Compendium of Wheat Diseases and Pests, Third Edition

Compendium of Wheat Diseases and Pests

THIRD EDITION

Edited by

William W. BockusKansas State University, Manhattan

Robert L. BowdenU.S. Department of Agriculture

Manhattan, Kansas

Robert M. HungerOklahoma State University, Stillwater

Wendell L. MorrillMontana State University, Bozeman

Timothy D. MurrayWashington State University, Pullman

Richard W. SmileyOregon State University, Pendleton

The American Phytopathological Society

Front cover photograph by Jeff Vanuga, USDA Natural Resources Conservation Service

Back cover photograph by William W. Bockus

Reference in this publication to a trademark, proprietary product, or company name by personnel of the U.S. Department of Agriculture or anyone else is intended for explicit description only and does not imply approval or recommendation to the exclusion of others that may be suitable.

Library of Congress Control Number: 2010900316International Standard Book Number: 978-0-89054-385-6

1977, 1987, 2010 by The American Phytopathological SocietyFirst edition published 1977Second edition published 1987Third edition published 2010

All rights reserved.No portion of this book may be reproduced in any form, including photocopy, microfilm, information storage and retrieval system, com- puter database, or software, or by any means, including electronic or mechanical, without written permission from the publisher.

Copyright is not claimed in any portion of this work written by U.S. government employees as a part of their official duties.

Printed in the United States of America on acid-free paper

The American Phytopathological Society3340 Pilot Knob RoadSt. Paul, Minnesota 55121, U.S.A.

PrefaceThe first edition of the Compendium of Wheat Diseases was

published in 1977, and the second edition in 1987. Dr. Maury Wiese, of Michigan State University and the University of Idaho, is to be commended for initiating and coordinating the preparation of those two editions. There are over 28,000 cop­ies in circulation, and they have been an excellent resource for researchers, students, diagnosticians, producers, and virtually anyone else in the wheat industry.

Because of the large amount of new information about wheat diseases that had been discovered since 1987, it became evident that a third edition was needed. The impetus for the third edition came from meetings of the North Central Edu­cation/Extension Research Activities committee number 187 (NCERA­187: Management of Small Grain Diseases). As a result of discussions at the June 2005 meeting in Ithaca, New York, I was recruited to oversee the production of the third edi­tion, with the understanding that the sister organization in the western United States, Western Education/Extension Ac tivities committee number 97 (WERA­97: Diseases of Cere als), would be contacted and a representative from that region recruited for the editorial team.

Some initial work had already been carried out by Dr. Rob­ert Bowden (USDA­ARS), Dr. Robert Hunger (Oklahoma State University), Dr. Gregory Shaner (Purdue University), and Dr. Richard Smiley (Oregon State University). Dr. Shaner do nated his list of potential chapters and authors for the third edition. The other three agreed to become associate editors to oversee the development of the sections on diseases caused by bacte­ria, viruses, and nematodes, respectively. Dr. Timothy Murray (Washington State University) was recruited to oversee the update of the section on fungal diseases and to represent the western United States in addition to Dr. Smiley.

The third edition is different from the earlier editions in that experts on each disease, insect, or disorder were recruited to

prepare the chapter on that specific problem. Additionally, the treatment of insects has been greatly expanded, and 16 chap­ters on insect and mite pests of wheat have been added. There­fore, an entomologist was needed on the editorial team, and Dr. Wendell Morrill (Montana State University) was recruited to serve as associate editor for the section on insects. To reflect this important addition, the title was changed to Compendium of Wheat Diseases and Pests.

Over 70 authors were recruited to update existing chapters or to prepare new chapters. Compared with the second edition, the third edition has over 30 new chapters, the number of illus­trations has been increased from 189 to 269, and the number of color illustrations has been increased from 74 to 246. Most of the illustrations are new. Another new feature of the third edition is that the color illustrations have been placed near the corresponding text rather than gathered in a separate section of color plates.

It is hoped that this third edition will be as useful as the first two to those interested in wheat diseases and insects. While the important diseases and insects have been included, it is recog­nized that even this comprehensive treatise is not an exhaustive treatment of all of the known pathogens and insects that have been documented on wheat. Similarly, the references that are cited after each chapter are designed to introduce the reader to the literature and are not exhaustive lists of all relevant publi­cations. However, it is the view of the editorial team that the use of recognized experts as chapter authors has produced an up­to­date treatment of each disease and insect that should prove to be a valuable resource to the wheat community.

Bill Bockus Kansas State University

iii

v

AuthorsMichael J. AdamsRothamsted ResearchHarpenden, Herts., United Kingdom

El­Desouky AmmarOhio State UniversityOhio Agricultural Research and Devel­

opment CenterWooster, Ohio

Michael L. AveryU.S. Department of AgricultureNational Wildlife Research CenterGainesville, Florida

Martin J. BarbettiUniversity of Western AustraliaNedlands, Western Australia, Australia

Gary C. BergstromCornell UniversityIthaca, New York

William W. BockusKansas State UniversityManhattan, Kansas

Nilsa A. Bosque­PérezUniversity of IdahoMoscow, Idaho

Robert L. BowdenU.S. Department of AgriculturePlant Science and Entomology Research

UnitManhattan, Kansas

Lee A. CalvertCentro Internacional de Agricultura

TropicalMedley, Florida

John L. CapineraUniversity of FloridaGainesville, Florida

Lori M. CarrisWashington State UniversityPullman, Washington

Brett CarverOklahoma State UniversityStillwater, Oklahoma

Xianming ChenU.S. Department of AgricultureWashington State UniversityPullman, Washington

Vijay Kumar ChoppakatlaOklahoma State UniversityStillwater, Oklahoma

Erica ClineU.S. Department of AgricultureSystematic Botany and Mycology Labo­

ratoryBeltsville, Maryland

R. James CookWashington State UniversityPullman, Washington

William T. CrowUniversity of FloridaGainesville, Florida

Ruth Dill­MackyUniversity of MinnesotaSt Paul, Minnesota

Mauro Di VitoIstituto per la Protezione delle PianteBari, Italy

Joseph P. DoskocilOklahoma State UniversityStillwater, Oklahoma

Etienne M. DuveillerCIMMYTMexico City, Mexico

Michael C. EdwardsU.S. Department of AgricultureNorthern Crop Science Research Labo­

ratoryFargo, North Dakota

Myriam R. FernandezAgriculture and Agri­Food CanadaSemiarid Prairie Agricultural Research

CentreSwift Current, Saskatchewan, Canada

Bruce FittRothamsted ResearchHarpenden, Herts., United Kingdom

Leopold A. FucikovskyInstituto de FitosanidadColegio de PostgraduadosMontecillo, Mexico

Denis A. GaudetLethbridge Research CentreAgriculture and Agri­Food CanadaLethbridge, Alberta, Canada

Rose C. GergerichUniversity of ArkansasFayetteville, Arkansas

Bikram S. GillKansas State UniversityManhattan, Kansas

Roy E. GingeryU.S. Department of AgricultureOhio State UniversityOhio Agricultural Research and Devel­

opment CenterWooster, Ohio

Stewart M. GrayU.S. Department of AgricultureCornell UniversityIthaca, New York

Steve HaberAgriculture and Agri­Food CanadaCereal Research CentreWinnipeg, Manitoba, Canada

