, i. 1). 1941. A Xylaria tuber rot of potato. Phytopathology 

31:936-939. 

SAIAI., 1). 1967. A newdisease of potato tubers caused by Gulmaniella 

hooicola Barron. Curr. Sci. 36:645-646. 

VESSEY, J. C. 1975. Some potato diseases of the Peruvian humid 

tropics. Plant Dis. Rep. 59: i004-1007. 


Mycorrhizal Fungi 

The role of these obligate symbionts in potato growth and 

particularly their relation to tuberization has been extensively 

investigated. Only recently has their beneficial effect on 

potatoes been established. Inoculation in the root hair region 

with the endomycorrhizal fungus, Glotnus .fasciculatus, increased 

tuber yields ant total plant weight. 


GRAHAM. S. 0.. N. E.GREEN. and ..W. HENDRIX. 1976. The 

Miscellaneous Diseases 

influence of vesicular-arbuscular mycorrhizal fungi on growth and 

tuberization of potatoes. Mycologia 68:925-929. 

PHILLIPS. J. M., and 1). S. HAYMAN. 1970. Improved procedures 

Tuber Rots 

for clearing roots and staining parasitic vesicular-arbuscular 

In Germianyv and Italy. (Ihmo.otachrs araariaevar. rosea 

mycorrhizal 

In IalyCermny 

fungi for rapid 

Chrwsuhv~ 

assssment 

nd 

of infection. 

arucuirn'var 

Trans. Br. 

roesMvcol. 

tuber rot occasionally 

Soc. 55:158-161. 

causes severe losses in storage following 

bad weather during harvest. Dark necrotic areas on tubers are 

(Prepared by W. J.Hooker) 

surrounded by white mycelium with abundant conidia. 

Armillaria dry rot isa minor problem in northern areas where 

potatoes are produced on recently cleared land. Armillaria 

,n.lea Vahl. ex Fr. causes hard brown, roughened areas some- 

Principles of Foliage 

what corky in texture. L.esions are usually shallow, with dark 

brown to black rhizomorphs attached to .:uch areas. 

Fungicide Application 

Xylaria tube- • it oc -urs in calcareous marl soils of Florida. 

Black rhizomo. ., tfireadlike to 3 mm thick, become firmly 

In most parts of the world, sprays have superceded 

attached 

dusts 

to 

in 

the tuber surface. In the field, tuber invasion slowly control of foliage diseases of potato. Dusts are 

progresses 

easily and 

as more or less semicircular lesions. The problem, of quickly applied without premixing with water, and dusters are 

minor importance, develops on recently cleared land. 

usually cheaper, lighter, and simpler in construction and 

Gilmaniella humicola causes minute brownish necrotic spots, maintenance than sprayers. However, dusts drift easily, do not 

2-6 mm in diameter, around lenticels and eyes. L.esions remain adhere well to foliage in the absence of moisture, 

shallow. 

and are 

Eyes 

not 

are killed, making tubers unfit for seed. 

well suited to large-scale outdoor crop protection. On the other 

Cyiudlrocarpontonkinesis dry rot develops during the rainy hand, sprays are less subject to drift, provide 

season 

more 

in India 

uniform 

as brown patches on skin, later with white coverage, and stick better to foliage than dusts do, but accurate 

mycelium in or on affected tissue, 

measurement and mixing of ingredients are essential to their 

te'erosporiutn sp., usually found on potato leaves, also effectiveness. 

causes lesions on tubers. 

With few exceptions, the fungicides used to control foliage 

diseases of potato are protectant in their action. 

Leaf 

This 

Spots 

means they 

must be applied to foliage before orat the same time as inoculum 

Periconia sp., IXetuspaerulinasp., and Diid'mella sp. are is deposited in order to prevent fungous spore germination,

penetration, and subsequent disease development. Because 

protectant fungicides are not absorbed and translocated 

through the plant to any significant degree, they must be applied 

uniformly to as much of the foliage as possible. This implies 

uniformity both in horizontal distribution of fungicide across 

the spray swath and vertical distribution (penetration) through 

the plant canopy. Coverage of both upper and lower leaf 

surfaces isalso essential. To achieve optimal coverage, attention 

should be paid to the following: use of the correct spray volume 

and pressure for which a sprayer has been designed; proper 

functioning of the sprayer as determined by cleanliness, wear of 

nozzle orifices, height of boom, accuracy of pressure gauge; 

spraying when the air is still; and not extending swath width 

beyond that specified for the sprayer. 

Traiditional hydraulic boom sprayers that apply large 

voluimes (70t 1170r L ha, 75-125 g A of dilute spray under 

high pressure (approximately 28 kg cm, 400 psi) provide good 

horizontal and vertical distribution of fungicides. However, 

weight, high cost, large water requirement, and frequent need 

for filling have decreased their popularity in recent years. The 

present, trend is towards low pressure (approximately 7.0-8.8 

kcn)-15pilwvlm(apoiaey45Lh,0 

kg cm -100-125 psi), low volume (approximately4651 ha,50 

g,A or less) spraying, either with hydraulic or airblast 

(atomizing) machines. These can be effectively used if the 

manufacturer's recommendations are followed, 

Spraying by aircraft has several advantages such as speed, 

saving of labor, ability to be used in fields too wet for ground 

equipment, absence of yield loss due to sprayer tracks, reduced 

spread of virus diseases, and low water requirements (usually 

28-47 1. ha, 3-5 g A). These advantages have increased accetance 

of aircraft application particularly among large growers, 

But again, certain disadvantages must be considered, such as 

wind iterference and risk of drift, unsuitability of small, 

irregularly shaped or topographically uneven fields, the hazard 

of physical obstacles, relatively poor vertical distribution of 

spray through the plant canopy, and sparse deposition of 

d3scr,;et particles of concentrated fungicide. This last makes it 

essential that fungicide deposits be redistributed, i.e., 

transferred from their original landing sites to unprotected leaf 

areas by moisture in the form of dew, rain, or irrigation. 

Although the addition ofadjuvantsto fungicide sprays has been 

promoted to improve redistribution, most fungicide 

formulations have adequate spreadability without being 

supplemented with such materials. 

To provide as complete a protective blanket as possible, 

fungicide sprays must be applied at regular intervals to protect 

newly-expanded foliage and to supplement fungicide activity 

lost to dilution, photodegradation, oxidation, etc. Frequency of 

application depends n weather conditions, presence of disease 

in the vicinity, tena,:ity of the fungicide, varietal resistance, 

sprayer capability, and other factors. The usual interval 

employed by growers ranges from 5to 14 days. In certain areas, 

disease forecasting systems are used to determine spray 

intervals, 

I se ofthe correct aimount offungicide per unit area isvital to 

effective disease control. This requires careful attention to 

spr,.ycr calibration and maintenance. Calibration means determining 

how much fungicide is applied by a sprayer to a particular 

area. 

In summary, the four basic requirements for success are to 

apply the right chemical in the right amount at the right time in 

the right way to obtain maximum coverage. 


IIJRSFA I.I. .1.G. 1956. Principles of Fungicidal Action. Chronica 

Botanica Co., Waltham, ME. 231 pp. 

MARlIN. II. 1959. The Scientific Principles of Crop Protection. 4th 

ed. EIdward Arnold, Ltd.. London. 359 pp. 

10RGESON,1). C.. ed. 1967. hIngicides An Advanced Treatise, Vol. 

I. Academic Press. New York. 697 pp. 

(Prepared by 0. Schultz) 

Tuber Seed Treatment 

Chemical treatment of seed tubers before planting is neithera 

cure-all nor a replacement for the use of high quality seed, 

properly stored and handled. Rather, it isinexpensive insurance 

that partially protects seed from invasion by microorganisms 

present in the soil and on the tuber surface. Unfortunately, it 

does not kill microorganisms present within seed. 

Possible benefits of seed treatment are: I) control of storage 

diseases such as Fusarium dry rot, 2)control of seed piece decay 

when cut seed has to be held for an extended period before 

planting. 3) control the soil (usually 

ol + seed piece decay inthsoluuay 

caused by Fusarium spp.) when planting is done under adverse 

soil conditions (cool and wet) that impair suberization of the cut 

surfaces, and 4) partial control of diseases such as Rhizoctonia 

stem canker, scab, Verticillium wilt, and blackleg. 

Prestorage treatment of seed, a relatively recent development, 

usually involves application of fungicides (e.g., thiabendazole) 

in the form of a fine mist as tubers enter the storage structure. 

Seed treatment after storage and before planting is most 

commonly don: by dusting with rotating drum dusters, which 

generally provide better coverage than do the shaker types of 

treaters. Several ethylenebisdithiocarbamate fungicides are 

useful for dip treatment of seed tubers. but they are not com 

monly applied in tis manner. 

When whole seed is planted, or when cut seed is planted in a 

warm, moist seedbed promptly after cutting, whole tubers may 

be surface disinfested by dusting or dipping. This is only 

partially effective in controlling diseases such as Rhizoctonia 

stem canker, scab, and Verticillium wilt because their causal 

agents are commonly soilborne. Where cut seed is 

predominantly used, treating seed immediately after, rather 

than before, cutting is advisable (dusts. are preferred). This 

protects the cut tuber surfaces from invasion by soilborne 

pathogens such as Fusarium spp. and provides partial surface 

disinfestation. 

Cut seed, whether treated or not, should be planted 

immediately. If this is impossible, it should he stored in open 

containers such as potato crates stacked to provide ample 

ventilation. Burlap bags should be only half filled and also 

stacked forventilation. Cut seed should be held at 10-16Cand 

high relative humidity (85-90%) for three to four days to allow 

wound cork to form over cut surfaces. If further stoage is 

necessary, temperatures can be dropped to 5 C, but seed should 

be warmed again before planting to ensure vigorous sprouting. 

Insects should be excluded from cut seed, particularly adults of 

the seed corn maggot. Cut seed held for some time before 

planting may develop considerable seed piece decay and give 

poor stands. 


BOYI). A. E. W. 1975. Fungicides for potato tubers. Proc. 8th British 

Insecticide and Fungicide Conf. 3:1035-1044. 

MOSHER, P. 1972. Treating seed potatoes for disease control. 

Spudlines. April 1972. Univ. of Maine. 3 pp. 

(Prepared by 0. Schultz) 

67

Virus diseases, although seldom lethal. reduce plant vigorand 

yield potential of seed tubers. Identification is complicated by 

wide symptom variation attributable to virus strain differences, 

plant response in relation to maturity and duration of infection, 

potato cultivar. and environmental influences. l)ifferentiation 

of viruses may involve purification, electron microscopy, 

comparison of physical properties, clectrophoresis. serology, 

and possibly other techniques. Recent developments in serology 

using the ELISA (eniyme-linked immunosorbent assay) 

,echnique provide an extremely sensitive test for virus presence 

and identity and have for the first time permitted serology with 

certain viruses difficult to detect in potato. 


BODE. 0. 1958, Die Virosen der Kartoffel und des'Tahaks. Pages 1-30 

in: M. Klinkowski, ed. i'lianliche Virologie. Vol. II. Akademie- 

Verlag. Berlin. 393 pp. 

CI.ARK. M. F., and A. N. ADAMS. 1977. Characteristics of the 

microplate method of eniime-linked immunosorbent assay for the 

detection of plant viruses. .1.Gen. Virol. 34:475-483. 

de BOKX, J. A.. ed. 1972. Viruses of Potatoes and Seed-Potato 

Production. Pudoc, Wageningen, The Netherlands. 233 pp. 

FERNANDEZ VAI.IEI.A, M. V. 1969. Introducci6n a la 

Fitopatologiii. Vol. I. Virus, 3rd ed. Pages 764-845. Inst. Nac. de 

lecnol. Agropecuaria. Buenos Aires. 1,011 pp. 

GIBBS. A.. and B. HARRISON. 1976. Plant Virology: The Principles. 

.Joh n Wiley and S o ns, New Y o rk. 292 pp . 

KI.INKOWSKI. M.. and 1H.KEGI.ER. 1962. Viruskrankheiten der 

Kartoffel. pages 1025-1138 in: R. Schick and M. Klinkowski. eds. 

Die Kartoffel, Vol. II.2.112 pp. 

MATItEWVS, R. E. F. 1970. Plant Vir,',,gy. Academic Press, New 

York. 778 pp. 

SMITH. K. M. 1972. A texlbook of .< virus diseases, 3rd ed. 

Longman, Iondon. 684 pp. 

Potato Leafroll Virus 

Potato leafroll, an aphid-transmitted disease is one of the 

most serious in potato and is responsible for high yield losses 

throughout the world wherever potatoes are grown. In 

Colombia and the Andes, the potato leafroll virus (PLVR) 

occurs in Solanum andigena potatoes: the disease has been 

known as "enanismo amarillo" for many years. 

Symptoms 

Primary symptoms (Plate 55) follow transmission by aphids 

Symptoms appear mainly in the young leaves, which usually 

stand uprigh:, roll, and turn slightly pale. In some cultivars, 

young leaves are pink to reddish starting at tile margins. Rolling 

sometimes affects only the base of the leaflet rather than the 

whole leaflet. These symptoms may spread later to the lower 

leaves. Primary symptoms may be lacking with late season 

infection, making diagnosis in seed stocks a major problem. 

Secondary symptoms (Plate 56) become evident when an 

infected tuber produces a plant. Lower leaflets are rolled and 

higher leaves are slightly pale. l.eaves are stiff,dry, and leathery 

and make a crisp, somewhat paperlike sound when touched. 

Older leaves of some cultivars are i..ak and or severely necrotic, 

especially at the margins. Plants are often noticeably stunted 

and rigid. Symptoms are less pronounced in the top of a plant 

with secondary infection than in one with primary irfection, and 

secondary infection is more damaging to the plant. Severity of 

symptoms depends on the isolate of the virus, the potato 

cultivar, and the growing conditions. 

In S. tuherosumssp. antdigena cultivars. secondary symptoms 

(enanismo amarillo) tend to be somewhat different from those 

in S. tuherosum ssp. tuherosutm, consisting of a marked upright 

habit of growth. stunting, and a marginal and interveinal 

68 

Viruses 

chlorosis of leaflets (Plate 57), especially of' dwarfed upper 

leaves. Rolling of lower leaves is often lacking. Secondary 

symptoms in hybrids of S. tuherosum ssp. andigena X S. 

tuherosum ssp. tuherosum consist of the rolling of lower leaves 

typical of S. tuherosuim ssp. tuherostni cultivars. In some 

cultivars, however, distinct interveinal and marginal chlorosis 

occurs as in S. tuherosumn ssp. antdigena cultivars. 

Internal net necrosis (Figs. 28B and 73A), visible to the 

unaided eye when the tuber is cut, is particularly marked in 

certain American cultivars such as Russet Burbank, Green 

Mountain, and Norgold Russet. This net necrosis is found in 

tubers from plants with primary, secondary, or tertiary 

infection. The color may vary from light translucent to dark. A 

definite trend toward a less severe type of infection from 

primary to tertiary has been found in tubers of Russet Burbank. 

Causal Agent 

PI.VR has icosahedral particles 24 nm in diameter(Figs. 73D 

and E). 

'ransmission is successful only by aphids and grafting; 

artificial inoculation by mechanical means has never been 

accomplished. The virus is transmitted by aphids in a persistent 

(circulative) manner (i.e.. after an aphid has fed on an infected 

plant it normally transmits the virus for the rest of its life). 

Isolates have not been differentiated by serological, physical, 

or chemical properties nor by vector specificity or transmission 

e mical No per ti ano r no All tra ns i ssi on 

efficiency. No differential plants are known. All strains give the 

same type of symptoms. Isolates vary in severity of symptoms 

on potato cultivars and on Ph'salisfloridana, but existence of 

strains has not been well defined. Some workers refer to three 

strains called severe, moderate, and mild; others refer to 

four strains called No. 1,2, 3, and 4. A fifth isolate, differing in 

symptom severity from No. I on P.floridana but not on other 

hosts, has been isolated. 


From the moment of symptom appearance, infections are 

always accompanied by phloem necrosis, which consists of 

thickening of the walls of the primary phloem cells in the stem 

and petioles (Fig. 73B). Accumulation of callose is often 

pronounced around the sieve plates in the phloem oftubersand 

stems (Fig. 73C). Stiffness of leaves in primary and secondary 

infections isaconsequence of starch accumulation in leaf cells. 

Epidemiology 

SThe virus istuberborne and isalso efficiently 

persistent 

transmitted 

manner 

in 

by 

a 

aphids that colonize potatoes, My'zus 

persicae being the most efficient. Infection efficiency increases 

with the length of feeding. The virus is spread over long 

distances by windborne winged aphids and over short distances 

by nonwinged aphids moving from plant to plant. Aphid 

transmission occurs from tuber t(. tuber during seed storage, 

especially in tropical countries. Plants from infected tubers and 

diseased volunteer potato plants also serve as virus sources. 

Moderate temperatures and dry weather favor spread. Plants 

become resistant to infection with age, and occasionally some 

tubers of plants infected late in the season escape infection. 

Other Hists 

Several plant species, mostly in the Solanaceac, are known as 

hosts. 

P.floridana is asuitable indicator, test, and propagation host 

that reacts with interveinal chlorosis, darkening of the veinal 

areas, and a slight cupping at the first two or three true leaves. 

Infections at a later stage cause plants to become somewhat 

pale. 

Datura siraionium is favored by some workers, especially in 

the more tropical regions, as a test and propagation host in 

which chlorosis develops. In Brazil, alternative hosts to PI.VR

have been demonstrated, including tomato, D. stranionium, 

and a Physalis species. D. stramoniutm also seems to be a 

reservoir for the virus in the Andean region, where it is a 

common weed. No evidence indicates that hosts other than 

potato act as a virus reservoir in the temperate regions. 

Nonsolanaceous hosts are found in the Amaranthaceae. 

Tuber Indexing 

Symptom development in eye sprouts can be used to index for 

virus infection in postharvest glasshouse tests. The often-used 

Igel-Lange test (deep blue staining of phloem sieve tubes after 10 

rin in Il " aqueous resorcin blue) is based on increased deposits 

of callose in the phloem (Fig. 73C). Neither method is 

completely reliable because symptoms are not always produced 

and because callose, which is not always observed in infected 

tubers, may also be found in healthy tubers. 

Electron microscope techniques alone are unreliable because 

of the low concentration of virus particles in infected plants. In 

combination with serological techniques, electron microscopy is 

efficient. 

The recent application of EI.ISA to detect the virus in 

tuber and other plant material has resulted in improved 

indexing techniques. A reliable method, although laborious to 

perform, involves aphid transmission tests on eye sprouts, using 

indicator plants such as P..1loridana. 

A technique in which leaves, stems, and small pieces of tuber 

are grafted to D.stramonium isnow used on a large scale in seed 

multiplication work in Brazil. This method is considered to be 

less time-consuming than that using aphids and P.floridana. 

Control 

I) Breeding resistant cultivars has met only limited success. 

Resistance is determined by many genes with additive effects 

and can only gradually be built up. Varying levels of resistance 

are found in some seedlings. Crossing of unrelated resistant 

parents may result in a higher proportion of resistant offspring 

than does inbreeding. Resistance isalso found in progenies from 

S. de'nissun, S. and(igena, S. acaisle, S. chacoense, S. 

stololnferunn, and S. etuherosuim. 

2) Disease-free seed tubers are essential for maximum 

production. Seed tubers with a low percentage of infection can 

be produced in areas where sources of virus are limited and 

aphids appear late in the season. Seed plots should be harvested 

as early as possible, compatible with reasonable yields, to avoid 

late season aphid transmission. Dates for lifting may be 

determined by the number of aphids caught in yellow traps or 

assessed by other methods. 

3) To minimi/e infection, measures such as clonal selection, 

early planting of virus-free tubers (from seed certification 

programs), and early lifting and roguing of infected plants and 

killing or removal of volunteer plants in and around the field can 

be Lused. 

4) Aphids should be controlled by toxic sprays or systemic 

insecticides. Application of granulated systemic insecticides has 

been successful in certain cases. Spread cannot be controlled by 

oil sprays. 

5)Tubers may be freed of the virus by heating, e.g., 25 days at 

37.50 C. 


BACON, 0. G., V. E. BURTON, D. .. McLEAN. R.H. JAMES, W. 

t). RII.EY, K.G.BAGHIOTT, and M.G.KINSEY. 1976. Control of 

the green peach aphid and its effect on the incidence of potato leaf roll 

virus. J. Econ. Entomol. 69:410-414. 

CHIKO, A. W.. and .1.W. GUTHRIE. 1969. An hypothesis for 

selection of strains of potato leafroll virus by passage through 

Phrsalisfloridana.Am. Potato .1.46:155-167. 

CUIPERIINO. F. I1.. and A. S. COSTA. 1967. l)eterminaciodo virus 

do enrolamento em hastas velhas de batalal para sementes. Bragantia 

26:181-186. 

l)AVI)SON.l-.M. W. 1973. Assessing resistance to leafroll in potato 

seedlings. Potato Res. 16:99-108. 

de BOKX. .1.A. 1967. [he callose test for the detection of leafroll virus 

I. .,.T. . 

:. ,.. " - 

Fig. 73. Potato leafroll virus (PLRV): A, phloem net necrosis of 

tuber; B, phloem necrosis in petiole (bar represents 10 pm); C, 

callose at stolon end of infected tuber (Igel-Lange stain); D,PLRV 

particles, 24 nm in diameter, negatively stained with 

phosphotungstic acid and (E)precipitated with PLRV antiserum 

and similarly stained. (C-E. Courtesy D. Peters) 

0 

69

in potato tubers. Eur. Potato .1.10:221-234. (primary) infection and in those from infected tubers (secondary 

)OUGI.AS, I). R., and .1..1.IAVEK. 1972. Net necrosis of potato infection). If infection occurs late in the season, foliage 

tubers associated with primary, secondary, and tertiary infection of symptoms may not appear. but tubers from such plants may 

leafroll. Am. Potato .1.49:330-333. " " 

MAAl. I). Z.. and .1.A. de I1(KX. 1978. Potato leafroll \irus: carry the disease. 

Antiserum preparation and detection in polato leaves aind sprouts Primary symptoms of PVY . depending on potato culti\ar. 

s,ith the en/\nme-linked immunosorbent assay ( II.SIA). Neth. . are necrosis, mottling, or yellowing of leaflets, leaf dropping, 

Plant Pathol. 84:149-156, and sometimes premature death. Necrosis, which starts as spots 

I'T FRS. 1). 1970. Potato leafroll virus. No. 36 in: Descriptions of or rings on the leaflets (Plate 58), may cause leaves to collapse 

Plant Viruses. (omnmonw. Mycol. Inst.. Assoc. Appl. Biol.. Kew, and either drop from the plants (IeafIdrop streak) or remain 

Surrey. Fngland. clinging to the stem, resembling paln trees. Sometimes these 

SNI Itt. K. NI. 1972. A Iexthook of Plant Virus Diseases, 3rd ed. symptoms appear only oil a single shoot in a hill. 

longman: london. 684 pp. lPlants with secondary PVY" infection are dwarfed, and 

leaves are mottled and crinkled. Sometimes foliage and stem 

(Prepared by I). Peters and R. A. C. Joines) necrosis occurs. Necrosis is usually more severe after primary 

Potato Virus Y 

Potato virus Y ( VY) causes rugose miosaic 

Common 

(Fig. 

strains 

74A). 

of the virus (PVY') are found worldwide, and 

necrotic strains (PVY 

than after secondary infection. The foliage symptom isa mosaic 

(Plate 59). which differs from that induced by potato virus A 

(mild mosaic) in that discolored areas are smaller and more 

numerous. l.eaf mottling may be masked at very low (10 C)and 

high (250 C) temperatures, but at high temperatures the disease 

can be identified by the crinkling and rugosity of the foliage 

(Plate 

byat 

60). 

the). 

" rnd in parts of Africa 

) occur 

and 

in Europe, including the USSR, 

[ne 

South 

typevirus 

America. 

C (PVY 

Strains 

) probah 

belonging 

occurinAustralia 

to 

and some 

PVY' evokes 

Affected 

stipple-streak 

plants 

symptoms 

are dwarfed 

in several 

and 

cultivars. 

A correlation 

may die prematurely. 

generally exists between symptoms in the 

the ypevirs )proablyoccr C( PY i Autraia nd ome 

parts of Europe. although extensive reports are not available. 

foliage and those in tubers. 

foliage 

Weak 

a s 

niosiac 

o se in 

symptoms 

ue d bamosia s tra 

in the 

foliage, as conimonily 

in t 

induced by P)VYN strains, are not 

Symptoms 

Svmiptoris in potato vary widely with virus strain and potato 

uthtivar, ranging in severity from weak symptoms to severe 

accompanied by symptoms in the tubers. Cultivars that react 

with necrosis in the foliage upon infection to [PVY') sometimes 

show light brown rings on the skin of tubers (Fig. 74B). PVY t 

foliage necrosis to death of infected plants. In general, PVY' 

and PVY( cause much more severe symptons than does PVY 

strains mal' induce internal and external necrosis in some 

5 . 

' 

PVY induces vague mottle in plants with current-season 

cultivars. 

Causal Agent 

PVY is a virus with flexuous, helically constructed particles, 

730 X II nm (Fig. 75A). 

Many groups of strains can be distinguished according to 

severity of systemic symptoms in tobacco, Physalisflridana, 

potato, and other hosts. The main groups are called PVY), 

. 

PVY and PVY(. Although aphids can transmit PVY 1 , they 

transmit sonic strains only with great difficulty, if It all, and 

others as readily as they transmit PVYN. 


Pinwheel inclusions observed in electron microscopy occur in 

tissue of tobacco and potato systemically infected with PVY 

p(Fig. 75). 

Spread of PVY depends mainly on the presence of winged 

aphids. The virus is borne on the stylet and is transmitted within 

a few seconds in a nonpersistent way by many aphid species. at 

least 25 are mentioned as capable of transmitting PVY, but little 

is known about their efficiency. Mt."us persicae is the most 

efficient species in many areas and seasons. 

PVY isconsidered one of the most damaging potato viruses in 

causing yield depression. PVY" and PVY t may cause complete 

failure of a potato crop. In combination with potato virus X, 

PVY is generally even more destructive, producing the rugose 

mosaic disease. 

Other Hosts 

Many plant species, mostly in the Solanaceae, but also in the 

Chenopodiaceae and I.cguminosae are hosts of PVY. 

Perennials seldom act as virus reservoirs in nature. In potatogrowing 

areas, the potato itself, as volunteer plants, may be 

considered a reservoir host. 

In Nicotiana tahacum (tobacco), most strains produce vein 

A clearing followed by mottling. The necrotic PVYN strain 

Fig. 74. Rugose mosaic: A, in cultivar Bintje; 6, tuber symptoms of induces mottling and bronzing of the niidribs and necrosis of 

unnamed seedling with potato virus Y". (Courtesy J. A.de Bokx) leaf ribs. 

70

In P..floridana,strains of PVY" and PVY cause local and 

systemic necrosis in young plants. Rapid death follows 

inoculation with PVY 1 , whereas PVY induces mosiac 

symptoms only. 

Potato cultivars, e.g., Duke of York. may be useful forfurther 

identification because after being grafted with P3VYN, PVy 

and PVY" , they react with mottling, rugose mosaic, and stipple 

streak, respectively. No hosts are known to separate the 

different strains, 

Solanum demissum "Y'of Cockerham or 'A6' (S. demissum 

X S. tuberosum 'Aquila') react to PVY with local lesions, 

Detached leaves are often used in routine tests, 

Datura stramonium or D. tatula are resistant to PVY and 

serve for elimination of PVY in certain virus complexes. 

Seed Propagation 

Mature plant resistance may be of'importance in seed-potato 

production procedures. When infection by aphids takes place in 

an advanced stage of plant growth, the virus may not spread to 

tubers: frequently only a few tubers per plant become infected. 

Mature plant resistance is much less effective against PVYN 

.. 

-; ' " - .)WARI)SON. Et .R.1974. 

Fig. 75. A, Electron micrograph of potato virus Y" (X40,OGO); B, 

pinwheel inclusion bodies demonstrated bythin section, electron 

microscopy (X72,000), in tissues infected with either potato virus 

Y or A.(A, Courtesy H. Huttinga; B, courtesy J. A. de Bokx) 

. 

than against PVY strains. 

Breeding and growing cultivars resistant to PVY is the best 

way of combating the disease. Extreme resistance, which 

protects plants from all strains of the virus, occurs in S. 

chacoense and S. stoloniferum. Seedlings with good 

commercial qualities have been derived from these. 

In areas where virus sources are limited and vectors are 

present only in certain periods of the growing season, seed with a 

tolerable percentage of infection can be produced. Certification 

schemes use combinations of measures such as clonal selection, 

planting virus-free seed at an early date, roguing, and early 

lifting. This may be followed by tuber indexing. Laboratory 

testing, such as leaflet inoculation of 'A6' and serology, can be 

included. 

Heat treatment and meristem culture may be used for freeing 

virus-infected clones. 

Preventing spread of PVY strains by chemical control of 

aphid vectors, including the use of systemic insecticides, is not 

possible because aphids have short periods of PVY acquisition 

and infection feeding. 

Control 

1) Plant clean seed free from tuberborne infection. 


3) Plant early, and rogue diseased plants. 

4) Prevent heavy aphid populations in the field by applying 

insecticides as foliage sprays and systemic soil treatments. 

Application of oil spray to the foliage has been useful 

experimentally. 

5) Time harvesting operations to precede heavy aphid flights 

as determined by yellow pan traps. 


COCK -RIIAM. (. 1957. Experimental breeding in relation to virus 

resistance. Pages 199-203 in: F. Quak, .1. )ijkstra. A. It. R. 

licejuster. and .1.P II. Van dcr Want. eds. 1958. Proc. Third Conf. 

P~otato Virus Dis.. 24-28 June. 1957. II. Veennian and Zonen, 

Lisse-Wageningen. lhe Netherlands. 282 pp. 

de BOKX. .1. A., ed. 1972. Viruses of Potatoes and Seed-Potato 

4-.. 

.A I' 

,, "' ,. 

ProduIction. Pudo(1C. Wageningeii. 'Ilie Netherlands. 233 pp. 

de B(OKY. .1.A.. and P. i. M. PIRON. 1978. t ransnission of potato 

iris Y' by aphids. EFor. Assoc. Potato Res. 7th 1riennial Conl. pp. 

244-245 (Absir.). 

1)1:ll(iAI)O-SANCII EZ.S.. and R.G.GROGAN. 19711. Potato Virus 

Y. No. 37 in: I)escripiions ol Plant Viruses. Comnmnw. Nivcol. 

Inst.. Assoc. Appl. BitIol. Ke . Surre. England. 

T*A 

EDl)WA)R SON. .1.R. 1974. Sone properties of the potato virus Ygroup. 

I1. Agric. E.xp. Sin. Monograph Set. No. 4. 398 pp. 

.:1'" ' ... 'r., ' ' 

.6 

I1.Agric. IExp. Sin. %Ion l1ost gnaph rangesol Ser. No. virusesin 5. 225p the . PVY-group. 

WE lilt. R. F.. and 1). R. WIISON. 1978. Solato demi.snml P. I. 

230579. attrue seed diagnosti I ost Ior potato %irus Y.Am. lPotato .j. 

55:15-23. 

(Prepared by J. A. de Bokx) 

Potato Virus A 

Potato virus A (PVA). which caiuses mild mosaic, is 

widespread in most potato-growing areas. PVA may decrease 

yield of infected potatoes by up to 40%. 

Symptoms 

The mild mosaic symptom induced in leaves of many potato 

cultivars is a chlorotic ,aottle, sometimes severe, in which 

yellowish or light-colored irregular areas alternate with similar 

areas of darker than normal green (Fig. 76A). Mottled areas 

vary in size and lie both on and between the veins. A slight 

rugosity of the leaf surface can usually be observed, and the 

margins of the leaflets may become wavy. Infected leaves as a 

71

whole look shiny. Severity of symptom expression depends 

largely on weather conditions, the potato cultivar, and the strain 

of virus A. 

Infected plants usually seem open because stems bend 

outward. At high temperaturesand in bright sunlight, symptoms 

are more difficult to recognize than in cloudy cool weather and 

may be completely masked. Normally, infected plants produce 

symptomless tubers, 

Causal Agent 

PVA, a member of the potato virus Y (PVY) group, has 

particles as flexuous filaments, 730 X 15 ni. PVA is 

serologically related to PVY, although the degree of 

relationship 

heterologous 

is 

tests 

diffficult 

do not give 

to assess 

the same 

because 

results. 

reciprocal 

According tesytso 

According 

n 

to 

potto 

synuptoms 

same rieasu 

in potato 

ralh 

and Nicandraph 

s 

isa/odes, 

strains 

moderately of PVA 

severe, may 

and severe. 

be classed into three groups: m ild, 


Pinwheel inclusions occur in tissue of tobacco and potato 

,A 

B 

Fig. 76. Potato virus A: A, mild symptoms in cultivar Saucisse 

Rouge; 8, necrotic local lesions in A6, a Solanum demissum x S. 

htiharnc-cr hhriA l- I -, - 

systemically infected with PVA (Fig. 7513). 

Epidemiology 

PVA is transmissible by at least seven species of aphids 

(including .Alphis frangudlav ,lacro.siphunrt eiquorhiae, and 

izuspersicae) in the nonpersistent manner, by grafting, and 

by inoculation with sap. lhe latter, however, usually yields poor 

results because of instability of the virus. Therefore, 

transmission hy foliage contact in the field probably does not 

take place. Many cultivars, e.g.. Ilintje, Katahdin, Kennebec, 

and Sebago, are field resistant (hypersensitive) to all known 

strains of PVA. For this reason. I'VA is considered less harmful 

thanPVY. llantsextrclielw.are also xtiyresistant troS. 

hVA r 

PA 

Testing for the presence of'MIA by using 'A6' or meristem 

clture for freeing virus-infected stock is useful in seed 

improvement i 

prograims. p o r m PVA cannot 

serological methods: however, for serological identification of 

PVA. the ELISA technique can be applied. 

b ed tectd b y 

e detcIed by present 

Other Hosts 

Hosts of PVA are limited to the Solanaccae. 

In Nicotiana tahacunt cv. Sanisun. virus strains produce vein 

clearing and diffuse mottle, whereas in N. tabacum cv. White 

Burley, vein clearing and vein banding are induced. 

'A6'(S. demnis.suin X S. tuberostum cv. Aquila) develops local 

lesions (Fig. 76B), which may be distinguished from those of 

PVY in detached leaf culture under controlled environment. 

S. denissum A' of Cockerham shows local lesions only after 

inoculation with PVA. 

Control 

I) Plant clean seed free from tuberborne infection. 


3) Plant early. and rogue diseased plarits. 

4) Prevent heavy aphid populations in the field by applying 

insecticides as foliage sprays and systemic soil treatments. 

Application of oil spray to the foliage has been useful 

experimentally. 

5) Time harvesting operations to precede heavy aphid flights 

as determined by yellow pan traps. 


lIAR I FRI S. . 1971. Votato irusA. \. 54 in: )escriptions ol Plant 

Viruse%. C(mrrrn . M~sl. losi. A oc. Appl. Itiol.. Ke\%. Surre\ r . 

[rilglanld. 

C()O(KI( R Il,,\. i. 1957. Fxpeiiicnial hreeding illrelatioi i virus 

Ieistndrce. l'ages 199 213 in: -. QOrik. .. I)iikslra. A. BI.R. 

Ilee lsan ler. lI. 1'. II. Van der Wan t. ds tlic. Ihi.d ('oi. Potato 

Virus t)is.. 24 28 tune. t957. It. Vec'nman adllZonen. lisse 

Wage.irgen. Ilie Nether lanrd.282 til. 

de B()KX..1.. A. cd. 1972. \'iirses of Ptliiiloc% and Seed-Pt)ajtlo 

Produciion. I'dhn . Wigenirrgen. Ihe Netherlands. 233 pp. 