Gary L. HeinUniversity of NebraskaPanhandle Research and Extension

CenterScotts Bluff, Nebraska

Ron HinesUniversity of IllinoisDixon Springs Agricultural CenterSimpson, Illinois

Charla R. HollingsworthUniversity of MinnesotaNorthwest Research and Outreach

CenterCrookston, Minnesota

Don M. HuberPurdue UniversityWest Lafayette, Indiana

vi

Robert M. HungerOklahoma State UniversityStillwater, Oklahoma

Barry J. JacobsenMontana State UniversityBozeman, Montana

Alexander V. KarasevUniversity of IdahoMoscow, Idaho

James A. KolmerU.S. Department of AgricultureUniversity of MinnesotaCereal Disease LaboratorySt Paul, Minnesota

Joseph M. KrupinskyU.S. Department of AgricultureNorthern Great Plains Research Labora­

toryMandan, North Dakota

Dale LeikamKansas State UniversityManhattan, Kansas

Roland F. LinePullman, Washington

Marcia P. McMullenNorth Dakota State UniversityFargo, North Dakota

Eugene A. MilusUniversity of ArkansasFayetteville, Arkansas

Wendell L. MorrillMontana State UniversityBozeman, Montana

Craig F. MorrisU.S. Department of AgricultureWashington State UniversityPullman, Washington

Christopher C. MundtOregon State UniversityCorvallis, Oregon

Gordon M. MurrayCharles Sturt UniversityNew South Wales Department of Pri­

mary IndustriesWagga Wagga Agricultural InstituteWagga Wagga, New South Wales, Aus­

tralia

Timothy D. MurrayWashington State UniversityPullman, Washington

Julie NicolCIMMYT InternationalAnkara, Turkey

Timothy C. PaulitzU.S. Department of AgricultureRoot Disease and Biological Control

Research UnitWashington State UniversityPullman, Washington

Analía PerellóUniversidad Nacional de La PlataLa Plata, Buenos Aires, Argentina

Dallas E. PetersonKansas State UniversityManhattan, Kansas

Margaret G. RedinbaughU.S. Department of AgricultureOhio State UniversityOhio Agricultural Research and Devel­

opment CenterWooster, Ohio

Jack H. RiesselmanMontana State UniversityBozeman, Montana

Ian T. RileySouth Australian Research and

Development InstitutePlant Research CentreUniversity of AdelaideUrrbrae, South Australia, Australia

Zoran RisticU.S. Department of AgriculturePlant Science and Entomology Research

UnitKansas State UniversityManhattan, Kansas

Roger RivoalInstitut National de la Recherche Agro­

nomiqueÉcole National Supérieure

Agronomique de RennesCentre de Recherches de RennesLe Rheu, France

Alan P. RoelfsGrantsburg, Wisconsin

Tom A. RoyerOklahoma State UniversityStillwater, Oklahoma

Edward P. RybickiUniversity of Cape TownRondebosch, South Africa

Dallas L. SeifersKansas State UniversityAgricultural Research CenterHays, Kansas

Gregory ShanerPurdue UniversityWest Lafayette, Indiana

James P. ShroyerKansas State UniversityManhattan, Kansas

Phillip E. SloderbeckKansas State UniversityGarden City, Kansas

Richard W. SmileyOregon State UniversityColumbia Basin Agricultural Research

CenterPendleton, Oregon

Mark SorrellsCornell UniversityIthaca, New York

Jeffrey M. SteinSouth Dakota State UniversityBrookings, South Dakota

Drake C. StengerU.S. Department of AgricultureUniversity of NebraskaLincoln, Nebraska

Erik L. StrombergVirginia Polytechnic Institute and State

UniversityBlacksburg, Virginia

Fiona TanzerUniversity of Cape TownRondebosch, South Africa

Sharyn TaylorSouth Australian Research and

Development InstitutePlant Research CentreAdelaide, South Australia, Australia

Timothy C. ToddKansas State UniversityManhattan, Kansas

Alfredo UrashimaUniversidade Federal de São CarlosAraras, São Paulo, Brazil

Robert VaseyLeicester, England

David K. WeaverMontana State UniversityBozeman, Montana

Robert J. WhitworthKansas State UniversityManhattan Kansas

Maurice V. WieseUniversity of IdahoMoscow, Idaho

Charles P. WoloshukPurdue UniversityWest Lafayette, Indiana

Hailin ZhangOklahoma State UniversityStillwater, Oklahoma

vii

ContentsIntroduction 1 Importance of Wheat 1 Wheat Production Losses 2 The Wheat Plant 3 Genetic Resources of Wheat

Diseases Caused by Bacteria 6 Aster Yellows 7 Bacterial Leaf Blight 8 Bacterial Mosaic 8 Bacterial Sheath Rot 9 Bacterial Streak and Black Chaff11 Basal Glume Rot11 Gumming12 Pink Seed12 Spike Blight13 Stem Melanosis

Diseases Caused by Fungi and Fungus-Like Organisms16 Alternaria Leaf Blight17 Anthracnose18 Ascochyta Leaf Spot19 Aureobasidium Decay19 Black Head Molds (Sooty Head Molds)20 Black Point (Smudge)22 Blast23 Brown Root Rot23 Cephalosporium Stripe26 Common Root and Foot Rot and Associated

Leaf and Seedling Diseases28 Dilophospora Twist and Leaf Spot29 Downy Mildew (Crazy Top)30 Ergot32 Eyespot (Strawbreaker Foot Rot)34 Fusarium Head Blight (Scab)37 Fusarium Root, Crown, and Foot Rots

and Associated Seedling Diseases39 Halo Spot40 Mycotoxins42 Phoma Spot42 Platyspora Leaf Spot43 Powdery Mildew45 Pythium Root Rot47 Rhizoctonia Root Rot48 Ring Spot50 Rusts53 Leaf Rust

54 Stem Rust 55 Stripe Rust 56 Septoria tritici Blotch 58 Sharp Eyespot 60 Smuts 60 Common Bunt (Stinking Smut) 62 Dwarf Bunt 64 Flag Smut 65 Karnal Bunt 66 Loose Smut 69 Snow Molds 70 Pink Snow Mold 71 Sclerotinia Snow Mold (Snow Scald) 72 Snow Rot 73 Speckled Snow Mold (Typhula Blight) 74 Southern Blight (Sclerotium Base Rot,

Sclerotium Wilt) 75 Stagonospora nodorum Blotch and

Stagonospora avenae Blotch 77 Stem Scald (False Eyespot) 78 Storage Molds 79 Take-All 82 Tan Spot (Yellow Leaf Spot) 84 Tar Spot 84 Zoosporic Root Colonizers

Diseases Caused by Nematodes 88 Cyst Nematodes 90 Root-Gall Nematode 91 Root-Knot Nematodes 92 Root-Lesion Nematodes 94 Seed-Gall Nematode 95 Stem Nematode 95 Stubby-Root Nematodes 96 Stunt Nematodes 97 Other Nematodes Associated with Wheat

Diseases Caused by Viruses and Viruslike Agents 99 Agropyron Mosaic 99 Barley Stripe Mosaic and Barley Yellow Stripe100 Barley Yellow Dwarf102 Barley Yellow Striate Mosaic103 Brome Mosaic103 Chloris Striate Mosaic (Australian Wheat Striate

Mosaic)104 Cocksfoot Mottle104 European Wheat Striate Mosaic105 Flame Chlorosis

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106 High Plains Disease107 Maize Streak109 Northern Cereal Mosaic109 Tenuivirus Diseases: Iranian Wheat Stripe

and Rice Hoja Blanca110 Wheat American Striate Mosaic111 Wheat Dwarf112 Wheat Soilborne Mosaic113 Wheat Spindle Streak Mosaic and Wheat Yellow

Mosaic115 Wheat Spot Mosaic115 Wheat Streak Mosaic117 Wheat Yellow Leaf118 Winter Wheat (Russian) Mosaic118 Yellow Head Disease119 Other Viruses Infecting Wheat

Damage Caused by Insects and Mites120 Armyworms and Cutworms (Lepidoptera:

Noctuidae)122 Cereal Aphids (Homoptera: Aphididae)124 Cereal Leaf Beetle (Coleoptera: Chrysomelidae)125 Grasshoppers (Orthoptera: Acrididae)126 Hessian Fly (Diptera: Cecidomyiidae)128 Mites Other Than Wheat Curl Mite130 Stored-Grain Insects131 Thrips (Thysanoptera: Thripidae)132 Wheat Curl Mite (Acari: Eriophyidae)133 Wheat Jointworm (Hymenoptera: Eurytomidae)133 Wheat Stem Maggot (Diptera: Chloropidae)134 Wheat Stem Sawfly (Hymenoptera: Cephidae)

136 Wheat Strawworm (Hymenoptera: Eurytomidae)136 White Grubs (Coleoptera: Scarabaeidae)137 Wireworms (Coleoptera: Elateridae) and

False Wireworms (Coleoptera: Tenebrionidae)

Other Pests and Disorders138 Air Pollution Injuries139 Albinism140 Birds140 Chemical Injuries143 Chloride- and Zinc-Deficient Leaf Spots144 Cold Stress147 Crinkle Joint (The Bends)147 Hail Damage148 Heat Stress148 Mammals149 Melanism (Pseudo–Black Chaff)150 Nutrient Imbalances153 Physiological Leaf Spots154 Preharvest Sprouting154 Soil Compaction154 Soil pH155 Water Stresses (Flooding and Drought)156 Wind Damage (Lodging)156 Witchweeds (Striga Species)158 Yellow Berry

159 Glossary

167 Index

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photosynthesis, while also removing water and nutrients needed for plant growth and reproduction. Overall, rusts reduce plant vigor, seed filling, and root growth. Rusted wheat plants are less palatable to livestock.

SymptomsRust symptoms and signs are most obvious in spring and

summer but may occur at any time, beginning shortly after seedlings emerge. All aerial parts of the wheat plant are sus­ceptible to infection, and more than one rust can occur on a single plant or leaf. Some infections are visible only as chlo­rotic flecks or brown, necrotic spots, whereas others may result in sporulating pustules of various sizes.

Causal OrganismsThe three rust diseases of wheat are caused by highly spe­

cialized fungi:

stem rust fungusPuccinia graminis Pers.:Pers. f. sp. tritici Erikss. & E. Henn.

leaf rust fungiP. triticina Erikss., with populations specialized for sur­

vival on Triticum aestivum (bread wheat) and others specialized for T. turgidum (durum wheat)

Rusts have been of great importance historically. These dis­eases are mentioned in the earliest records of wheat cultivation. Wheat rusts changed the course of early civilizations by de­stroying their major food source. The potential for wheat rusts to develop into widespread epidemics is well documented. In past decades in North America, it has been conservatively esti­mated that rusts have decreased wheat yields by over 1 million metric tons annually. Similar statistics could be quoted for most wheat­ growing regions of the world. By a wide margin, most of the scientific literature on wheat diseases concerns rusts.

Three different rust diseases occur in wheat—stem rust, leaf rust, and stripe rust. They are named for the dry, dusty, yel­low red or black spots and stripes (sori or pustules) that erupt through the plant epidermis. The size and surrounding color­ation of urediniospore pustules (uredinia) determine the specific infection type, which can vary with different wheat cultivars, temperature, and races of the rust pathogen (Figs. 76–78).

Rust epidemics that occur before or during flowering are the most damaging. Stripe rust infection of the wheat head is espe­cially damaging, even if no infection occurs elsewhere on the plant. Rusts reduce seed yield, lower the forage value of the crop and diminish its winterhardiness, and predispose plants to other diseases. Rust infection modifies the host epidermis, re­sulting in increased transpiration and respiration and decreased

Rusts

Fig. 76. Stem rust infection types, in infection of wheat culms by Puccinia graminis f. sp. tritici: R = resistant; MR = moder-ately resistant; MS = moderately susceptible; S = suscep-tible. (Reprinted from Rust Scoring Guide, by permission of the Research Institute for Plant Protection, Wageningen, the Netherlands, and CIMMYT, Mexico City)

Fig. 77. Leaf rust infection types, in infection of wheat leaves by Puccinia triticina: R = resistant; MR = moderately resistant; MS = moderately susceptible; S = susceptible. (Reprinted from Rust Scoring Guide, by permission of the Research Institute for Plant Protection, Wageningen, the Netherlands, and CIMMYT, Mexico City)

51

additional urediniospores in intervals of as little as 7 days. P. tritici­ duri produces fewer urediniospores, but this inoculum can be supplemented by aeciospores from newly formed aecia.

Urediniospores are one­ celled, spiny­ walled, and dikaryotic (Figs. 80 and 81). They are nutrient­ independent and germinate in contact with a film of water. Germ tubes penetrate the plant by means of an appressorial peg or penetrate stomata directly (in the case of the stripe rust pathogen). The pathogen then forms substomatal vesicles and intercellular hyphae with glo­bose or lobed haustoria, which establish physiological contact with host cell membranes, to complete the infection cycle.

Urediniospore production on host plants may be followed by teliospore development within uredinia or within separate telial sori. Teliospores are brown black, binucleate, and two­ celled and have thick, smooth walls (Fig. 80). In P. graminis and P. triticina, teliospores remain within the sorus and persist over the winter. They germinate in spring, by a process of nuclear fusion, reductive division (meiosis), and production of a promy­celium (basidium) with four haploid sporidia (basidiospores). Basidiospores cannot re­ infect wheat but are carried by the wind to alternate hosts (Fig. 79). Basidiospores of P. striiformis are presumed functionless, because there is no known alternate host. In most wheat­ producing areas worldwide, the alternate host plays little direct role in epidemics. The exception is P. tritici­ duri, which may cycle to its alternate host throughout the growing season.

Infection of alternate hosts produces yellow orange sori (pyc­nia, a type of spermagonium) on the upper surface of leaves. Within the pycnia, uninucleate, hyaline spores (pycniospores, a type of spermatium) and receptive hyphae fuse in compatible pairs when brought into contact by rain or insects. Their fusion restores the dikaryon, which proliferates and erupts through the opposite leaf surface as an aecial cup. Dikaryotic, dry, yellow spores (aeciospores) are liberated from aecia and are carried by wind to wheat plants. Aeciospores germinate and penetrate plants by entering through stomata, and infection results in the production of urediniospores.

EpidemiologyRust epidemics develop when compatible wheat plants and

rust fungi are both present over a large area. With free moisture and temperatures between 15 and 25°C, infection is completed in 6–8 h, and urediniospores are produced in 7–10 days. Ure­diniospores are numerous and are readily disseminated over vast distances by wind, so that a small fungal population can rapidly increase within a few weeks (one uredium can produce up to 10,000 urediniospores). This combination of large num­bers of viable spores and efficient dissemination by wind makes the rust fungi remarkably successful parasites.