FERNANI)I1Z VA.\I ItLA. M. V. 1969. Inir ducci61n i.1,1 

Filpat ,ogi~i. VI. I. Virus..31d ed. Pages 704-845. Inst. Nile. 

crnol. Agropecuaria, Buenos Aires. 1.011 pp. 

MAA. I). . -and I. A. de lit uX. 1978+ In/ynre-iinked 

irnnrl unosoirhent aJssi\ (1:1 1 SA l I tie dlerectioni of potato %iruses A 

and Y in potato tea es and %pl ts. Nellh .. t. Plant I'athol. 

84: 167- 173. 

WIlBB. R. -.. :lnd R. W B1K..Ir. 1955. A diagnostic tust otr potato 

,, tirus . \AIn. t'tor t .1, 32:248 252. 

Prepared by J. A. de Bokx) 

Potato VirusX 

Potato virus X (PVX) occurs wherever potatoes are Lyrown. It

infects certain comnie,-cial stocks, ith yield reductions 

estimated to range tp to more than l5('. 

Symptoms 

FVX Ina\ be atent. without foliage s)nptois or apparent 

effect on plant igor except when closely conpared tcPVX-frce 

stocks, or it may s h % mild uotte {Ilate 61 ) to sc ere or rugose 

iosaic (Fig. 77A),.sith (hkarling of the plant and reduced 

leaflet site. 'ertain combinations ol PVX strain and host 

genotype cause extensive top necrosis (Fig. 771B). shich may 

kill part or all of' the plant and cIuse tuber necrosis. In 

comhination \ ithpotto \ iruses A or Y. crinkling !,:gosity. or 

necrosis may :c\elop. 

Causal Agent 

PVX particlc~s a-e Ilexuous filaments. 515 < 13 mil. with 

helical (pitch, 3.4 ni) substructure (Fig. 781)). Single-stranded 

ribonucleic acid, ith molecular %%eightof 2.1 X 10' , compries 

6:, of the particle \seight. Ihermal inctikation is 68-76, 

depending on tie s"ain: dilutioniend point is 16'--10': 

longe\i.tv in \ttr i-sc\eral e .ks. 

PVX is strongly imutnogenica ind s sulTficientl ,yho moge,-ous 

to permit se\ eral serolotal methods to be used inidentification 

of naturallv inlec:ed plants. 

I'VX isolatcs ha.c been grouped into itrains by cross 

absorption scrolog\ (four groups), tcoperatur' of inactivatiot 

(three groups). and necrotic reaction within S. tzluro.oum spp. 

tuhero.mum (11r grotips). Strains related by allty of, the ;e 

groupings tna\ \iary considerably in the irtensity of, tlt 

synptonis the cause. 

Within potatto leaf cells. IPVX forms large ar orphou:i; 

inclusions readily o.serva ble .vith light microscopy. These 

inclusions. exaittined itt thin sectiot by electron microscopy, 

contain \irUs particles itttersper,;ed between altertivting layers 

0I curved or rolled laminate inclusion components. 

Epidemiology 

k)\ X is with few exceptions. transo, .ttcd by tubers in 

susceptible cutltivars. lransmission through sap inoculation is 

readilv aeccnip!isltid by centact of plant pars in tilefield due to 

wind, atnimal.. or machinery: by root contact: by sprout to 

sprout contact; by the cutting knife before planting; and by 

biting insects (grasstoppers). Zoospores of' Sv'ipchvriwm 

elohiofictm ate reported to transmit the virus. Anhids are not 

knovtn to transr.i. PVX. nor is the virus known to be 

transmitted through true seed. 

.007 

Symptoms inmost plants are enhanced by low temperatures 

oi 16-20'C and are mild or may be masked at temperatures 

above 28' C. 

Culi /ars may be freed from PVX by meristem culture of 

sprout tip:; grown at 32-36'( ". 

Other Hosts 

PVX isolates cause widely different symptom severity ranging 

from rild to severe. Mild isolates may spontaneously become 

severe or vice versa. PVX is chiefly systemic in tite Solanaceae, 

usually produces local lesions in the Chenopodiaceae or 

Amaranthaceae, and also infects certain Leguminusae. 

In Nicoia:a Iahacuin (White Burley 01 Samsun types), 

infection i,systemic, with mottles or rin, spots (Fig. 78B and C, 

Plate 62). 'I he plant is useful for virus prolpagation. 

laturastramonium and I). taiula show systernic infection, 

latent to severe mottle, and some leaf necrosis. 

Gomphrenaghhosa is a local lesion host (Fig. 78A) useful for 

quantitz'tive infectivity assay. 

" 

Resistance 

Compreltensixe or extreme resistance, earlier called 

"immunity,"is determined by a singl dominant gene(Rx). This 

gene or one similar confers resistance to all strains of PVX 

except one recently isolated in the Andes. It is present in 

selections of Solanuim acaule and its derivatives, including the 

zultivar Saphir, and incertain selections of S. tuherosum ssp. 

atdfiget'a, which include C. P. C. 1673, tite cultivar Villaroela, 

and its Irobable derivative S.41956. 

Field immunity itt S. tutierosu.m ssp. tuoerosui.,determined 

by dominant genes, is a strong necrotic, often top necrotic, 

reaction to infection. The Nx:nb genetic type confers resistance 

to Cockerham's (1954) PVX ,'roips I and 3,nx:Nb to groups I 

and 2, -.nd Nx:Nb to groups 1-3. Genes conferring similar 

rt'iistdnce are present in -ertain other tuber-bearing Solanum 

sp}p. 

Certain cultivars, although susceptible, apparently prevent 

completely free PVX movement within the plant, permitting 

certain plant parts to escape infection. By contrast, other 

cultivars are so thoroughly invaded that obtaining virus-free 

parts for propagation is difficuli. 

A strait, of PVX (XI 1 i) recently isolated in the Andean 

highlands differs markedly from previously descr;bed PVX 

strains by infecting I) plants with the Rx gene (USDA S.41956, 

Saco, Saphir, and resistant selections of S. acaule) and 2) G. 

glohosa without symptoms in inoculated leaves. This strain does 

not become systemic in G. glohosa. 

Fig. 77. Potato virus X: A, tatent strain in branch at right a id severe rugose strain at left; B, top necrosis 'n fie!d-resistant Epicure following 

graft inoculation with potato virus X. (A, Courtesy J. Munro) 

73

Control 

I) Use IPVX-free seed and avoid contamination through 

contact with infected plants or tubers. 

2) Use resistant cultivars where possible. Tolerant cultivars 

are useful. Many high yielding seed stocks, completely infected 

with PVX, produce plants with excellent vine type and high 

tuber quality. 


BERCKS. R. 1970. Potato Virus X. No. 4 in: Descriptions of Plant 

Viruses. Commonw. Mycol. Inst., Assoc. Appl. Biol.. Kew,Surrey, 

England. 

COCKERItAM, G.1954. XIII. Strains of potato virus X. Pages 82-92 

in: E. Streutgers. A. B. R. Beemster. 1). Noordam, and 1.P. H. Van 

der Want, eds. 1955. Proc. Second Corf. Potato Virus Dis., 25-29 

June, 1954. H. Veenman and Zonen, lisse-Wageningen, rhe 

Netherlands. 193 pp. 

COCKERIHAM, G. 1970. Gcenetical studies on resistance to potato 

viruses X and Y. Hteredity 25:309-348. 

DEI.HEY. R. 1974. Zur Natur der cxtremen Virusresisten, bei der 

Kartoffel. Phytopathol. Z. 80:97-119 

MEI.LOR, F. C., and R. SIACE-SMIIlI. 1970. Virus strain 

differences in eradication of viruses X and S. Phytopathology 

60:1587-1590. 

MOREIRA, A.. R. A. C. JONES. and C. E. FRIBOURG. 1980. 

Properties of a resistance-breaking strain of potato virus X. Ann. 

Appl. Biol. 95:93-103. 

MUNRO,,1. 1954. Maintenanceof virus X-free potatoes. Am. PotatoJ. 

31:73-82. 

MUNRO. .1.1961. The importance of potato virus X. Am. Potato J. 

38:440-447. 

SHALLA. "L A.. and .1. F. SHEPARD. 1972. The structure and 

antigenic analysis of amorphous inclusion bodies induced by potato 

virus X. Virology 49:654-657. 

SHEPARDJ. F.and G.A. SECOR. 1969. )etection ofpotatovirus X 

in infected plant tissue by radial and double-diffusion tests in agar. 


WRIGHT, N.S.1970. Combined effects of potato viruses X and S on 

yield of Netted Gem and White Rose potatoes. Am. Potato J. 

47:475-478. 

(Prepared by J. Munro) 

Potato Virus M 

Potato virus M (PVM) isfound worldwide in potato cultivars. 

It is more important in Eastern Europe and the USSR than in 

other parts of the world. Its economic significance in North 

.- ~c:..America is uncertain. 

The disease was first named potato leafrolling mosaic. Early 

descriptions were probably not made on PVM alone because the 

J%. virus frequently occurs with potato viruses X and/or S. The 

identity of PVM has only recently been clearly established. 

7 "PVM causes the latent paracrinkle disease in the King Edward 

cultivar. 

K 

. . 

Symptoms 

Aboveground symptoms range from very slight to severe 

(Fig. 79 A-C, Plate 63) and include mottle, mosaic, crinkling, 

and rolling of leaves; stunting of shoots; leaflet deformation and 

twisting; and some rolling of the top of the plant. Severity is 

influenced by virus strain, potato cultivar, and environmental 

conditions. Necrosis of petioles and stems may develop in 

certain potato cultivars. 

- .PVM 

S -nm. 

Fig. 78. Potato virus X infections: A, Gomphrena globosa; B, 

Causal Agent 

particles are straight to slightly flexuous rods 650 X 12 

The thermal inactivation point is between 65 and 70°C; 

dilution end point is 10-2-10-4; 

20 

and infectivity is retained at 

0 Samsun tobacco; C, Havana tobacco inoculated leaf with 

clear ring spots and leaf of same plantwith systemic vcin clearing. 

D,Electron micrograph of potato virus X particles (X83,000). (B, 

Courtesy J. Munro) 

C for two to four days. The virus is a good immunogen. 

Cytopathology and Histopathology 

Numerous PVM rods and virus aggregates occur in the 

74

cytoplasm of infected potato cells (Fig. 79E). These include or approximately 24'C and abeve. 

neither pinwheels nor pinwheel-related structures. No virus 

particles and or aggregates are found in chloroplasts, Other Hosts 

mitochondria, or nuclei. PVM infects mainly the Solaraceae but also members of the 

Epidemiology 

Transmissi ,i by mechanical inoculation with infective sap or 

by tuber or stem grafting can be achieved with ease. True seed 

transmission has not been demonstrated. Most PVM strainsare 

aphid-transmissible in the nonpersistent manner by Myzus 

persicae and less efficiently by Macrosiphum euphorbiae, 

Aphisfrangulae, and A. nasturtii. Strains differ in efficiency of 

transmission by aphids. Symptoms are masked at temperatures 

I, ,1_4French 

Fig. 79. Potato virus M (PVM): A, mild symptoms; B, healthy 

control; C, severe symptoms in Kennebec; D, local necrotic 

lesions of PVM on red kidney bean; E,aggregate of PVM particles 

(v)and mitochondrion (m)in potato parenchyma cells. (Dand E, 

Courtesy C.Hiruki) 

Chenopodiaceae and Leguminosae. 

Local dark green or yellow 

local chlorotic 

spots in Chenopodium 

rings or necrotic 

quinoa and 

spots in Gomphrenaglobosa are 

produced by some PVM isolates only. Symptoms in Datura 

meiel are local chlorosis or necrosis and later, systemic necrosis. 

Lycopersicon chilense exhibits epinasty, distortion, stunting, 

and abscission. L. esculentum (tomato) is susceptible to PVM 

but remains symptomless and is immune to potato virus S. 

In Solanum rostratum, necrosis is systemic. In Nicotiana 

debnevi, local brown ringlike nccrotic lesions are produced by 

some PVM isolates only. Phaseo'us vulgaris cv. Red Kidney 

exhibits local necrotic lesions on the primary leaves (Fig. 79D). 

bean is a convenient and reliable local lesion host for 

quantitative investigations of PVM. 

In Vigna sinensis, local brown necrotic lesions are produced. 

N. tahacum and Ph"vsarisfloridana are nonsusceptrible. 

To distinguish between PVM strains. L. chilense and the 

potato cultivars Kennebec and Prinslander are useful. 

Control 

I) Use disease-free virus-tested seed tubers. 

2) Cont'ol aphid populations. 

3) Rogue infected plants when first found in the field. 

4) Infected potato can be freed by apical meristem culture 

only or by combining heat treatment vith axillary bud culture. 


BAGNAIL, R. H., R.H.LARSONand J.C.WALKER. 1956. Potato 

viruses M, S and X in relation to interveinal mosaic of the Irish 

Cobbler variety. Wis. Agric. Exp. Stn. Res. Bull. 198. 45 pp. 

BAGNALI., R. H.. C. WETTER, and R. H. LARSON. 1959. 

Differential 

potato virus 

host 

S and 

and serological 

carnation 

relationships 

latent virus. 



potato virus M, 

V ~49:435-442. 

BAWDEN. F. C., B. KASSANIS, and H. L. NIXON. 1950. The 

mechanical transmission and some properties of potato paracrinkle 

virus. ..Gen. Microbiol. 4:210-219. 

HIRUKI. C., E. POUNTNEY, and K. N. SAKSENA. 1974. Factors 

affecting b'oassa:, of potato virus M in red kidney bean. 


KOWALSKA, A.. and M. WAS. 1976. Detection of potato virus M and 

potato virus S on test plants. Potato Res. 19:131-139. 

ROSENDAAL, A.,and t). H.M. VAN SLOGTEREN. 1958. Apotato 

virus identified with potato virus M and its relationship with potato 

virusS. 

J. 

Pages 

P. 

20-36in: 

H. 

F.Quak,J. 

Van 

Dijkstra, 

der Want, 

A. B.R. Beemster,and 

eds. Proc. Third Conf. Potato Virus Dis. 

24-28 June, 1957. H.Veenman and Zonen, Lisse Wageningen. The 


TU, C.. and C.I IRUKI. 1970. Ultrastructure of potato infected with 

potato virus M. Virology 42:238-242. 

WETTER, C. 1972. Potato Virus M. No. 87 in: Descriptions of Plant 

Viruses.Commonw. Mycol. Inst., Assoc. Appl. Biol., Kew. Surrey, 

England. 

(Prepared by C. Hiruki) 

Potato Virus S 

Potato virus S(PVS) occurs worldwide wherever the potato is 

grown. In the temperate zones, it is confined to the potato. 

PVS was first detected not through symptoms but through 

serology during efforts to produce an antiserum to potato virus 

A. 

Symptoms 

PVS is virtually symptomless in most of the common potato 

75

cultivars. Symptoms are slight deepening of veins and rugosity 

of leaves and possibly stunting and a more open type of growth. 

Some strains may cause mottling or bronzing in certain cultivars 

and, when severe, may cause necrotic spots oti the upper 

surfaces. Older leaves in the shade may develop greenish spots 

instead of turning uniformly yellow. Controversy exists as to 

whether PVS alone consistently reduces yield, but losses of 

10-207 have been reported. 

CatLsal Agent 

PVS particles are straight to slightly curved filaments, 

approximately 650 X 12 nm. Thermal inactivation is 55-6 0 ' Q 

dilution end point in crUde potato sap is about 10 U;and 

longevity in vitro at 20'C is about four days. 

PVS isstrongly antigenic, and for convenience and reliabdlity 

in diagnosis, serology is generally used. Plants in the field are 

best tested just before flowering by sampling lower and middle 

leaves. Viru:s concentration may be low early or late in the 

season. 

In tube tests, the precipitate is flocculent. The simple slideagglutination 

test can be used under ideal conditions, but 

inicroprecipitin, bentonite, or latexflocculationorgel-diffusion 

tests are preferred. 

Epidemiology 

PVS is tuber-perpetuated, readily transmitted mechanically 

by infective sap, and reputed to be spread in nature primarily 

by contact with diseased plants. Certain strains are transmitted 

by the aphid I' :rs persicae in a nonpersistent manner. 

Transmission tests with true seed have been negative. 

Other Hosts 

Ir. Nicotiana dehne'vi, systemic vein clearing occurs after 20 

days, spreading from the leaf tip toward the base (Fig. 80A). 

Later, leaves develop interveinal or veinbanding mottle at 200 C 

with a 16-hr day at 1,000 FC. Andean isolates give mild mosaic 

or are sy(ptomless. 

So/anum rostratunm and Saracha un/re/lata (affected by sone 

strains only) show necrotic spotting on inoculated leaves in 20 

days, and later, on systemically invaded leaves. Andean strains 

do not cause necrotic spotting. 

Datura meteI, Pi.vsalis philadelptica.aind P. puhescens are 

systemically infected without symptoms. 

Capsicum annuurm, Lycopersicon esctuh'nltun, Nicandra 

pnhrsalode is,N o aa glutinu, A'. sar'eesris, N. abacu, 

and Ph/'Vsa/is floridlata are immune to infection. 

Local lesions occur in Chenopoditim album and C. 

amaranticolor after 40 days (Fig. 80B and C), in C. quiroa 

16-20 days), and in C'antopsis tetragonoloha(6-10 days). 

Most Andean strains (but not all) are systemic in C. quinoa 

and C. amaranticolor. 

Resistance 

Well-defined mature plant resistance is present in potato, so 

ransissionmst occur relatively early in the season if tuhcrs 

are to become infected. 

Certain cultivars, including Bintje, Katahdin, aid Kennebec, 

are moderately resistant to reinfection. [he cultivar Saco and 

some of its progeny hiave' strong general resistance, which is 

inherited as a simple recessive: this resistancc can be overcome 

by grafting, and plants carry the virus virtually without 

symplams. 

Resistance ofthe hypersensitive type ispresent in a cultivar of 

Solanumt tuberosum ssp. antdigena this characteristic has been 

brought through several crosses with S. tuerosum. A similar 

type of resistance has been reported in the diploid S. 

11egistacrolohbtum. 

Control 

o) VS-fr e clones (f susceptible cultivars have been 

esta blished by rneristcm tip culture. In some regions these can be 

maintained relatively free from reinfection, but in other regions 

this is rlot so. possibly due to an insect vector. Indexing tubers 

and testing mother plants intended for production of stem 

cuttings, followed by release of elite seed. are the accepted 

practices. 

2) Roguing is not effective. 


BAFRE(KE, M. .. 1967. t'"berempfindlichkeit gegen das S-Virus der 

Kartoffel i.i cineh boliviarischcn Andigena-Kion. Ziichter 

37:281-286. 

BAGNAI.I., R. II.. C. W- ILR.art'l R. Il. LARSON. 1959. I)ifferential 

and host 

carnat and serological relationships i n late n 


t 

potato \ irus 

\i 

10, potato virus S, 

I\ h\ topa tho logy 49:435 

BAiNAI.I.. R. -442. 

H.,and I). A. YOt NG. 1972. Resistance to virus Sin the 

potato. Am. Potato .l. 49:196-201. 

de ()KX. .1 A.. ed. 1972. Viruses of Potatoes and Seed-Potato 

Production. Pudoc. Wagcningei. Ihe Netherlands. 233 pp. 

MacKIN)NON. I. P.. aid R. H. BA6iNA1.1. 1972. Use of Vicotiana 

dehoevii to detect \iruses S. X. and Y in potato •d stocks, and 

relative susoe,,Ihibility of six cointion varieties to potato virus S. 

Potato Res. 15:81-85. 

SII IPA R1). .1.I.. and I.. 

principles 

F. (.A I-I. 

ol seed 

N. 1975. 

potato 

Critical 

certification. 

analses of 

Ana.i. 

the 

Re. PIhitropathol. 

13:271-293. 

STACF-SMIr11. R.,and F. C. MEI.OR. 1968. Eradication of potato 

viruses X and S by ihermotherapv and axillar' bud culture. 

Plrytopathology 58:199-203. 

Fig. 80. Potato virus S: A, systemic vein clearing in young leaves of Nicotiana dobneyi; B, local lesions in young and old leaves of 

Chenopodium amaranticolor. (A,Courtesy R. H. Bagnall) 

76

WETTER, C. 1971. Potato virus S. No. 60 in: Descriptions of Plant 

Viruses. Commonw. Mycol. Inst.. Assoc. Appl. Biol., Kew, Surrey, 

England. 

(Prepared by !,.1.1agnall) 

Potato Virus T 

Potato virus T (PVT) occurs in Peru. Bolivia, and probably 

elsewhere inthe Andes. 

Symptoms 

PVI produces no :-;'ous symptoms in several ituherosumn 

and andmiena types but may produce mild mottle or slight vein 

necrosis and chlorotic spots, and sone andigena types may 

develop top necrosis after grafting. New shoots are symptomless 

bi: infected. 

Causal Agent 

PVI particles are flexuous filaments 640 X 12 rim, helically 

constructed %%ith3.4 tim pitch: their substructural detail differs 

from that of other viruses (Fig. 81 ). P'V] is serologicallv related 

to. but distinct froni. the apple stem grooving virus. Its thermal 

inactivation point is about 65°C: dilution end point is 10-5and 

hotgevitv in vitro is twvo to four (lay's. 

Epidemiology 

I'V I isreadily transmitted mechanically by tubers and sap. It 

is[ot transmitted by the aphids Mivzus'persicae or ilacrosiphum 

eulthor!iae. It is seed-transmitted in Vicandra ph.tisa/odes, 

)atura strantonium, and Solanumn demissuin, pollentransmited 

to seed but not to mother plants inS. demissum, 

ari( not pollen-transriitted in X. ph.rs'alo'es and D. 

.vlrtmonlium~. 

Other Hosts 

I hese include the tuber-bearing S. demissin, S. 

.steitotonum,. cIiaico n'i, S. spegaz:inii, S. vernei, and S. 

acaule. PVF is readily transriitted by inoculation with sap and 

has a wide host range. infecting 43 of 56 species tested. Most 

solainaceois species remain svmptoniless or develop on!y mild 

symptotms. 

I'/ia.solu.%vularis c\. Piinto and Prince are good local lesion 

hosts when heavily shaded after inoculation, later developing 

svstemic necrosis followed by plant recovery, 

Chenlopodittni quinoa, a good host lor propagating the virus, 

is svstemically infected. 

C. anaranticlor is the best diagnostic host: it develops 

svsteiric distortion and necrosis. 

Control 

Little is know about diseases caused by PVT. Infected plants 

in stocks can be identified by visual in.pectior, by inoculation 

tests using suitable indicator plants, or by serological tests. 

Infected plants should be destroyed. 

1 / .Phytopathology 

" 

-.."" .. ":.FRIBOURG.C. 

Fig. 81. Particle of potato virus T. Note unusual substructural 

detail. Bar represents 100 rim. (Courtesy L. F.Salazar and B. D. 

Harrison) 


SAI.AZAR. L. F.. and 13.1). HARRISON. 1977. Two previously 

undescribed potato viruses from South America. Nature 

265:337-338. 

SALAZAR. I.. F.,and 13.I). HARRISON. 1978. Host range, 

purification and properties of potato virus T. Ann. Appl. Biol. 

89:223-235. 

'Prepared by L. F.Salazar and B.D. Harrison) 

Andean Potato Mottle Virus 

The Andean potato mottle virus (APMV) is present in Peru, 

Bolivia, probably throughout the Andean region at elevations of 

2,000-4,000 m, and in Andean germplasm collections in 

Europe. 

Symptoms 

Primary symptoms are usually mild patchy mottle and, in 

sensitive cultivars, strong mottle, leaf deformation, systemic 

necrosis, and or stunting. Strong secondary mottle is normal, 

but sensitive cultivars also show delayed emergence, leaf 

deformation, and severe stunting (Plate 64). 

Causal Agent 

Cua 

APMV 

gn 

is a member of the cowpea mosaic virus (comovirus) 

group. Particles are isometric, approximately 28 nm in 

diameter, some full and some empty (Fig. 82C). Two types of 

proteins, small and large, have molecular weights of 20,800 and 

40.100, respectively. The virus is strongly immunogenic and is 

serologically related to some members of the comovirusgroup. In 

N. higelovii sap. the thermal inactivation point is 65-701C; 

longevity in vitro, four to five weeks; and dilution end point,> 

10 . 

Epidemiology 

APMV produces symptoms and multiplies best under cool 

conditions. It is readily transmitted by contact between plants 

and probably also by animal and machinery movement. 

However, a beetle vector is possible because beetles 

characteristically vector the comovirus group. 

Dissemination is through infected seed tubers. 

Other Hosts 

APMV can be transmitted mechanically only to solanaceous 

hosts. 

Nicotiana higelo'ii shows a mosaic of dark green blotches 

(Fig. 82A and B). Leaf tips develop necrotic areas and holes at 

1518o C. 

Lrcopersicon chilense exhibits veinclearing, interveinal 

mosaic. chlorotic spotting, and sometimes epinasty. 

Andean weeds, Nicandra phyisalodes, Datura siramonium, 

Ph'.salis peruviana, and L.pimpinellfoliutn are susceptible to 

mechanical inoculation. 

Control 

Roguing is effective because APMV induces conspicuous 

symptoms. 


FRIBOURG, C. E., R.A.C. JONES, and R. KOENIG. 1977. Andean 

potato mottle, a new member of the cowpea mosaic virus group. 

67:969-974. 

E.. R. A. C. JONES. and R. KOENIG. 1979. Andean 

potato mottle virus. No. 203 in: Descriptions of Plant Viruses. 

Commonw. Mycol. Inst.. Assoc. Appl. Biol., Kew, Surrey, England. 

4 pp. 

(Prepared by C. E. Fribourg and R. A. C. Jones) 

77

Andean Potato Latent Virus 

Andean potato latent virus (APLV) is common throughout 

the Andean region at 2,000-4,000 m and occurs in collections 

of Andean germplasm in Europe. 

Symptoms 

Primary infection is often symptomless but may cause 

V. 

: 

.V 

' 

mosaics and or chlorotic netting of minor leaf veins (Plate 65). 

Secondary infection normally causes mild mosaics, but 

chlorotic netting of minor le.f veins and rugosity may occur. 

Cool conditions favor symptom de\clopment. 

Causal Agent 

APLV resembl_2s members of the turnip yellow mosaic group 

and is therefore considered a strain of eggplant mosaic virus. 

Particles are isometric and about 28 nm in diameter; some are 

full and some empty. The molecular weight of the protein 

subunits is 19,600-20,700. The virus is strongly immunogenic. 

Two serologically distinct strains are recognized (Col-Caj and 

Hu). 

Dilution end point is 10-7-10 ' and longevity in vitro is up to 

three weeks. Thermal inactivation ranges from 65 to 80'C, 

depending on the strain. Survival to 90' C has been claimed for 

Col-Caj in Nicoiiana glutinosa sap. 

Epidemiology 

APLV produces symptoms and multiplies best under cool 

conditions. It is readily transmitted by contact between plants 

and probably also by animal and machinery movement. The 

potato flea beetle. Elfitrix, is a vector of low efficiency. 

Transmission from infected potato ploits to their tubers is 

erratic. The virus is transmitted at low frequency in potato true 

seed. 

Other Hosts 

APIV has been found occurring naturally only in potato. It 

can be transmitted mechanically to species of the Solanaceae, 

Chenopodiaceae, Cucurbitaceae. and Amaranthaceae, 

including the Andean crop plants ('henopodiwm quittoa and 

A ,naranthus edulis. 

AIn higeloi'ii. mosaic and characteristic netting of minor leaf 

veins develops with all isolates (Fig. 83), and most isolates also 

cause faint to distinct local lesions in inoculated leaves. More 

virulent isolates may also cause systemic necrotic flecking and 

starlike lesions. 

N. clevelamli exhibits faint necrotic or chlorotic spots or 

rings on inoculated leaves with most isolates. Systemic 

symptoms are mosaic and necrotic orchlorotic netting of minor 

leaf veins. 

Control 

I) Clonal selection during initial multiplication of seed 

stocks is most effective. Tubers from infected plants often 

escape infection. 

2) Roguing iseffective only when conspicuous symptoms are 

present. 

Fig. 82. Andean potato mottle virus in Nicotiana bigelovii, causing 

systemic necrotic areas and holes (A), or dark green blotchy 

mosaic (B). C,Virus particles in apartially purified preparation. 

The empty shells are dark colored. (A and B, Courtesy C. E. Fig. 83. Andean potato latent virus mosaic and necrotic netting of 

Fribourg; C and D, courtesy E. Lesemann) minor veins in Nicotiana bigelovii. (Courtesy C.E. Fribourg) 

78

3) Resistance has not been identified. 

4) Applications of insecticides may help decrease spread 

when populations of Epitrixare high. 


FRIBOURG. C'.E.,R. A. C. tONES, and R. KOENIG. 1977. Host 

plant reactions, physical properties and serology of three isolates of 

Andean potato latent virus from Peru. Ann. Appl. Biol. 86:373-380. 

GIBBS. A. ... E. HECHIT-POINAR, R. I). WOODS, and R. K. 

McKEE. 1966. Some properties of three related viruses: Andean 

potato latent, l)ulcamara mottle and Ononis yellow mosaic..I. Gen. 

Microbiol. 44:177-193. 

JONES, R.A. C'..and C. F. FRIBOURG. 1978. Symptoms induced by 

Andean potato latent virus in wild and cultivated potatoes. potato 

Res. 21:121-217. 

(Prepared by R. A. C. Jones and C. E. Fribourg) 

Cucumber Mosaic Virus 

Cucumber mosaic virus (CMV) causes chlorosis and a 

blistering mottle of leaves. Leaflet apices are usually elongate 

and margins distinctly wavy. Following mechanical 

inoculation, mild delimited chlorosis develops over a large part 

of the leaf surface as intense yellow flecks. Yellowing spreads 

slowly from the inoculated leaf to the petiole and isfollowed by 

complete collapse of the leaf'. Symptoms successively develop on 

each higher leaf. The virus is recovered only from plant parts 

with symptoms. CMV on potato occurs naturally in England 

and Scotland. Itis readily transmitted by rubing with infective 

sap and by aphids in the nonpersistent manner. 

CMV i:usually not transmitted by tubers and has not 

become an economic problem. 


MacARTHUR, A. W. 1958. A note on the occurrence of cucumber 

mosaic virus in potato. Scott. Plant Breeding Sin. Rep. pp. 75-76. 

(Prepared by W. J.Hooker) 

Tobacco Mosaic Virus 

Tobacco mosaic virus (TMV) is not a problem in potato 

production, having been reported once in field plants and in the 

wild in S. contmersonii. 

Mechanical inoculation of commercial cultivars results in 

localized infection, local lesions or blotches, drop of inoculated 

leaves, and rarely with systemic invasion in the current year. 

Usually infection is not tuberborne into the second year. 

Green strains 

Green strin 

of TMV may be almost 

rugoseMmaic 

latent or cause 

symptoms suggestive of rugose 

virulmst lafletorcas 

curl, and malformation. Yellow strains may exhibit striking 

yellowish flecking and leaflet malfo'mation. Infected tubers 

develop multiple thin, weak stems, resembling those of witches' 

broom. Mosaic symptoms of TMV infection vary with the 

potato cultivar and virus isolate and may resemble those of 

potato viruses X. Y, or A. 

Although resistance is present in commercially available 

cultivars of S. tuberostin, the virus is a potential threat, 

Susceptible commercial cultivars have apparently not been 

developed. Systemic infection readily transmitted through seed 

tubers occurs both within selections of S. tuberosum and also 

within certain wild species, including S. acau. 

Severity of reaction is greater at 24-28°C than at lower 

temperatures. 

Potato plants may be killed when doubly infected with potato 

virus X and TM'V. 


HANSEN,H.1.1960. Tobacco mosaic virus carried inpotato tubers. 

Am. Potato .1.37:95-101. 

L.UI. K. C., and J. S BOYI.E. 1972. Intracelluli., morphologN of two 

tobacco mosaic virus strains in,and cytological responses of, 

systemically susceptible potato plants. Phytopathology 

62:1303-1311. 

SIEMASZKO. J. 1961. Wirus mozaiki tytoniowej na ziemnaikach. 

Biul. Inst. Hodowji Aklimatyzacii Roslin 5:13-18. 

(Prepared by J. S. Boyle) 

Potato Mop-Top Virus 

Potato mop-top virus (PMTV) occurs in the Andean region 

of South America, in Northern and Central Europe, and 

probably also in other parts of the world where the powdery 

scab fungus, Spongospora subterranea, occurs. 

Symptoms 

PMTVcauses yield decreases ofup to 26Vi insensitivecultivars 

and can have severe effects on tuber quality. Influenced by 

cultivar and environment, it causes variable symptoms. The 

most important of these are: I) bright yellow (aucuba) 

markings: blotches, rings, or diagnostic V-shapes (chevrons), 

especially in lower leaves; 2) pale V-shaped markings in upper 

leaves; and 3) stunting of stems and shortening of internodes, 

involving some or all of the stems of a plant and giving the 

disease its name (Plate 66). 

Primary infection from soil to tuber rarely spreads to the rest 

of the plant. Tubers are infected symptomlessly or with raised 

rings on the surface that, in sensitive cultivars, may be 

associated with necrotic arcs in the flesh (Plate 67). These arcs 

are induced at the virus invasion front in the tuber bya sudden 

drop in temperature, but they do not limit further virus spread. 

Secondary infection occurs only in some of the tubers produced 

malformation, 

by an infected gross plant. or In fine sensitive superficial cultivars. cracking, it maysurface 

cause 

blotching, and' or necrotic arcs centered on the stolon (Plate 

68). 

Causal Agent 

Particles are elongated, have ahollowcore, and are normally 

defective because of terminal uncoiling of the protein helix. 

They are 18-20 nm wide, but of many lengths. frequently 

250-300 or 100-250 nm. The helix pitch is2.4-2.5 nm, and the 

molecular weight of the protein subunits is18,500-20,000. The 

virus is moderately immunogenic and seems to be distantly 

related serologically to the tobacco mosaic virus. 

Thermal inactivation is 75-80'C; dilution end point, 

0--10' and longcvitinvroupo10wes 

ty in vitro, up to 10 weeks. 

Disease Cycle 

PMTV survives inside Spongospora subterranea resting 

spores for several years and is transmitted to roots by zoospores. 

The most important means of long-term survival in infested 

land is in dormant resting spores. Weed and other crop species 

in the Solonaceae and Chenopodiaceae, which are hosts of both 

virus and vector, are potential alternative natural hosts. The 

virus is introduced to uninfested fields when infected seed tubers 

carrying powdety scabs are planted. Also. short-distance 

movement may occur in infested soil transported on farm 

machinery or on the feet of farm animals. Healthycrops become 

infected when planted on infested land. 

Epidemiology 

Symptom production is especially sensitive to light and 

79

temperature eonditions. S'ystemic ioNsellet seenlls to occur 

through the X\ll and not lie plloent. PMIV caises distinct 

symptoms in potlato onl under cOol conditions, and cold datap 

clilttS tli\Ol its spread b scctor /oospoies. II Northern 

Europe. the disease seldoni occiis in areas witlt all annual 

rainfall of less than 760 inun. 

Other Host% 

PMTV is kno\n naturally onl[\ in potato bitt can be 

transmitted inechanicall\ to spcCies of the Solanaceae. 

Chenopodiaccae, and r\i/oace;ic 

[il 0tenol)

nm), which do code for coat protein synthesis (Fig. 85C). 