Uredinia have limited survival ability, compared to telia, but can survive year­ round on hosts in milder climates. Ure­diniospores of the stripe rust fungus maintain their infectiv­ity at lower temperatures than those of the leaf rust and stem rust fungi. Urediniospores often serve as sources of primary inoculum in spring and summer by virtue of long­ distance dispersal by wind. The annual progression of urediniospores across continents is well documented. Thus, teliospores and al­ternate hosts are required for the completion of pathogen life cycles but not for disease initiation. P. tritici­ duri epidemics start with airborne aeciospores from its alternate host, Anchusa italica, growing near durum wheat. A few urediniospores are produced, which can re­ infect wheat, but abundant teliospores are also produced, and they can germinate immediately, pro­ducing basidiospores, which re­ infect A. italica, resulting in another generation of aeciospores.

Alternate hosts support the sexual stages of rust fungi and thereby are sources of new virulence combinations and of early spring inoculum (aeciospores). It may be possible for new races of rust fungi to develop apart from alternate hosts, through mu­tation and parasexual mechanisms in the uredinial stage.

P. tritici­ duri Viennot­ Bourgin (a member of the P. re­condita complex), specialized for survival on durum wheat

stripe rust fungusP. striiformis Westend. f. sp. tritici Erikss.

Each species comprises numerous physiological races, dis­tinguished by their patterns of pathogenicity on differential hosts. The interaction of specific pathogen avirulence genes and specific host resistance genes determines the infection type (Figs. 76–78) and distinguishes races of rust fungi. Many races that were prevalent in the past are insignificant today, because specific resistance genes have been incorporated into modern wheat cultivars by breeding. However, because of the capacity for genetic change through mutation and sexual reproduction of these pathogens, new races of rust fungi continually surface to threaten wheat production.

Disease CyclesWheat rust fungi are considered obligate parasites, although

a few strains have been grown vegetatively on agar media. A few unique strains can sporulate and complete their life cycle apart from host plants.

Wheat rusts have complex life cycles that can involve alter­nate hosts and up to five spore stages (Fig. 79). Urediniospores are produced in great number. They are dispersed by wind to other wheat plants, where they generate new infections and

Fig. 78. Stripe rust infection types, in infection of wheat leaves by Puccinia striiformis f. sp. tritici: R = resistant; MR = moderately resistant; MS = moderately susceptible; S = susceptible. (Reprinted from Rust Scoring Guide, by permission of the Research Institute for Plant Protection, Wageningen, the Netherlands, and CIMMYT, Mexico City)

52

by breeders to develop resistant cultivars. However, resistance based on a single gene of the host is often rendered ineffective by shifts in pathogen virulence. Destroying alternate hosts in­terrupts the life cycle of rust fungi, limits their diversity, indi­

ManagementPlanting resistant cultivars is the best method of control­

ling wheat rusts. The heritability of rust resistance in wheat has been known for over 100 years and has been widely used

Fig. 80. Urediniospores of (left to right) Puccinia triticina, P. graminis f. sp. tritici, and P. striiformis f. sp. tritici. (Cour tesy R. L. Bowden)

Fig. 79. Disease cycle of stem rust of wheat. (Reprinted from G. N. Agrios, Plant Pathology, 5th ed., copyright 2005, with permis-sion from Elsevier)

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Leaf RustLeaf rust (also called brown rust and orange rust) may be the

most widely distributed disease of wheat. It is most prevalent in climates where wheat matures at temperatures of 25–30°C, as in the Great Plains of North America and the steppes of central Asia. Yield losses due to leaf rust can vary from trace levels to over 50%, depending on the stage of plant development when the initial infection occurs and the resistance of the wheat cultivar.

The causal organism is the fungus Puccinia triticina Erikss. (syns. P. recondita Roberge ex Desm. f. sp. tritici (Erikss. & E. Henn.) D. M. Henderson, P. rubigo­ vera (DC.) G. Winter). It produces orange red, round to ovoid uredinia, up to 1.5 mm in diameter, which are scattered or clustered primarily on the upper surface of leaf blades (Figs. 77 and 81). They are erum­pent, but unlike the uredinia of the stem rust pathogen (Fig. 76), they do not cause conspicuous tears in the epidermal tissues at the uredinium margins (Fig. 77).

Urediniospores are subgloboid, 15–30 µm in diameter, and red brown, with three to eight germ pores scattered in their thick, echinulate walls (Figs. 80 and 81). The optimum temperature for the germination of urediniospores and infection is 18°C, with free moisture on the leaf surface for at least 6 h. Temperatures in the range of 20–25°C are best for the development of uredinia.

Telial sori develop beneath the epidermis, principally on leaf sheaths and blades. Telia are the size of uredinia, glossy black, and not erumpent. Teliospores are round or flattened at the apex, like those of P. striiformis. They are sometimes not produced in some environments or if plants become infected near maturity. Teliospore germination requires alternating pe­riods of wet and dry.

P. triticina reproduces in almost all wheat­ growing regions by clonal production of urediniospores. The main alternate host, Thalictrum speciossimum, is found in Spain and Portugal. Isopyrum fumarioides has also been described as an alternate host in Siberia.

Collections of P. triticina that are highly virulent to durum wheat and mostly avirulent to common bread wheats have been described. A leaf rust fungus affecting durum wheat and having an alternate host in the genus Anchusa has been described in Mo­rocco; the pathogen is most likely a different species, P. recon­dita, but it has been referred to as P. tritici­ duri Viennot­ Bourgin.

Selected References

Anikster, Y., Bushnell, W. R., Eilam, T., Roelfs, A. P., and Manister­ski, J. 1997. Puccinia recondita causing leaf rust on cultivated wheats, wild wheats, and rye. Can. J. Bot. 78:2082–2095.

Ben­ Ze’ev, I. S., Levy, E., Eilam, T., and Anikster, Y. 2005. Whole­ cell fatty acid profiles—A tool for species and subspecies classification in the Puccinia recondita complex. J. Plant Pathol. 87:187–197.

Huerta­ Espino, J., and Singh, R. P. 1994. First report of virulence to wheat with leaf rust resistance gene Lr19 in Mexico. Plant Dis. 78:640.

Roelfs, A. P., Singh, R. P., and Saari, E. E. 1992. Rust Diseases of Wheat: Concepts and Methods of Disease Management. CIMMYT, Mexico City.

Samborksi, D. J. 1985. Wheat leaf rust. Pages 39–59 in: The Cereal Rusts. Vol. 2. A. P. Roelfs and W. P. Bushnell, eds. Academic Press, Orlando, Fla.

Sayre, K. D., Singh, R. P., Huerta­ Espino, J., and Rajaram, S. 1998. Ge­netic progress in reducing losses to leaf rust in CIMMYT­ derived Mexican spring wheat cultivars. Crop Sci. 38:654–659.

Singh, R. P., Huerta­ Espino, J., Pfeiffer, W., and Figueroa­ Lopez, P. 2004. Occurrence and impact of a new leaf rust race on durum wheat in northwestern Mexico from 2001 to 2003. Plant Dis. 88:703–708.