Protein-coated 

noltUm on tins+ long particiles and short of rods hoth are lengths. produced ManlV on 1 strains %'lcitlhe of 

I RV are known and illOCILIII paricle may i e COI~fiWbth of differentiated lngth. surologicall. Man'v trais OfCuIL 

Isolationti Of I RV from potato is ustl Ujl difficult, and 

diflicult increases \ ith time after har\ est. IR V is isolated from 

soil b mechanically inoculating leaves oftest plants with roots 

of hailt plants (tobacco Or ciucunber triturated in buffer, 

Epidemiology 

Incidence Of spraing is liglcst ill Sandy ',oils. I\e le species 

of sttubh \ tomll u nr ~itide ( Trich/ro r s or -Iaratr/icodorusl 

transm it I RV: io \c\c . riot ill f these feed oil potato. 

od-i rU. sPp. gcnerallI Icc- ill sands, opeln-textured soils 

and ha.\e been found at depths of 8f0- 100 cm. Populations of' 

"'iulh:,ori.% hac renlfiaied inftcti\c in moist soil ma rintained in 

the lhoirator\ lfo as long as like \Cars in tie absence Of athost. 

I lie \ iruns is not retained throughfilt egg Or the molt. 

Priimar\ tuber infect ion follows inemathodes feeding directly 

oi uhers. Ssfsernic rnfectioin Oiftubers fromi rioot feeding sites 

has not beeun deonoi rated. . slt\nfrtile m CitClt o01"R N occurs 

iost olien l 21-25 '' and is sometimes enhanced by pruning. 

A, hliugh tile discase can he transrmitted through seed tubers, 

transmiussuion in this minriner is infrequent, and te virus is 

iuhltiniatcls sel-eitiiatil. Nuns iruilicroLus populatiorns of tile 

Irihiul,rol rilrll\ acquire the \iri, frot infected potato 

plirits. and tuher dissCmililation Of I RNV from infected to virus- 

Irce ficlds has not been deinonrstated. Opinions differ as to tile 

irrrpiOr ltaiC,(f tulbetr disserinatir. I lic \irus can be SeedrIrIlI'rniid 

iii fhosts. 

other Mo\ement iif sioil infested \with 

k i hlferoti,s ltierialodcs is priibaihl. t. liost effective nleans if 

if isse iiiinil i . 

Other losts 

I 10 can infect inore thran 400 ninocotyledonous and 

LlnCOr\ ledilorUS spcies in user 51) ~airrilies. Often it does trot 

hconlc ssstrlnlic. re-rlainrill in otlls iof plants that Show' no 

foliage s\ tritorris. 

In ( ]t tt;'v oiiudm amaranicolor,t lie si rils prod rices necrotic 

local lesions. soie spreading, bit the sirus is not systernic. I lie 

hist Is used for diagnosis indf for local lesion assay. 

In ( iil lim iis.,.i 'l hilorotic or Iccrotic local lesions occuir. 

I his is i diagnrostic houst, used for local lesiion assay, and is a 

go id hait pla tt Is roots become infected from nemalode 

feed i itu. 

11 .irofiall'i' ch'elandii.inoiculated lea\ es are sVmptonless 

or lia\e ehirtotie ir necrotic lesions. Systenicalis infected 

Iea\e,, ts'\clp e\\ syvniptltois orr variable ailnounts of necrotic 

flecing and distortion. I his is a diagnostic host, alsi used for 

increasii g 5iris titer. 

Necrotic loc-ral lcsions are formed Onl Phl.u ,olux vnaris ill one 

o thrCC d;1\s. Ilie diseise is iot s\stelenic. 

V tata

WAI.KINSHtAW, C. ].. and R.11.LARSON. 1959. Corky ringspot of 

potato. A soil-borne virus disease. Wis. Agric. Exp. Sin. Res. Bull. 

217. 31 pp. 

(Prepared by 1). P. Weingartner) 

Potato Yellow Dwarf Virus 

Potato yellow dwarf virus (PYDV) occurs in Canada and in 

the United States in Michigan, New York. and Wisconsin. 

Disease outbreaks have not been reported for almost 40 years. 

Symptoms 

Vines from infected seed pieces are dwarfed and brittle, and 

Vine eedpiees frm ifeced re wared nd ritleand 

the entire plant has a yellowish cast. I.eaflet margins roll 

upward, but the longitudinal axis of the leaflet curves 

downward (Plate 71). Pith necrosis of stems is common, 

appearing shortly after foliage chlorosis. Necrosis beginning 

near the growing point may eventually extend the length of the 

stem (Fig. 86). 

Tubcrs are usulally few, small, and deformed. A dark brown 

necrosis, which may easily he confused with heat necrosis, 

occurs 

i 

throughout the tuber, with only the xylem elements 

apparently unaffected (Fig. 86). Failure of infected tubers to 

germinate, resulting in widespread stand reduction, is 

characteristic. 

Causal Agent 

'YI)V isbacilliform, with particles measuring about 380 X 75 

It. 

*; 

fVirology 

Fig. 86. Yellow dwarf virus: tuber surface cracking, internal 

necrosis, and pith necrosis of stem. (Courtesy J. H. Muncie) 

82 

nm. Virions are closely associated with the nucleus of infected 

cells. Approximately 20%' of the virus is lipid. Of the four major 

structural proteins (with molecular weights of 22, 33, 56, and 78 

X 10 ). the largest is a glycoprotein. The virus contains singlestranded 

ribonucleic acid (molecular weight 4.6 X 10"'). 

Infectivity of PYI)V in Nicotiana rustica sap is retained for 

2.5-12 hr at 23-27 - 

0 C. Dilution end point is usually about 10 

and thermal inactivation, about 50'C. IPYDV does not 

withstand desiccation in N. rustica leaves nor prolonged storage 

in frozen leaves. Purification of PYI)V is difficult because the 

virus is quite labile. 

Epidemiology 

PYDV, the only known virus borne by leafhoppers that isalso 

mechanically transmissible, consists of two closely related 

forms, one transmitted by Aceratagallia sanguinolenita but not 

byrAgalona 

by Agallia 

transmittedand another transmitted wit t nr 

constrictaand another tiansmitted with tile inverse 

vector relationship. Agalha quadrupuncata has been reported 

to transmit both forms. PYDV is propagative in the vector. No 

transmission through true seed his been recorded. PYDV is 

c r m o erion t oee xt in poaor . 

carried from one generation to the next in Potato tubers. 

High temperatures enhance vine symptoms and reduce plant 

emergence from infected tubers, whereas low temperatures 

increase plant or sprout emergence and suppress vine 

s p l s mu s 

symptoms. 

Other Hosts 

In addition to solanaceous plants, vectors have transmitted 

the virus to members of Compositac, Cruciferae, Labiatae, 

Leguminosae. Polygonaceae, and Scrophulariaccae. 

N. rushica and N.glutinosa can be mechanically inoculated by 

rubbing. 

In N. rustica, primary lesions Occur, followed by systemic 

invasion. This host serves for virus assay and propagation. 

hChr.santhemtnn leucanthetan var. pinnatqiidn, oxeye 

daisy. is the principal source of infection for potato crops. 

Control 

I) Plant certified seed produced in areas where PYDV is not 

found. 

2) Plant certified seed produced as far as possible from clover 

fields in infested areas to avoid the clover leafhopper, 

Aceratagallia sanguinolenta, which can harbor the virus 

through the winter. Table stock potatoes should not be planted 

adjacent to clover fields in infested areas. 

3) Plant tolerant cultivars. Cultivars shown to be fieldtolerant 

are Chippewa, Katahdin. Russet Burbank, and Sebago. 


BI.ACK, I.. M. 1937. A study lof'potato yellowdwarf in New York. N.Y. 

Agric. Exp. Sin.. Cornell. Mem 209. 23 pp. 

BLACK. I..M. 1970. Potato yellow dwarf virus. No. 35 in: Descriptions 

of Plant Viruses. Cormonw,. Mycol. Inst., Assoc. Appl. Biol., Kew, 

Surrey. England. 

HStU, II. T.. and .. M. BI.ACK. 1973. Polyethylene glycol for 

purification of potato yellow dwarf virus. Phytopathology 

63:692-696. 

MacI.EOI), R., . M. BL+ACK, AND F. H. MOYER. 1966. The fine 

structure and intracellular localiation of potato yellow dwarf virus. 

29:540-552. 

tMUNCIE, .1.II. 1935. Yellow dwarf disease of potatoes. Mich. Agric. 

Exp. Stn. Spec. Bull. 260. 18 pp. 

WAI.KER,-1. C.. and R. II. I.ARSON. 1939. Yellowdwarf ofpotato in 

Wisconsin. .1.Agric. Res. 59:259-280. 

(Prepared by H. Darling and S. Slack) 

Alfalfa Mosaic Virus 

Alfalfa mosaic virus (AMV) is found worldwide but is 

generally considered of little economic importance in potatoes.

Symptoms 

AMV may induce 

Other 

predominantly 

Hosts 

calico symptoms on foliage Natural 

(Plate 

infection 

72) or necrotic 

is known 

symptoms 

for 47 plant 

in tubers. 

species 

Calico 

in 12 familiessymptoms 

are over 300 species 

pale 

have 

to bright 

been 

mottling 

experimentally 

or blotching 

infected. 

ofpotato 

AMV 

leaflets, 

is 

with all or highly variable, with numerous 

large 

strains 

sectors 

causing 

of leaflets 

different 

yellow. The plant may be slightly 

stunted. Leaflet 

reactions 

necrosis 

on test 

is 

plants. 

common and may extend into 

stems 

the 

and to the tubers. 

Phaseolus vulharis (French bean) and Iligna sinensis 

Tuber necrosis, 

generally show 

usually 

local 

visible 

lesions 

by 

and or 

harvest, 

systemic 

begins 

infection 

just 

and 

beneath 

serve 

gs diagnostic and assay p orts. 

the epidermis at tile stolon attachment and later spreads i'ciafahaand Pisim satitnu 

throughout 

exhibit black, 

the tuber, 

necrotic, 

leaving 

local 

scattered dry, corky areas. Tubers 

may be 

lesions 

misshapen, 

and stem 

cracked, 

necrosis; 

and 

plants 

few per 

die. 

plant. Disease severity In Chenopodium ainaranticolorand 

varies with virus strains 

C. quinoa. 

and 

local 

potato 

lesions 

cultivars. and systemic chlorotic and necrotic flecks are produced. 

Causal Agent 

Nicotiana tabacum is a good propagation 

necrotic or chlorotic 

species, 

local 

with 

lesions and systemic 

AM 

mottle. 

Vconsists of sc\eral differently sedimenting nucleoprotein 

species (Fig. 87), each with a width of about 18 

containing 

nm and 

about 

Control 

18"i ribonucleic acid (RNA). The larger I) Potatoes should 

particles 

not 

appear 

be planted 

to be bacilliform, 

adjacent to 

with 

known 

approximate lengths of reservoir 

58, 49. 38. 

hosts 

and 

such 

29 nm, 

as alfalfa 

whereas 

or clover, 

the smallest 

especially 

particle, 

when cultural 

19 rim in practices promote 

diameter, 

aphid movement 

is probably 

into 

icosahedral. 

tie potato 

Molecular 

crop. 

weights for the 2)Volunteeralfalfa, 

encapsidated 

clover, 

RNAs 

or potato 

are about 

plants 

1.3, 

that 

1.1. 

may 

0.9. 

serve 

and 

as 

0.3 X 10'. A an initial source of inoculum should be removed 

single structural 

from a 

protein 

potato 

with a molecular weight value between 

24,500 and 32.600 

field. 

has been reported. The largest three 3) Visibly infected potatoes should 

nucleoprotein 

be rogued 

components 

during the 

or all four RNA molecules are 

necessary 

growing 

for infection. 

season. 

The structural or coat protein can be 4) Certified 

substituted 

seed 

for 

should 

the smallest 

be planted 

RNA 

each 

molecule 

year. 

to initiate infection. 5) Spraying to reduce vector 

AIMV 

populations 

is moderately 

is of dubious 

inmunogenic. 

value 

and no serological because of the short time required for transmission. 

relationship to other viruses has been found. 

Thernal inactivation is usually between 60and 65'C but may 

range from 50 to 75'C. The dilution end point isgenerally in the 

\icinity of 10 


. and longevity in vitro is from 4 hr to four days. BEEMSFiER, 

Infectivity 

A. 1. 

in leaves 

R.. and 

persists 

A. ROZENDAAI. 

at -18C for 

1972. 

more 


than 

viruses: 

a year. Properties and symptoms. Pages 115-143 in: .1.A. de l3okx, ed. 

Viruses 

Epidemiology 

of Potatoes and Seed-Potato Production. Pudoc, 

Mechanical inoculation 

Wageningen. The 

with 

Netherlands. 

sap by rubbing 

233 pp. 

is generally BLACK, I.. M., and 

effective. 

W. C. PRICE. 

AMV 

1940. 

is 

The 

transmitted 

relationship 

in 

between 

tile styletborne or viruses of potato calico 

nonpersistent 

and alfalfa mosaic. 

manner 


by as many as 16aphid species, including 30:444-447. 

Myzusersicae. rcgrfigand In pota potao.ed to, AMV AfM may may es he transmitted tansmitted by b tuber-. tuber- 1OI. J. F.,I.. ;VI.0iTEN-I)OIING. and F.M..J.JASPARS. 

core 

.Afunctionalequivalence 1971. 

graftitg and can becarried 

of topcornponent 

fromseason 

aRNA 

to season 

and coat 

in 

protein 

tubers, in the initiation of infection by alfalfa mosaic 

Although 

virus. 

AM 

Virology 

Vis seed-transmitted in some alfalfa varieties 

in chili 

and 

pepper, trarsmission 

46:73-85. 

through true potato seed has not 130S, I.,and E. M.J.I ASPARS. 

been demonstrated. 

1971. Alfalfa mosaicvirus. No. 46in: 

criptins of Plant Viruses. Commonw. Mycol. Inst., Assoc. 

. , • .%, * 4 . 9 

Fig. 87. Alfalfa mosaic virus particles: A,of various sizes in purified preparation, fixed in 2%glutaraldehyde and negatively stained in 1% 

phosphotungstate; B, one type of particle aggregation occurring in infected tissue (ch = chloroplast, v = virus). Note the pronounced 

swelling of virus particles in A versus those in B. Bars represent 100 nm. (Courtesy G. A. de Zoeten and G. Gaard) 

.4

Appl. Biol.. Kew. Surrey, England. 

CERVANIES. J., and R.11.I.ARSON. 1961. Allala mosa: Oirus in 

relation to tuber necrosis in the potato xariet\ Red L.a Soda. is. 

Agrie. Exp. Sn. Res. ull. 229. lip. 

lUt+L. R. 1969. Alfala mosaic ,itus Ad\, Virus Res. 15:365-433. 

OS\ Al.1)..I, W. 1950. A strain ol the allatta-mosaic virus causing %,inc 

aid tither necrosis il potato. Pl,,topatltholhg, 40:973 -991. 

(Prepared by S. Slack) 

Potato Aucuba Mosaic Virus 

Potato aucuba mosaic virus (PAM V) is found worldwide but 

is not common. It is also called tuber blotch. 

Symptoms 

These depend bit itotn Nirs strainaand potato cultivar( Fig. 88 

A and B). They include bright yellow spots, mostly on the lower 

leaves: deformation and stunting \without Vello" spots: mosaic 

and top necrosis: and necrosis and sometimes deformation of 

the tubers (tuber blotch) (l'ig. 88(). 

Foliage symptoms may be lacking in the second \ear after 

infection and later. liher necrosis generally de\clops duiring 

storage and its de\elopaient is more sexere at higher 

temperatures (20-24°C) than at lower ones. Necrosis of the 

tubers can be both on the surface lbrown patches and sunken 

brown areas) atnd in the flesh. 

AB i 

!;" 

1 

. " .!Bright 

C W 

Fig. 88. Potato aucuba mosaic virus: A, bright yellow mosaic 

mottle; B, deformation; C, tuber necrosis; D, necrosis of 

inoculated leaves and systemic leaf necrosis in pepper. (Courtesy 

J. A. de Bokx) 

84 

Originally. P)AM V (potato virus G) and potato tuber blotch 

virus (potato virus F) were described as different viruses. Now 

the latter isconsidered to bea strain of PAM V. Many strains are 

known and can best be differentiated by using various potato 

cultivars. 

Causal Agent 

PAMV has filamentous particles. 580 am long and 11-12 nrn 

wide. The virus istransmitted mechanically and by aphids in the 

nonpersistent manner (stVlethorne) when aided by "helper" 

viruses, including potato viruses Yor A. 

The virus is strongly immunogenic. Antisera can be used for 

identificatiotn by the precipitina test. 

Other Hosts 

On CapCsium annuun, brown, irregular concentric local 

lesions appear after 8-10 days. followed by systemic symptoms 

such as vein clearing, deformation, and severe necrosis (Fig. 

88D) and sometimes by complete killing of the plants. PAMV 

can be differentiated from mop-top virus, which produces 

similar symptons on potato, because the latter does not infect 

C. annu 1 systemically. 

Nicotiana glitinosa exhibits mottle and vein banding. 

In N. tahacum. PAMV usually produces symptomless 

systemic infection. 

Some strains produce small round yellow spots on lower 

leaves of LYcolersicon em-ulentum. 

Control 

Remove infected plants from seed fields. 


BEEMSTER. A. B. R., and A. ROSENDAA,.. 1972. Plotato viruses: 

lProperties and symptomns. Pages 115-143 in: .1.A. de Bokx. ed. 

Viruses of Potatoes and Seed-Polato Production. Pudoc, 

Wageningen. The Netherlands. 233 pp. 

KASSANIS. B.. and 1). A. (i()VIIER. 1972. Pt.to aucuba mosaic 

si , No. 98 in: I)escriptions of orus. Ilant Viruses. Coanmonw. NIycol. 

Inst.. Assoc. Appl. Riol.. Key,. Surrey, Fngland. 

Mt NRO. .1.1960. lhe reactions of some potato varieties and seedlings 

to potato virus F. Aam. P:ota to .1.37:249-256. 

SMITH. K. M. 1972. A Textbook of Plant Virus Diseases, 3rd ed. 

I orignian. London. 684 pp. 

(Prepared by A. B. R. Beemster) 

Tobacco Ringspot Virus 

So far, Andean potato calico caused by tobacco ringspot virus 

(TRSV) has been confirmed only in Peru, but preliminary tests 

indicate its presence in other Andean countries. 

Symptoms 

yellow areas on the margins of middle and upper leaves 

gradually increase in siue to form large patches or even to affect 

the whole leaf (Plate 73). Most of the plant foliage may 

eventually turn yellow without stunting or leaf deformation 

(Plates 73 and 74). In experimentally inoculated potato, the 

primary reactions are local and systemic necrotic spots, 

ringspots, and sometimes systemic necrosis. 

Particles are isometric, about 28 nm in diameter. Purified 

Causal Agent 

preparations show empty particles and particles with infectious 

or noninfectious nucleoprotein. The virus is highly 

immunogeric. TRSV occurs in nature as six well-characterized, 

serologically related strains. The Andean potato calico strain is 

serologically related, but not identical, to the others. In tobacco 

sap its thermal inactivation point is 55-60' C: longevity in vitro, 

9-Il days; and dilution end point, I0 - 

- 10 - ' . TRSV is similar in 

certain respects to potato black ringspot virus.

Disease Cycle I)escriptions of Plant \'iruscs. Comll nwv,. NIycol. Inst., Assoc. 

The virus is probably introduced to uninfcsted soil when Appl. Biol., Kcy. Surrey, England. 

infected seed tubersare planted. Seedlings from infected seed of 

some weed species may also act as virus reservoirs. (Prepared by '. F. Fribourg) 

Iransmission to potato plants has not been investigated, but the 

virus is transmitted in other crops by the nernatode, .Vilhinemca 

americanum; thrips, 7hrit.s taha'i; the tobacco flea beetle, Tomato Black Ring Virus 

lt'itrixhirtipnni.s;and other vectors. Iowever. sporadic field 

occurrence of calico fits the pattern of spread by a nernatode Tomato black ring irus (IBR V) affects potato in Northern 

vector. and Central Europe bt normally is uncommon. 

Epidemiology Symptoms 

Cool temperatures favor disease development in potato Primary systemic s~mptonis, necrotic spots and rings on 

plants. Iigh soil moisture may favor the nematode. leaves. (eve"lop in only a few plants. Often plants are 

Other |osts symptomless the fiist year of infection. 

TRSV 

Il the second 

transmits 

year, 

mechanically to at least 38 genera in 17 chronic shpdadslgtynsspnwhnericpoigad 

symptoms develop: tip leaves ma\ be cupped (spoonfamilies. 

usually inducing symptoms of chlorotic or necrotic s and slightly iissiapen, wh necrotic spotting and 

spotting. plants sornev hat stunted (boUtUqet) (Fig. 91). In the third year, 

In Vicotiana taatuni, it prodtices local and systemic 

plants de~clop 

pat 

only 

c 

chronic 

lpol 

s~riptoris. 

hoi 

Blhight yellow 

smtis lih 

leaf 

markings are produced elwla 

by the 

chlorotic 

pseudc-aucUba 

and necrotic ringspots and line patterns, followed by infected synponlessl, 

strain. 

and Some tubers from diseased 

Tubers 

plants 

are 

syvstemic svmnptomless infection F ig. 89A). in-ce 

sytemic 

s-polsladsm 

s ies nftrdin 

uesfo 

necotic 

iesdpat 

lesions 

I o,'na 

nino 

sinunsi.c\eiibits 

atare 

reddish necrotic lesions 

healthy. Although 

ill noculated secondaiy 

loss of 

symptoms 

yield in individual 

averages 20--30) 

plants 

, this is 

with 

not a major 

leaves, follo, cd by systemic apical necrosis (Fig. 891). disease because it occurs only sporadically. 

In ('utctojis saivus. symptoms are chlorotic or necrotic 

lesions in inoculated leaves, systemic chlorotic spots, mottling, Causal Agent 

and apical distortion. Particles are isometric and about 30 nm in diameter. Some are 

Control Controltobacco full and some sap, thermal empty. 'he inactivation virtis is strongly is 60-65°C; immunogenic. dilution end In 

I) Roguing infected plants is effective because the disease is point, 0-I0 and longcvity in vitro, two to three 

sporadic 

weeks. 

and susceptible cultivars show conspicuous symptoms. 

2) IRSV is sometimes controlled ii other crops by treating 

infested fields with nematicides. 


FRIBHOtURG, C'. F. 1977. Andean potato calico strain of tobacco 

ringspot %irus. I'htopathology 67:174-178. 

GOOI)ING. i. V., .tr. 1970. Natural serological strains of tobacco 

ringspoi ,irus. Phytopathology 60:708-713. 

SAIAZAR. I.. F.. and B. I). HARRISON. 1978. The relationship of 

potato bhlack ringspot ,irus to tobacco ringspot and allied viruses. 

Anti. Appl. Iliot. 90:387-394. a 

STACF-SM ITH, R. 1970. lohacco ringspo" virus. No. 17 in: 

B 

' '. 

Fig. 89. Tobacco ringspot virus: A,systemic symptoms intobacco 

leaf; B, local necrotic lesions and systemic apical necrosis in Fig. 90. Tomato black ring virus systemic necrotic spotting in 

cowpea (Vigna sinensis). (Courtesy C. E. Fribourg) naturally infected Majestic variety. (Courtesy S. D.Harrison) 

85

Disease Cycle 

TBRV is soilborne and transmitted by Longidorus spp. 

nematodes. L. attenualus transmits the bouquet strain and L. 

elongatus the pseudo-aucuba strain. The virus is not retained 

through the moult, and infective nematodes kept in fallow soil 

lose infectivity after about nine weeks, 

The most important means of survival in infested land is in 

infected weeds and their seeds. TBRV isseed-transmitted in at 

least 24 species in 15 families. Seeds also serve as vehicles for 

dissemination of the virus to new sites, as do infected seed 

tubers. Short distance movement may occur by nematodes in 

infested field soil. Healthy crops become infected when planted 

on infested land. 

Epidemiology 

Cool climates favor development of disease in potato plants. 

Activity of the nematode vector is favored by high soil moisture, 

with resultant spread to healthy potato plants. 

Other Hosts 

TBRV can be mechanically transmitted to a wide range of 

hosts in at least 29 families and naturally infects many weed and 

crop plants. 

Chenopodiuntamaranticolor and C. quinoa exhibit chlorotic 

or necrotic spots and rings in inoculated leaves and systemic 

necrosis or chlorotic mottle. 

Nicotiana rustica and N. tahactm show necrotic or chlorotic 

spots or rings in inoculated leaves and systemic spots, rings, and 

line patterns with variable amounts of necrosis. Leaves 

produced later appear normal but contain virus. 

Cuctumis sativus is a useful bait plant for virus detection in soil 

samples, producing chlorotic or necrotic local lesions and 

systemic mottling. l.eaves produced later may develop enations. 

Control 

I)Roguing is effective if seed stocks are not later reinfected by 

being planted in infested land. 

2) Nematicide soil treatments decrease incidence of infection 

when healthy crops are planted. 


BERCKS, R. 1962. Scrologische Uberkreuzrcaktionen zwischen 

Isolaten des Tomatenschwar/ringflecken-Virus. Phytopathol. Z. 

46:97-100. 

HARRISON. B. I). 1958. Relationship between beet ringspot, potato 

bouquet and tomato black ring viruses .1. Gen. Microbiol. 

18:450-460. 

MURANT. A. F. 1970. Tomato black ring virus. No. 38 in: 

Descriptions of Plant Viruses. Commonw. Mycol. Inst.. Assoc. 

Appl. Hiol., Kew, Surrey, England. 

(Prepared by R. A. C. Jones and C. E. Fribourg) 

Potato Yellow Vein Virus 

Vein yellowing, caused by the potato yellow vein virus 

(PYVV), is very common in the highlands of Ecuador and 

southern Colombia. Apparently PYVV ispoorly invasive in the 

plant: tuber transmission is not regular and tuberboriie 

infection may be very slow in symptom expression. 

Newly developed symptoms are bright yellow veins and, in 

some ctultivars. interveinal ycllowing. I.ater the leaves become 

yellow and the veins may turn green (Plate 75). These colors are 

most distinct in leaves that had expanded before the onset of the 

disease. Affected plants are spectacular because of the intensely 

bright yellow color, which remains distinct throughout the life 

of affected leaves. Lcuves with symptoms are somewhat rougher 

than are leaves that appear healthy. Some rugosity and necrotic 

spotting may also develop. Tubers are deformed, with eyes 

protruding as knobs suggestive ofsecond growth. Yields may be 

86 

reduced by 50%. 

The PYVV particle is isometric and 26 nm in diameter 

(Salazar, L. F., and B. D. Harrison. 1980. Personal 

communication). The vector in nature has not been identified. 

The disease is graft-transmitted and can be mechanically 

transmitted to Datura stramonium only with difficulty. 


DIAZ, MORENO, .1.1965. El virus del amarillamiento de las papas. 

Cicnc. Nat. (Quito) 8:25-37. 

VEGA. J. G. 1970. Transmissi6n, purificaci6n y caracterizaci6n del 

agente causal del "amarillamiento de %enas"enpapa. Tesis, M. S. 

Universidad Nacional InstitutoColombiano Agropecuario. Bogat,. 

47 pp. 

SMITH, K. M. 1972. A Textbook of Plant Virus Diseases, 3rd ed. 

Academic Press, New York. pp. 427-428. 


Tobacco Necrosis Virus 

Tobacco necrosis virus (TNV) occasionally affects the 

cultivars Duke of York (Eersteling) in the Netherlands and 

Sieglinde in Italy. 

Symptoms 

Only tubers react to infection (Fig. 91). The skin of recently 

lifted tubers shows dark brown lesions with radial or reticular 

cracks. Parallel or star-shaped cracks may resemble scab 

lesions. Superficial lesions are circular or bandlike, and light 

brown patches about the same size as the radial cracks occur. 

Blisters, sometimes visible at harvest, may develop during 

storage and later become sunken, covering most of the tuber 

surface. 

Causal Agent 

TNV has a wide host range, and little is known about the 

disease of potato. Inoculation of Duke of York tubers with 

TNV has been unsuccessful. Diseased tubers produce a healthy 

or nearly healthy progeny. 

TNV rarely becomes systemic, is transmitted naturally to 

plant roots by zoospores of Olpidium brassicae,infects both 

monocotyledonous and dicotyledonous plants, and after 

mechanical inoculation typically produces local lesions on 

" , 

V: 

Fig. 91. Tobacco necrosis virus: early and late symptoms on 

tubers. (Courtesy D.Peters)


KASSANIS, B. 1970. TFbacc ecrosis virus. No. 14 in: Dt'scriptions 

of Plant Viruses. Common". Mycol. Inst.. Assoc. Appl. Biol.. Ke . 

Surrey. England. 

NOOPDAM. 1). 1957. Tahaksnecrosevirus in samenhang met een 

opperslakkigc aantasting Nan aardanpelknollen. Tijdschr. 

Planteickten 63:237-241. 

(Prepared by I). Peters) 

Deforrming Mosaic 

Relatively little is known about this disease, although it is 

economically important in Argentina. 

Secondary symptoms appearing soon after plant emergence 

are severe mosaic and irregular occurrence of' yellowish green 

patterns, leaves are distorted, and leaf surfaces are ;ough, with 

interN eiaial tissue extending above the veins. Later in the season, 

severity of svmptonis lessen, and infection may be masked, 

Tubers are symptomiess, internally and externally. Tuber 

transmission of the virus is not consistent, and up to a third of 

the tubers from infected plants may produce healthhy plants. 

The disease isgra ft-t ran.,mitted to Solaniont demissum and S. 

Itahtoen.se and then readily transmitted to potato. It has not yet 

bc .i transmitted mechanically nor by aphids. The potato 

cultivar Huinkul is rapidly infected in the field. with losses of 

20' or more (Fig. 92). Others, Kennebec and Pontiac, usually 

do not show%synipioios under similar exposure. 

Early roguing of diseased plants in seed fields is 

recommended. 


CAL.I)tFRONI. A. 1965. An unidentified virus of deforming mosaic 

typc in potato variclies in Argentina. Am. I'otato.l. 42:257 (Abstr.). 

(Prepared hy W. .1.Hooker) 

Tomato Spotted Wilt Virus 

The tomato spotted wilt virus (TSWV) occurs worldwide but 

is more frequent in subtropical and temperate region,, of the 

African, American, and Australian continents than in Europe 

and Asia. Losses in potato can be extensive. 

Symptoms 

Primary symptoms are necrotic spotting of leaves, stem 

necrosis, death of the top of one or more stems, and occasionally 

death of the whole plant (Plate 76). More frequently, however, 

only the upper parts die. 

Local chlorotic or necrotic lesions may appear at points of 

thrip feeding (Fig. 93A and I)). Pale green upper growth may 

precede the onset of systemic necrotic spotting. Leaf lesions 

appear as single necrotic rings around a central green area with 

or without a central dot, as concentric necrotic ri tg, interspaced 

with green tissues, or as solid necrotic spots with concentric 

zonation soeewhat resembling Alternaria ,cal spot. Necrotic 

lesion.i appear also in the petioles and veins and in the stem 

(cortex and or pith). A:illarv buJs may sprout in necrotic 

plants with chlorotic concentric ringspots. 

Tubers produced by infected plants may appear normal or 

they may be malformed, with cracks and internal rusty or dark 

necrotic spots. Spots are visible when the tuber is cut or may be 

visible through the skin. sometimes as concentric patterns (Fig. 

93B and C). 

Secondary syriptotns on shoots from infected tubers may 

include necrosis, early death, varying degrees of stunting, or a 

rosette type of growth with coarse, dark green leaves. Leaves 

may show necrotic spotting or chlorotic concentric ringspots. 

Many diseased plants survive with minimal yield of tubers, 

which are generally small and malformed. 

Causal Agent 

TSWV consists of isometric particles 70-100 nm in diameter 

(Fig. 93F). [hey contain ribonucleic acid and 19% lipids. 

Particles occur singly or in clusters inside membrane-bound 

structures that correspond to cisternae in the endoplasmic 

reticulum or nuclear envelope. The virus membrane may be 

partly of ccllular origin. Virus particles occur in leaf, stem, and 

root tissues and are present in all types of leaf cells except 

tracheids. 

TSWV is unstable in plant extracts but mare stable with 

buffers near pH 7containing a reducing system such as sodium 

sulfite, thioglycollate, or cvsteine. Inactivation isat 500 C for 10 

min; longevity in vitro is 2-5 hr: infectivity is lost at relatively 

low dilutions. -ISWV is serologically active. 

The virus occurs in nature as a series of strain complexes with 

certain strains predominating in potato and thus differing, in 

part, from those affecting other crops. Some strains tend to 

become localized in potat.o leaf tissues when inoculated 

individuall,' but may invade the plant systemically in the 

presence of others that act in an auxiliary capacity. 

Epidemiology 

The spotted wilt virus is vectored by thrips: Thrips tabaci, 

Frankliniella schulizei, ' fusca, and F. occidentalis. The first 

two are involved in spread in potato. The virus is acquired only 

bv immature stages of thrips and transmitted only by adults. 

Therefore, symptoms of a new infection transmitted from other 

potato plants by thrips may not appear for several wecks while 

the vector is developing. 

Transmission is unlikely through true seed of potato, 

although some transmission through seed of other plants has 

been reported. 

Virus perpetuation in either normal or malformed tubers may 

reach 30-40j but generally does not exceed 5C. Some tubers 

from a diseased hill may be virus-free, and some buds from a 

diseased tuber carry the virus whereas others do not. 

The spotted wilt virus can be transmitted mechanically with 

relative ease if infected leaves are triturated with a reducing 

substance. 

Mechanical transmission in potato apparently does not occur 

Fig. 92. Deforming mosaic in cultivar Huinkul. (Courtesy A. V. 

Calderoni) 

87

naturally. Potato, more resistant to mechanical inoculation 

than most other suscepts, is most effectively inoculated on the 

young tips of plants near the flowering stage with virus from 

potatoes rather than from other hosts, 

Spotted wilt in potato is seasonal. Spread generall% occurs in 

late spring and early summer. occasionally later, and sometimes 

erratically. 

Most field infection occurs as viruliferous vectors move into 

potato from outside sources. Field incidence may be patchy, 

especially during early growth or when incidence is low. H igh 

densities of the vector, even if present for only short periods, 

seem more necessary for widespread potato infection than for 

infection of other crops such as tobacco and tomatoes, 

In Australia, thrip populations increase when the rainfall is 

satisfactory without being excessive and when the temperture 

steadily rises as summer 'pproaches. In contrast, high 

temperature and lack of moisture are adverse to vector 

breeding. Elsewhere, potato spotted wilt is more prevalent in 

dry rather than in wet seasons, 

Other Hosts 

TSWV infects dicots and monocots of more than 30 families, 

annuals and perennials, and many crop, weed, and ornamental 

plants. Tomato and tobacco are much more severely damaged 

than is potato. 

Petunia hyhrida is a,local lesion host. (Lesions appear in two 

to four days on intact or detached leaves.) It is usually not 

systemical!y infected. 

Phaseolus vulgaris (Manteiga and related cultivars) exhibits 

chlorotic local lesions in three to six days (Fig. 93E). 

Nicotiana tahaeum (Samsun NN, Turkish NN, Blue Pryor), 

A'. clevelandii, A'. giinosa, and N. rustica show local lesions, 

systemic necrosis, and leaf deformation. They are used for local 

lesion assay and %irus purification. 

Tropaeolum najus, Cucumis sativus, and Vinca rosea are 

good diagnostic species. 

L tmajus and Gomphrena glohosa are used for maintaining 

cultures. 

Resistance 

Some field resistance is present in Kathadin and Snowflake, 

in some of their hybrids, and in Brownell, Brown's, and Epicure. 

This level of field resistance breaks down easily under severe 

exposures. Potato is more susceptible to infection during the 

growing phase than it is after flowering, when plants become 

increasingly resistant. 

Fig. 93. Tomato spotted wilt: A and D,lesions on potato leaves; Band C,symptoms within and on tubers; E,local lesions on bean leaves; F, 

purified virus. Bar represents 1jim. (A-E, Courtesy A. S. Costa; F,courtesy E. W.Kitajima) 

88

Control 

1)Avoid locations in wkhich severe outbreaks have occurred 

frequently, and because of virus reservoirs in ornamental and 

vegetable plantings, aN oid locations near residences. 

2)Select higher elevations when possible. 

3) Earlv cultivars and early plantings may escape infection, 

4) Insecticides (foliage sprays or systemic granulated 

cortpounds) in the planting or on border catch crops have been 

used vith varying effectiveness in various crops. 


1IE . R .1. 1968. loniato spotted %%iltsirus. Ads. Virus Res. 

13:65-146 

COSA, A. S.. andCO~A. .1. 1. KlflIl.. . I EIll. S. aid 1938. t938 1 I'mia trolestia mlesja dla a btatnha batatinlia 

"necrose do topo" causada pelo virus de vira-cabeqa. J. Agron., 

I'iracicaha 1:193-202. 

IF. . S. 1970. tomiato spotted \%ilt \irus. No. 39 in: l)escriptions of 

Plant Viruses. ('omnoni. M col. Inst.. Assoc. Appl. Biol., Key'. 

Sur-ci,\. iai l. 

KII A.lIM A. F. W. 1965. Electron microscopy ol vira-cabega (Brazilian 

Spottled %ill\irr,,) \0ithin the host cell. Virology 26:89-99. 

MA(i( pII C. .1. 1936, Spotted %oilt disease of lettuce and potatoes. 

Agric. (ia.\.S.\'. 47:99- 1011. 

NORRIS.1). 0. 195. Spoiled ill oh potato Ast. .t. Agric. Res. 

22S. I'.. to.. I. I . ItIFRIAN and . P1tERS. 1977. Purification 

AS A 

arid 

n 

sciologicalanall\ 

).Il 

sis 

R.17. 

ofto nato spotted 

1rfc 

%ilt virus. 

( 

Neth... 'lant 

t'ath. 83:61-72. 

shows PSTV nucleic acid produced by all strains of PSTV as a 

band additional to those in healthy plants. 

Epidemiology 

Transmission is largely mechanical. principally by man 

himself and to a lesser extent by chewing insects. Eidence that 

sucking insects are involved is inconclusie. This is one of the 

few potato diseases transmitted readily by pollen and true seed. 

Other Hosts 

About two to three weeks after inoculation of L'copersicon 

esculentut with severe strains, new leallets show marked 

rugosity, epinasty. and down-curling (Fig. 951)). Internodes 

become shorter, forming a rosette or bunch\- top. Later veinal 

necrosis can become very severe. With mild strains, syvmptorns 

are slight epinasty and stunting. Bunchy top is increased in 

continuous light of 1,000 FC or more. Mild strains temporarily 

cross-protect against later inoculation with severe strains, and 

the reaction calr be used to demonstrate the presence of mild 

strains in otherwise syrnpton less plants. 

Scopolia sinensis responds with dark brown, necrotic local 

lesions in two or three weeks and later with systemic necrosis 

(Fig. 95C). Severe strains cause symptoms earlier than do mild 

strains. Optimrium conditions are rnanganese-rich soil nutrition. 

18-23'C' incubation in not over 300-400 FC of light. 

preinoculation shading, and inoculuri in 0.05,1f K 2 H P04, pH 

9.0, buffer. Certain insecticides severely impair local lesion 

formation. 

Many plant species belonging to most genera of the 

Solanaceac are syiptomlessly infected. PSTV also infects 

members oftbe Amaranthaceae, Boraginaceae, Campanulaceae, 

Caryophyllaceae. Compositac, Convolvulaceae. Dipsaceae, 

Sapindaceae. Scrophulariaceae, and Valeriaceac. 

Control 

I) Use seed tubers known to be free from PSTV, such as 

government-inspected certified seed. 

2) Avoid mechanical transmission by planting whole, rather 

than cut, seed, and avoid leaf contact by equipment in field 

operations. 

3) Decontaminate knives and other equipment by dipping 

them itt or \\aishin tlttu \\ilhi odium h.tpocltlorite 11 ).25I ol 

calciiih l\hpochloritc 11.1 ,1. 

4) Roguing of diseased plants in seed fields is ineffective 

because of indistinct plant symptoms. 

5) Plant seed fields with whole (uncut) tubers and wide 

spacing for large tubers or by the tuber unit method: the latter 

aids in disease identification but introduces the danger of 

transmission during cutting. 


)IENER. 1. 0.. and A IIAI)II)I. 1977. Viroids. Comp. Virol. 

11:285-337. 

DIENER. T. 0.. and W. I3. RAYMER. 1971. Potato spindle tuber 

'virus.- No. 66 in: I)escriptions of Plant Viruses. Coin on . 

Mycol. Inst.. Assoc. Appl. 13iol.. Vey. Surrey. England. 

FERNOX\. K. H. 1967. Toinaitoas a test plant fordeteciing mild strains 

ol potato spindle tuber \irus. Phytopathology 57:1347-1352. 

McCI,.'AN. A. P. I). 1948. Bunchv-top disease of the tornliat: 

Additional host plants, and the transmission oi the \irus through the 

seed of infected plants. S. Afr. Dep. Agric. Sci. Bull. 256. 28 pp. 

MORRIS. 1. I.. and N. S. WRI(ilII. 1975. l)etection on 

polyacrylarinide gel of a diagnostic iucleic acid Ironi tissue inIected 

with potato spindle tuber siroid. /\il. Potato .1. 52:57-63. 

SINGH. R. P. 1973. Experimental host range of the polato spindle 

tuber "virus. An. Potato .. 48:262-267. 

SINGI. R. P.. R. E. FINNI E.and R. If. HAGNAII.. 1971. lossesdue 

to the potato spindleItuber \irus. Ani. Potato .1.48:262-267. 

YANG. T. C., arnd W. .1.1100K ER. 1977. Albinism of potato spindle 

tuber viroid-inlected Ruitgers totmato in continuous light. Amn. 


90 

(Piepared by R. '. Singh and K. H. Fernow) 

Sugar Beet Curly Top Virus 

Curly top. caused by the sugar beet curly top virus (BCIV), 

mvssol 

thlrough the pota to plant and isapparently uotnc 

littemp onc 

Current season syrptoms consist of dwarfing. yellow,ing. 

elongation, and upward rolling of tie midrib of terminal 

leaflets, leaflets near the gro\ing point ha\e marginal 

yellowing, elongation. cupping, rolling. twisting. bulging, and 

roughness ( Fig. 96). lu her-pcrpet uated sv nptorns are 

extremely \ariaible. Tubers from infected plants may produce 

healthy appearing plants. sproits delayed in emiergence or 

failing to emerge, (r sprouts having extremely short shoots \with 

unmottled lea\es ranging from dark to light green and yellow. 

The green dwarf symptom consists of shoots dela" ed in 

emergence with leaves failing to unfold completely aInd 

remaining stiff and erect. As stenis elongate, they stav stiff and 

erect, with the growing point pinched together. 

Symptorsare remarkab!y similar to certain svmptoris of the 

mvcoplasma vellows disease and therefore ma\ ha\e escaped 

identification. 

Transmission in nature is ,,y the leafhopper. Circul~ir 

(Neoliturus) tenelu.s, in which the virus is circulati\e. 


BENNI: . C. W. 1971. The curly top disease (i stigarber and other 

plants. Monogr. 7.Am. Phytoparhol. Soc.. St. Paul, MN. 8t pp. 

GARDNER. W. S. 1954. Curly top of the potato in tIah and its 

possible relationship to hayvwire." Plant l)is. Rep. 38:323-325. 

GII))NGS N. .1. 1954. !ioie studies of curl\ rop on potaloes. 

Plhytopatlology 44:125-128. 

STOKER, G. I... and 0. S. CAN)NON. 1962. Ctirrent-season arnd 

tuber-perpetuated s.ni ptonis o! portaro cirly it)p. Plant I)is. Rep. 

46:176-180. 

(Prepared by W. .I. Hooker) 

Fig. 96. Sugar beet curly top virus, showing leaf rolling and 

dwarfing, (Courtesy N.J. Giddings, from Bennett, C. W., 1971)

The "yellows" types of disease, characteristic of mycoplasma 

infections that have been studied in some detail possess rather 

broad host ranges. Some have been reported to infect potato in 

the field or have been transmitted to potato experimentally. 

Unfortunately, disease symptoms in the potato itself are hardly 

of diagnostic value except to distinguish two large groups of 

agents, those causing the aster yellows and the witches' broom 

types of disease. 

Mycoplasma-like organisms (M 1.0). formerly considered 

viruses with somewhat unusual characteristics, were first 

demonstrated in plants in 1967 by electron microscopy. Actual 

proof that MI1.0 cause disease in potato is needed by Koch's 

postulates, although the presence of MLO in plant tissue 

constitutes the best evidence so far available. More accurate 

methods of differentiating between these pathogens are urgently 

needed, particularly because potato is a relatively incompatible 

host. 

None of these diseases is contact-transmissible. Grafting is 

often used for experimental transmission. All of the pathogens 

rely on leaflioppers for transmission and dispersal, and their 

occurrence and distribution is determined by lealfiopper 

activity. Variations in symptomatology, host range, or vector 

relations of different source materials of each disease suggest 

that strains of these pathogens occur. 

Symptoms and M I. may be suppressed by antibiotics of the 

A7 

Mycoplasmas 

tetracycline group. and individual plants may be cured by heat 

therapy. 

Aster Yellows and Stolbur 

Aster yellows and its allied diseases occur worldwide. Stolbur 

is found in Europe, tomato big bud in Australia, purple top roll 

in the Indian peninsula of Asia, and parastolbur and 

metastolbur in Europe. In the western hemisphere, aster yellows 

has been variously called purple top wilt, yellow top, bunch 

top. purp!e dwarf, apical leafroll. haywire, latebreaking virus, 

blue stem, and moron. 

Symptoms 

Upper leaflets roll and develop purple or yellow pigmentation 

(Plate 77). Aerial tubers are common, and occasionally some 

proliferation of axillary buds occurs (Plate 78). Often only a 

single stem in a hill isaffected. Plants are often stunted and may 

die prematurely(Fig. 97A and B). Under field conditions, lower 

stems frequently develop cortical necrosis, shredding of tissue, 

and vascular discoloration. 

At harvest, an affected hill usually has some normally mature 

and some immature tubers. In stolbur, flaccid (gummy) tubers 

Fig. 97. Aster yellows mycoplasma in potato: A, primary symptoms; B,advanced wilting of stolbur in left stem with stem at right unaffected; 

C, aster yellows mycoplasma in infected tissue of aster (electron microscope photograph, bar represents 1pm. (A and C, Courtesy N. S. 

Wright; B,courtesy V. Valenta) 

44; 

91

may form. 

When the causal agents survive storage in seed tubers. plants 

in the second year develop symptoms. In the more usual 

situation, in which causal agents failto survive in seed tubers. 

plants in the second year may he normal, lack diagnostic 

symptoms, be smaller than normal, or failto emerge. Hair 

sprouts frequently develop on tubers from infected plants (Plate 

79). Plants with stolbur may bear simplified "round" leaves, but 

this symptom disappears in subsequent years. 


Mycoplasmalike organisms (MLO) occur in phloem sieve 

cells and occasionally in phloem parenchyma cells of infected 

plants (Fig. 97C). They ,are pleomorphic, lack a cell wall. and are 

bounded by aunit membrane. M I.O vary in diameter from 50 to 

1,000 nm. The larger, more prevalent forms are roughly 

spherical and contain a central fibrillar network of strands, 

presumably DNA. and a peripheral area of ribosomelike 

granules. The presence of elongate forms and small, dense 

"elementary bodies" suggests propagation by binary fission. 

budding, or fragmentation. 

Epidemiology 

The principal leatfhopper vector ol aster yellows. .iacrosteh's 

fascifrons,overwinters on weeds, grasses, and small grains. The 

favorite host of tile main vector of stolbur, Iiraesthe.s 

obsohtus, is perennial hindweed, (on volvulu arven.sis, which 

simultaneously acts as the main inoculum reservoir plant. 

All pathogens are transmitted by and propagative in 

lea fh oppers. Potato is not a fhavored host and usualIv escapes 

extensive disease incidence. Stolbur is an exception that, in 

certain European regions, mav become ,cry destructive. 

Leafhopper vectors do not complete their life cycles on potato. 

Neither nymphs nor adults can acquire the pathogen from 

potato. Transmission to potato occurs only when the leafhopper 

has fed on some other infected host. two to three weeks before 

feeding on potato. 

Other Hosts 

Many vegetable. ornamental, field crop plants, and weeds tire 

among the 350 species froni at least 54 families susceptible to 

aster yellows. 

Witches' Broom 

Witches' broom. also called northern stolbur and dwarf shrub 

virosis, has been reported from North America, Europe, and 

Asia but is of minor economic importance. Several distinct 

pathogens or strains of a single pathogen may be involved in 

different geographical areas. 

Symptoms 

Symptoms are generally similar. Plants have many axillary 

and basal branches with simple "rotnd" leaves, which may he 

chlorotic (Fig. 98A). This disease is distinct from wilding, a 

somatic aberration. Current symptoms appear late. if at all. and 

consist of an upright habit of growth. rolling of leaflets, and 

some chlorotic or anthocyanin discoloration in apical leaves. 

Most strains cause no flower symptoms. but witches' broom 

strains of central and eastern Europe are characterized by 

virescence, phyllody, and associated flower symptoms (Fig. 

98B). 

Mycoplasmas offwitches' broom are tuber-perpetuated, in 

contrast to those of aster yellows, which usually are not. 

Affected hills usually produce tubers that appear normal during 

the year of infection hut gIive rise to plants with advanced 

symptoms the subsequent 'ear. Tubers from infected plants 

frequently produce hair sprouts. Such plants have many small 

tubers and an abnormally high number of sprouts with 

simplified, small leaves. Occasionally these sympt(ms follow 

92 

early infections during the current season. Infected tubers 

usually lack dormancy. 


Pathogens are mycoplasmalike organisms, such as those that 

cause aster yellows. 

Epidemiology 

The pathogens are transmitted by leaf hopper vectors, 

Ophiola (Scleroracus)lavopitu.s, S. dasidus (Fig. 98C),and S. 

halli, in which they are propagative. In most areas, the vectors 

are not yet known, nor are the natural host ranges of the 

pathogens. 

lcafhuoppers are unable to acquire the pathogen from potato. 

Spread to potato occurs when a vector feeds on oth-r infected 

hosts several days before feeding on potato. Witches' broom in 

perennial legumes isusually more serious than in potato because 

the former are preferred hosts by the vector and inoculum is 

usuall, available within the crop. 

Other Hosts 

L.r,'oliervicon escuhe'ttm, C, 'vphomandra betacea, and 

Nicotiana tahactum have been used to distinguish between 

strains. 

ifedicago sativa, Jelilotus alba, or l.otus corniculatusserve 

as natural reservoirs and may be used as indicator plants. 

Trifolium r 'ens isalso susceptible. 

Control 

I) Generally these diseases are of minor importance and do 

not justify elaborate control measures. 

2) Control leafhopper migrations into potato fields by 

,, .. 

C 

Z 

Fig. 98. Witches' broom: A, in potato plant; B, current season, 

medium intensity flour phyllody of Czechoslovak type II; C, 

Scleroracus dasidus female, one of the leafhopper vectors. (A, 

Courtesy N. S. Wright; B, courtesy V. Valenta: C, courtesy J. 

Raine) 

:.

modifying cultural practices and by using insecticides. 

3) Spread from potato to potato is believed not to occur. 

4) Heat treatment may be useful on individual plants, 

5) Remission of symptoms often follows treatmlent with 

tetracclines 

tetracy lines.6 


BRCAK. ..O. KRAI.'IK. J.I. II fERK. and NI. LI.RYCIOV,. 

1969. Mycoplasm-like bodies in plants infected %% ith pota:o witches' 

br ,o disease and the response of plants to tetracycline treatment. 

Biol. plant. 11:470-476. 

CIHAI'MAN. R. K., moderator. 1973. Smrnposiunm: Asteryvelloss. Proc. 

N. Cent. Branch. Fntomiol. Soc. Am. 28:38-99. 

l)Ol. Y.. M. ITRAMAKA, K. YORA. and if. ASLYAMA. 1967. 

MNcoplasma or PI. group-like microorganisms found in the 

phloem elements totplants infected % itt mulberr \dwarf, potato 

%% itchtes' broon. aster ,sellosiss, or Paulo%%nia \sitches' broom. Ann. 

h'livtopailhol. Soc. .apan 33:259-266. 

I:FtKt;SIl. I..I. SIIIKAIA. II. SHIO).A. F. SFK'YANI.A, I.. 

TANAKA, N. ()SIINIA. and Y. NISIIIA. 1955. Insect transmission 

of poltato silches' broomn in lapan. Proc .. Ipn. Acad. (Nihon 

(akusiNj.... .31234-236. 

N.A(iAICtI, I). B..I. K. PI'RI. R. C. SINIIA. N1 K. )l1INGRA, and 

V. It. LI.AR I)\VA,\.l. 1974. %tscoplasna-like organisms inplants 

affected %%itht purple top-roll, marginal flasecence and 

broott 

,itcltes' 

diseases ofpotatoes. 'hs%tmpalthol. Z.81:273-279. 

Psyllid Yellows 

This disorder results from insect feeding, and no infectious 

microorganism is involved. 

()trs ines. \Ong leis es. shIcll arC Ofteni rCL O purple. he1otte 

erect and hasc ctppedf basal portitm . Nodes of Nuitng stetts 

hecote cnlargcd: [lte a\illars angle bet %ccnstctIs ami pettiles 

is larger than lustual: and aerial tuhcrs ,,tistocks sltots. Irequct 

t11.. 1k tlci, i Ito Inat 

tle Iaf a \ils. Plants ha\c a p ramidal 

shape and are gcncrall% scllos tobitolttd. lit ad\a cctdstages, 

oldCr lCaCs rll Up\sard. become ello\ \ith necrotic areas.,t 

break dti \s rapidll. I lie tip lea\cs Iot-it a rosette (PlaC 80). 

Plants do[l tgenciralls*\\sill cn under escttcc dttght. 

Iorder parcicht \tia surrounding the phlcli is first allected. 

atd later tissue breakdti\s.t extends laterally. causing phllt 

necrosis. Abtirillh large dcptisits of starch dcvclop inthe 

Corte\ anid pith. 

I-\ if an\ tubers are set oinplants attacked in early 

de\clpmntnt. When older plants are affected, stolon tips may 

produce sprouts and secondary sho.ots that emerge front the soil 

as smiall plants. Masses tif small tubers mav orn oi secondary 

stolon bra nches. or successi\c tubers nas forn oila stolon in a 

chain or beadlikc arrangement. 

Abnormnalls small tubers sprout without a dormant period. 

Similarly. trnancv may be lacking iii tubers that appear 

normal. IBecause (t tie nman\ small tubers. tie number of 

inarketa ble tubers is greatly reduced. 

1he disorder is not tuber-transinitted. Artificial methods of' 

transmission from plant to plant have not been successful. 

Insect Toxins 

Nematodes 

RAINE. .J.1967. Ieafhlopper transmission of vitchos'broomand clover 

phyllod %iruses frotm British Columbia to closer, alfalfa. and 

potato. (an..I. Bot. 45:441-445. 

SENIAN('K. .J. S.. and .1. PI [RSON. 1971. Association of a 

mycopsna ih havsire disorder of polatoes. Phytopathology 

1':1316--1317. 

VA. EN IA. V. 1957. Potat o "itches' bro o i %j rus in Cech oslo va kia. 

Pages 246-250 in: I..Quak..I. l)ijkstra, A. II. R. licemster. and J. P. 

II. Van der Want. eds. Proc. Ihird (ont. Potato Virus Dis. 24-28 

June, 1957. If.Veenman and Zonen. Lisse-Wageningen, The 


VA I.E NI A, V. 1969. Vergleich cines aus Niedersachsen stammenden 

Kartoffelhexenhesen-Virus mit anderen aus Europa bekannten 

Viren dieser (iruppe, Zentralbl. Ifakteriol. Parasiteuk. Infektionskr. 

1lyg. Alt. 2. 123:352-357. 

VAI.ENIA. V., M. NI SII.. and S. MIS.IGA. 1961. Investigations on 

European veIlos, s-tpe\iruses. 1.lhestolhur virus. Phvtopathol. Z. 

42:1-38. 

VA NIA. V..dand M. MI I.. 1963. Investigations otnEuropean 

yellowks-type iruses. II. 1he cloer dwarf atnd parastolbur viruses. 

Phytopathol. Z.47:38-65. 

\VR1(Ill. N.S. 1957. Potato witches'broom in North America. Pages 

239-245 in:1-.Quak..I. l)ijkstra. A. If. R. FHeemster. and J. P. H. Van 

der \Vant. eds. Proc. third Cont. on Potato Virus Dis. 24-28 June, 

1957.11. Veenmanand Zonen. lisse-Wageningen, The Netherlands. 

282 pp. 

(Prepared by N. S. Wright, J.Raine, and V. Valenta) 

Tubers from affected plants produce plants that appear normal 

except for a slightly spindly or weakened appearance. Seed 

tubers from affected fields are not of satisfactory quality. 

[he disease results from toxic substances introduced during 

feeding of nymphs of Paratrio:a cockerelli, the tomato or 

potato psyllid. also known as the jumping plant louse. As few as 

three to five n\'nplts may cause car. symptoms, but higher 

populations (15-30 per plant) are required for full symptom 

expression. Adults tip to 1.00 per plant do not induce 

symptoms. Progress in symptom development is stopped 

abruptly svhen nymphs are removed, and affected plants 

frequently recover. 

During the 1 9 30s, the disease caused considerable damage in 

the United States vest of the Missouri Riverand extending from 

New Mexico into Canada. In certain areas it was the most 

destructive disease. Symptoms are most severe in high intensity 

sunlight, at high field temperatures, and during drought. 

Similarity between psyllid yellows, the mycoplasma disorder 

haywire, leafrolls of various types, and Rhizoctonia has caused 

some confusion in diagnosis. 


EYIRS,.1.R. 1937. Physiology ofpsyllid yello's of potatoes. J. Econ. 

RICIIAIS,.If.I.., 

IAntArIl. 30:891-898. and II.L. BLIOOD). 1933. Psyllid yellows of the 

potato... Agric. Res. 46:189-216. 

SCIIAA I.. L A. 1938. Some factors affecting the symptoms of the 

psyllid yellows disease tif potatoes. Am. Potato .1.15:193-206. 


Nematodes pathogenic to potatoes (Table II) occur in all appear on aboveground parts of the plant except for unthrifty 

climates and cause serious crop losses, but much of this damage top growth resulting from poor root systems. Low densities in 

is unrecognized or attributed to other causes. Because the soil cause no top symptoms but may reduce tuber yields. As 

nematodes attack roots and tubers, no diagnostic symptoms the world population increases, soil suitable for potato culture 

93

will become more scarce. Consequently, potatoes will he grown 

more frequently on the best potato land, and because 

monoculture encourages nematode population increase, 

nematode damage to potatoes will increase dramatically. 

Confining nematode populations to areas where they already 

exist by restricting movement of infected seed tubers and plants 

may be the most effective way of preventing loss of productive 

land. Care in purchase of seed and prevention of shipment of 

infected seed into nematode-free areas cannot be over 

emphazied. 

in southern Europe, Newfoundland, British Columbia. Greece, 

Israel, Tunisia. South Africa. Nes% Zealand, and.lapan. Reports 

from Asia are incomplete. 

Both G. rostochiensis aad G.pallida occur in South America 

and Europe. Only G.pallida has been identified in Colombia, 

Ecuador, and in most of Peru. In southern Peru. Boliva, and 

Argentina, G.pallida and G. rosto/hiensis occur together, and 

in Chile. Vereiuela. Central America, and Mexico, only G. 

rostochitensis has been found. Both species occur in the central 

and western European countries. In the south and east of 


Europe, only G. rostochiensis isfound. In the United Kingdom, 

certain potato-growing areas have predominantly either G. 

WINSLOW, R. ).. and R. .1.WI ILIS. 1972. Nematode diseases of 

potatoes. Pages 17-48 in:.I. M. Webster, ed. Economic Nematology. 

Academic Press. London and New York. 563 pp. 

rostochiensis or G. pali/a. Only G. rostochtiensi occurs in the 

United States. In many countries and areas of countries, species 

determinations have not been made. 

Symptoms 

Cyst nematodes do not cause specific abo'eground symptoms 

Potato Cyst Nematodes of diagnostic value, but root injury causes infected plants to 

seem to be under stress from water or mineral deficiency. 

Cyst nematodes, Glohodera(Heterodera)spp..also known as Foliage is pale, and severe wilting occurs under drought. Large 

golden nematodes or potato root eelworms. are present in most nematode populations cause stunting, early senescence, and 

countries of northern and central Europe and to a lesser extent often proliferation of lateral roots. At flowering, minute 

TABLE II. Nematode Pests of the Cultivated Potato 

Distribution ' 

Scientific 

Transmission by 

and Common Names H C S T Tubers' 

Behmolaimus logicaudatoA (sting nematode) 

Ditt'h'ncltus t'.lirti'ior I potato-rot nematode) 

Ditylnchut.% /il,.a(i (stem and bulb nematode) 

Ieh'uictrh'onch spp. (spiral nemalodes) 

hi)hodera spp. Iround cyst nematodes) 

t 

h 

c 

c 

s 

s 

t 

T 

t 

t 

 

+ 

+ 

+ 

(i1 pal/ida potato cyst nematode Iwhite immature females) 

G.ro. ochien.is potato cyst nematode (golden immature females) 

Ihexat'llu vign.v 

L.ongidorms maimu.s (needle nematode) 

.feloidogne spp. (root-knot nematodes) 

C 

C 

T' 

T' 

t 

t_ 

+ 

+ 

+ 

M. acrotea 

M. africtana 

M. arenaria 

,t. hala 

A. incognita 

M. javanua 

.M1.thamle.ii 

Mehm)in a sp. 

Vacohhus aerran.s (false root-knot nematode) 

Veot.t''letttu.%ahulho.s 

Paralt/h,tchu.%spp. (pin nematodes) 

Pratvh'ntchus spp. (root-lesion nematodes) 

h 

h 

H 

H 

h 

h 

c 

C 

c 

c 

C 

c 

s 

s 

S 

S 

s 

s 

t 

t 

T 

T 

T 

T 

t 

t 

T 

t 

t 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

-+ 

P. anmditu.% 

P.brachi'trit 

P. crenal.s 

P. coffeae 

P. ifltt. 

. pemtrans 

. praten.ti.% 

P. scrihneri 

P. thornei 

Rot/lenchulus spp. (reniform nematodes) 

Roo'lenchus spp. (spiral nematodes) 

Trichodorusspp.. Paratrichodorus spp. (stubby toot nematodes) 

h 

h 

I 

h 

h 

C 

C 

C 

c 

c 

e 

c 

c 

s 

s 

S 

s 

S 

s 

s 

t 

t 

t 

t 

T 

t 

t 

t 

t 

t 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

T. allius 

P. christiei 

P. pachyiermus 

T. primtiivus 

P. teres 

c 

c 

c 

t 

d 

t 

td 

d 

t 

td 

- 

- 

 

_ 

T'enc'horhntchus spp. (stunt nematodes) 

T. cla tioni 

T. duhius 

Xiphinena spp. (dagger nematodes) 

h 

h 

c 

c 

c 

s 

s 

s 

t 

t 

d 

t 

- 

 

- 

H = hot tropical. C = cool tropical. S = subtropical. T = temperate zone. When capitalized, as shown. thejudged relative importance is greater than 

when small letters are used. All attack potato and additional members of the Solanaceac as well as plants outside the Solanaceae. 

'None are known to be transmitted by true botanical seed. 

'Limited to the Solanaceae. 

'Plant virus vectors. 

94

immature females in the white or yellow stage erupt through the 

root epidermis. Yield losses vary according to nematode 

densities, and complete economic crop failure can result when 

densities are high. Potato cyst nematodes may increasc 

incidence of Verticillium wilt and bacterial wilt (brown rot). 

and mate with the females. Fertilized females increase in size to 

become subspherical. Mature females measure between 0.5 and 

0.8 mm in length and greatly vary in size, probably due to the 

type of host and amount of nutrition during their development. 

Eggs are produced and retained within the female. The female 


G. rostochiensis and G. pal/ida become round cysts upon 

maturity. Cysts are light to dark brown with an irregular pattern 

of subsurface punctuations over most of the body. 

Cysts of G. rostochiensis differ from those of G. pallida by a 

greater average anal-vulval distance, 60 compared with 44 pm, 

and a greater average number of cuticular ridges between anus 

and vulva, 21.6 compared with 12.2. G. rostochif'nsis females 

develop through a golden yellow phase before turning brown. 

hence tihe common name. golden nematode: G. pallida females 

are white or cream before turning brown (Fig. 99A, Plates 81 

and 82). I.engths of larval body, stylet, and tail are usually 

longer in G.palla than in G.rostocliensis. 

Races are differentiated by ability to multiply on resistant 

cultivars of S. tuberosum ssp. antligena, S. mulidissectui, S. 

verm'i, or S.kurtzianum. 

Disease Cycle 

In the spring, over 50('i of the second stage larvae inside eggs 

within a cyst are stimulated to hatch. They enter the host plant 

roots, feed, and develop through a series of three molts. The 

females enlarge and rupture the root tissue but remain attached 

to the root by their heads and protruding necks, which stay 

inserted in root tissue. Mature wormlike males leave the root 

cuticle darkens and hardens, becoming the cyst, which may 

contain as many as 500 eggs (Figs. 9913 and I00A). Cysts remain 

in the soil when the crop is harvested. 

M ultiplication rate and sex ratio are influenced by population 

density of the nematode and host crop. An ample food supply 

favors a multiplication rate up to 60-fold. When food is limited 

and the population islarge ( 100 eggs pergram of soil) nematode 

density may decline. 


Glohodera spp. are stimulated to hatch by exudates from 

plant roots. Second stage larvae usually enter the root hair zone. 

As larvae move through cortex cells of potato roots, feeding 

may cause some limited necrosis in susceptible cultivars. 

The female feeds near the vascular cylinder, resulting in 

multinucleate units called syncytia (giant cells) near the 

nematode's head. Syncytia are formed by incorporation of 

adjacent cells following cell-wall dissolution, which begins in the 

cortex. Cell walls ofa column of cells toward the vascular tissue 

are then dissolved. In the vascular cylinder, syncytia are limited 

by lignified xylem, so incorporation of new cells proceeds 

parallel to the root axis (Fig. 10013). 

Syncytia may be formed in the cortex, endodermis. pericycle, 

and parenchyma of the central vascular strand. Cytoplasm of 

syncytia becomes dense and granular in structure. 

A 

Fig. 99. Potato cyst nematode (Globodera rostochiensis). A,immature swollen females attached to potato roots. B, diagrammatic life 

cycle of potato cyst nematodes: 1,cyst showing enclosed eggs; 2, enlarged egg showing enclosed, coiled larva; 3, larvae entering root; 4 

and 5, swollen females feeding in root; 6, mature female breaking through root surface. (Courtesy W. F. Mai, B. B. Brodie, and M.B. 

Harrison) 

B 

. 

.*... 

95

Syncytia usually are elongate, with ends merging with normal 

tissue, and each syncytium is generally associated with one 

larva. When multiple infections occur within a small area of root 

tissue, syncytia may coalesce. Nuclear hypertrophv is followed 

by decrease in size and number of plastids, breakdown of 

chond riosomes (mi tochondi ra). polyploid y of nuclei, and 

nuclear disintegration, 

Ingrowths or protuberances d'eslop next to xylem vessels; 

"boundary formations" and microtubules are associated with 

the ends of these protuberances. Ihey serve to increase the 

surface area of the syncytial cell wall relative to its volume and to 

allow for increased flow of solutes across the plasmalemma. The 

cell wall becomes tip to 10 times its normal thickness. 

Epidemiology 

Although populations of cyst nematodes do not increase as 

rapidly as do fungal and bacterial pathogens of potatoes, once 

well established in a potato-growing area, they arc. with present 

technology, inipossihlc to eradicate. The environmental 

conditons providing successful cotomLr'iAl potato production 

also provide optimum conditions for their multiplication and 

survival. Potato cyst neniatodes flourish where soil 

temperatures are cool. Although they have been found in 

tropical and warmer temperate climates, they. do not generally 

become established and are of lesser economic importance than 

in cool climates, larvae become active at IO C. and maximum 

invasion of roots occurs at 160 C. Soil temperatures of 260 C for 

prolonged periods of time reduce development and limit 

reproduction. 

Cyst nernatodes develop well in soils suited for surviva! and 

movement of wormlike stages, such as medium to heavy clay 

soils and well-drained and aerated sands, silts, and peat soils 

with a moisture content of 50-75(i of water capacity. Soil pH 

valles that are tolerable to the potato plant can apparently be 

tolerated by the nematodes. Nutritional status of the soil 

.pp. 

_l • 

Fig. 100. Potato cyst nematode (Globodera rostochiensis): A, 

mature cyst with enclosed eggs; B,sectien of potato root showing 

syncytia. (Courtesy W.F. Mai, B. B. Brodie, and M. B. Harrison) 

96 

;10 

appears to have little or no effect on nematodes other than that 

caused by crop performance. 

Encysted eggs withstand desiccation and can remain viable 20 

years or more in soil under severe environmental extremes. 

Moving infested soil such as that clinging to equipment, seed, or 

storage containers is the most important means of local and long 

distance spread. Planting contaminated tubers provides ideal 

conditions for spread and is thought to be a primary factor in 

nematode dissemination throughout the world. Birds are not 

considered important in long-distance spread. 

Other Hosts 

These include tomato, eggplant, and a number of 

Solanaceous weeds. 

Resistance 

Resistant cultivars and nonhost crops cause an average of 95 

and 50i reduction in populations, respectively. Excellent 

sources of resistance to G. rostochiensis(race R A) are available 

in commercial varieties in Europe and North America. Good 

resistance has been found to some, but not all, races of G. 

pallida. Resistance to G.pallida (race P 4A) is available in some 

ne%%er Dutch varieties. 

Control 

I) Restrict shipments of seed tubers and plants of other types 

from infested areas. 

2) Except for high dosages of soil fumigants, chemical 

treatments usually reduce densities only slightly, if at all. 

Although some organic phosphate and carbamate nematicides 

provide good protection against infection by active larvae, 

nematode density in treated soil usually remains the same or 

slightly increases during growth of a potato crop. 

3) Crop rotation has been widely used but is often 

uneconomical because ofthe length of rotation required. When 

nematode densities are high, rotation with potatoes grown once 

in five years is necessary to assure profitable potato yields. 

Resistant potato cultivars in rotation with susceptible cultivars 

and nonhosts considerably reduce the required length of 

rotation. 

4) Combining different control mcasures is necessary for 

keeping populations below damaging levels and for preventing 

establishment of nematodes in new areas. Key components of 

nematode management are: extensive surveys to determine 

distribution of cyst nematodes, soil fumigants to reduce 

numbers of nematodes in the soil, resistant cultivars to prevent 

density increase, carbamate nematicides to suppress density 

increases, prohibition of potato seed production in known 

infested or exposed land, and regulation of reuseable containers 

and movement of farm machinery, top soil, and plant material. 


C111TWOOD. B.Gand E.M. BUIIRER. 1946. The life historyofthe 

golden nematode of potatoes, leterodera rostochiensis 

Wollenweber. under Long Islana. New York, conditions. 


ENDO, 13.Y. 1971. Nematode-induced svncvtia (giant cells). Pages 

91-117 in: B. M. Zuckerman. W. F. Mai. and R. A. Rohde, eds. 

Plant Parasitic Nematodes, Vol. 2.Academic Press. New York. 347 

EVANS, K., .1. FRANCO. and M. M. de SCURRAII. 1975. 