Yehuda, P. B., Eilam, T., Manisterski, J., Shimoni, A., and Anikster, Y. 2004. Leaf rust on Aegilops speltoides caused by a new forma specialis of Puccinia triticina. Phytopathology 94:94–101.

(Prepared by James A. Kolmer)

rectly increases the stability of resistant cultivars, and prevents the production of early spring inoculum (aeciospores). In the United States, a program to remove barberry, the alternate host of the stem rust fungus, has achieved these goals.

Protective or eradicative fungicides have been used for rust control. They are applied as foliar sprays where cost­ benefit analyses show that they are profitable. Systemic foliar fungi­cides are used in some regions, and systemic seed treatment show promise for controlling rust in seedlings.

Early­ maturing cultivars should be grown where possible. Spring wheat should be sown as early as possible and given ade­quate phosphorus to ensure early maturity and perhaps escape peak rust periods. Autumn rust infections can be reduced by late­ autumn seeding. Self­ sown or volunteer wheat is a major source of urediniospores, which serve as inoculum in the next crop, and therefore volunteer plants should be destroyed.

Selected References

Anikster, Y., Bushnell, W. R., Roelfs, A. P., Eilam, T., and Manister­ski, J. 1997. Puccinia recondita causing leaf rust on cultivated wheats, wild wheats, and rye. Can. J. Bot. 75:2082–2096.

Chen, X. M. 2005. Epidemiology and control of stripe rust [Puccinia striiformis f. sp. tritici] wheat. Can. J. Plant Pathol. 27:314–337.

Kolmer, J. A. 2005. Tracking wheat rust on a continental scale. Curr. Opinion Plant Biol. 8:441–449.

McIntosh, R. A., Wellings, C. R., and Park, R. F., eds. 1995. Wheat Rusts: An Atlas of Resistance Genes. Plant Breeding Institute, Uni­versity of Sydney, CSIRO, Melbourne, Australia, and Kluwer Aca­demic Publishers, Dordrecht, Netherlands.

Nagarajan, S., Singh, H., Joshi, L. M., and Saari, E. E. 1976. Meteoro­logical conditions associated with long­ distance dissemination and deposition of Puccinia graminis tritici uredospores in India. Phyto­pathology 66:198–203.

Roelfs, A. P. 1985. Wheat and rye stem rust. Pages 3–37 in: The Cereal Rusts. Vol. 2. A. P. Roelfs and W. R. Bushnell, eds. Academic Press, Orlando, Fla.

Roelfs, A. P., Singh, R. P., and Saari, E. E. 1992. Rust Diseases of Wheat: Concepts and Methods of Disease Management. CIMMYT, Mexico City.

Samborski, D. J. 1985. Wheat leaf rust. Pages 39–59 in: The Cereal Rusts. Vol. 2. A. P. Roelfs and W. R. Bushnell, eds. Academic Press, Orlando, Fla.

Stubbs, R. W. 1985. Stripe rust. Pages 61–101 in: The Cereal Rusts. Vol. 2. A. P. Roelfs and W. R. Bushnell, eds. Academic Press, Or­lando, Fla.

(Prepared by Alan P. Roelfs)

Fig. 81. Urediniospores of Puccinia triticina erupting through the epidermis of a leaf. (Photo by M. F. Brown and H. G. Brotzman, reprinted from D. M. Rizzo, comp., 1997, Phytopathogenic Fungi: Scanning Electron Micrographs, APS Press Slide Collections, American Phytopathological Society, St. Paul, Minn.)

54

a specialized pathogen, with each forma specialis and race having a narrow host range. P. graminis f. sp. tritici completes part of its life cycle on alternate hosts, especially barberries (Berberis vulgaris and B. canadensis) and certain species of Mahonia, in addition to wheat.

B. vulgaris is an erect woody shrub that reaches a height of 3 m. It bears prominent spines and clusters of two to six leaves at stem joints (Fig. 82). It has gray bark and yellow, inconspicu­ous flowers in long, drooping clusters. Red berries, formed in late summer, overwinter on the plant. Barberries are cultivated as ornamentals or grow wild in clusters on uncultivated land. The Japanese barberry, B. thunbergii, appears to be immune to stem rust.

The disease cycle of stem rust is depicted in Fig. 79.P. graminis f. sp. tritici forms uredinia on wheat stems,

leaves, and leaf sheaths and occasionally on glumes, awns, and even seeds. The uredinia are conspicuously erumpent, with tat­tered epidermal tissues at their margins (Fig. 76). They may erupt through both leaf surfaces, but they tend to be larger on the underside. The pustules are oval, elongate, or spindle­ shaped and up to 3 × 10 mm. Numerous infections on a stem can weaken it and cause the plant to lodge. Urediniospores are oval, oblong, or ellipsoidal, 15–24 × 21–40 µm, orange red, and dehiscent (Figs. 80 and 83). They have thick, spiny walls in­dented with four median germ pores.

Host maturity and the aging of uredinia initiate the formation of teliospores in uredinial sori or in separate erumpent telial sori. Teliospores are ellipsoidal to clavate, 15–20 × 40–60 µm, black brown, two­ celled, and tapered at the apex, with smooth, thick walls and a slight constriction at the septum (Fig. 83). They have a terminal germ pore in the upper cell and a lateral germ pore in the lower cell.

Teliospore germination normally follows a period of cold dormancy and yields a hyaline basidium (promycelium) on which four hyaline sporidia (basidiospores) develop on sterig­mata. Basidiospores infect barberry and give rise to small, flask­ shaped pycnia (spermagonia), which are sunken except for the ostiole (Fig. 84). The supporting leaf tissues are typi­cally discolored yellow red. Pycnia exude slender, hyaline pyc­niospores (spermatia) and receptive hyphae in small, sticky droplets that attract insects. Pycniospores fertilize compatible

Stem Rust

Stem rust was recognized in classical Roman times as the “greatest of plant diseases.” However, detailed characteriza­tion of the disease cycle did not begin until 1767. Stem rust of wheat (also called black rust and black stem rust) is caused by Puccinia graminis Pers.:Pers. f. sp. tritici Erikss. & E. Henn., which also parasitizes certain barley and rye cultivars and some grasses, especially wild barley (Hordeum jubatum) and goat grass (Aegilops spp.).

The relationship between the various forms of P. graminis is uncertain. The species can be subdivided according to mor­phology, pathology, and genetics; pathology and genetics pro­vide the most similar classifications. The stem rust fungus is

Fig. 82. Aecial stage of Puccinia graminis f. sp. tritici, the wheat stem rust fungus, on a barberry leaf. (Cour tesy B. J. Steffenson, reprinted from D. E. Mathre, ed., 1997, Compendium of Barley Diseases, 2nd ed., American Phytopathological Society, St. Paul, Minn.)

Fig. 84. Pycnium (spermagonium) (top) and aecium (bottom) of Puccinia graminis f. sp. tritici, the wheat stem rust fungus, in a bar-berry leaf. (Cour tesy W. W. Bockus)

Fig. 83. Teliospores (above) and urediniospores (below) of Puccinia graminis f. sp. tritici, the wheat stem rust fungus. (Cour-tesy A. P. Roelfs)

55

chlorotic areas. Each uredinium contains thousands of yel­low orange, spherical urediniospores, 20–30 µm in diameter, with thick, echinulate walls and six to 12 scattered germ pores. Urediniospores are yellow to orange in mass and powdery (Fig. 85A, B, and D–F).