)istribution of species of potato cyst-nematodes in South America. 

Nemnatologica 21:365-369. 

HOOPES, R.W. 1977. [he internal response of several resistant and 

susceptible potato clones to invasion by the potato cyst nematode 

IUniversity. I'ieroderarostochiensis 61 pp. 

Woilenweber. NIS thesis. Cornell 

MULVEY, R. II.. and A. R. STONE'.. 1976. Description of Punctodera 

maladorensis n. gen.. n. sp. (Nematoda: fleteroderidae) from 

Saskatchewan with lists of species and generic diagnosis of 

(ilobodera In. rank). Ileterodera and Sarisodera. Can .1.Zool. 

54:772-785. 

SPEARS, .1. F. 1968. The Golden Nematode Handbook: Survey,

l.aboratory, Control. and Quarantine Procedures. U. S. Dept. 

Agric. Handbook 353. 81 pp. 

SIONE. A. R. 1972. Ilterod.ra pallida n. sp. (Neiiatoda: 

Nfeteroeridae). a wcolg species 4 par-to cyst nerialatde. 

Root-Knot Nematodes 

One or more species of Meloido,'iyne are known to attack 

almost all major crop plants and many weeds species. Vegetable 

crops, inclhding potatoes. are extensi\ely damaged. with potato 

losses reaching 2511 or more. Although species differ in their 

abilitv to attack certain \cgetable crops, no vegetables go 

Ln harned. 

Root-k not ne matodes are wo rid wide in d isti but ion but are 

limited in specific areas b\ tem perature and cropping practices, 

lhe .Il. hi'ognitagroup is. perhaps. the most \widely distributed. 

l. hapla is the dominant species on potato in Europe arnd North 

America folhoscsd by .l. incognita and M. intog'niaacrita. InA 

Africa and Asia. . /arvalicaand Al. iio, nlita are domi nalt. 

follo\ed b\ . incognitaacrita and Ml. hap/a, tile latter being 

found il .Japan. .1. itcogtital. incognta acrita, Al. [avanica. 

and Ml. hap/a atrack potatoes in South America. 1 . arenari/ 

has been found ii potatoes ol most continents. 

Symptoms 

Aboveground syniptonis are not diagnostic. l)epending upon 

nematode dcnsity, infected plants may show .arving degrees of 

stuintinig arid a terideicy to \wilt under mnoisture stress. 

K nots or galls of varying si/es and shapes are present on tile 

roots (Fig. 101A). When neriatode densities are fiigh and 

enirloniental conditions favorable. tubers are infected and 

display galls that give themi a wart\ appearance (Fig. 101I). 

Galls. containing white. pear-shaped. mature feriale 

nemiatodes, range frori an almost spherical shape (in M. 

arciraria) to averv rough arid irregular appearance (ilr M. 

ha/il/a). Iidiidual gall si/ec(peids upiio neiiiatodedensityanid 

species, root size. teriperiattire. and other environmental 

factors. In :,dtition to galling . h01la caurses initiation of 

extensi\e lateral root formltio,,. 

Disease Cycle of Causal Organism 

I lie disease cycle of root-knot nematodes on potato is similar 

to thal on oitler crops arid plants. I lie first miolt occurs within 

tile egg: the second-stage larsa emerges from the egg and invades 

the host root near the rip. Iar\ac rligrate through the root to the 

\ascular tissue. shere they become stationary. Feeding injury 

and glandular sccretion by arsrae cause host cells surrounding 

the reriatode head to undergo cell division a nd cell 

enllargentcir. Ilnteraction of neriaolde anrid host causes 

deselopniri ut mutiriucleate giant cells. fron which tie 

neriaiode obtains its I od. After feeding, the larvae begin to 

swkell. Sexes become distinguishable in fourth-stage larvae 

within tile host tissue. I-eiiales continue to swell and at 

riituritvare hrite. pear-shapedarid about I-2 rni long. After 

the fourth stage, riales become \\ orrilike, about 1-1.5 riri flng. 

al(n migrate out oftthc roots. Males are comrimon in some bot ri.t 

all species and are functional in reproduction ill sWie bur not all 

species. Feniah's remain in roots, and each may produce up to 

I.000 eggs in a gelatinous matrix that is ofiten pushed out of tie 

100t tissue. Eggs hatch inl the gelatinous matrix: young larvae 

ererge arnd invade newv sites of tile silare root or new roots. 

I)cpendi;, upon hosts, tempera ture, and nematodes species, 

geecrathii time is usually 20-60 days. 

Epidemiology 

In ge.neral. root-knot nematodes reproduce most rapidly, 

survive lInger. and cause tile most damage iii coarse-textured 

soils. However. tile\t arcapparently limited more by 

temperature requirements, which vary with species, than by soil 

type. The "northern" root-knot nematode, AM.haplu, has an 

optimum temperature of 200C. Other species have higher 

temperature requirements and cannot withstand cold 

temperature. Hence. root-knot nematodes are of greatest 

economic importance in tropical and warm temperate climates 

and of lesser importance in northern latitudes and high 

elevations of tropical latitudes where soil temperatures are cool. 

Because potatoes are predominately grown in tie cooler 

climates, root knot of potato is not a major economic problem. 

Potato culture in warmer climates could drastically change this 

situation. Furthermore. environmental races exist in M. 

javanica and possibly iii other species. Such strains could adapt 

to cooler climates and cause severe damiage. For example, A'. 

incognita has become well established in the nidhill elevations 

of lIndia and causes severe damage to potato. Meloidogvnespp. 

enhance disease development by other pathogens. On potato. 

development of brown rot bacteria ( Pseudo/onaiotros solatracearum) 

is enhanced by ,I. incognitaacrita. 

,. / 

# 

Fig. 101. Root-knot nematodes (Meloidogynespp.): gallson roots 

(A) and tubers (B). (Courtesy P. Jatala) 

'A, 

97

Resistance 

Limited research has been done on developmlent of potato 

cultivars resistant to Meloidogrnespp. In India, poato cultivar 

11-294 is resistant to Jl. incognita, and moderate to high 

resistance exists in several wild diploid species of S lanun. In 

Peru, resistance to If.incognita inhybrids of S. denissum was 

found. Also, high resistance to 'ieloidogrnespp. in S. torvum 

and partial resistance in S. psealoluloand S. quitoense has been 

reported. More recently, the International Potato ('enter 

reported resistance in a number of noncultivated Solanum spp. 

lithe United States, resistance to Jf. hapla, Jl. javanica, V. 

incognia. 3f. arenaria, and Jl. incognita acril, has been found 

in clones of S. tuherosun ssp. andigena. 

Control 

I) Because Ih'lohdogrne spp. deposit theireggs in an external 

egg mass that is relatively unprotected, chemical control has 

been more successful than vith cyst nematodes. Ii sonic 

countries %%here .eloihlogyne spp. cause serious damage to 

potatoes, economic control has beer, achieved through the use 

of soil fumigants or the newer organic phosphate or carbamate 

iiema t icides. l)osage lee ls depend upon soil type, 

environmental conditions, and type of crop. 

2) The wide host range of ih'hidogyne spp. has made 

selection of suitable crops for rotation schemes difficult, 

although using grasses has been successful. li Rhodesia, 

weeping lovegrass. Katabora lRodesgrass. or Baibatsi 

Panicuiiigrass provide good control of ,f.javanica. Beca use of 

tle relatively rapid decline of Ihhidogyne spp. in the absence 

ofla suitable host. nonlost crops cai be grown fora shorter tiiiie 

for root-knot nematode control than that required for potato 

cyst nematode control, 


BROt)IE, .BI.. and R. I.. PI.AISTEI). 1976. Resistance to root-knot 

ri2atodes in So/wru, tuhrrur ssp. Nematol. 

RANK.N. . I. 1971. laxonivyrf teteroderidae. Pages 39-162 

in: It. M. Zuckernian. W. F.Mai. and R. F.Rohde. eds. Plant 

Parasitic Neriatodes. Vol. I. Acadeinic Press. New, York. 345 pp. 

IA IALA. P.. and I'. R. ROWE. 1977. Reaction of 62 tuber-bearing 

,Sohrnu species rO root-knot neiatodes. ,ih'oidogyne incognita 

acrita. .1.Nerniatol. 8:290. 

False Root-Knot Nematodes 

Information on distibution of false root-knot nematodes is 

incomplete and warrants attention. This nematode isapparently 

native to the Andean regions of Peru and Bolivia, where losses 

of up to 55(i are not uncommon at altitudes of 2.000-4.200 m 

aind occasionally at lower altitudes. It also occurs in Argentia, 

Chile. Ecuador. the United States. Mexico, England. Ilolland, 

India, and the USSR. 

Symptoms 

No specific abo\cground symptoms are diagnostic, although 

infected plants are stunted and tend to wilt under moisture stress 

as I result of poor root growth and or root damage. Galls oti 

roots are similar to those produced by root-knot nematodes, 

and infected plants lack normal fibrorus root growth. Larval 

invasion can cause death and deterioration of the small roots. 

Galls occur ina beadlike fashion, and, inBolivia and Peru. they 

are comnonly called "'rosario." referring to rosary heads (Fig. 

102). 

Individual gall size depends upon nenatode density, root size, 

and the race of the nematode. Gall shape isusually spherical and 

similar to that caused by ieloidogyne arenaria. but extension 

of lateral roots on tilegalls is usually lacking, depending upon 

the nematode race and host type. Although the false root-knot 

nematodes do not cause easily recognizable symptoms on 

98 

potato tubers. they attack tubers and usually penetrate under 

the skin to a depth of approximately 1-2 mm. 

Disease Cycle of Causal Organism 

.Vacohhusah rranson potatoes has a disease cycle somewhat 

similar to that on sugar beets. The first molt occurs within eggs; 

second-stage larvae emerg,. invade small roots, and establish 

themselves in a faorable location. Cells of the feeding site 

(vascular cylinder) increase in size, followed by necrosis of the 

cortical cells, larvae feed and undergo two molts. They either 

leave the roots as preadults or continue feeding in the already 

established site, develop galls on roots, and, complete the life 

cycle. A portion of those that leave the roots complete the final 

molt and become males or active females. Sex 

distinguished 

can be 

at the end of the third stage. Young female 

nematodes love to large roots and establish themselves with 

their heads near the vascular tissue. Surrounding cells enlarge 

and a gall develops. Posteriors of the females extend to.vard the 

outside. and an opening is formed on the root surface, where a 

portion of the eggs are deposited intoi a gelatinous matrix. 

Preadult anrid active females also invade tubers and penetrate 

approximately 1-2 mm below the skin surface. Although a few 

develop to maturity, the majority remain in itsemiquiescent 

stage for long periods and serve as tle primary means ofdisease 

dissemination. Larvae lay also infect tubers, but these seldom 

develop beyond the larval stage and may be disseminated in that 

form. l)epending upon host, temperature, and race of 

nematode, generation time is usually het\meen 25 and 50 days. 

Epidemiology 

False root-knot niematodes have wide temperature 

adaptability, surviving and reproducing most rapidly at a 

temperature range of 20-26'C . Thus, they could become a 

limiting factor to potato production in warm climates. 

However, in the Andes they 

at 15-18'C 

are associated 

and 

with 

are not 

potatoes 

limited 

erown 

by soil type. N. aherrans 

odigeia..t. ccurring in the Andes contains two or more races differing in 

pathogenicity and is often found with Glohodera and 

Al'logrm' spp. Obtainiig resistance to Glohodera or 

leloihlogne spp. might therefore alter tilecompetition for 

Nacohbus spp. or \ice versa. :Vacohhus-induced galls are often 

infected with Spongospora suhterranea,tile fungus of powdery 

scab. 

Other Hosts 

False root-knot nematodes have arelatively wide host range. 

Fig. 102. False root-knot nematode (Nacobbus aberrans) on 

potato roots. (Courtesy P.Jatala)

They attack many major crops in the Andean region and many 

weed species, causing extensive damage to members of the 

Solanaceae. Races differ in their ability to attack certain crops. 

Resistance 

Limited work has been done ol development of resistance to 

N. aberrans. A native Solantr tu erosum ssp. amligena 

cultivar shows a high level of resistance, and excellent resistance 

exists in S. sparsipiluni. 

Control 

II In preliminary experiments in South America, economical 

control has been achieved through the use of'organophosphates 

and oxime carbamates. 

2) Because of'a relatively wide host range, selection of suitable 

crops for rotation schemes isdifficult, although members ofthe 

Gramineae and most of the Leguminosae are no nhosts. 

Populations decline rapidly in the absence of a suitable host: 

therefore, rotations can be shorter than those required for the 

potato cyst nematode. 

3) Quarantine and restriction of potato seed tuber shipments 

into disease-free areas should be strictly enforced. 


AI.AR)N. C., and I'. IA I ALA. 1977. Afecto de la temperatura en la 

resistencia da Solanuon ardi,en a it Nacoblbu aherras. 

Nematropica 7:2-3. 

CLARK, S. A. 1967. [he development and life histor' of the false 

root-knot nematode. 'ah, .serendipiticu.s. Ne'natologica 

13:91-11). 

IATAIA. P.. and M. de SC1R RAIl. 1975. Mode oftdissenlination 

ol Nacotbu. spp. in certain potato-grossing areas of Peru and 

Bolikia. I. Nenratol. 7:324-325. (Ahstr. . 

,JAILA,IP.. and A. M. GOIL)EN. 1977. laxonomic status of 

\acothrts species attacking potatoes i South America. 

Nenatropica 7:9-10. 

LaROSA, t). i., and I'. IA AI.A. 1977. Depth of penetration of 

.\acobhu.aherran.s in potato tuhers. Ncratropica 7:11, 

LORI)EI.I.O. I.. 6. F.. A. P).I.. ZAMITII. and 0. J. BOOCK. 1961. 

f-No nematodes found attacking potato in Cochaha mba. Bolivia. 

Ain.. Acad. Bras. Cienc. 33:2)9-215. 

SIER. S.A. 1970. Revision of tile genus ,acoth-o Ihorne and Allen. 

1944 (Nematode: lvlernchoidea). .1.Neniatol. 2:228-235. 

Lesion Nematodes 

Of the several Pratrhnchiuns spp. known to damage potatoes, 

P. penetrans is the most important in North America and in 

Europe. Species in other areas are P. crefratms, P. mittyu's, P. 

thornei,and P. scribneri in Europe; P. crenatts, P. hractlvurts 

and P. scribneri in North America: P. anclinus, P. scrihneri,P. 

penetrans,and P thornei in South America: P.hrachvurusand 

P. scrihneri in Africa: and P. vunus and P. coffeae inI Japan. 

Symptoms 

High populations of lksion nematodes cause areas of poor 

growth: plants are less vigorous, turn yellow, ard cease to grow. 

Damage is caused by direct feeding, and usually only cortical 

tissues are affected. Large numbers of nematodes cause 

extensive lesion formation and cortex destruction of 

unsuberizcd feeder roots (Fig. 103A). Affected roots are 

commonly invaded and damaged by other soil iicroorganisms, 

thus increasing root destruction. Rhizomes are not attacked as 

severely as roots. 

In general, P. penetrans in primarily aroot pathogen, whereas 

other species such as P. brachi.urtus and P. scribneri cause 

serious tuber damage. Lesions on tubers become visible when 

nematode numbers in a small area of the tuber are high enough 

to cause a number of adjacent cells to die. In South Africa, 

symptoms on tubers caused by P. brachyurutsare purple-brown 

areas about 0.5 nim in depth, irregular in shape.and surrounded 

by a slightly depressed border. Raised wartlike protuberances, 

unsightly lesions, pimples, and weight loss and withering 

in storage reduce tile market value of tubers and make infected 

seed potatoes worthless (Plate 83). 

Lesion nematodes are often associated with wilt-causing 

fungi such as Fusaritjnrspp. and J'eriicillium spp. Other fungi 

and bacteria are frequently present in potato tissue damaged by 

these nematodes. 

Disease Cycle of the Causal Organism 

The first molt occurs in the egg, and the second-stage larva 

emerges from the egg. All stages are wormlike and active. They 

enter plant roots usually just behind the root cap but may enter 

through other u,nsuberized surfaces of roots. rhizomes, and 

tubers (Fig. 10313). Entry of, and movement through, roots may 

be intercellular or intracellular. Entry is apparently 

accomplished largely by mecha nical pressureaid cuttiig actioI 

of tie stylet rather than by enzymatic action. lesion formation 

and root death usually occur ahead of the area penetrated. In 

tubers, cells surrounding nematodes are brown: cytoplasm is 

granular: and nuclei are reduced in size. 

Males are common in some species but not in others. Bisexual 

reproduction occurs in species in which males are abundant. 

Gravid females lay eggs in the soil and roots, either singly or in 

small groups. (ieneration time is from four to eight weeks, 

depending uponi factors such as temperature, nematode species, 

and host. 

Epidemiology 

Soil temperature requirements vary greatly with species. 

Optimum temperature for reproduction of P. petetrans is 

16-20' C: it is anrimportant pest in regions of Europe and the 

United States that have this temperature range. In warmer 

climates, species with higher temperature optinia (25-28°C), 

such as P. hractitrrus in Africa and R coffeae in southern 

.Japan replace P. pe slerans. 

Damage to potatoes by lesion nematodes is usually associated 

with coarse-textured soils. This may be partly because some of 

the species involved, e.g., P. penetrans, are favored by sandy 

soils and partly because such soils are preferred for potato 

culture. 

Soil moisture influences movement and other activities of 

Prat lenchusspp. In general, favorable soil moisture level isone 

Fig. 103. Root-lesion nematode (Pratylenchus penetrans): A, 

damage on the roots; B, adults, larvae, and eggs inside root. 

(Courtesy W. F. Mai, B. B. Brodie, and M. B. Harrison) 

AP

at which the soil particles and aggregates are surrounded by a 

film of water but the intercellular spaces are free of water. 

Other Hosts 

Species of' Praty'lenchusthat attack potatoes have wide host 

ranges. More than 164 hosts have been recorded for P, 

Iwnelr 

an s 

. 

Resistance 

A high degree of resistance in potato has not been identified, 

although Peconic and IHudson have some resistance, Lower 

population increase with certain resistant cultixars is due to 

fewer numbers of eggs produced per female, 

Control 

I )Soil fumigation decreases populations of Pratilhlchts spp. 

and often increases potato yields but is practical onuly x\hen 

yields and prices of potatoes are high. Soil tnmigants are further 

limited becatuse thtv are ineffective in fine-textured and cold 

soils. Nonfulnigant ncinlticides have little or no phytotoxicity, 

are easier to apply, may be applied at planting time, and are 

more ellectis c in a wider vatricty of soil types. Such nematicides 

are usuall*V more practical than fumigants for controlling rootlesion 

nemat odes. 

2)Controlling root-lesion nematodes by crop rotation is not 

effectix e because tile species hatc a wide host range. Rye is an 

excellent host of A penetrans. Secere plant danage and yield 

reductions follo%, rye is a winter co\er crop. 

Selected Reference% 

IICKI RSuN. (I. .I \1 I)\RI I\(,. -ind (, I) (Gl1llt.1\ 1964. 

PlI[hoge.nicli\ , 

and po)Ii;kitonI l1ctlt0l h1all h'/I Ilshtl-IIan oil 

POUa iI d Corn1.1.. pithlIogx 34: ; .32. 

I)['\ ,\. \Is 73 t. O t lCc inl lotal h (. /.tIll tl IIn/'r,' i toI) 

PrIl /' 11h'l/s ls 'IrIIoj \ 1 1tm lnCI \ . 18ll6 .:10 8 II: \h ill ilci 

Papers. 2nd Intl. Cong. Plant Ilathol.. Minneapolis. MN. 

KII\. II I',Q1,7 \oc, oli tie 1h.,l lance, ec,lo, and ,1Ialll 

d,\ailll I /ral ll/n I( II,./ih l(/,r r . \cm/llh 131 I 124, 

MILLIER. P. %I..and A. IIAWKINS. 1W69. L.ong terni effects of 

ptplnf f lllal'illntiu oin potrlo licldi .\I. PotI o .I.46-1187 .197. 

Potato Rot Nematodes 

Ditlenchus destructor is primarily ar important potato 

pathogen inthe temperature regions of Europe and, especially, 

in the USSR, probably due to its inability to withstand drying 

rather than toa direct tnemperature relationship. It also occurs in 

Soutl Africa, some areas of' tile Mediterranean region, a few 

isolated regions of North America, and in South America. 

Symptoms 

No specific abovegrouinul syiptols exist. It confines its 

attack to underground part:, of the plant, pritiarily the stolons 

and tubers but not the roots. [ie earliest belowground 

symptoms are small, white, chalky or light colored spots just 

below the surface of the tuber when it is peeled (Fig. 104A). 

Affected tissues ar, dry and granular. As aflected areas coalesce, 

tissues dharken and are invaded by fiungi and bacteria. 'Iliber skin 

becomes paper thin and cracks as tie underlying tissues dr. 

and shrink (lFig. 11411 and C). I nder suitable environnental 

conditions in the field or in storage. bacterial wet rot nay cause 

complete tuber destruction. 


The causal organism is now known as D.destructorThorne 

(syn. ,Angui/lu/adlipsaci K in. 7'henclus dlevastatrixv, K h i,1). 

dipsaci Filipjev). 

Disease Cycle 

Nematode inoculunl may survive intile soil, on fungi, or on 

100 

weed hosts, or it nlay be introduced by planting diseased seed 

tubers. 1). desiructor enters small potato tuhers thirough 

Icnticels or the skin near the eves. Nematodes at first exist singly 

or in small numbers in the tissue just beneath the skin of the 

tuber, and small white lesions are present during ear!', to 

midseason tuber fornation. Great numbers of nematodes are 

present in advancing margins of the lesions where the tissue is 

soft and mea ly.More tuber tissue becomes involved as 

populations increase. [issue becomes darker in color as 

secondary organisms that cause dry or wet rots follow. The 

nematode continues to live and develop in harvested tubers. 

Low temperatuic o,erwiintering probably occurs in the egg 

stage. 

Epidemiology 

The potato rot nematode survives in soils as low as -28* C. 

Greatest infestations occur at 15-20'C and at high relative 

humidity, 90-I1001". l)evelopment occurs in the range from 5 to 

340 C. The nenatode cannot sti rvive under drought or low 

relati\e hunidity (below 40(' ).Spread of the nrematode to new 

areas is primarily by tile use of infested potato seed. 

Other Hosts 

1). detstructorhas a very wide host range of higher plants and 

soil-inhiabiting fungi. 

Control 

1)Use only uncontaminated seed. All known potato cultivars 

are to some degree Susceptible. 

2)Soil fumigation isan effective control measure and call be 

used where it is econonically feasible. 

3) Crop rotation isdifficult oriimpossible because of the wide 

host range of the nematode. Ilowever. rotation is reported to be 

an eficetive practice in the USSR. 

4) lot water seed treatm ent has not vet been developed for 

seed po ta toes. 

5) Control isdifficult, but unknown factors must be operating 

because spread has not been extensive, and in some previously 

C 

B 

Fig. 104. Nematode (Dilylenchus destructor) tuber rot. Note 

white chalky area (A) and surface cracking (B and C). (A, 

Courtesy L.R.Faulkner and H.M.Darling; B and C, reprinted by 

permission of Phytopathology) 

. 

/

infested areas of North America severity of the problem ias 

declined. 


ANI)ERSSON, S. 1967. Investigationson the occurrenceand behavior 

of Ditvlenchus destructor in Sweder. Nematologica 13:406-A 16. 

FAU.KNER, L. R.. and H. M. DARIJNG. 1961. Pathological 

histology, hosts, and culture of the potato rot nematode. 


SMART, G.C.. Jr, and H. N1.)ARi.ING. 1963. Pathogenic variation 

and nutritional requirements (f Dityilenchus destructor. 

Phytopathoiogy 53:374-381. 

THORNE, (. 1961. Pages 138-148 in: G. Thorne, ed. Principles of 

Nematology. McGraw-Hill. Inc., New York. 553 pp. 

Stubby-Root Nematodes 

Stubby-root nematodes have a very wide host range in the 

temperate regions, and they transmit virus in many different 

types of plants. 

Symptoms 

No diagnostic aboveground symptoms exist except stunting. 

Roots cease elongation, resulting in numerous stunted "stubby 

roots" which show little or no necrosis, discoloration, or other 

injury symptoms. 


Paratrichordorus pachyvderm us, P.christiei, and Trichodorus 

primiivusattack potatoes. 

Disease Cycle 

Eggs are deposite! in the soil. Immature and adult forms 

migrate through the soil and feed superficially on roots without 

becoming embedded in the plant tissues. When soil temperature 

is 15-20' C. the life cycle is completed in about 45 days. These 

nematodes most frequently occur in light, sandy soils, although 

they have also been reported in other soil types. 


Feeding activity of the stubby-root nematode occurs 

principally at root tips. Epidermal and outermost cortical cells 

are punctured: as feeding proceeds, the protoplast shrinks from 

the cell wall. After 5-10 sec, the nematode moves on to another 

cell. Feeding activity is followed by a loss of meristematic 

activity. Parasitized roots lack a root cap and a region of 

elongation. Differentiation of protoxylem elements occurs 

almost at the root apex. Apparently, therefore, new cell 

production is halted but differentiation of existing cells 

continues. 

Epdemiology 

In the Netherlands, nine species of stubby-root nematodes 

transmit tobacco rattle virus. A close relationship exists 

between populations of Trichodorus and the virus is')Iates. 

Tobacco rattle virus is probably not readily spread for long 

Aphids 

distances by virus-infected plant material because the strain of 

the virus would probably not be suitable to the nematode 

population of the new location. Activity of stubby-root 

nematodes, as determined by virus spread, is affected by soil 

moisture, type, and temperature. Greatest activity occurs in 

sandy soil at 15' C with 16.7% moisture; as soil moisture 

decreases, activity decreases. Very little more is known about 

the influence of the environment on these nematodes. 

Control 

1)Soil fumiga!nts have been used to control Trichodorusspp. 

and thereby reduce spread of tobacco rattle virus. 

2) Not :nough is known about the host range of the nematode 

and the virus, advise rotation as a control measure. 


HEWITT, W.B.,D.J. RASKI, and A.C.GOHEEN. 1958. Nematode 

vector of soil-borne fanleaf virus of grapevines. Phytopathology 

48:586-595. 

RASKI, D.J.,and W. B.HEWIT. 1963. Plant-parasitic nematodesas 

vectors of plant viruses. Phytopathology 53:39-47. 

ROHDE, R.A.,and W. R.JENKINS. 1957. Host range of a species of 

Trichodorus and its host-parasite relationships on tomato. 


VAN HOOF. H. A. 1968. Transmission of tobacco rattle virus by 

Trichodorusspecies. Nematologica 14:20-24. 

Nematicides 

Control of nematodes in soil can be achieved through use of 

nematicides, of which only a limited number are presently 

available. All should be considered potentially hazardous, and 

some are difficult to apply. They must be applied correctly and 

under suitable environmental conditions in order to obtain their 

full nematicidal potential. 

Dispersion through the soil and activity of most soil-applied 

nematicides is enhanced when soil tilth, moisture, and temperature 

are in the proper range. Dosage level and technique of 

application will depend on the nematicide, soil type, rate of 

control desired, and economic considerations. Nematicides may 

be gases, liquids, or granular solids. A well-qualified, experienced 

person should be consulted before applications of 

nematicide are attempted. 

Some nematicides are fumigants, which volatilize in soil and 

become gases that move through soil. Others are nonfumigants, 

which depend upon external forces such as soil water for 

movement. Another category of nematicides consists of those 

that move systemically in the plant and can be applied to foliage. 

Most currently available ner.aticides are either halogenated 

hydrocarbons, organic phosphates, or carbamate compounds. 

Some are phytotoxic. All are toxic to humans. Therefore, 

caution must be exercised in their use. Label directio,!s must be 

carefully read and strictly followed. 

(Prepared by W. F. Mai, B. B. Brodie, M. B. Harrison, 

and P. Jatala) 

Several potato virus diseases are transmitted by aphids, and Others, although seldom establishing colonies on potatoes, are 

identification of the vector involved is often necessary. Those vectors of some nonpersistently transmitted potato viruses 

that commonly colonize potato (Table I1)can be easily (Table i11).M)'zuspersicaeisthemost efficient aphid vector and 

identified by morphological characteristics (Figs. 105 and 106) is found worldwide. 

that are visible to the naked eye or visible when magnified by a Aphid species differ not only in morphology and ability to 

hand lens (Table IV). These aphids may transmit both transmit potato viruses but also in form (morph), life cycle, and 

circulative (persistent) and stylttborne (nonpersistent) viruses, behavior, depending on the environment (temperature, relative 

101

humidity, photoperiod, and host plant condition) to which the Where winter conditions are severe, most potato-infesting 

aphid or its mother is exposed. Thus. the life cycle of any aphids overwinter as sexually produced eggs laid on the rough 

particular species riaN not be the same in different parts ofthe bark of a woody host or on the crown and leaves of an 

world. Aphids may he winged (alate) or wingless (apterous), herbaceous biennial or perennial plant. A female nymph 

male or emale. Females may he o%iparous (sexually producing hatches from each egg in the spring, feeds on the expanding 

fertili/ed oxer%%intering eggs) or parthenogenetic and viviparous foliage, and after molting four times, develops into a nature, 

(asexually producing living young, called nymphs), wingless, parthenogenetic female. She gives birth to female 

TABLE i11.Aphid Pests of Potato and Known Vectors and Nonvectors of Potato Viruses' 

Virus Transmitted" 

Aphid 


Leafroll Y 


A M 

Potato Acuba 

Mosaic 

Alfalfa 

Mosaic 

Coloni/ers ol potatoes 

,.lphi. iA..rpii-fI;'at/ae. cornplex' (melon) 

.-IIhi. na.turtif buckthorn) 

.Aulacorthui. lani' (Ioxgloye) 

.t/a(rophtint euirhiae'(conmmon potato) 

./it: atcalon 'io (shallot) 

.1/ii. per.%iat' (green peach) 

lIhopahemiiphonimi lati.hsipion(bulb and potato) 

Ihoah.oiphumruiabtdominali. (rice root 

- 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

_ 

+ 

_ 

- 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

+ 

'Smri ihio 'he Icuj 

I'rconiniton ctloniicrs of or visitors on potatoes 

,-I(irhin il)hito pt.uttm' 

.. i rthoipio pri t/ac 

Aphi. /ia'at 

("avariella ' 

i,%tiliateae 

lit dto eri.knit 

.lacro.ilhontiilla .%an/orni 

r ttro. 

.Ilizt.u hiuoitl 

+ 

_ 

+ 

+ 

+ 

+ 

+ 

+ 

- 

+ 

_ 

+ 

. rnala s + + _ 

.\m'o:Ii 4ctil//t',ilds 

Rhohinu,,s '.itmiia tialhrleaeta/ipaelhts 

Rholi wmpntm pad, 

I-rm Kennel\ cit a 11962) and Beemsier and Ro/endaal (1972). 

+ 

+ 

+ 

+ 

+ 

+ 

+ = \ector. -- -- nonector, I 

Ma o\crinter as eggs. 

incficient or inconsistent vector. 

TABLE IV. Key to Wingless Viviparous Female Aphids Colonizing Potato 

I. Siphunculi absent. Cauda small, rounded. On stolons. Smynithurodes hetae. 

II. Siphunculi present. Cauda extended, not rounded. 

A. Antennae always much shorter than body: head without prominent anten,;al tubercles, front of head slightly convex, almost flat. Siphunculi 

slightly longer than cauda. 

I. Body and antennae with long hairs; green with deep orange markings between and at bases of ,iphunculi; siphunculi almost cylindrical, 

thinner iust before flange. On roots. R/opalosilium ruflahdotoinalis. 

2. Hody and antennae without long hairs; yellow to green, without deep orange markings on posterior; siphunculi cylindrical. 

a. On overwi nteri ng host, bodydeep green and, on potato, lemon yellow to green; siphunculi pale to light brownish with dusky tips; cauda 

y'clloss to light brown. same color as basal portions of siphunculi. On leaves and flowers. Aphis nasturtii (Plate 84), 

b. Body pah: yellow, yellow-green to mottled blackish green, siphunculi black, cauda dusky green to black. On leaves. Aphis gossl'fi 

/ani.dae'complex. 

B. Antennae usually as long as or longer than bodv: head with prominent antennal tubercles; front of head broadly concave; siphunculi much 

102 

longer than cauda. 

I. Siphunculi shiny black, cxtremely swollen: swollen part over four times as wide as the basal 1/3and distal I / 10 part, with a well-developed 

flange. Body pale olivc green to shiny dark olive green with a brown to black sclerotic patch covering most of the dorsum of the abdomen. On 

sprouts and subterranean parts. Rholao.silgto/nin. lahiyrp/ton. 

2. SiphunCuli brown to pale yellow-green: if black, then siphunculi cylindrical; on most, siphunculi only slightly swollen on distal half. 

a. Body clongated. wedge-shaped. Largest of potato-infesting aphids. Body shades of green, pink, or yellow with a darker dorsal ridge. 

[lead with prominent, outward sloping antennal tubercles. l.egs long, antennae longer than body; siphunculi cylindrical, flared outward, 

about 1.25 times as longas the distance between their bases. Siphunculi light brown, sometimes with darkerapices. On leaves, stcms,and 

flowers. .1facro.ip/tium euphorhiae(Plate 85). 

b. Body ovoid or pear-shaped, antennal tubercles prominent and converging inward or with parallel sides. 

1.) Body pear-shaped. globular. widest just ahead of siphunculi. flead with prominent parallel, straight-sided antennal tubercles. 

Siphunculi straight, with prominent dark flanges at tips. Body shiny light yellow green to dark green, sometimes brownish, usually 

with darker pigmented areas around base of siphunculi: legs and antennae with dark joints. On leaves and flowers. Aulacorth,o 

.oltani (Plate 861. 

2.) Body ovoid, almost same width from thorax to base of siphunculi. then sides gently rounded to abruptly meet thecauda. Head with 

prominent in-pointed antennal tubercles. 

a.) Body deep pink, peach, yellowish, light green to almost colorless. Siphunculi same color as body with the tips darker; slightly 

swollen on apical half. Cauda short. On sprouts, foliage, and flowers. iaus persicae(Plate 87). 

b.) Body dull yellowish brown to greenish brown. Siphunculi same coloras body without the tips darker, swollen towards the apex. 

Cauda upturned, hardly visible from above. On sprouts. M v:us a.calo'tiCus. 

+

antennal tb l 

tuberce 

u 

antenna 

eye head 

-torax 

cuasiphunculus 

- 

abdomen 

Fig. 105. Parts necessary for identification of a wingless aphid. 

(Courtesy M.E. MacGillivray) 

Fig. 106. Outline of head region of wingless potato-infesting 

aphids showing shape of antennal tubercles. Left to right: Myzus 

persicae, Aulacorthum solani, Macrosiphum euphorbiae, Aphis 

nasturtii. (Courtesy M. E.MacGillivray) 

Because the potato plant atd its tubers are vulnerable to 

many diseases and pests, seed quality, as determined by relative 

freedom from these entities, is of major importance in potato 

production. This became apparent during the latter part of the 

19th century when pests and disease organisms were 

disseminated in seed stocks that were allowed to move freely 

throughout the world during the rapid expansion of potato 

culture. Because of this seriously developing dilemma, the 

United States established the National Plant Quarantine Act of 

1912. prohibiting the importation of potatoes infected with 

black wart (Stncht'irium endohioticum (Schilb.) Perc.), an 

embargo that is still in effect. An embargo preventing 

importation of potatoes from countries harboring powdery scab 

(Spongos)wora subterranea(Wallr.) Lagerh.) was enacted two 

%,earslater. 