Distinct stripes are not formed on seedling leaves (Fig. 85B), but they develop on upper leaves after stem elongation (Fig. 85D and E). Depending on temperature and the resistance of the host plant, chlorotic or necrotic spots or stripes of vari­ous sizes develop, with or without sporulation (Fig. 85G). In

receptive hyphae, which give rise to aecia on the underside of the leaf. Aecia on barberry leaves are yellow and hornlike, pro­jecting up to 5 mm from the leaf surface (Figs. 82 and 84). Aeciospores are subglobose, 15–19 × 16–23 µm, smooth, light orange yellow, and formed in long, dry chains. They infect wheat and give rise to uredinia, completing the disease cycle.

Urediniospores released from uredinia on wheat leaves initi­ate new infections, from which new uredinia are formed, so that several cycles of urediniospores can be produced dur­ing the growing season. In most areas, urediniospores are the major means of survival and spread of the pathogen and serve as inoculum in the development of epidemics.

The optimum temperature for the development of stem rust is near 26°C. Disease development is seriously hampered below 15°C and above 40°C. The optimum conditions for infection by urediniospores are a temperature of 18°C and the presence of dew (free water) for 6–8 h, followed by a 3­ h gradual warming with light, while free water is present.

Delayed crop maturity especially favors stem rust develop­ment, so late planting and growing late­ maturing cultivars in­creases the risk of stem rust.

Stem rust has been controlled by planting resistant cultivars. However, sexual reproduction where barberry is present and mutation during the urediniospore cycle generate new viru­lence combinations, which can result in epidemics in previously resistant cultivars.

Selected References

Abbasi, M., Goodwin, S. B., and Scholler, M. 2005. Taxonomy, phylog­eny, and distribution of Puccinia graminis, the black stem rust: New insights based on rDNA sequence data. Mycoscience 46:241–247.

Bhardwaj, S. C., Nayar, S. K., Prashar, M., Kumar, J., Menon, M. K., and Singh, S. B. 1990. A pathotype of Puccinia graminis f. sp. trit­ici on Sr24 in India. Cer. Rusts Powdery Mildews Bull. 18:35–37.

Leonard, K. J., and Szabo, L. J. 2005. Stem rust of small grains and grasses caused by Puccinia graminis. Mol. Plant Pathol. 6:99–111.

McIntosh, R. A., Wellings, C. R., and Park, R. F., eds. 1995. Wheat Rusts: An Atlas of Resistance Genes. Plant Breeding Institute, Uni­versity of Sydney, CSIRO, Melbourne, Australia, and Kluwer Aca­demic Publishers, Dordrecht, Netherlands.

Pretorius, Z. A., Singh, R. P., Wagoire, W. W., and Payne, T. S. 2000. Detection of virulence to wheat stem rust resistance gene Sr31 in Puccinia graminis f. sp. tritici in Uganda. Plant Dis. 84:203.

Roelfs, A. P. 1985. Wheat and rye stem rust. Pages 3–37 in: The Cereal Rusts. Vol. 2. A. P. Roelfs and W. R. Bushnell, eds. Academic Press, Orlando, Fla.

Roelfs, A. P., and McVey, D. V. 1979. Low infection types produced by Puccinia graminis f. sp. tritici and wheat lines with designated genes for resistance. Phytopathology 69:722–730.

Roelfs, A. P., Singh, R. P., and Saari, E. E. 1992. Rust Diseases of Wheat: Concepts and Methods of Disease Management. CIMMYT, Mexico City.

(Prepared by Alan P. Roelfs)

Stripe Rust

Stripe rust (also called yellow rust) has been reported in more than 60 countries and on all continents except Antarctica. In the United States, the disease occurred mainly in the Pacific Northwest and California until 2000. Since then, it has become increasingly important in the South Central states and the cen­tral Great Plains. The disease thrives where winters are mild and summers are cool.

SymptomsInfection can occur throughout the life of a plant. Symp­

toms first appear as chlorotic patches on leaves. Tiny, yellow to orange uredinia (0.3–0.5 × 0.5–1 mm) then develop in these

Fig. 85. Stripe rust of wheat. A, Infected seedlings in the field. B, Uredinial pustules on a seedling leaf, not forming stripes. C, Stripe rust foci early in the disease season. D, Uredinial pustules forming a stripe on a mature leaf. E, Heavy sporulation on leaves of mature plants, with few obvious stripes. F, Infected glumes and immature kernels. G, Necrotic stripes with few or no uredinial pustules on a wheat cultivar with durable, high- temperature adult- plant resistance. H, Black telial pustules on a leaf sheath. (Cour tesy R. F. Line; composite by J. Foltz)

56

ManagementStripe rust can be managed by growing resistant cultivars,

the use of fungicide seed treatment, timely application of fungi­cides, and appropriate cultural practices, such as late planting, eliminating volunteer plants, and avoiding excessive water and fertilizer. High­ temperature, adult­ plant resistance, which is non­ race­ specific and durable, may provide sustainable control of stripe rust.

Selected References

Chen, X. M. 2005. Epidemiology and control of stripe rust [Puccinia striiformis f. sp. tritici] on wheat. Can. J. Plant Pathol. 27:314–337.

Chen, X. M., Line, R. F., and Leung, H. 1995. Virulence and poly­morphic DNA relationships of Puccinia striiformis f. sp. hordei to other rusts. Phytopathology 85:1335–1342.

Chen, X. M., Moore, M., Milus, E. A., Long, D. L., Line, R. F., Marshall, D., and Jackson, L. 2002. Wheat stripe rust epidemics and races of Puccinia striiformis f. sp. tritici in the United States in 2000. Plant Dis. 86:39–46.

Coakley, S. M., Line, R. F., and Boyd, W. S. 1983. Regional models for predicting stripe rust on winter wheat in the Pacific Northwest. Phytopathology 73:1382–1385.

Line, R. F. 2002. Stripe rust of wheat and barley in North Amer­ica: A retrospective historical review. Annu. Rev. Phytopathol. 40:75–118.

Mares, D. J. 1979. Light and electron microscope study of the inter­action of yellow rust with a susceptible wheat cultivar. Ann. Bot. 43:183–189.

Milus, E. A., and Line, R. F. 1986. Number of genes controlling high­ temperature, adult­ plant resistance to stripe rust in wheat. Phyto­pathology 76:93–96.

Mulder, J. L., and Booth, C. 1971. Puccinia striiformis. Descriptions of Pathogenic Fungi and Bacteria, no. 291. Commonwealth Myco­logical Institute and Association of Applied Biologists, Kew, Sur­rey, England.

Rapilly, F. 1979. Yellow rust epidemiology. Annu. Rev. Phytopathol. 17:59–73.

Stubbs, R. W. 1985. Stripe rust. Pages 61–101 in: The Cereal Rusts. Vol. 2. A. P. Roelfs and W. R. Bushnell, eds. Academic Press, Or­lando, Fla.

(Prepared by Xianming Chen)

wheat heads, uredinia normally occur on the ventral surface of the glumes, and immature seeds are sometimes infected (Fig. 85F).

The pathogen utilizes water and nutrients from the host plant and can desiccate the plant quickly.