/ 

Seed Potato Certification 

nymphs, some of which may develop wings. Eventually, in later 

generations, most of the aphids will be winged and fly to 

herbaceous plants, weeds, and horticultural flowers or 

vegetables, including potatoes. ilere the winged forms deposit 

female nymphs that, when mature, produce additional females 

by parthenogenesis. in late summer, when the length of the night 

extends past II hours and night temperatures decrease, sexual 

morphs (males and oviparous females) are produced. Winged 

viviparous females usually fly to the overwintering host and 

deposit nymphs that develop into oviparous females. In the 

meantime, males (winged and wingless) arrive on the host plant 

and mate with the oviparous females, after which the fertilized 

eggs are deposited to complete the cycle. Eggs are pale green at 

first and later become shiny black. 

In mild cli. ates, sexual aphids and eggs do not occur, and 

parthenogenetic, viviparous females are produced throughout 

the year. Some species, such as Myzus persicae, Macrosiphum 

euphorbiae, and Aulacorthum solani, which normally 

overwinter as eggs in colder climates, survive as viviparous 

females in sheltered places such as greenhouse and storage 

cellars. 


BANZIGER, H. 1977. Keys for the identification of aphids 

(Homoptera). 11.Field identification of common wingless aphids of 

crops in Thailand. Dept. Agric. Minist. Agric. and Cooperatives, 

Bangkok, Thailand, and UNDP FAO Th. A. 74/019. Plant Prot. 

BEEMSTER, 

Serv. Tech. Bull. 36:1-41. 

A. B. R.. and A. ROZENDAAL. 1972. Potato viruses: 

Properties and symptoms. P'ges 115-143. in: J. A. de Bokx, ed. 

Viruses of Potatoes and Seed-Potato Production. Pudoe, 

Wageningen. The Netherlands. 233 pp. 

COTTIER, W. 1953. Aphids of New Zealand. N.Z. Dep. Sci. Ind. Res. 

Bull. 106. 382 pp. 

EASTOP, V. F. 1958. A study of the Aphidae (Hornoptera) 

Africa. 

of East 

Her Majesty's Stationer), Office, London. 126 pp. 

EASTOP. V. F. 1966. 

(Homoptera). 

A taxonomic 

Aust. 

study 

J. 


Zool. 

Australian 

14:399-592. 

Aphidoidea 

HILLE RIS LAMBERS, D.. and M. E. MacGILLIVRAY. 1959. 

Scientific names of potato-infesting aphids. Can. Entomol. 

91:321-328. 

HOLMAN, J1.1974. Los dfidos de cuha. Inst. Cubano Del Libro, La 

Habana. 304 pp. 

KENNEDY, J. S., M. F. Day, and V. F. EASTOP. 1962. A conspectus 

of aphids as vectors of plant viruses. Commonw. Inst. Entomol., 

London. 114 pp. 

PRIOR, R. N. B., and J. R. MORRISON. 1977. Key for the field 

identification of brassica. potato and sugar beet aphids with 

photographic illustrations. Minist. Agricul. Fish. Food, London. 

(Prepared by M. E. MacGillivray) 

Origin of Seed Potato Certification in North America 

In 1904, while studying potato diseases in Europe at the 

request of the U.S. government, Professor L. R. Jones of 

Vermont observed seed improvement programs, he later 

persuaded Dr. W. A. Orton of the Bureau of Plant Industry of 

the U.S. Department of Agriculture (USDA) to visit Germany in 

1911 to observe potato diseases and study the seed potato 

inspection program initiated by Dr. Otto Appel. On his return 

from Europe, Dr. Orton, with Dr. William Stuart of the USDA, 

developed a plan for the inspection and certification of potato 

seed stocks based upon the German system. During the next few 

years, they presented their proposal to growers, potato 

specialists, ad state agricultural experiment station officials 

and at the annual meetings of the American Phytopathological 

Society and the National Potato Association of America (now 

103

the Potato Association of America). 

In 1914, Dr. Orton, accompanied by Dr. Appel of Germany, 

Dr. H. T. Gussow of Canada, Dr. Johanna Westerdijk of 

Holland, and potato specialists from the USDA. visited the 

principal potato-growing areas of 13 states extending from 

Maine to California to study disease and other problems related 

to seed production. This study stimulated interest and added 

impetus to the movement for organized inspection programs. 

These efforts culminated i. the first official Potato Seed 

Certification Conference, which was held in Philadelphia, PA, 

on December 28, 1914. Representatives from Canada. 

Germany, Ireland, the USDA, and 12 states participatud. At 

this conference, the basic framework of the present seed potato 

certification programs was formulated, 

Dr. Orton recommended that "a system of official inspection 

and certification" be established in each of the seed-growing 

states, with emphasis being placed on "freedom from disease, 

varietal purity and vigor." The suggestion was also made that 

programs be administered by a "state agency such as an 

Experiment Station and protected by suitable legislation 

penalizing misu.,- of certificates." The proposal, which 

suggested that programs be operated on a voluntary basis and 

that growers stand the cost of inspection, also outlined 

procedures for making field inspections, established disease 

tolerances, suggested the use of certificates and official tags for 

inspected seed, and proposed size and quality of tubers. Even 

though virus infections were not suspected at the time, the 

proposal recognized that "degeneration" or "running-out" of 

seedstocks was tuber-transmitted and suggested that "seed" 

tubers be selected from healthy-appearing stocks. 

Seed potato certification programs in North America became 

a reality during 1913-1915, when Canada (New Brunswick and 

Prince Edward Island), Idaho, Maine, Maryland, Vermont. and 

Wisconsin established official programs. Ten more states 

started programs between 1916 and 1919, followed by three 

additional Canadian provinces and eight states during 

1920-1922. 

In the early days of certification in North America, inspectors 

were confronted with the problems of varietal mixtures, varietal 

synonyms, and degeneration ur "running-out" of seed stocks. 

The confused picture of the degeneration complex started to 

clear when Quanjer et al in 1916 first established the infectious 

nature of potato leafroll by graft transmission; shortly 

thereafter, Oortwijn Botjes (1920) and Schultz and Folsom 

(1921) reported independently that the aphid Myzus persicae 

transmitted the causal entity of leafroll from plant to plant. 

Subsequent investigations exposed the involvement of 

numerous tuberborne virus diseases, such as mild and severe 

mosaic and spindle tuber (the causal agent of which is now 

known to be a viroid), with seed degeneration. Recognition of 

these diseases by certification personnel provided the ba,: far 

their subsequent control. A tremendous improvement in yield 

and quality ofseed stocks occurred after certificatior personnel 

had mastered the diagnosis of virus diseases, 

Present Day Seed Potato Certification 

eent DaypSdPotato Certification ayand 

Seed potato certification today represents a voluntary 

agreement between the seed grower and the certif.ing agency. In 

the United States, programs are handled by individual states 

TABLE V. Field Tolerances (%)for Certified Potatoes, as Required 

by Wisconsin Certified Seed Potato Agency, Madison 

Disease or Varietal Inspection 

Mixture First Second or Subsequent 

Leafroll 1.5 1.0 

Mosaics 2.0 1.0 

Spindle tuber 1.0 1.0 

Total 3.0 3.0 

Bacterial ring rot 0.0 0.0 

Varietal mixture 1.0 0.1 

104 

and administered by state departments of agriculture, land 

grant universities, grower associations, or various combinations 

of these agencies. In Canada, seed potato certification is a 

federal program carried out hythe Plant Quarantine Division of 

the Department of Agriculture. Since all agencies have been 

given official status by their respective state or national 

governments, protection against the fraudulent use of the term 

"certified seed potatoes" has been assured. Disclaimer clauses 

limiting liability to the value of the seed are commonly used by 

all agencies to protect both the grower and the agency. 

Each agency publishes certification standards outlining 

eligibility requirements for inspection, grower fee schedule. 

disease tolerances, grade requirements, winter tests, and rules 

governing sale of certified seed. Application inspection forms 

are sent to individual growers before the planting seaso n 

requesting alisting of cultivars, classification and source of seed 

lots, acreage, field numbers and location, previous crop history 

of fields, and date of planting. This information is used by the 

agency to determine eligibility for inspection. 

Fields are planted with pretested and approvea seedstocks. 

Practicesareadopted that minimizethespread ofvirusesand of 

pathogens borne by soil and debris. Procedures for inspections 

vary among states but, in general, are quite similar. A minimum 

of two field inspection- is made during the growing season at a 

time most opportune for detecting diseases and varietal 

mixtures by visual examination. Field tolerances fordisease and 

varietal mixtures vary among agencies but, in general, are quite 

similar. Those currently used in Wisconsin for the Certified class 

are fairly typical (Table V). 

Failure to meet the tolerances is cause for rejection and, in 

addition, certification may also be denied for the prevalence of 

other diseases such as blackleg, haywire, or wilts. Lack of 

isolation, unsuitable cultural conditions, high aphid 

populations, nematodes, unsatisfactory performance of test 

samples, orotherfactorsthat mayimpairseed valuemayalso be 

cause for rejection. Of the acreage rejected from 1968-1972 in 

North American agencies certifying over 1,000 acres per year, 

bacterial ring rot, leafroll, varietal mixture, mosaic, and 

blackleg accounted for 5.6, 0.8, 0.7, 0.5, and 0.4(,', respectively. 

Harvest inspections are required by some agencies, whereas 

others require both a harvest and a bin inspection, which 

identifies the stored seed and includes estimates of volume, 

grade, and tag eligibility. Certification is not complete until the 

seed has been graded for quality and size in conformity with seed 

grades and identified with official tags and seals and has passed 

inspection by the State-Federal Inspection Service. Inspection 

reportsare issued to the grower by the inspectoraftereach field, 

harvest, and bin inspection. 

Most agencies in North America certify two basic classes of 

seed potatoes-"Foundation" and "Certified." Requirements 

for the production of Foundation class seed are much more 

rigid, e.g., Foundation class seed growers mus, enter their entire 

acreage for inspection, field tolerances for disease are 

approximately one fourth of those allowed for Certified classes; 

and requirements for seed source, land, isolation, sanitation, 

the handling and storage of the crop are much more 

stringent. This class of seed isused to plant certified seed potato 

fields, Many certifying agencies require a winter test as part of 

their Foundation class requirement. A few agencies have made 

it compulsory for all seed lots, irrespective of class. These tests, 

which are conducted in Alabama, California, or Florida, where 

wing conditin f a , Caiforia, o dieasere 

growing conditions favor symptom expression of diseases, 

consist of field planting 300-800 tubers per lot and reading the 

resulting plants for disease content, primarily 'irus, and other 

factors pertinent to seed productivity. To receive Foundation 

designation, most agencies require that a seed lot shall not show 

a total in excess of 0.5% of the diseases mosaic, leafroll, and 

spindle tuber in the winter field test. 

Because of the short interval between harvest and planting of 

the winter test in Florida, dormancy ofcertain cultivars must be 

broken. Rindite, a 7:3:1 mixture of ethylene chlorohydrin (2chloroethanol), 

ethylene dichloride (I ,2-dichloroethane), and

carbon tetrachloride, applied at the rate of 141 ml m' (4 cc, ft') 

of treatment chamber (container), is one of the most effective 

chemicals used. The total dosage is applied at 24-hr intervals 

over a three-day period in an air-tight chamber filled to not 

more than one-third to one-half of its total volume. Samples are 

stacked at a uniform height of approximately 4 ft (1.2 m) on 

6-in. (15-cm) pallets arranged in rows that allow for ample air 

circulation provided by fans. Before treatment, samples are 

warmed for five days at 24-25'C, and during treatment 

temperature is maintained at 25-26'C; higher temperatures 

may result in injury. Rindite is placed in pans above the 

potatoes, and burlap bags are arranged to dip into the chemical 

and act as wicks. Rindite is highly toxic to humans and proper 

safety precautions must be taken. 

Certified seed is packed and shipped in clean, new bags or in 

bulk in clean, disinfested carriers. Individual bags and carriers 

containing bulk shipments are tagged, indicating cultivar, crop 

year, seria! or certification number, and grower's name and 

address. Tags are attached to each container so that neither can 

be opened without breaking the seal. 

In the United States all certified seed potatoes are graded in 

conlormity with standards established by individual states; in 

Canada they are established by the federal government. Grades 

vary among states but basically are quite similar to the federal 

grade of"U.S. No. I Seed Potatoes" established in 1972, which 

serves as a relerence point for marketing seed potatoes, 

replacing the U.S. No. I table grade. Most certifying agencies in 

North America have several grades, with a blue tag most 

frequently representing top quality and other colors for grades 

with less stringent standards. Size restrictions, which can vary if 

specified, usually range from 111'-3 1 in. (3.8-8.3 cm) in diameter. 

with a maximum weight of 12 oz (340 g). 

In the United States, fees for certification services are borne 

by individual growers, whereas in Canada they are absorbed by 

the federal government. Fees cover thecost of application, field 

inspections based on acreage, v:rus tests, shipping point 

inspections for individual bags or bulk shipments, winter tests, 

tags and seals. 

Following completion of field and harvest inspections, 

agencies publish crop directories listing growers and all varietal 

acreages that have met certification standards. Directories are 

also released by agencies following completion of the southern 

winter tests. Both of these publications, which are widely 

distributed within the potato industry, serve as an important 

tool in locating reliable seed sources, 

Seed potatoes in North America are produced primarily in 

the northern states along the Canadian border, in areas of high 

elevation in certain western states, and in all Canadian 

provinces except Newfoundland. At one time as many as 36 

states certified seed potatoes. However, the rapid spread of virus 

diseases was the primary reason that southern states dropped 

out of seed production. The spread of virus is considerably less 

apt to occur in northern areas, primarily because of lower 

populations of viruliferous insects, such as the green peach 

aphid, which spread many of the viruses that attack potato. 

From 1968 to 1977, approximately 78;i of the total seed 

production in the United States was produced in Maine (25%), 

Idaho (22%), North Dakota (17%), and Minnesota (14%). In 

1977, 19 states produced atotal of 230,458 acres of certified seed 

potatoes, of which these four states accounted for 

approximately 77%,. Prince Edward Island and New Brunswick 

are the leading seed-producing provinces in Canada, accounting 

for approximately 86%*-of the total acres (66,888) passing 

certification in 1977. During the past 10-year period, they have 

produced approximately 84% of Canada's seed acreage. 

Seed Improvement Programs 

Seed improvement programs are constantly striving to 

upgrade the quality of nuclear (elite) seed stocks, which serve as 

the basis for certified seed potato production. 

In an attempt to more effectively control several virus diseases 

and bacterial ring rot, four states and four Canadian provinces 

have established official Foundation (elite) seed farms where 

nuclear seed stocks are developed for their respective seed 

industries. The practice of planting cut seed in North America 

favors rapid spread of several diseases because the causal 

organisms are easily transmitted mechanically; such spread is 

curtailed by the planting of whole seed. 

These official seed farms are located in well-isolated areas 

that havea history of low insect populations and are staffed with 

personnel having the expertise to perform the technical 

procedures required for development of nuclear seed stocks. 

Practices involving strict sanitation, application of systemic 

insecticides at planting, and rigid spray schedules for control of 

insects and foliar diseases are adhered to at all times. 

In recent years, considerable time and effort have been 

devoted on these farms to developing nuclear seed stocks free 

from such latent viruses as X,S,and M. Virus-free programs 

have been developed primarily because of potato virus X 

(PVX), which causes latent mosaic. PVX, known as the "healthy 

potato virus" because of its symptomless characterisitics, 

produces visible symptoms only under certain environmental 

conditions, making control by roguing extremely difficult. 

Partly for this reason, seed potato certification personnel 

welcomed the introduction of virus X-free certification 

programs; they fully appreciated that the developing virus Xfree 

projects of the 1 9 30s in Europe, which led to such official 

programs in America after 1945, were big steps forward in seed 

potato improvement. In North America, seed specialists are not 

in complete agreement as to the desirability of maintaining 

totally virus-free seed stocks. some feel that advantages exist in 

the cross-protection provided by mild strains of PVX. 

Procedures for the development of nuclear seed stocks vary 

on these official seed farms, but in general, programs are based 

on clonal selections. A clone is a stock of tubers or plants 

derived from the same mother plant by vegetative propagation. 

Clonal selection implies the increase of stocks from selected 

healthy plants of desirable varietal type and their subsequent 

multiplication. 

In recent years, meristem and shoot tip culture have been used 

to obtain virus-free stocks of standard cultivars, old cultivars of 

historical interest, and promising new seedlings. This procedure 

is based on the fact that cells in the growing tips ofaxillary buds, 

as well as in tips of sprouts, may, by exposure of the plant or 

tuber to high temperatures, "grow away" from viruses even 

though the plant or tuber is systemically infected. By removing 

the meristem tips and allowing them to develop on special 

media, virus-free plantlets can be obtained. In practice, a high 

percentage of success in obtaining virus-free plants has been 

achieved when meristem tips have been taken from rooted stem 

cuttings or sprouting tubers that have beenexposed to 35-38 0 C 

for 4-6 weeks before bud excision. 

Plantlets produced in vitro by meristem tissue culture are not 

necessarily pathogen-free and so should be thoroughly screened 

for freedom from bacteria, fungi, viruses, and viroids. Some of 

the diseases or pathogens for which screening is conducted and 

the testing procedures used to detect them are: bacterial ring rot 

(eggplant and tomato as indicator plants and the broth test for 

plantlets produced in vitro); potato virus X (Gomphrena 

globosa as indicator plant and serology); potato virus S 

(serology): potato virus A (plant indicator'A6') and potato virus 

Y (serology, indicator plants'A6,'and Solanumdemissum P.1. 

230579); leafroll (aphid transmission to indicator plant Phisalis 

floridana); and spindle tuber (polyacrylamide gel electrophoresis). 

In the latter test, the pathogen (viroid) is aribonucleic 

acid that differs significantly from the nucleic acids that occur in 

healthy plants. Separation by electrophoresis and subsequent 

staining permits reliable detection of the viroid. including 

strains that cause no visible symptoms. 

Stem cutting, which was developed as ameans of eliminating 

bacterial and fungal pathogens normally carried over by tuber 

propagation, isarelatively new procedure that has proven to be 

a valuable tool in seed improvement. Plants from selected tubers 

are grown in the greenhouse and then topped when they are 

105

15-40 cm high so as to stimulate the growth of axillary shoots. 

These shoots, which are used as cuttings, are removed when they 

are 5-7 cm long (treating with a rooting hormone is optional) 

and transplanted to moist, sterile sand or vetmiculite (held under 

intermittent mist in some institutions) until rooting occurs, 

usually 10-12 days. Following an optional hardening-off period 

in a cold frame, they are transplanted to the field. In the 

meantme the "mother" plants. from which the cuttings were 

taken, are screened thoroughly to assure freedom from the 

various pathogens. In 1970, Scotland became the first country 

to require that all seed lots entered for ce,'tification be derived 

from nuclear stocks developed from virus-tested stem cuttings. 

Once disease-free material has been obtained, procedures for 

further increase of nuclear seed stocks on official seed farms 

vary; however, a thorough indexing program (greenhouse and 

winter field test). utilizing various combinations of tuber, hill, 

and tuber-unit indexing, is used in all programs. These stocks 

are increased primarily as four-cut tuber units (four consecutive 

hills per tuber) for two years before being sold to foundation 

growers. During this increase period, they are rogued 

intensively during the growing season and screened thoroughly 

for the presence of viruses. Foundation seed growers are 

encouraged to use a "flush-out" system that entails purchasing 

nuclear stocks each year from official seed farms and increasing 

them for no more than 2-3 years. 

Certifying agencies, which do not have official seed farms, 

must rely on a few selected growers for the increase of nuclear 

seed stocks 

The production of top quality seed potatoes has become a 

highly sophisticated and technical procedure that undoubtedly 

will become more complex as new technology isdeveloped. It is 

imperative that all those associated with seed production be 

receptive to technological improvements to ensure continuous 

progress in the seed industry. 

106 


DARLING H. M. 1977. Seed potatocertification. Pages 405-416 in: 0. 

Smith, ed. Potatoes: Production, Storing, Processing, 2nd ed. Avi 

Publishing Co.. Westport, CT. 776 pp. 

HARDIE. J. .. 1970. Potato Growers' Guide t) Clonal Selection. 

McCorquodale l.td., Glasgow., Scotland. 20 pp. 

MELLOR, F. C.,and R.StACE-SMITIH. 1977. Virus-free potatoes by 

tissue culture. Pages 616-646 in: J. Reinert and Y. P. S. Bajaj. eds. 

Applied and Fundamental Aspects of Plant Cell. Tissue, and Organ 

Culture. Springer-Verlag, New York. 803 pp. 

MOREL. G. and C. MARIN. 1955. Guison de pommes de terre 

atteintes de maladies i virus. C. R.ttebd. Sanc. Acad. Agric. Fr. 

41:472-474. 

MUNRO,J. 1954. Maintenanceofvirus X-freepotatoes. Am. Potato.. 

31:73-82. 

OORTWIJN BOTJES. I. G. 1920. t)e bladrolziekte van de 

aardappelplant. M.S. thesis. Iandbouwhogeschool, Wageningen. 

136 pp. 

ORTON. W.A. 1914. Inspection and certification of potato seed stock. 

Phytopathology 4:39-40 (Abstr.). 

QUANJER, H. M., H. A. A. VAN DER LEK, and J. G.OORTWIJN 

BOTJES. 1916. Aard, verspreidingswijze en bestrijding van 

phloemnecrose (bladrol) en verwante ziekten. Sereh. Meded. 

Landbouwhogesch. 10:1-138. 

RIEMAN. G. H. 1956. Early history of potato seed certification in 

North America, 1913-1922. Potato Handbook. Vol. I, pp. 6-10. 

Potato Assoc. Am., New Brunswick, NJ. 

SCHULTZ, E.S., and D. FOISOM. 1921. leafroll, net-necrosis. and 

spindling-sprout of the Irish potato. .1.Agric. Res. 21:47-80. 

SEED REPORT. 1977. Spudlight. Certified Seed Edition, Part 2.United 

Fresh Fruit Veg. Assoc., Washington, DC. 15 pp. 

(Prepared by E. D. Jones, James Munro, and H. M. Darling)

Diagnostic Microbial Structures 

Sclerotia 

Black - white mold, gray mold, Rhizoctonia, charcoal rot 

Purplish black- violet root rot 

Very small, black black dot 

ran - stem rot 

Bacterial Exudate from Vascular Tissue 

Abundant, gray -- brown rot 

Sparse, white ring rot 

Prominent Mycelium in or on Soil 

White white mold 

White, fanlike-- stem rot 

Grayish white ---Rosellinia 

Brown, in strands near or on tubers-Xylaria, Armillaria 

Entire Plant 

Distinct Symptoms Lacking 

Unusually large - giant hill 

Off-color, poor growth --general nutrient deficiency, several nutrient 

imbalances 

Bronzing 

General or of old leaves- photochemical oxidant air pollution, 

potassium or zinc deficiency, Fusarium wilt 

Of tip leaves psyllid yellows 

Upright growth habit - PI.RV in andigena types, PSTVL 

Stunting and/or Poor Growth 

Beginning in localized areas of field --nematodes (cyst, root-knot, false 

root-knot, stubby-root, lesion). 

4 

Mild ,o%evere --several virus diseases (PLRV, PVY, PVM,APMV, 

TBRV,PSTV, PYDV, BCTV) 

Pale light green to yellow leaves, later necrotic -magnesium deficiency 

Dark green several mosaic viruses 

Early in season---potassium deficiency 

Lusterless phosphorus deficiency 

Dwarfing BCTV, PYDV, PMTV 

Early maturity - several nutritional deficiencies 

Lower leaves mature, speckled - photochemical oxidant air pollution 

General chlorosis, usually from base upward-Verticillium wilt 

Key to Disease 

Necrosis 

Systemic (top necrosis)-PVX, PAMV,APMV, PVT, TSWV 

Defoliation from bottom toward top of plant-early blight, 

photochemical oxidant air pollution, powdery mildew, pink rot, PVY 

Deformed 

Internodes shortened 

Downward leaf curl -potassium deficiency 

Bushy appearance--boron defiiency, PYDV, Fusarium wilts 

Spindly, crinkled leaves-chemical injury 

Chlorotic to necrotic margins phosphorus deficiency 

Numerous stems, bushy-- genetic abnormalities, mycoplasmas 

Rosette 

At tip-calcium deficiency 

With dwarfing-ring rot 

Red pigmentation or chlorosis of apical leaves, stunting, general 

chlorosis, thickening of nodes, aerial tubers, vascular necrosis, basal 

stem necrosis, or early death--blackleg, Rhizoctonia, mycoplasma, 

Fusarium wilts, BCTV, psyllid yellows 

Stem 

Numerous-coiled sprout 

And thin-genetic abnormalities, hair sprout, mycoplasmas, TMV 

Stoentlng 

Of some stems--TRY 

And internodes shortened-PVY, PMTV, PYDV 

Lesions Originating Below Ground 

Black, extending upward from seed tuber, pith dark, cortical 

decay-blackleg, pink rot 

Brown-common scab, skiii spot, black dot 

Girdling of stem- Rhizoctonia 

Rot, with dry shredding--Fusarium wilts, mycoplasmas 

With prominent gray fungus, mold growth- Rosellinia 

Lesions at or Near Soil Surface 

Girdliog and collapse, bleached color-heat injury 

White pi . -mis at soil line, cross-hatched collapse of pith-lightning 

injury 

No underyling necrosis on stem surface 

Red to purple mycelium-violet 

Surface 

root rot 

moldy, white at soil line, watery rot, stem collapse 

Late maturity, larger than normal-genetic abnormalitiesRetoprlmylim-oltotrt 

Wilt 

With drought stre! -nematodes (cyst. root-knot, false root-knot) 

Chlorosis, wilt, and early death-- black do., violet root rot. brown rot, 

charcoal rot 

In groups in the field- -Rosellinia 

With vascular discoloration Verticillium wilt, Fusarium wilts 

Wilt or chlorosis 

Of one stem or on one side of leaf, stem, or side of plant-brown rot, 

Fusarium wilt, Verticillium wilt, ring rot 

Of green leaves and stems, later chlorosis and necrosis-ring rot, 

brown rot, pink rot, stem rot 

Rapid green collapse and death of some or all plants in localized areas 

of field-lightning injury 

Black sclerotia--white mold 

Tan sclerotia-stem rot 

Lesions Above Soil Surface 

Epidermis white, underlying tissue usually unaffected-sunscald, hail 

injury 

Necrosis, black to brown 

Extensive--late blight 

Restricted in size-early blight 

Stippled flecks--powdery mildew 

Also of petiole, stem brittle-manganese toxicity 

Brown necrotic streaks on stems and petioles-PVY, TSWV 

At petiole attachment-blackleg, late blight, gray mold 

Light brown broad zonation-white mold 

107

Vascular Discoloration 

Brown, most severe in lower part, extending also above 

ground - Fusarium wilts. Verticillium wilt 

Black - brown rot. blackleg 

Pith Necrosis 

Brown, near tip- PYDV 

Black at base blackleg 

At nodes- Fusarium wilts 

Aerial Tubers and/or Enlarged Nodes--pink rot, Fusarium wilts, 

mycoplasmas, psyllid yellows. Rhizoctonia 

Galls - wart, smut 

Swelling, Twisting, and Deformation-rusts, coiled sprout 

Mosaic Mottles 

Symptomless, very mild to severe rugosity - PVX. PVS. PVM, PVY. 

PVA. PVT. APMV. API'. CMV, TMV, TRV. AMV, PAMV, 

deforming mosaic frost injury 

On tip leaves fusirium wilts 

Netting of minor eafsins AP 

And veinal necrosis PVT 

Rough, crinkly P'Y. PVM. PYVV 

Yellow areas. pale to bright AMV. TRV, PMTV, TBRV, PYVV. 

TR SVsp 

More severe on lower leaves PAM 

Chlorosis 

General Fusarium wilt. Verticillium wilt 

Greenish spots on low shaded leaves PVS 

Interveinal Chlorosis or Necrosis 

Of tip leases manganese deficiency 

Of lower leaves ring rot 

To white yellow chlorosis sulfur oxide air pollution, manganese 

toxicity, magnesium deficiency 

Deformed 

Crinkled. rugose PVY. PVA. deforming mosaic 

Small. twisted. possibly with short petioles and stem internodes 

PAMV. PVM, IMV. CMV, TBRV, TRV, PMTV, APMV, PSTV, 

genetic abnormalities, chemical injury 

Young leaves twisted and cupped zinc deficiency 

Cupped phosphorus delicienc' 

On tip leaves iBRV 

Irregular holes, banded, mottled low temperature vine injury 

Flongate. puckered, pinched, veins prominent -chemical injury. CMV, 

TMV, loss- temperature nitrogen toxicity 

Pustules. orange, red to brown enlargements, or twisting--rusts 

Small with fluted margins, acute petiole-stem angle -- PSTV 

Small, numerous thin stems mycoplasmas 

Many leaves, simple (not compound) genetic abnormalities, 

witches' broom, stolbur 

Upward Rolling 

Stiff, papery texture, pale color PLRV, boron deficiency 

Throughout plant, downward roll of petioles - PYDV 

Of tip leaves, possibly pink at margins PLRV, manganese deficiency, 

PVM. mycoplasmas, BCTV, psyllid yellows 

With chlorosis zinc deficiency 

Of lower leaves or throughout the plant. chlorosis absent to 

mild nonvirus leafroll, PI.RV, PVM, potassium, phosphorus, or 

boron deficiency 

Chlorotic or necrotic margins calcium deficiency 

Upward rolling severe at plant tip. chlorosis orred at bases of tip leaves. 

may be accompanied by aerial tubers blackleg. Rhizoctonia. 

mycoplasmas, Fusarium wilts 

Dwarfing, marginal and interveinal chlorosis - PI.RV in andigena types 

Thick. brittle, interveinal chlorosis or necrosis-- magnesium deficiency 

Tattered edges or with holes wind or hail injury, Ulocladium blight 

Necrosis 

At tip of plant-- frost injury 

108 

Bronzed 

On upper surface and margins -- photochemical oxidant air 

pollution 

Necrotic - potassium deficiency 

And necrotic spots PVS 

And extensive systemic necrosis- Fusarium wilt 

On epidermal surface or extending through the leaf-wind injury 

Of veins- PVT 

And stem streak PVY 

Flecks to streaks manganese toxicity 

Systemic leaflet and petiole necrosis AMV, APMV, TSWV 

And leaf drop -PVY 

Necrotic I Pqions 

SpecKling ot lower leaves but also on upper leaves--- nitrogen deficiency 

chemical injury. photochemical oxidant air pollution, manganese 

toxicity 

Necrotic spots and rings TBRV, TRSV, TSWV, PVY 

Necrosis of petioles and leaflets TSWV, PVY 

Without concentric zonation 

Black when wet, brown when dry, with or without sparse white 

Initially sporulation, 

water-soaked 

possibly yellow halo -late blight 

large necrotic lesions-- Choanephora 

Yellowish to purple 

blight 

Ccr:ospora leaf blotch 

Tan. angular Stemphr-lium consortiah. 

At mechanical wounds, dark to black Ulocladium blight 

Green to black. white to gray-brown sporulation---powdery mildew 

Light colored Pleospjora herharuot 

With concentric zonation 

Broad zonation, wedge-shaped, circular to irregular, tan 

sporulation -gray mold 

uato gry m d 

Narrow 

Round, zonation 

brown Phoma leaf spot 

Round or angular lesi'ins with pycnidia-Septoria leaf spot 

Brown black- TSWV 

Angular (limited by veins) -- early blight, Alternwria ahernata 

Tuber 

Small Size-- various viruses. genetic abnormalities, nutrient imbalances 

Many tubers -- witches' broom, psyllid yellows, second growth 

Flaccid or Wilted--mycoplasma 

Forming Secondary Tubers or Plants Prematurely- second growth, 

secondary tubers 

Galls 

Green, brown to black--wart 

Tuberlike, deformed-smut 

Raised. pimplelike, purple-brown-powdery scab, skin spot 

White tufts-enlarged lenticels 

To brown galls later becoming necrotic depression-powdery scab 

Warty-- root knot nematode 

Also pimples --lesion nematode 

Deformed 

Irregular shape -second growth, compacted soil, PAMV, PSTV, 

Rhizoctonia. mycoplasmas 

Set close to stem, stolons very short-Rhizoctonia, blackleg, 

mycoplasmas 

Protruding eyes- second growth, PYVV 

Pointed ends--second growth. PSTV 

Elongate, round in cross-section-- PSTV 

Dwarfed, deformed, possibly cracked, with internal necrotic 

spots--AMV. PYDV, TRV, TSWV, PSTV, chemical injury 

Internal arcs or rings - TRV. PMTV 

Warty with internal black, scattered areas-smut 

Normal Tuber Shape, Surface Unblemished 

Black sclerotia on tubersrlace (soil that will not wash off)-Rhizoctonia 

Interior glassy or watery throughout orat stolen end--second growth, 

frozen tissue 

Starch deposition irregular to very low-second growth, immature 

tubers 

Sugar in tissue -- low temperature storage

Surface and or interior 

Shades of green tuber greening 

Underlying tissue collapsed sunscald 

Subsurface tissue 

Blue to black blackspot 

Dried. soft or sunken wind injury 

Brown at stolen attachment stem-end browning 

Necrotic arcs to flecks TRV, PMTV 

Center. hollo or cracked hollow heart 

Interior firm 

Necrotic trust colored) spots or flecks principally in medullary 

tissue internal heat necrosis, phosphorus deficiency, calcium 

deficiency. AMV. PAMV. PYDV. TRV 

Necrotic to tan discolored areas PVY' 

Rust colored arcs or rings I'RVPMTV 

Net (phloem) scattered necrosis PI.RV. low temperature injury. 

stem-end browning, PAMV 

At stolon attachment stem-end browning, chemical injury, low 

temperature injury, calcium deficiency, Fusarium wilt, Verticillium 

wilt 

Mahogany colored interior low temperature injury 

With glassy texture, starch depletion second growth 

Interior firm to solt 

Smoky gray discoloration low temperature injury, leak 

Black medulla blackheart 

Vascular discoloration 

Soft texture, ooze \;hen squeezed ring rot, brown rot 

Firm to soft. dark low temperature injury 

F-irin. confined to vascular area, brown to black possibly with watersoaked 

border FtUsariuni wilts 

Firm near stolon attachment calcium deficiency, stem-end 

browning, Fusarium ssiIs 

Netlike. more severe near stolon end Verticillium wilt, chemical 

iniury, stei-end brow.ning 

Discoloration evident through skin 

Indistinct lines, arcs, or blotchy areas TRV. PMTV, TSWV. 

PAMV 

As raised rings PMIV 

(iras-brown discoloration brown rot, pink rot, pink eye 

Chalky 

Normal Tuber 

white 

Shape, 

spots 

Surface 

belosw skiti. 

Blemished 

later 

Without 

dry' granular. 