Dark brown to black telial pustules, which are persistently subepidermal and often form streaks on leaves and leaf sheaths (Fig. 85H), appear late in the crop season under moist condi­tions. Teliospores can germinate without cold treatment to pro­duce basidiospores under laboratory conditions.

Causal OrganismStripe rust is caused by Puccinia striiformis Westend. (syn.

P. glumarum Erikss. & E. Henn.). It is not known to have an alternate host or to complete a sexual cycle.

P. striiformis is subdivided into formae speciales based on virulence to different genera and species of cereal crops and grasses. For example, P. striiformis f. sp. tritici Erikss., the wheat stripe rust pathogen, mainly infects wheat and sometimes species of Aegilops, Agropyron, Elymus, and wild Hordeum, but rarely infects cultivated barley. P. striiformis f. sp. hordei, the barley stripe rust pathogen, mainly infects barley and occa­sionally infects wheat and some grasses. The wheat and barley stripe rust pathogens do not cause disease in bluegrass or or­chard grass, and the bluegrass and orchard grass pathogens (P. striiformis f. sp. poae and P. striiformis f. sp. dactylidis) do not cause disease in wheat and barley. Numerous races of the wheat stripe rust pathogen have been identified, distinguished by their differential ability to infect wheat cultivars with different genes for resistance.

Disease CycleStripe rust of wheat originates from mycelium that overwin­

ters in leaf tissues and, especially, from urediniospores that survive locally or are windborne from distant hosts. Infection may occur throughout autumn and winter, because mycelium remains viable to –5°C. Urediniospores lose viability rapidly at temperatures above 15°C. Neither urediniospores nor mycelia survive temperatures above 32°C. The optimum temperature for urediniospore germination is between 7 and 12°C, with lim­its near 0 and 21°C. Disease development is most rapid between 10 and 18°C with intermittent rain or dew.

Septoria tritici Blotch

Septoria tritici blotch is one of several leaf spot diseases of wheat occurring in most wheat production areas. It tends to be more severe in wet areas, particularly when the weather is cool and rain is frequent during the vegetative and early reproduc­tive growth stages. Mycelium of the fungus proliferates within the apoplast of the wheat leaf, where it establishes a parasitic relationship. Lesions eventually become necrotic. The disease normally does not become severe until after flowering, so para­sitism and destruction of photosynthetic area impede grain filling rather than reduce the number of heads or number of grains per head. Shriveled grain results in lower yield and test weight.

SymptomsIn winter wheat, lesions appear in early spring on the blades

of lower leaves, which emerged the previous autumn. Lesions often appear first on areas of leaves that are in contact with the surface of the soil. Lesions on these seedling leaves are broadly

elliptical with a tan center (Fig. 86) and usually have a dis­tinct yellow margin. Pycnidia are readily visible as small, black specks in the necrotic area of the lesion.

If the weather remains conducive to infection during stem elongation and flowering, lesions develop on successively higher leaves. Lesions on upper leaf blades tend to be straight­ sided (Fig. 87), without a distinct chlorotic halo. Lesions may coalesce to kill large areas of leaves or entire leaf blades. Le­sions also develop on leaf sheaths.

In spring wheat at higher latitudes, the disease may not ap­pear until the plants are in the boot stage, and then lesions will form simultaneously on several layers of leaves.

When the relative humidity is high but the leaf surface is not actually wet, a curved cirrhus extrudes from the ostiole of the pycnidium (Fig. 88). Cirrhi are easily visible with a hand lens and can often be seen with the unaided eye as coiled, translu­cent bands. When rain or dew wets the cirrhi, the gel matrix dissolves quickly.

It can be difficult to distinguish Septoria tritici blotch from Stagonospora nodorum blotch, tan spot, and other leaf spots late in the season, when necrosis is extensive. Microscopic ex­

57

Septoria tritici blotch is a polycyclic disease. Rain splashes spores produced on lower leaves, carrying them to upper leaves. Thus, the disease typically shows a vertical gradient, with the amount of leaf area with symptoms being greater on lower leaves. If weather favorable for infection persists through the development of the flag leaf, all leaves eventually become severely blighted. By then the lower leaves have shriveled. Pseudothecia may develop on these lower leaves and contribute ascospores to the pool of secondary inoculum.

Hyphae grow intercellularly until the onset of necrosis, about 10 days after infection. By that time, mesophyll cells in the infection site become disorganized and collapse. From about 10 to 14 days after infection, pycnidia develop in substomatal cavities in the lesion. The ostiole of the pycnidium develops be­neath a stomatal opening. The minimum latent period is about 11 days when daily temperatures are in the range of 15–25°C but is substantially longer at lower temperatures.

Plants inoculated in a greenhouse or growth chamber must remain in a moist chamber for at least 48 h for lesions to de­velop. Very few lesions develop when the moist period is only 24 h long. A moist period of 72 h will usually result in more lesions than a 48­ h moist period. Leaves need not be wet dur­ing the moist period, but the relative humidity must be very high. Rain falling for more than a few consecutive hours is rare in nature. However, infection will occur if a “wet” period (in which the humidity is very high) is broken by a period of lower humidity (50 or 75%) followed by an additional wet period.

In nature, if rain falls on two or more days, even though not continuously, the relative humidity may be sufficiently high for at least 48 h to allow infection to occur. This may explain why epidemics develop when there are several periods of rainy

amination of necrotic tissue will readily distinguish Septoria tritici blotch from other diseases. A small piece of necrotic tis­sue can be placed in water on a microscope slide. The mor­phology of the spores that are extruded from the pycnidia will permit reliable identification of the pathogen (Fig. 89).

Causal OrganismThe pathogen is Mycosphaerella graminicola (Fuckel)

J. Schröt., a fungus present in most wheat­ producing areas. The anamorph, Septoria tritici Roberge in Desmaz., is more commonly found in living wheat, although the teleomorph may be found on necrotic lower leaves. Pycnidia are 60–200 µm in diameter and form in substomatal chambers with the ostiole beneath the stomate. Conidia are long and slender (20–98 × 1.4–3.8 µm) and multiseptate, with tapered ends (Fig. 89). The fungus is heterothallic. Pseudothecia become laterally compressed, measuring 76–80 × 77–100 µm. Asci are bitunicate and obpyriform (34–41 × 11–13 µm). Each ascus contains eight ascospores, which are hyaline, ellipsoidal (10–15 × 2.5–3 µm), and one­ septate, generally with one cell larger than the other.

Disease CyclePrimary infection of winter wheat occurs in the fall, mainly

from ascospores produced on residue from the previous sea­son’s crop. Germ tubes grow over the leaf surface, at random, and penetrate stomates. Depending on the climate where wheat is grown, these primary infections produce lesions in early win­ter or not until the following spring. As the air and soil surface become warmer in the spring, lesions on overwintered leaves mature and produce pycnidia.

Fig. 86. Young, oblong lesion with black spots (pycnidia) on a leaf with Septoria tritici blotch. (Cour tesy W. W. Bockus)

Fig. 87. Old, straight- sided lesions with black spots (pycnidia) on a leaf with Septoria tritici blotch. (Cour tesy W. W. Bockus)

Fig. 89. Spores released from pycnidia of Septoria tritici. (Cour-tesy W. W. Bockus)

Fig. 88. Cirrhi emerging from the ostioles of pycnidia of Septoria tritici. (Cour tesy W. W. Bockus)

58

Infection early in the growing season, after prolonged cool, wet, overcast weather or snow cover, results in spring blight (also called winter­ kill), with symptoms resembling those of snow mold. The disease can severely reduce stands and yields of winter cereals.