Active Rot 

becoming 

darker rot newiatode 

rlisters I NYV 

Bros n rings to necroic areas PVY'. PMI Y. TRY 

Skin cracked tither cracks, Rhioctoni, PYI)Y, PSTY PMTY 

INV, boron deficiency 

Or feathered surface abrasions 

lenticels affected enlarged lenticels, bacterial soft rot, powdery scab, 

sten rot, charcoal rot, gangrene, PSTV 

( t nderyling tissue brown to black pink rot 

Stolon attachment discolored chemical injury.jelly end rot, stem-end 

browning, brown rot, ring rot, stein rot, Verticillium wilt, 

Fusarium wilts, horon deficiency, charcoal rot, pink rot 

Also of nedullarv areas soft rot, blackleg 

Eves discolored 

Principally at tuber tip pink eve. Verticillium wilt 

Anywhere charcoal rot, Fusarium wilts 

)ark colored gangrene 

With soiladhering browuri rot 

Purplish black raised spots skin spot 

With watery exudate frozen tubers 

Wounds infected bacterial soft rot,powdery scab, leak. Fusarium 

tuber rots, gatngrene 

tubrlowsnganyre 

Shalhiss- lesiorvs anywshereBrwlein 

Necrotic skin, dark gangrene, sunscald. high temperature field 

injury. low temperature injury, wind injury. TNV 

Silvery sheen to light brownish surface silver scurf 

Silvery to brown with very small black scerotia--- black dot 

Irregular purplish brown lesion nematodes 

Raised lesions 

Purplish corky to necrotic spots. sometimes around eyes --skin 

spot 

Circular lesions Ihecaphora smut 

Reddish purple mycelium and sclerotia on surface, sunken areas 

below violet root rot 

Brown sunken blotches PAMV 

Brown to dark sunken pits, russet or raised lesions or russet 

discoloration 

Underlying tissue firm. corky, at stolen end - potassium deficiency 

Tan brown to black--common scab, TNV 

Raised pustules white, later depressed, dark brown-powdery scab 

Pitted Rhizoctonia 

Necrotic often in bands. scablike---chemical injury 

Firm lesions, slightly sunken, relatively shallow 

Reddish brown--late blight 

Black--early blight 

Purplish mycelial mat- -violet root rot 

Circular---Fusarium wilts, Fusarium tuber rot 

Active Rot 

Skin cracks, discolored- -ring rot 

Cavities spongy, shrunken--Fusarium tuber rots 

With white mycelium and black sclerotia-white mold 

Cortex less severely rotted than medulla--ring rot leak 

Possible holes through the tuber--lightning injury 

Gray smoky discoloration 

Of cortex, vascular ring. or medulla--low temperature injury 

Black medulla -- blackheart 

Anywhere bordering rotted tissue- leak 

Water% 

At stolon end - -jelly end rot 

On exposure to air shades of pink. brown to black-frost injury 

Charcoal rot. later spongy -leak, pink rot 

Later chocolate brown dries as zonate lesions--- Rhizopus 

Semiwatery 

Brown flabby decay--gray mold 

Light gray, cavities with mycelium, and black sclerotia-charcoal rot 

Advancing margin clearly delimited--.-white mold. Fusarium tuber rot 

Dark line -leak. pink rot 

Tissue firm to dry, punky with cavities 

Pustules of spores on surface--- Fusarium tuber rot 

Dry granular, shrunken - rot nematode 

Vascular tissue discolored reddish brown to black-brown rot, ring rot 

Lesions thumbnail to deep. dark cavities --gangrene 

Loose gray white mycelium on surface and in soil, rot black, 

carbonaceous-- Rosellinia 

Fanlike mycelium on tuber and on soil surface, semifirm decay, cheesy 

rot- stem rot 

Tuber shell remains -- leak 

Secondary Rots 

Slimy, cream to tan. often foul odor-bacterial soft rot. Fusarium 

tuber rots. These and others follow primary pathogens such as brown 

rot, ring rot, low or high temperature injury, blackheart, late blight, 

stem rot, charcoal rot. Rhimopus rot, and rot nematode. 

Seed Tubers 

Decay-oxygen relations, blackheart, ader e temperature (low or 

high), Fusarium tuber rots, leak, bacterial soft rot, stem rot 

Dormant, or delayed in germinating- PYDV.APMV, mycoplasmas 

Dormancy lacking-- psyllid yellows, witches' broom, second growth 

Abnormally thin--genetic abnormalities, hair sprout, mycoplasma 

Many- witches' broom 

Growing into the tuber--- internal sprouting 

Forming tuber directly--second growth, secondary tubers, hair 

sprouts, calcium deficiency 

Swollen, curved--coiled sprout 

Necrotic 

.Just below tipi--calcium deficiency 

Soft, progressing from seed piece -blackleg 

Brown lesions 

In storage, transverse cracks-- skin spot with girdling 

In field-- Rhizoctonia 

Stolons 

Short---potassium deficiency 

Numerous. long---genetic abnormalities 

Dark, covered by gray-white mycelium--Rosellinia 

Necrosis -pink rot 

Brown lesions skin spot 

And girdling Rhizoctonia 

With dotlike sclerotia- black dot 

109

110 

Galls 

White to brown-powdery scab. smut 

On tips-wart 

Roots 

Galls 

White to dark brown-powdery scab, root-knot nematode 

As beads along root-false root-knot nematode 

Cysts, white to brown-cyst nematodes 

Brown lesions-skin spot 

Cortical decay 

Dotlike sclerotia-black dot 

Large sclerotia--- Rhizoctonia 

Cortical injury- lesion nematodes 

General rot-Fusarium wilts 

Necrosis 

Brown to black -pink rot 

Dark, covered by gray white mycelium--Rosellinia 

Poor development- potassium deficiency, phosphorus deficiency, 

nitrogen toxicity 

Stunted--magnesium deficiency, boron deficiency, aluminum to:(icity, 

cyst nematodes. stubby-root nematode 

Proliferation of lateral roots--cyst nematodes, root-knot nematode 

(Prepared by W. J. Hooker)

Equivalent Names of Potato Diseases 

(ommon Name 

Causal Factor Other Names Spanish German French 

Air pollution nitury 

Ihotochemical oxidants 

Sulfur o~xides 

l)ahos prov:cados por 

contaminaci'n ahnbienial 

Oxida ntes fotoqumicos 

Gases sulfurosos 

Alfalla mosaic Lucerne mosaic Mosaico de la Kalikokranklhcit 

%irus Calico alfalfa 

A M V Tuber necrosis 

virus 

A.ndean potato Virus latente de los Andes 

latent %irus 

A P1 V 

Anride n potato Moteado andino 

mottle virus 

APMV 

Arrnillaria dry rot 

.Armillariamella 

Aster \ello%%s. stolhur. 

and allied diseases 

NIycoplasma 

lacterial soft rot 

Erwiniatiarotovora 

Black dot 

(olhioiri/n 

atramenntirittin 

Purple top wilt 

Tormato big bud 

Purple top roll 

Ilaywire 

late breaking virus 

IBlue stein 

Moron 

Purple dwarf 

Yellowv top 

Blunch top 

Apical leafroll 

Punta morada 

Amarillamiento 

apical violIcco 

liallimasch Pourridie-agaric 

Armillaire 

Stolhurkrankheit 

P'alrastolbur 

Metastolbur 

Solt rot Pudrici6n blanda Knollennassfliule 

Nassliule 

Antracnosis 

Punteado negro 

Colletotrichum- 

SchaIlennekrose 

Colletot rich um- Welke 

Pourriture molle 

bactrienne 

Dartro~e 

Anthracnosc 

Blackheart Cora/6n negro Schwar/herzigkeit Coeur noir 

Blackleg Pierna negra Schwar/beinigkeit .ambe noire 

Ilackspot Internal bruising 

Enivrnatic graying 

Blue bruise 

1I1uespot 

Brown rot 

I'teldonwina.% 

.%olanaceatit 

(ercospiira leaf 

blotches 

('erco pora spp. 

Charcoal rot 

thacrolihminapIahe.woli 

Blacterial wilt 

Southern bacterial wilt 

Mancha negra 

infecciosa 

Marchite, bacteriana 

Pudrici6n pitrda 

no (irauflckigkeit 

Schwar/fleckigkeit 

Blaumerflirbung 

Schleimkra nkhcit 

Baktriellc Hraunliule 

Cercospora leaf spots Manch6n foliar (ielbflcckigkcit 

Cercospora- 

Blattlleckenkrankiheit 

Pudrici6n carbonosa 

Chemical iniury Iatos por ageltes 

Choanephora blight 

('hoinephora 

quilaicos 

Muerte regresiva 

Coiled sprout Brote doblado 

Taches cendrcs 

Tachetures bleues 

[aches plombes 

Pourriture brune 

Taches foliaires 

Cercosporiose 

(continwed on next page) 

111

Common Name 

Causal Factor Other Names 

Common rust 

Puci inia pitlieriana 

Common scab Scab 

Slreplon'ime.%s uh'ie. 

Cucumber mosaic 

CMV 

Deforming mosaic 

PDMV 

l)eforming rust 

.Ai'hilon c'antsisA 

Early blight 

.hernaria .%)ani 

False root-knot nematode 

Vai obhux aterrans 

Fusarium dry rots Fusarium storage rots 

Fusaritni .soani Seed piece decay 

F. roseti 

Fusarium wilts 

1o.arioto euntartii 

F. o.\iAj'orumi 

F, a* 'a*.a' tlt 

I .dolani 

Gangrene 

Iqhonla exil,a 

Gray mold 

Botr tis cierea 

Ilail injury 

flair sprout Spindle sprout 

High temperature 

field injury 

Hollow heart 

Internal beat necrosis Internal brown spot 

Internal rust spot 

Internal spotting 

Internal sprouting Ingrown sprouts 

l.ate blight 

Phytophthorainfeisans 

Leak Watery, wound rot 

PI'ti/uIio spp. 

Lesion nematodes 

Pratihnchusspp. 

Lightning injury 

Low temperature 

foliage injury 

112 

Spanish 

Rova comin 

Sarna 

Sa rna comn ~in 

Mosaico del pepinillo 

Mosaico deformante 

Roya peruana 

rizdn temprano 

Mancha negra de la 

hoja 

Falso nematodo del 

nudo de la rai z 

Rosario 

Pudriciones secas por 

Fusarium 

Marchitez por Fusarium 

Gangrena 

Cancro 

Pudrici6n de ]a ra~z 

Pudrici6n gris 

Moho gris 

Dahos provocados por 

granizo 

Brotes filiformes 

I)ahos a la planta 

por alta temperatura 

Coraz6n vacto 

Necrosis interna de 

los tubrculos 

Brotamiento interno 

Tiz6n tardro 

Hielo 

Gota 

Rancha 

Pudrici6n acuosa 

Gotera 

Nematodo de la lesien 

radicular de racines 

Dahos provocados 

por relfimpagos 

Dahos en el follaje por 

baja temperatura 

Heladas 

German French 

Kartoffelschorf Gale commune 

Curkenmosaikvirus 

Ddirrfleckenkrankheit Rrflure alternarienne 

Dbrrfleckenkrankheit Maladie des 

taches brunes 

Nematode c&cidogene 

de Cobb 

Nematode de gales 

velues 

Fusarium-Trockentijule Fusariose 

Fusarium-Weissfiiule Pourriture s'eche 

fusarienne 

Fusarium-Welk FI6trissure fusarienne 

Phoma-Stengelbraune Gangrene 

Phoma-Trockenfliule Pourriture phom;enne 

Phoma-Knollenfiiule 

Grauschimmel Pourriture grise 

Pustelfiiule Moisissure grise 

ftagelschiiden Dgiits de grle 

Fadenkeimigkeit 

tiohlherigkeit Coeur creux 

Eisenfleckigkeit Taches de rouille 

Braunherzigkeit 

Kringerigheid 

(Dutch) 

Innerer Germination introrse 

Keimdurchwuchs 

Krautfiiule Mildiou 

Knollenfi ule 

Braunfliule 

W'issrige Wundfiiule Pourriture aqueuse 

Nematode des lesions 

de racines 

Frostschliden an Dgfits de froid 

der Pflanze 

(contlilued oil llext page)

Common Name 


low temperature 

tuber injury 

Nonvirus leafroll 

Nutrient imbalance 

Phoma leaf spot Black blight 

Phmna anclina 

Pink eve 

IP'l, n0oMOMIS 

Red xylem disease 

Bruise infection 

fItre.t lin 

Brown eve 

Pink rot Watery rot 

PhIlt tithora 

Wilt 

erti/ro.wptica 

P1htI ophithra spp. 

PleJm'pra 

twr/'aruin 

Potato aucuba Pseudo net necrosis 

mosaic Tuber blotch 

PAMV Viruses Fand G 

lPotato cyst neinatodes Golden nematodes 

(Glho,/era spp. P'otato root eelworm 

( 1Ihi'trleraspp.) 

P~otato leafroll virus Potato phloem necrosis 

P1RV Tuber net necrosis 

l'otato mop-top Mop-head 

PM IAV Yellow mottling virus 

Potato rot nematode 

I)it.venhus dletructor 

Potato spindle tuber Unmottled curly 

viroid dwarf 

PST V 

Tomato bunch top 

Gothic 

Potato virus A Mild mosaic 

PVA 

Potato virus M Potato leafrolling 

PVM mosaic 

Interveinal mosaic 

Paracrinkle 

Potato viruses E and K 

Potato virus S 

PVS 

Potato virus T 

PVT 

Potato virus X Potato latent 

PVX Potato mild mosaic 

Potato simple mosaic 

Healthy potato virus 

Potato viruses B and D 

Spanish 

Dahos en el tubrculo por 

baja temperatura 

Enrollamiento no viral 

Desbalance nutricional 

liz6n foliar 

Tiz6n negro 

Ojo rosado 

Pudrici6n rosada 

Podredumbre 

rosada 

Mancha foliar 

por Pleospora 

Mosaico aucuba 

Mosaico necr6tico 

Nematodo del quiste 

Nematodo dorado 

Enrollamiento 

Enrollado 

Lnanismo amarillo 

Mop-top de la papa 

Nematodo de la pudricion 

de ]a papa 

Pudrici6n seca de la papa 

Tub~rculo ahusado 

Mosaico suave 

Mosaico crespo 

Mosaico latente 

Mosaico leve 

German French 

Frostschliden an 

der Knolle 

Kalteschaden an 

den Knollen 

Physiologisches 

Blattrollen 

Rosissement 

des yeux 

Rotfiule Pourriture rose 

Rosafiiule Pourriture humide 

Akuba Mosaik Mosaique d'auchuba 

Aucubamosaik 

Gelber Kartoffel Maladie de la pomme 

nematode de terre 

Kartoffelzystenalchen Nematode sur pomme 

de terre 

Blattrollkrankheit Enroulement 

Blittrollvirus 

Knollennetznekrose 

Kartoffelkriitzealchen Pourriture du 

Nematodenfiiulc der tubercule 

Kartoffel Nematode de la 

pourriture du 

tubercule de 

pomme de terre 

Spindelknollen- Tubercules en fuseau 

krankheit Tubercules fusiforme 

Rauhmosaik Frisolhe mosaique 

Rollmosaik 

Kartoffel X-Mosaik Mosaique ligbre 

Leichtes Mosaik 

(continued on next page) 

113

Common Name 


Potato virus Y Rugose mosaic 

PVY Streak 

Potato yellow dwarf 

PYDV 

l.eatdrop Ytreak 

Stipple streak 

Potato virus C 

Potato yellow vein Vein yellowing 

PYVV virus 

Powdery mildew 

Er~~siphe 

ci'icorac',rumo 

Powdery scab Corky scab 

Spongo.ora .mthierraneu 

Ps)'llid vellows 

Rhioctonia canker Black scurf 

R/izoctonjia .%olni 

Rhi/opus soft rot 

Rliz/opispp. 

Ring rot Bacterial ring rot 

C"ornelbac'terittn 

vepedotic'ton 

Root-knot neniatodes 

.thloilo.,ime spp. 

Rosellinia black rot Torbo 

Rio.oellioiaspp. 

Second grohth 

Icily end rot 

Secondary tubers No-top 

Little potatoes 

Septoria leaf spot 

Septoria II'opei'r.ii 

Silser scurf 

Ihehninthoporiun,.olani 

Skin spot 

Oompora p/oaolthi 

Smut Tiecaphora smut 

ihe'cap/tora solani 

Stem rot Southern blight 

.Sch'roiiun,rolfnij 

Stem-end browning 

S/enplIctlinm,, cousortiah, 

Stubby-root nematodes 

Tric/mlorA irintiti.s 

Paratric/hodoritm spp. 

Sugar beet curly top Green dwarf 

BTid 

114 

Spanish 

Mosaico rugoso 

Mosaico severo 

Enanismo amarillo 

Amarillamiento de 

las nervaduras 

Oidiosis 

Mildiu pulverulento 

Roha 

Polvosa 

Sarna polvosa 

Arnarillarnientos por 

ps(llidos 

Rhi/octoniasis 

Costra negra 

Pudrici6n blanda por 

Rhizopus 

Pudrici6n anular 

Nematodo del nudo de 

la ralz 

Torbo 

Mortaja 

Lanosa 

Crecimiento secundario 

Pudricion apical 

gelatinosa 

Tubrculos secondarios 

Mancha anular de la hoja 

Costra plateada 

Mancha plateada 

Caspa plateada 

Mancha de la cAscara 

Carb6n 

Buha 

Pudrici6n basal 

Bronceado de la base 

de los tubrculos 

Nematodes de la atrofia 

radicular 

Punta crespa 

German French 

Strichelkrankheit Bigarrure 

Frisol~e 

Gelbzwergigkeit 

Echter Mehltau Ozdium 

Pulverschorf Gale poudreuse 

Kartoffelriiude Gale spongieuse 

Riude 

Wurzeltiterkrankheit Rhizoctone brune 

Kartoffelpockcn 

Pockenkrankheit 

Bakterienringiule Fl~trissement 

Ringr~ite bact rien 

Bakterielle Schleimtliule 

Wurzelgalleniilchen Nodosite des 

racines 

Glasigkcit Anomalie tie 

Durchwuchs croissance 

Zwiewuchs Aspect vitreux 

Kindelbildung 

Knillchensucht Boulage 

Couveuse 

Silberschorf Gale argentee 

Silberflecken Tache argentee 

Tiipfelfleckenkrankheit Tache de la peluce 

Moucheture du tubercule 

Sklerotium-Knollen-idule 

Brunissement du talon 

Tache stemphylienne 

(continueld on nuxi page)

Common Name 


Surface abrasions 

Iobacco mosaic 

TMV 

Tobacco necrosis potato ABC disease 

TN V 

Tobacco rattle Stem mottle 

TRV Spraing 

Corky ringspot 

lobacco ringspot Andean potato calico 

I RSV 

Tonato black ring Bouquet 

iBRV Pseudo-aucuba 

Iornato spotted wilt Spotted wilt 

IS W\V 

Tuber cracks 

luber greening Sun-green 

Sunscald 

Illocladium blight 

( locladittn; alrtom 

Verticillium wilt 

Ferticilliumalbo-airum 

I'.dah/i'av 

Violet root rot 

Rhi:ocitioia 

i'ro(orto 

Wart Black wart 

Srnc/ vritt 

rnm/otioti .m 

White muold Stalk break 

S'lvroinia 

.ilerotiorooi 

(also S. minor, 

S(ermjiia spp. ) 

Wind injury 

Witches' broom Northern stolbur 

Mycoplasma Dwarf shrub virosis 

Spanish 

IPcladura 

Mosaico del tabaco 

Virus de ]a necrosis 

del tabaco 

Bouquet 

Pseudo-aucuha 

Marchitei apical 

Necrosis de los 

brotes 

Necrose do topo 

(Portuguese) 

Viracabeja (Portuguese) 

Agrictadura de los 

tuhbrculos 

Verdearmiento 

Escaldadura 

Kasahui 

Marchitez por 

Verticillium 

Verticilosis 

Pudricibn 

radicular violeta 

Verruga 

Rohta negra 

Esclerotiniosis 

Moho blanco 

Pudricibni dura 

Dahos provocados por 

el viento 

Escoba de brujas 

German 

Tabaknekrosevirus 

Ratel-Virus 

Proplenbildung 

Profenkrankheit 

Stengelbuntkrankheit 

Stengelbunt 

Taha kmauchevirus 

Bukettkrankheit 

Bukettvirus 

Gelbfleckigkeit 

Bronzelleckenkrankheit 

Rissigkeit 

Wachstumrisse 

Griinverflirbung 

der Knollen 

Welkekrankheiten 

Wirtelpilz-Welkekrankheit 

Verticillium-Welke 

Violetter Wur/eltciter 

Violette Wur/,elfiiule 

Kartoffelkrebs 

Sklerotinia- 

Stengelliiule 

Windschiiden 

Hiexenbesenkrankheit 

French 

Tacheture de la tige 

Bouquet 

Craquelement 

Verdissement 

Insolation 

Maladie du jaune 

Fltrissure verticilliene 

Verticilliose 

Rhizoctone 

violet 

Gale verruqueuse 

Tumeur verruqueuse 

Gale noire 

Porriture du collet 

Pourriture sclerotique 

D~gfits de vent 

Balai de sorciiere 

115

Glossary 

abraded-rubbed or worn away, especially by friction; eroded of chemicals (insecticides) or as ribonuclease inhibitor in virus 

acervulus (pl. acervuli)-saucer-shaped or cushionlike fungus fruiing extraction 

body bearing conidiophores, conidia, and sometimes setac bi- (preflx)-two 

acre-unit of land area 43.5601t1(0.40469 hectare; 4,046.87 m) bicollateral-vascular bundle having phloem both outside and inside 

acute-developing suddenly; severe, e.g., symptoms of disease; or less the xylem 

than 90", describing an angle binary fission-division of a cell into two daughter cells by simple 

adjuvant-a substance added to a medicinal to aid its action division of the nucleoplasm and cytoplasm 

advenitious-a rising not at its usual site; e.g., roots originating from biotype-subspecies of organisms morphologically similar but differing 

stems. tubers, or leaves physiologically, particularly in ability to selectively parasitize plants 

aerial tuber-a tuber developing in the axils of leaves aboveground on with specific resistance 

potato sterns blight-a disease characteried by rapid and extensive death of plant 

aerobic-requiring the presence of elemental oxygen for survival foliage 

agar-solidifying component ofmicrobial culture media derived from 

certain marine, red algae 

akaryoi:--describing a cell without well-differentiated nucleus 

amorphous-lacking a definite form or shape 

AM V-alfalfla mosaic virus 

anaerobic-living and surviving in absence of elemental oxygen 

anastomoses (sing. anastomosis)-interconnections between branches 

ol the same or different hyphae (or other structures) to make a 

network 

broadcast application-fertilizer application by spreading or scattering 

within or on the soil 

buffer-a 

surface 

substance capable in solution of keeping hydrogen-ion 

concentration constant and thereby avoiding rapid changes in 

acidity or basicity of a solution 

0 C- Celcius (formerly' Centigrade), unit of temperature 0.01 between 

boiling and freezing points of waterat standard press-ire. 'C =(o F 

32) 59 and 0 antheridium (pl. antheridia)-fungus structure producing male gametes 

(male gametangium) 

anthocyanin-blue, purple, red, or pink water-soluble flavenoid 

pigment in cell sap 

antigen (adj. antigenic)-a foreign chemical, usually a protein, that 

induces antibody formation when injected into an animal body 

antiserum (pi. antisera)-serum containing antibodies 

apex (pl. apices, adj. apical)-tip of root or shoot containing the apical 

ieristem 

aphid-a small, sucking, homopterous insect living on plant juices and 

capable of transmitting viruses 

APIA'-andean potato latent virus 

APMV-andean potato mottle virus 

apothecium (pl. apothecia)-open cuplike or saucerlike, ascus-bearing 

fungus fruiting body 

appressorium (pl. appressoria)-swelling on a fungus germ tube or 

hypha, especially for attachment to a host in an early stage of 

penetration 

ascospore-spore formed within an ascus 

ascus (pl. asci)-saclike cell in which ascospores (typically eight) are 

produced 

ash-the solid, noncombustible residue left after burning 

attenuated-reduced in virulence 

aucuba-bright yellow mosaic leaf variegation of genetic or virus origin 

avirulert-nonpathogenic 

F = 9/5 (°C)+ 32 

calcareous-rich in calcium, often as carbonate, lime 

callose-a carbohydrate component of plant cell walls often forming 

over sieve plates and in calcified cell walls 

callus-a mass of parenchymatous cells formed over or around a wound 

camblum-lateral meristematic layer of stems and roots, giving rise to 

secondary xylem, secondary phloem, and parenchyma and 

responsible for secondary growth 

canker- necrotic, localized, diseased area 

carbohydrate- various chemical compounds of carbon, hydrogen, and 

oxygen, such as sugars, starches, or cellulose 

catenulate-formed in chains or in an end-to-end series 

cellulose-a carbohydrate comprising the primary cell wall substance 

certification scheme-a governmentally supervised procedure of seed 

propagation to insure high quality, varietal purity, and freedom 

from disease 

chelate-relating to or having a ring structure that usually contains a 

metal ion held by coordination bonds 

chimaera-plant with several tissues or tissue layers differing in genetic 

constitution 

chip-in this text, a thin slice of potato tuber fried in deep fat 

chlamydospore-thick-walled, asexual, resting spore formed by 

rounding up of a hyphal cell 

chlorosis (adj. chlorotic)-abnormal plant color of light green or yellow 

due to incomplete formation or destruction of chlorophyll 

chondriosones-a generic term for small cytoplasmic structures 

including mitochondria 

bacilliform-a blunt, thick rod shape, rounded on the ends; 

bacillus-shaped 

bacillus-type of bacterium, rod-shaped with rounded ends 

bacterium (pl. bacteria)-typically, a single-celled microorganism 

lacking chlorophyll and increasing by simple cell division 

bar-metric unit of pressure, I bar = 0.987 atmosphere pressure, 106 

dynes/em' 

basidium (pi. basidia, adj. basidial)-a short, club-shaped fungus cell on 

which basidiospores are produced 

BCTV-sugar beet curly top virus 

bentonite-an absorptive and colloidal clay used especially as a carrier 

chromosome-elongate aggregate of genes formed within nuclei at 

certain stages of cell division 

circulative-describing viruses that must accumulate within or pass 

through the lymphatic system of their insect vector before 

transmission to plan. 

clsterna (p. clsternae)-a cavity within a cell enclosed by a membrane 

clavate-club-shaped 

cleistothecium (p]. cleistothecia)-closed usually spherical, ascus 

containing structure of powdery mildew fungi 

clone-group of vegetatively (asexually) propagated plants derived 

from a single original plant or plant part 

CMV-cucumber mosaic virus 

117

coalesce-union of similar structures merging or growing together into 

a larger similar structure 

coenocytic-multinucleate; e.g., a multinucleate plant body enclosed 

within a common wall or a fungus filament lacking cross walls 

comovirus-a virus within the group to which cowpea mosaic virus 

belongs 

conidilophore-specialized fungus hypha on which conidia 

(conidiospores) are produced 

conldlum (pl. conidla)-anyasexually produced spore germinating by a 

germ tube 

cortex (adj. cortica!)-parenchymatous tissue between the epidermis 

and phloem in stems, tubers, and roots 

cotyledon-seed leaf; primary embryonic leaf within the seed in which 

nutrient for the new plant is stored 

cupulate-cuplike, cup-shaped 

cuticle-water-repellent waxy covering (cutin) of epidermal cells of 

plant parts such as leaves, stems, or fruits; also the outer sheath or 

membrane of nematodes 

cv. (cultivnr)-a plant variety, a cultural selection 

cwt- 100 lb, 45.45 kg 

cyst-a capsule around certain cells, as bacteria in aresting spore stage; 

also the egg-laden carcass of a female nematode 

cystosori-a group of sporangia formed after division of a single 

protoplast 

cyto- (preflx)-referring to cell 

cytoplasm-substance of a cell body exclusive of the nucleus 

damping off-rapid destruction and collapse of seedling plants near soil 

level due to cortical decay 

decortication-loss of cortex due to rot 

dehydrate-to reduce water content, to become dry 

density gradient 

centrifugation 

centrifugatlon 

in a column of a 

-separation 

solution of increasing of components density by 

desiccate-to dry out 

diagnostic-a distinguishing characteristic important for identification 

of disease or other condition 

dicotyledons (adj. dlcotyledonous)-plants having two cotyledons (seed 

leaves), in contrast to monocotyledons (the grasses and cereals) 

dilution end point-the point at which infectivityor other activity is lost 

due to dilution 

diploid-having two sets of chromosomes (in potato 2n 2x = 24) 

distal-far or opposite distal-far~tha 

from fro the ormioppowth end enplantshen 

of attachment or rrii origin 

dolomitic limestone-limestone rich in magnesium carbonate, CaMg 

(CO10. dormant-resting, living but in a state of reduced activity 

electrophoresis-movement of charged particles aad macromolecular 

ions under the influence of an electric field 

ELISA-enzyme-linked immunosorbent assay, an extremely sensitive 

serological test for virus or other antigens 

elite seed-seed oiected from basic stocks of known origin, varietal 

purity, and freedom from disease and protected from contamination 

by sanitation and isolation 

encapsidated-enclosed as if in a capsule 

encyst (n. encystment)-to become enclosed in a cyst, a capsule 

endemic-native to or peculiar to a locality or region 

endoplasmic-pertaining to the inner granular, relatively fluid part of 

the cytoplasm 

enzyme-protein that catalyzes a specific biochemical reaction, 

epicotyl-describing the portion ofa plant embryo or seedling above the 

cotyledonary node 

epidemiology-study of disease initiation, development, and spread, 

particularly as influenced by environment 

epidermis (adj. epidermal)-outer layer of cells usually one cell thick on 

plant parts. On tubers, the epidermis is very short-lived 

epinasty-downward c-irvature of leaf, leaf part, or stem due to rapid 

expansion of the upper surface 

erose-having the margin irregularly notched as if gnawed 

erumpent-breaking out or erupting through the surface 

exudate-usually an ooze or slime discharged from a diseased plant part 

facultative-capable of changing life style; e.g.. from saprophytic to 

parasitic or the reverse 

fallow-describing plant-free cultivated land kept free from a crop or 

weeds during the normal growing season 

fasciated-malformed by growing together of plant structures, stems, 

or buds 

filament (adj. fllamentous)-thin, flexible, threadlike structure 

fllform-threadlike 

fixation-preservation of biological structures for microscopic 

118 

examination by killing in suitable chemicals or physical conditions 

so as to avoid changes in structure 

flaccid-wilted, lacking in turgor 

flagellum (pl. flagella, adj. flagellar)-hairlike or whiplike appendage of 

bacterial cells or fungus zoospores providing movement 

flocculation-aggregation into a loose fluffy mass 

fructification-in fungi, a sporc-bearing structure 

fumigant-a vapor-active chemical used in the gaseos. ;-base to kill or 

inhibit growth of microorganisms or other pests 

fungicide-a substance killing fungi; sometimes broadly used also for 

substances inhibiting growth of fungi or spore germination 

fungus (pl. fungl)-spore-producing plant lacking chlorophyll, often 

causing disease of higher plants 

g-gram, a unit of metric weight, approximately I/29 -z 

galls-localized enlargements (overgrowths) on plants 

gelatinous-resembling gelatin or jelly 

gel-diffusion-a type of serological assay for virus identification 

gemmation-in potato. successive production of tubersona stolon ina 

beadlike manner 

genetic-relating to heredity; describing heritable characteristics as 

influenced by germplasm 

genotype-the entire genetic constitution of an organism 

geotroplc-plant growth directed toward the force of gravity; e.g., roots 

germ tube-initial hyphal strand from a germinating fungus spore 

germplasm-material capable of transmitting heritable characteristics 

sexually or asexually 

giant cell sncultinucleate cells formed by disintegration of cell walls; 

also called syncytia in nematode infections 

glycoprotein-a conjugated protein in which the nonprotein group is 

carbohydrate 

Gram stain-a stain for differentiating bacterial types 

greening-development of chlorophyll in tubers after exposure to light 

ha-hectar, 10,000 m (2.4b acres) 

haploid-having the single basic chromosome numberas in most germ 

cells 

haulms-plant stems or stalks, vines of potato 

haustorium (pl. haustoria)-specialized fungus protuberance into a 

host cell, probably functioning in food absorption 

herbaceous-nonwoody; e.g., a plant or plant part 

herbicides-chemicals that suhh kill herbaceous plants; also applied to those 

that limit growth of such plants 

heteroiogous-different although apparently similar; e.g., the reaction 

between an antiserum and an antigen closely resembling but not 

identical to the antigen causing the production of antibody 

hexaplold-having six sets of the basic number of chromosomes (in 

potato. 2n = 6x = 72) 

histopathology-study of pathology of cells and tissues; microscopic 

changes characteristic of disease 

homogeneous-similar in certain characteristics, such as in chemical 

nature or physical properties 

host-plant that furnishes a medium suitable for development of a 

parasite 

hyaline-colorless, transparent 

hybrid-sexually produced offspring of parents differing genetically. In 

potato, further vegetative propagation may continue as a clone. 

hydrated-having absorbed water 

hydrolyzed-having undergone chemical decomposition involving 

splitting of a bond and addition of hydrogen and oxygen 

hyperplasla-abnormal increase in the number of cells, resulting in 

formation of galls or tumors 

hypersensitive-extremely or excessively sensitive; having a type of 

resistance resulting from extreme sen-itivity to a disease 

hypertrophy-abnormal increase in the size of cells, resulting in 

formation of galls or tumors 

hypha (pl. hyphae)-tubular filament of a fungus 

hyphal fusion-joining of fungal hyphae, usually with some exchange of 

cell contents 

hypocotyl-the part of a plant embryo or seedling below the cotyledons 

icosahedral-describing a regular polyhedron with 20 equilateraltriangular 

faces 

Immunity-high resistance against a disease, exemption from infection; 

or in an animal, having developed antibodies against a foreign 

substance (usually a protein) 

immunogenic-producing immunity, usually describing a protein 

(antigen) capable of causing antibody formation when injected into 

an animal 

in vitro-in an artificial environment, usually outside the living body

in vivo-in a living body 

incipient-ecarly in development (ola disease or condition) 

inclusion-nonprotoplasmic structure inside a cell 

indicator host-plant that responds specifically to a particular 

infection, used to detect a disease or to identify the pathogen 

indigenous-nat i%e 

infection-entrance and subsequent multiplication ofa microorganism 

in a plant 

infection court-site in or on host plant where infection can occur 

infection propagules-inlectious units of inoculum 

inoculum-parts of a pathogen capable of infecting a host 

intercalary-situated between existing layers or plant parts 

intercellular-blLween cells 

intercostal-between veins, interveinal 

internode-portion of the stem between joints or leaf attachments 

interveinal-between veins 

intracellular-within cells 

irradiation-exF.osure to radiant energy of various types 

isometric-equally !ong, as a virus particle with all axes of equal length 

(essentially spherical) 

kg-kiogram, 1,000 g (2.2 Ib) 

labile - unstable 

lamina (pl. laminae)-a laver; the broad expanded part of a leaf 

larva-juvenile stage of certain animals (e.g., nematodcs and aphids) 

occurring between the embryo and the adult 

latent-present but invisible or inactive 

lateral buds-buds formed on stems at the axils of leaves 

latex -ru bberlike 

leaching-removal of a chemical through solubility, usually in water 

legumes-plants 

alla tits 

behnginlg 

bhe 

ti the l.egumiaosae, 

g tsuperficially 

including beans, peas, 

,illaillf, and clover 

lenticel-natural opening in surface of leaf, stem, or tuber permitting 

gas exchange 

lenticular-lens-shaped (convex oi, both faces) 

lesion-distinict diseased area 

leucoplast-colorless plastid 

lipid-generic term for oils. fats. waxes, and related products found in 

living tissues 

local lesion host-a host (usually ofa virus) responding by lesions at the 

site (f infection 

locule (adj. locular)-a cavity, especially one in a fungus stroma 

lysogeny-dis.olution; cell destruction by dissolution 

macerate-to cause to become softened and desintegrated as by steeping 

or soaking it. fluid 

marl-a type of soil. rich in lime, formed in the bottom of a lake or 

swarmp 

mechanical injury-injury of a plant part by abrasion, mutilation, or 

wounding 

medullary-of or relating to the pith of a plant 

melanin-dark to black pigment 

meristem-pla nt tissue functioning principally in cell division 

meristem culture-aseptic culture ol a plant or plant part from a portion 

of the meristemO 

mesophyll-central, internal, nonvascular tissue of a leaf, consisting of 

the palisade and spongy mesophyll 

microbial-pertaining to or relating to microbes or microorganisms 

microorganism-an organism of microscopic size 

microprecipitin test or precipitin test-a type of serological test for virus 

microsclerotia-very small sclerotia 

microtubules-any of the minute cylindrical structures ofa cell that are 

widely distributed in protoplasm and are made up of longitudinal 

fibrils 

mildew--superficial (surface) fungus growth 

mitochondria-various long or round cellular organelles that are feund 

outside the nucleus of a cell, produce energy for the cell through 

respiration, and are rich in fats, proteins, and enzymes 

MLO-mycoplasmalike organisms 

mm-millimeter, I 1000 of a nieter, approximately V:25 in. 

pm-micron or micrometer, 10 m. approximately I 25,000 in. 

molecular weight-thie weight of a molecule expressed as the sum of the 

atomic weights (If its coInstituent atoms 

molecule-the smallest particle ofa substance composed of onc or more 

atoms that retains the properties (if the substance 

monocotyledons (adj. monocotyledonous)-plants (including the 

grasses) with one seed leaf 

monogenic resistance-resistance determined by a single gene 

morphology-study of form and structure 

mosaic-disease symptom usually of a virus; nonuniform foliage 

coloration; a more or less distinct intermingling of normal, light 

green, or yellowish colored patches; a mottle 

motile-exhibiting or capable of movement 

mottle-discase .ymptom comprised of light and dark areas, an 

irregular pattern on a leaf 

muck soil-soil similar to peat soil, often having a lower percentage of 

organic materials 

multinucleate-having more than one nucleus enclosed within a cell 

wall 

muriform-having cells like bricks in a wall with both longitudinal and 

transv.rse septa 

mutation-heritable genetic change in a cell 

mycelium-hyphae compromising the thallus or body of a fungus 

mycoplasma (mycoplasm)-procaryotic organism, smaller than 

bacteria and larger than viruses, without rigid cell wallsand varying 

in shape, reproducing by budding or fission 

necrosis (adj. necrotic)-death of plant cells or plant parts, usually 

accompanied by darkening or discoloration; a symptom of disease 

nematicide-chemical agent that kills nematodes 

nematode-threadlike round worms of the order Nematoda, usually 

soilborne, of which a number of microscopic size attack potatoes 

net necrosis-necrosis of phloem tissues within tubers causing a netlike 

pattern of internal discoloration 

nm-nanometer, 10 9m, 0.00O1pm 

node-joint in a stem, also the eye of tuber at which leaves and axillary 

buds are formed 

nonpersistent-short-lived; said of viruses that are infectious for only 

short periods when transferred in or on insect mouthparts 

nonseptate-describing fungus filaments without cross walls 

nymph--juvenile stage of insect with incomplete metamorphosis but 

resembling the adult 

obovate-egg-shaped with wide end outward 

obovoid-egg-shaped with narrow end outward 

omnivorous-feeding on substances of both animal and vegetable 

origin 

oogonium (pl. oogonia)-the female egg cell of oomycete fungi 

oospore-thick-walled, sexually derived resting spore of phycomyceteous 

fungi 

organelle-delimited membranous structure within a cell having a 

specialicdl tunction 

ostiole-pire; opening in a perithecium or pycnidium 

ozone-O, a photochemical oxidant air pollutant 

palisade-a layer or layers of columnar cells rich in chloroplasts present 

beneath tie upper epidermis of plant leaves 

PAMV-potato aucuba mosaic virus 

papillum (pl. papilla)-small, round or nipplelike projection 

paracrinkle-a symptom of mild crinkle in virus infections 

paragynous-having the antheridium at the side of the oogonium 

paraphyses-hairlike cells within a fungus fruiting structure 

parasite-organism that lives with, in, oron another organism (host)to its 

own advantage and to the disadvantage of the host 

parenchyma-saft tissue of living plant cells with undifferentiated, thin, 

cellulose walls 

pathogen (adj. pathogenic)-the causal agent of a dise--.se 

peat soil-a soil type, high in organic materials conisting of partially 

decayed, moisture-absorbing plant materials, formed in bogs or 

swamps 

pectolytic-enzyme capable of dissolving pectin (the substance that 

normally cements plant cells togetler) 

pedicel-stalklike structure 

pentaploid-having five sets of chromosomes = 

(in potato, 2n = 5x 60) 

peptone-any of various water-soluble products following partial 

Lydrolysis of proteins 

perennial-a plant naturally persisting vegetatively for more than one 

year or growing season 

periclinal chimaeras-plants with inner tissues genetically different 

from outer tissues 

peridial-referring to the outer envelope of the sporophore of many 

fungi 

pericycle-a thin layer of parenchymatous or sclerenchymatous cells 

that surrounds the stele in most vascular plants 

permeability (adj. permeabile)-the quality or condition allowing a 

fluid or substance in a fluid to pass or diffuse through a membrane 

persistent-describing a relationship between virus and vector 

characterized by a lapse of several hours between acquisition and 

first transmission and the continuation of virus transmission for 

119

many days following removal of the insect front the virus source 

petiole-stalklike portion of a leaf attached to the stem and supporting 

the lamina 

pH-measurement of acidity or basicity. pil7 being neutral, values 

below being acid, and those above being basic (alkaline) 

phenol (adj. phenolic)-a toxic acidic compound. CHOH, used as a 

disinfectant or protein denaturant 

phenolase-an enzyme capable of degrading phenolic compounds 

phloem-vascular tissue consisting usually of sieve tubes, companion 

cells, and parenchyma that conducts elaborated food materials 

photochemical oxidants-highly reactive compounds formed byaction 

of sunlight on less toxic precursors 

photodegredation-degredation due to light, usually sunlight 

phyllody-change of a plant organ into a foliage leaf 

phytotoxic-harmful to plants; usually describing a chemical 

pigmentation-colora tion 

pinnate-describing leaves having similar parts arranged on opposite 

sides ifthe axis 

pitch-in a filamentous virus particle, the axial distance between 

adjacent turns of a row of capsids 

pith-loose. spongy tissue in the center of certain stems 

plasmodium (pl. plasmodia)-naked mass of protoplasm without cell 

walls containing nuclei and cytoplasm. usually of itfungus 

plastid-any of various cytoplasmic organelles (chloroplasts, 

leucoplasts, etc.) that 

metabolic 

serve in many cases as centers 

activities 

of special 

pleomorphic-with various shapes; of nonnstant form 

PlRV-potato lea ri virus 

PMV-potato leaf-tolp virus 

podzol--ype of light colored, relatively infertile soil of cool, coniferous 

forests poor in lime and iron 

pollen-male sex cells produced by anthers of flowering plants 

polymerize-to subject to or undergo a chemical reaction in 

or 

which 

more similar 

two 

molecules combine to formlrger molecules of 

repeating situctural units 

polyploidy-stat of having more than two chromosome sets 

polysaccharide-a carbohydrate that can be decomosed by hydrolysis 

into two or more molecules of monosaccharides 

ppm-parts per million 

primary inoculum-inoculum usually from an verwintering source, 

that 

primry inoului. 

initiates 

noclumsualy 

disease in the 

fom 

field, rather 

n oerwnteingsouce, 

disease during 

than 

the 

that 

seasonpragtoofoao 

which spreads 

primary symptom-the symptom produced soon after infection, in 

crimasymtom-henda symptom roducd 

Contrast 

solows 

to a secondary 

aftrinfectompby 

symptom, which follows more complete 

prinium (adj. primordial)-stil ridientarv or initiating portion 

progmii-dcscpndana'S 

front which it plant par'tIrmed . preng hsfo 

propagule-an. part of an orgalnism capable of independent growth 

protein-anyacidr 

prot1inanf no o'l nncrousare 

whi naturaly tessentiacuirrituencomplexllolbinationl 

occurring, complex combinations 

o aiiino acids. -hich areessential constituents ofall living cells 

protox rn athe first-I ornugd x veni. with anntlar. spira. or 

pseudosclerotia-sclcroliaik structures 

I'SlV-postato spidlc iiiher iroid 

psdid-ip planl w c he hily Iylasomatic-relating 

ps) Ilids -0iuping planti lice of i he fami ly Ps vI (lidae 

punctate-dotlike. iiarked vith dots or tiny spots 

pustule-blisterlikc: small crumpent spot. spore mass, or sorus 

IVA-potuto \irus A 

IVM-potato irus M 

PVS-potato virus S 

'1VT-potato virus I 

PVX -potato virus X 

l'V-potato virus Y 

pycnidiospores-sporcs (conidia) produced in i pycnidium 

pycnidium (pl. picnidia)-asexual. globose or flask-shaped fruiting 

body of fungi producing conidia 

IVV-pota IIYD')V--potato t yell yellow ow dwarl vfi irus virus 

IN~V-potato vellosv vein viruseniom 

quinones-any of various (usually yellow, orange, or red) quinonoid 

compounds, including several that are biologically important as 

coenzymes. hydrogen acceptors, or vitamins 

race-biotype 

reducing sugars-sugars with free carbonyl groups such as fructose, 

formed from hydrolysis of complex sugars 

resistance (adj. resistant)-property of hosts that prevents or impedes 

infection or disease development 

120 

resorption-the action of absorbing again a substance previously 

differentiated 

respiration-enzymatic reactions within a living organism utilizing O2 

and releasing CO., usually for production of energy 

resting spore-temporarily dormant spore, asually thick-walled, and 

capable of surviving adverse environments 

reticulum (adj. reticular, reticulate)-netlike or weblike structure 

rh-relative humidity 

rhizome-horizontal underground stem of more than one year's 

growth, possessing buds, nodes, and usually scalelike leaves 

rhizomorph-fungus mycelium arranged in strands, rootlike in 

appearance 

rhizosphere-microenvironnient in soil near to and influenced by plant 

roots 

ribonucleic acid-any of a number of nucleic acids containing ribose, 

uracil, guanine, cvtosine, and adenine and associated with control of 

cellular chemical activity; the nucleic acid type of most plant viruses 

RNA-ribonucleic acid 

rogue (noun)-diseased or abnorm;,l plant; (verb)-to remove rogues 

during their growth 

root cap-protective cap covering apical meristem at root tip 

rosario-arranged as heads on a string (Spanish for rosary) 

rugose mosaic-severe mosaic accompanied by deformation such as 

leaf crinkling, curling, or roughening of leaf surface 

saprophyte--nonpathogenic plant that obtains nourishment from the 

products of organic breakdown and decay 

scald-a necrotic conditiin of tissue, usually bleached in color, with 

appearance of having been exposed to high temperature 

sclerotia-drought-resistant or heat-resistant form of fungus structure, 

usually with thick, hard cell walls permitting survival over adverse 

environments 

second growth-resumption of growth after normal growth has ceased 

secondary organism-organism that multiplies in already diseased 

tissue; aot the primary pathogen 

secondary rot-rot caused by Isecondary organism 

secondary symptom-symptom of virus infection appearing after first 

(primary) symptoms; in potato, a symptom often from infection 

borne by seed-tubers 

seed tubers-tubers or tuber parts planted as seed for asexual 

propagation of potato 

senesce (n. senescence)-to decline with maturity orage; often hastened 

stress from environment or disease 

septum (pl. septa)-cross wall 

serological method-several types of tests for identifying viruses by 

using an antiserum that reacts specifically with a given virus protein 

serum-colorless, liquid component of blood used in serological tests 

for viruses 

seta (pl. setae)-bristelike fungus structure 

sieve tube-a tube consisting ofan end-to-end series of thin-walled cells 

in the phloem, with ends (sieve plates) perforated and thickened, 

functioning chiefly in translocation of organic solutes 

solanine-a potentially toxic glycoalkaloid present in plants of the 

Solanaceae, including potato 

to the body, especially body cells as distinguished 

from germ plasm 

som aerraim 

somatic aberration-mutation orabnormality ina somatic celland its 

progeny 

sorus (pl. sori)-a group of spores that is formed within plant tissue and 

that may erupt through the surface 

sp. (singular, pl. spp.)-species 

specific gravity-in potatoes, dry matter content of tubers expressed as 

weight per unit of volume; used as an indication of starch content 

sporangium (pl. sporangia)-a type of fungus structure producing 

asexual spores, usually zoospores 

sporangiophore-a sporangium-hearing body of a fungus 

spore-reproductive one or more cells; body a bacterial of fungi and cell other 

modified 

lower 

to 

plants, 

survive 

containing 

adverse,. 

environment 

sporiferous-bea ring or producing spores 

sporophore-a spore-bearing body in fungi 

sporulating-producing and often liberating spores 

ssp.-subspecies 

sterigma (pl. sterigmata)-small, usually pointed protuberance on 

which basidiospores are borne 

sterile-free from contaminant organisms; incapable of propagation; 

infertile 

stolon-type of underground stem on the tip ofwhich. in potato, tubers 

are formed 

stomate (pl. stomata)-opening in the epidermis of a plant part

surrounded M gaid cellsitnd Icalditg to ilnintercellullar ,pace 

through Maich gases dilluttse 

strain-a selection of ai oiganisii %kithpecuiliar claractertlti s: race: 

biot.ype 

stylet-slender Itihlar tnoulltparls inplant-part+ttc nenaltodes or 

aphids 

subcullure-at culture (l.g.. of bacteria or fungi) t rIdesed fronm antiother 

culttre 

suherin-wa\x, wVaner-it.,rsiattas stbstrtce associated with corky 

tisste deposit d iltor rita planrat cells 

suberjied-inlilri.ti loalcell ssalls natlh suberitt 

,ul)tsidalitil-dcl.,:icyc\ at oxygeat that impairs ritrinatal respiratiot 

suhsrtte-thc suhslance iilt\sitich aitorganism li\es or frttm which it 

oblaitts raiarnicants: cherrtical suibstanice acted utponr. oalteta by att 

cni/ri 

mcculeilt (Inoit r dj.)-plaiar. oir planat part \witll tetder, iuicy. or 

waterls tisuC 

superctaioled-describiltag liquid coled beltas its Iree.itg ptint withutt 

foiarmtratioift tce crs s\tals 

surfaclaint-at rllace-aclise sitlbstarice ttailyifing sUIrlace aetasitn of 

liquid, atd their abilit* tai \%ct tihcr natcrials 

sutscellile-lacking rsiltace: plitre ta itlection 

ia ryrttr In s 

s)n)iUi (Ill. i nci till) -n tilltrttlcatc mass o pttlaplasrill resulting 

rarrt cantini al ucit .ear alis stori or cell \%'all breakdownri arad 

a seLu.ii'l I saOn t plathlaplasts anlt strroaunlideil by atcomtton cell 

\%all.alsi callel giant cells itt iteliatode irlfeciots 

'lIIHV-trniatl black ritng siri 

tenile strenglh--Ie greatcst lengthwise strcss i sabstance can hear 

wititltlut teari rg ;lapjrt 

felrapluid-having four sets oafchlmorsimes (inpotaia. 2n = 4x = 48) 

Ilbernal inactihatin lentperature-the tnlttperalare at %hich infectiatus 

entitieN are inacti ated tasiaually witihit a giiven time periad 

Iitt-latc art sail aggregation or corsistencc; goard tilth imtplying 

parrr ats. lriatlc texture 

"IAMV-thbaicco lltit:il iirus 

lNV-tibacct tnecrosis s rils 

tltlerance-capacit tat a plalnt air crap ta) sistairn disea air entdure 

astl.re eresirirrraeatt \\ithol lseriols daaage tar irtiry 

tlo\ic-capabte artcaIIuIg intir tara lisilrg tirgatritn 

htxitt-pnistorttiils substance itbiolhgical orrigin 

Irttnslatcale (at. tratislucaliotn)-t trasfer Irtarn oie locatint otalsor 

an tier itllhe plant bo daf 

Fannlucenl-pernitiing liglt tanslinre throuigh is lilltuseil light 

trasmanil-tr spread s asatl intectiout 

ritial r,a patlrgetn Itlrn plant tat 

paIt or rtlir irtle planat genteratiorn tat ,aoiatther 

tricharute-platat epidetiral halr , f sstich eei I.vl types exist 

triplaid-hasiitg thrce sets rt chromilotsomraaaes (in potator. 2nl 3.\ -- 36) 

triturate-to griand as withl a nortarand pestle 

lRSV-tobacco rittgspot \irus 

true seed-sceud resiltirg rout scxual lusion an ganetes (incontrast to 

secd tuKrs ofpotato. \Mtucharc produced aSexually) 

TRV-tobacco rattle sirs 

7.SW\\-toiato spotted \ilt \irus 

luher-slhort. thickened. Il.sr\' unraderground sten, borne usually at the 

end ofl a stolon 

tuber iuadexing-prapagatior ofl a1plant frot a tither ori titber parl to 

deter inc p resenrace ol I tliherhorate disease 

tuberije-io lorri lubcrs 

turgid-f istensitn olcellk rtistt die taowater absarption 

turgar pressure-inteirnal pressa r within plarnt cells. Lack of turgor 

catuses plils it)will. 

I[,eiraasinase-a rteta/,iiic widcspica f itt plantts ;itd a niaitals that catalye.s 

txidation of tyrosine 

tyroaine-i atetaholicall- iaatptitaartt plhtnolic aiuitto acid 

uninucleate-ta'ing ane tcticleis 

vascular-pelrtaining toictnductive (xvIcn " and pthlcin) tissues 

vascular ring-circular arranragemtrenta tal osascular trands within a stem 

ot tiher 

vascular sirtmnd-grtip tof .ltaligated cells intcludirng xylcaa, phlettn, andrid 

parelchylatotatis tissue. pro\iding tor irtttetni.ert of water anld 

soaltutes and lair mttecharical ,aipporl 

vectur-agetat that trai rits irtarculuri atd is capable of disseninating 

disease 

vegetltive-rele-rirg tat statatic air asexual parts of the plant It 

insolta'ed insextal Ieprtdulictitirt 

viroid-ib, smallest kllaiawi inlectitrat agernt caaaasistingt nucleic ti acid 

and lacking tire i ,isal protein carat atf \irtje,, 

virulent-pathlrgenic: ha\ing capacity lir cai sing discase 

viruliferous-irus-ca rryirg tig ,tsaall art insect or nremattde 

virus-an inifectise particle smtaaller than a bactcritina cotrtairaiig prateira 

antd nucleic acid antdilcapable tal mnultiplying \itlhinplant tar alinial 

cells 

volunteer plant -a latatr ptaIr growing Iroan tlnatrirestedwther as a 

weld 

xyleni-ctlnph.x \wotady tiSslte crsisting tat resCIs. tracheids. fibers. 

ail parerch'lYtia that tranrrsporrts witer antd salites antadnay serve 

tar matelcharnical sutppoart 

inate (n. zonalin)-niarked \iih stripes air lincs natare tr less parallel 

ta tire edge o Ile lesion 

ioosparangjuni -a spoare ease tar sptrangitna-heariag /oa spores 

zooaspore-I'lugUS spore with flagella capa ble of' locoarmoaation in water 

zygote-scxually prodttcedf cell forned by tlhe union of two gamaites 

121

Index 

Abrasions, tuber surfaces. 14 Botrris cinerea 

Aceratagallia 

Erytsiphe 

saguinohnta, 

cichoracearum, 

potato 

powdery 

)ellow 

mildew 

gray mold caused by, 48 

dwarf virus vector. 

caused 

82 

by, 43 

o7one predisposing to infection by, 

Atinomices.xcahie,,seeSireitonii, 

21 Ethylene, coiled sprout 

rsscahies 

role, 18 

Brown rot Eumartii wilt, see Fusarium 

.-trrtriosiphon 

wilts 

spp.. 102 ring rot compared 

-1ecidiuln 

to, 29 

'anitesis,rust from, 65 symptoms. 29 

.gallia 

False 

quadrijupwtaia. 

root-knot nematodes. 

potato yellow 

98 

dwarf Browning 

virus vector, 

Flavohacterium 

82 

sp. 

internal mahagony, temperature 

.'tgrobac'erium 

relation, 9 

sp., in healthy 

in healthy 

tubers, 

tubers, 

33 

33 

stem-end, symptoms, 22 

Air pollution, 

per'lilovoruni,soft 

injury from. 

rot 

20 

from, 28 

Bunch top. 91 

Alfalfa mosaic 

Foliage, 

virus. 

temperature 

82 

effect on, 9 

Foundation 

symptoms, 83 

seed. 104 

Calcium deficiency, symptoms, 23, 24 

control. 

Frankliniella 

83 

spp., tomato spotted wilt virus 

Catechol test, use of. 15 

.Ahernaria vector, 87 

Cavariellapastinacae, 102 

ah,'rnata,44 

Frost injury 

Cerco.spora foliage, 9 

'olani. 43 concors, leaf lotch caused by, 47 tubers, 

lenuis. 

9 

44 solawi-Ihero.vi. 

Aluminum, 

leaf blotch 

toxicity 

caused 

from. 

by. 47 

24 

Fungicide application, principles, 

Cercospora 

66 

leaf blotch 

Andean potato latent virus 

Fu.saritm 

cause and symptoms. 47 o.insporunm 

symptoms. 

f.sp. 

78 

iuberosi, 61 

control. 47 

control. 78 ro.seuin 

Certification, seed potato. 104 

Andcan 

'Avenaceum', 

potato mottle 

59. 

virus 

61 

Certified seed potato, fraudulent use, 104 

symptoms. 

'Sambucinum', 

77 

59 

Chaetomitn spp., leaf spots from, 66 

control. 77 

solani. 61 

Charcoal rot 

..Itgio'or 

'Coerulcum', 

.5ohi, smut 

59 

caused by. 64 cause and symptoms, 56 

Aphids f. sp. eumariti, 61 

control, 57 

description. 

Fusarium dry 

101 

rots 

Chemical injury, symptoms. 21 

table, key to wingless 

cause. 

forms, 

59 

102 Chimacras. periclinal. 7 control, 59 

..phi,% ('hoanephora blight, 48 symptoms, 

102 

58 

/ratgtila', potato virus 

Ci/a. (hoantep/ora 

M vector, 

ucur/'ritartt, 

75 

48 

('irru/ifi,rten,/h, 

Fusarium wilts 

sugar beet curly top virus 

o'~rli-fran,tiho. 

cause, 61 

112 vector. 90 

,attorii. po ato virus 

control, 

M 

61 

vector, 75 Cono.%tashr.%arautariue,tuber rot from, 66 symptoms. 

Apical 

60 

Icafrll. 91 C/ostridium spp.. solt 

.Armilhr 

rot relation, 

a elh,Ia. 

28 

tuber rot from. 66 Colhetoric'huo, 

Aster y'ellows. 

Gangrene 

sympt ms. 91 aranmentarium,55 

Iuto1'rthut 

cause and 

.uhmi, 

symptoms. 

102 

57 

coceot,/s. 55 

Asc naccu m " 

control, 

ill. we 

58 

Ftusarium wilts Common scab. se Scab Gemmation, 12 

Corticium,.we 

11(il/t-b 

Rli'?/ 

srp. 

ttonia 

Genetic abnormalities. 

Corineatcterioum 

7 

.sepedonitim ring rot 

soft 

Giant 

rot caused 

hill, genetic 

by, 28 

abnormality, 7 

caused by. 31. 32 

oegate'rium, 

Gilmanielha huinticola 

in healthy 

tuber 

tubers, 

rot 

33 

from, 66 

Cucumber mosaic virus. 79 

Bacterial 

Globoderaspp., 

wilt. symptoms. 

94 

29 Cr/lindro'arp/on totikine-ij, dry rot from, 

/iltlaimun 

66 pallida. 

/rngicattdailt% 

95 

94 

Black dot 

roslochiensis, 95 

Deforming mosaic, sy.mptoms. 87 

C(//cloirichot 

Gloius 

cause, 

fasciculatus, 

55 

66 

Difirmell sp.. eal splot from. 66 

silver scurf 

Gram 

similarity, 

stain, recipe, 

55 

31 

I)iirhnchu.s spp.. 94 

Black scurf 

Gray mold 

de.struc'tor, 101 

cause, 53 

cause and symptoms, 48 

Dwarf shrub virosis, 92 control, 48 

control. 54 

symptoms. 52 Early blight 

Blackhcart 

iHail injury, 19 


-ause and symptoms. 

Haywire. 

10 

91 

control, 44 

temperature relation. 

leat necrosis, 

9 

internal, symptoms, 

Eisenfleckigkeit, 

I I 

II lhelicohasidiuitpurpuretm, 

Blackleg, symptorms, 27 

violet root rot 

lEnanismo amarillo, 68 

Blackspot, potassium 

caused 

deficiency 

by, 54 

predisposing I.piirix sp. 

to. 23 

Ile/icoiltc/us spp., 94 

Andean potato latent viru:, vector. 78 Heninittosporium 

Blight. vee Early 

.solanti,silver 

blight or L.ate 

scurf 

blight 

caused 

hirtipennis, tobacco ringspot vector. 

Itlitecast. 

85 

late blight 

by, 55 

epidemic forecasting, 42 Erwinia 

Blue stem. 91 

Ifeterodhera, see Glohodera 

carotovora, blackleg caused by, 27 

Boron 

Ihte'rosporiun 

deficiency, 

sp., 

symptoms. 

on leaves 

24 

and tubers., 66 

chrrsanthemi. blackleg caused by, 28 Ihexat.i/us vigissi, 94 

123

[follow heart, cause and symptoms. 13 

Iiratha)hi.%'ri..nioi 102 

Ihah.tsihe o).oh'un. stolbur vector, 93 

lirloc'hnt.,. weeRhi:octonia 

Igel-lange test. tuber indexing, 69 

Importance ol potato, worldwide. I 

Insect toxins. 93 

Internal net necrosis, 68 

Late blight 

cause and s"vnptorns 41) 

control. 42 

latcbrcaking ViMS.91 

I.cafrall 

non irus. I8 

,irus.e Itato lealroll virus 

I eat spots. 66 

Leak 

cause and s'm aiptonis. 38 

control. 39 

I .cticels. infection role. 4 

I.'Ip/t(U'toha tO sp.. lealspot from. 66 

Lesion nematodes, 99 

Lightning injury. 19 

Ioni tlri.% maoxmtin.. 94 

ihu'roltontna Iph wolt, charcoal rotcause. 

56 

.Mautro.q)tonielta .manb orai, 102 

,fac'roiitim etpIdiorliae, 1(12 

potato %irus M vector. 75 

Eapro.orittnta/wa. wes'.'IIrara %.lani 

lfarrte'e..la ilri.%, aster vellows vector. 93 

M:agnesium deficiency, symptoms, 24 

Manganese deliciency. symptoms. 26 

tIfelhha ~,gnt %pp.,94. 97 

.Ih'loit'ma sp., 94 

tit rEm'oat sp.. i healthy tubers. 33 

Milde%. we IPowders nildes, 

M rnt). 9 

Mitation. somatic, importance. 7 

ilticlta aerilia. black rotcaused bv. 51 

M\'cophrsmas. description. 91 

vcotrrhi/ae. 66 

,iticvelloila ('oncor. leafblotch caused 

by. 47 

.Iv:tu. spp., 102 

aE a/oanai'v. potato lealroll vector. 102 

pt'rvcae, 102 

potato leafroll vector. 68 

potato virus M vector. 75 

,Vattrhhtu ahtrrait.%, 94 

false root-knot cause. 98 

.asonewia lacticae, 102 

National Plant Quarantine Act. 104 

Nematicides, description, 101 

Nematodes 

cyst, description, 95 93 

rot o1,9 

table of, 94 

Neohiirus tenllu, sugar beet curly top 

vector. 90 

1cticfle.rs. 102 

Neolnenchs. ahulhow turu, 94 

Net necrosis, low temperature causing, 8 

Nitrogen, 

symptoms. 

requirements 

22, 23 

and deficiency 

Northern stolbur, 92 

Olpidiuat hrassicae,tobacco necrosis virus, 86 

Oasporaptistulans,see Poat'suitaluapurtsulans 

Ophiolafalvopictus,witches' broom vector, 92 

Oxygen requirements, tuber effect, 8 

Oxysporum wilt, .ee Fusarium wilts 

Ozone injury,symptoms, 20 

Parastolbur, 91 

124 

Paratrihtodoru. spp.. 94. 101 

tobacco rattle virus vector, 81 

Paratrio:a ockerelli,psyllid yellows cause. 93 

Parau'hir/et/ht. spp.. 94 

'ellicularia. %v' Rhi:octonia 

Pericotnia sp.. lealspots from, 66 

Pcroxyacetyl nitrate. injury trom. symptoms, 

20 

Phoma 

anlina,. leaf spot caused by, 47 

eXigua. gangrene caused by. 57 

Phoma leat %pot 

cause and synptoms, 47 

control, 47 

Phosphorus. requirements and deficiency. 23 

I'/topithora 

errltroeptima.pink rotfrom. 39 

in/ie.ani, late blight from. 41) 

Pink eye. symptoms. 32 

Pink rot 


control, 41 

Pleo.s)ora herhartmt. symptoms.46 

IPo/tr %ctta/to,Inituhtai, skin spot caused by. 

.7Rhopalosil)honinus 

Potassium deficiency, symptoms. 23 


cultivated types. 2 

flowers, fruits, stems, roots. 2 

impartance, worldwide, I 

tuber., .weITuber 

Potato aucuba mosaic virus 

control. 84 

symptoms. 84 

Potato cyst nematodes 

cause. 95 

contral, 96 

symptoms, 94 

Potato leafroll, control. 69 

Potato leafrall virus, symptoms, 68 

Potato mop-top virus 

control, 81 

symptoms. 79 

Potato rotnematodes 

control. 100 

symptoms, 100 

Potato spindle tuber viroid 

control. 90 

symptoms, 89 

Potato tuber blotch virus, 84 

Potato virus A 

control. 72 

symptoms, 71 

Potato virus G. 84 

Potato virus M 

control. 75 

symptoms. 74 

Potato virus S 

control. 76 

Potato symptoms, virus T 75 

control. 77 

symptoms, 77 


control. 

virus X, 

74 

72 

symptoms. 73 

Po.lnt.usvirus Po- 

Y 

co,trol, 71 

symptoms, 70 


Ptt 

yellow 

elwdafvrsSpoi 

dwarf virus 

control, 82 

symptoms, 82 

Potato yellow vein virus, symptoms, 86 

Powdery mildew 

cause, 43 

control, 43 

symptoms, 42 

Powdery scab, see Scab 

Pratylenchus spp., 94 

control, 100 

symptoms from, 99 

IPstioeonons sp. 

in healthy tubers. 33 

Ifuorescen., pink eye caused by, 32 

soatacearuin,brown rot caused by. 30 

F'syllid ycllows 93 

'uct'ciniapittieriana, rust caused by. 65 

Purple dwarf. 91 

purple top roll. 91 

Purple top wilt, 91 

Prthium spp.. leak caused by, 8, 38 

Rhi:octonia 

crovorun, 54 

oslani, black scurf caused by, 53 

Rhi"ctonia canker 

cause. 53 

control, 54 

symlptoms, 52 

R/i:opu. 

arrhizs. 52 

.stoloniftr,52 

Rhizopus soft rot 

cause and symptoms. 52 

control. 52 

spp., 102 

Rto 1 wlosil)hu spp.. 102 

Rindite. 105 

Ring r)t 

brown rotcompared to, 29 

cause and symptoms.31 

Root-knot nematodes 

control. 98 

symptoms. 97 

Rosario. 98 

Rasellinia spp.. 5I 

Rosellinia black rot 


control, 52 

Roit'lenchulus spp.. 94 

Rot'nchu.s spp.. 94 

Rust 

common 

control. 65 

symptoms, 65 

deforming 

control. 66 

symptoms, 65 

Scab 

common 


control, 34 

powdery 


control, 36 

Scleracus.flavopictus, witches' broom vector, 

92 

Scleroractus spp.. witches' broom vectors, 92 

Sclerotinia 

bataticola, 56 

minor, 49 

selerotiorum, white mold caused by, 49 

Selerotium rolfrii, stem rot cause, 50 

Seed improvement programs. 105 

Seed treatment, tubers, 67 

Septoria leaf spot 


control, 46 

Storia h'coptr. 

yoesc 

it'i 

control, 46 

symptoms, 46 

Silver scurf, Helminthosporium solani 

causing, 54 

Skin spot 


control, 38 

Smut, Thecaphora causing, 63 

Sint'nthurodes hetae. 102 

Solanum 

acaaule. 73

Irost tolerance in. 9 

aniligena. 68 

,pp., comparison. 2 

hacm'nxn. 71.72 

dh'i'. Lum,. 71, 72 

late blight resistance in. 42 

.pecies comparison. 2 

hybrids., diploid%, triploids. tetraploids, 

pentaploids. hexaploids. 2 

kurtziatnm, 95 

iultdjix.ieiUm. 95 

pIhurea. spp. comparison. 2 

ro.straint. potato virus S host. 76 

spp.. comparison of. 2 

.itenoloown, spp. comparison. 2 

%Ioloniftrum. 71. 72 

ilhero.sum, 68. 73. 76. 95 

spp. comparison. 2 

verner. 95 

Southern bacterial wilt 

symptoms. 29 

synonyms. 29 

SlpondihlocdiOm atrovirens.55 

.Spogotoora oi'tlterrawi~a 

powdery scab caused by, 35 

quarantine lor. 104 

Spraing. tobacco rattle virus causing. 80 

Sprout 

coiled, cause and symptoms, 17 

hair, cause. 18 

Sprouting, internal, in storage. 17 

Stem rot 


control. 51 

Stem streak necrosis, Mn toxicity causing. 26 

Stem-end browning 

control. 22 

symptoms. 22 

.Semphrlilni 

atrum, symptoms. 46 

hotr osum. symptoms, 46 

con,ortiahl, symptoms. 46 

StolhIJI, symptoms. 91 

Strepionrces stahies. common scab caused 

by. 33 

Stubby-root nematodes 

control, 101 

symptoms. 101 

Sugar beet curly top virus, 90 

Sulfur 

deficiency. symptoms, 24 

oxide, injury Irom, 21 

Sinc/i'trium elohimi'um 

potato virus X vector. 73 

qIa rantinc for. 10t4 

wart caused by. 36 

Tall types, genetic abnormality, 7 

Temperature 

foliage affected by. 9 

of soil. injury from. I1) 

tubers affected by, 8 

77tanetephorus,see Rhi.Toctonia 

Thecaphora .solani, smut caused by. 64 

77trips tahaci 

tobacco ringspot virus vector. 85 

tomato spotted wilt vector. 87 

lobacco black ring virus 

control. 86 

symptoms. 85 

Tobacco mosaic virus. 79 

Tobacco necrosis virus, symptoms, 86 

Tobacco rattle virus 

control. Kl 

symptoms. 80 

Tobacco ringspot virus 

control. 85 

symptoms, 84 

Tomato big bud. 91 

Tomato black ring virus 


control. 86 

Tomato spotted wilt virus 

control, 89 

symptoms. 87 

Toxins, insect. 93 

Tricho(dorus spp.. 94 

Prifiniti.6s. I01 

tobacco rattle virus vector, 81 

Tubers 

abrasions. 14 

blotch. 84 

bruising. 16 

cracks. causes. 14 

description. 3 

greening and sunscald, 16 

indexing, viruses, 69 

respiration in storage, 5 

rots, 66 

secondary, field and stored, 17 

seed treatment, 67 

wound healing. 3 

7Trenc'horhrnch spp.. 94 

Uloclaiuim 

atrum, symptoms. 46 

'onsortiale, symptoms. 46 

Ulocladium blight. cause and symptoms, 46 

Variation. see Genetic abnormalities 

Verticilliun, 

albo-atruin, wilt caused by. 62 

dahliae, will caused by. 62 

Verticillium wilt 


control. 63 

Violet root rot 


control. 54 

Virus diseases. 68 

Wart 


control. 37 

Whet:elinasch'rotorunt. 49 

White mold 

cause. 48 

control, 50 

symptoms. 49 

Wildings. true and feathery, 7 

Wilt, see Fusarium wilts and Verticillium wilt 

Wind injury. 19 

Witches' broom. 79 

control. 92 

symptoms, 92 

Wound healing, in tubers, 3 

Xatthomonas sp., in healthy tubers, 33 

Xiphinema spp., 94 

anericantint, tobacco ringspot virus vector, 

85 

X.laria sp.. tuber rot from, 66 

Yellow top, 91 

Yield, worldwide. I 

Zinc deficiency, symptoms, 25 

125

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