With the increased control of eyespot (strawbreaker foot rot) in Europe and the United States, sharp eyespot has become more common. Spring blight has been a primary reason for the abandonment of 10–40% of the winter wheat planted in the U.S. Midwest in some years.

SymptomsSymptoms of sharp eyespot, like those of eyespot, usually

appear first on an outer leaf sheath near the base of the plant. A circular or elliptical, light brown area circumscribed by a thin, necrotic, dark brown border develops on the leaf sheath. Af­fected leaf sheaths may rot, and the rotted tissues leave a char­acteristic hole (rather than a fibrous net, as with eyespot), but generally the leaf sheaths remain intact. Several lesions, ranging up to 1 cm in diameter, may occur on the lower leaf sheaths of the same plant and, in contrast to eyespot lesions, can occur up to 30 cm above the soil line. Severe infection causes the death of late tillers or seedling blight of late­ seeded winter wheat, but most main culms of infected plants survive to maturity.

Lesions on culms are light brown or straw­ colored with a sharply defined, dark brown border (Fig. 90). The lesions may resemble those of eyespot but are more superficial, less lens­ shaped, and more sharply delineated. On maturing culms, the area beneath a lesion is often covered with abundant ash white mycelium, in which small, light brown sclerotia are sometimes present. Severe infection causes a loss of tillers, premature rip­ening, and lodging. The culms of lodged plants often bend at the second or third internode as they attempt to right them­selves. The sharp eyespot pathogen is less able to mechanically weaken infected culms than the eyespot pathogens.

Spring blight lesions are initially small, water­ soaked, ne­crotic spots, which then expand to rot carbohydrate­ depleted leaves (Fig. 91). These initial symptoms are similar to those of snow mold. The disease is sometimes referred to as winter­ kill, but it is independent of the temperature­ hardiness of a cultivar. Under optimal conditions for disease development, all foliage may be killed, but some plants may recover as temperatures rise and photosynthesis resumes, unless the crown tissue has been completely destroyed. Late­ seeded winter wheat plants that fail to develop adequate crown carbohydrate reserves for prolonged respiration during the winter are especially suscepti­ble. Losses due to spring blight, as in the case of sharp eyespot, are generally due to the death of tillers and thinner stands, but the disease may make entire fields unprofitable to harvest.

The sharp eyespot pathogen is a common rhizosphere colo­nizer, but it rarely causes significant damage to root systems, and it has been promoted as a biological control for other soil­borne root pathogens, including Rhizoctonia solani.

weather that last for more than 1 day. Looked at from the op­posite way, the severity of Septoria tritici blotch is inversely related to the number of 2­ day periods in which no rain falls during early spring.

ManagementResistant cultivars provide control of Septoria tritici blotch.

Several major race­ specific genes confer a high degree of re­sistance to avirulent races. Although this resistance is race­ specific, there has been less dramatic loss of effective resistance because of the adaptation of races of the pathogen, as com­monly occurs with rusts and powdery mildew. There is also a partial, quantitative resistance. Resistance to Septoria tritici blotch may be obscured in the field by the presence of other leaf spot diseases, particularly Stagonospora nodorum blotch and tan spot, because all three often constitute a disease complex.

Fungicides provide effective control if used in a timely man­ner. They have the advantage of controlling several diseases simultaneously, but they add to the cost of production of wheat. Application at flag leaf emergence or shortly after is generally most effective, but if a period particularly favorable for infec­tion precedes fungicide application by a few days, control may not be satisfactory.

Selected References

Chungu, C., Gilbert, J., and Townley­ Smith, F. 2001. Septoria tritici blotch development as affected by temperature, duration of leaf wetness, inoculum concentration, and host. Plant Dis. 85:430–435.

Coakley, S. M., McDaniel, L. R., and Shaner, G. 1985. Model for pre­dicting severity of Septoria tritici blotch on winter wheat. Phytopa­thology 75:1245–1251.

Cunfer, B. M., and Ueng, P. P. 1999. Taxonomy and identification of Septoria and Stagonospora species on small­ grain cereals. Annu. Rev. Phytopathol. 37:267–284.

Eriksen, L., Shaw, M. W., and Østergård, H. 2001. A model of the effect of pseudothecia on genetic recombination and epidemic de­velopment in populations of Mycosphaerella graminicola. Phyto­pathology 91:240–248, 519 (erratum).

Eyal, Z. 1999. The Septoria tritici and Stagonospora nodorum blotch diseases of wheat. Eur. J. Plant Pathol. 105:629–641.

Kema, G. H. J. 1996. Mycosphaerella graminicola on wheat: Genetic variation and histopathology. Ph.D. thesis, Wageningen Agricul­tural University, Wageningen, Netherlands.

Sanderson, F. R. 1972. A Mycosphaerella species as the ascogenous state of Septoria tritici Rob. and Desm. N.Z. J. Bot. 10:707–710.

Scott, P. R., Sanderson, F. R., and Benedikz, P. W. 1988. Occurrence of Mycosphaerella graminicola, teleomorph of Septoria tritici, on wheat debris in the UK. Plant Pathol. 37:285–290.

Shaw, M. W. 1991. Interacting effects of interrupted humid periods and light on infection of wheat leaves by Mycosphaerella gramini­cola (Septoria tritici). Plant Pathol. 40:595–607.

Shaw, M. W., and Royle, D. J. 1989. Airborne inoculum as a major source of Septoria tritici (Mycosphaerella graminicola) infections in winter wheat crops in the UK. Plant Pathol. 38:35–43.

(Prepared by Gregory Shaner)

Sharp Eyespot

Sharp eyespot is a disease of wheat, barley, and rye in China, Europe, North America, and most other temperate wheat­ growing regions. Strains of the sharp eyespot pathogen also cause yellow patch of turfgrass and spring blight of winter wheat.

Severe sharp eyespot in wheat causes the death of late tillers, premature ripening (formation of whiteheads), and lodging. Sharp eyespot lesions are often superficial and inconsequential when spring weather is optimal for plant growth, and thus con­trol measures are generally not justified. Fig. 90. Sharp eyespot lesion on a stem. (Cour tesy D. M. Huber)

59

of leaf tips or leaves near the soil or by soilborne inoculum splashed onto them during prolonged cool, wet, or heavily over­cast weather or after prolonged snow cover in late winter and early spring.

Sharp eyespot especially affects cereals grown continuously on the same land and is more severe in crops grown in untilled or acidic soils. R. cerealis is difficult to isolate from lesions later in the season. Sclerotia develop during the summer and are a principal source of inoculum in residue returned to the soil after harvest.

The importance of the teleomorph, C. cereale, in the epide­miology of sharp eyespot is unknown.

ManagementSeveral wheat cultivars are resistant to sharp eyespot, and

various degrees of tolerance of spring blight are known. Toler­ance of spring blight is not related to winterhardiness.

Early autumn seeding of winter wheat results in less disease but may also favor take­ all. Late seeding of spring­ sown wheat may avoid seedling development under environmental condi­tions conducive to severe disease.

Manuring and fertilization to ensure that sufficient zinc is available to enable carbohydrate storage in crown tissues dur­ing a long winter period increases tolerance of spring blight and sharp eyespot. Early autumn seeding is associated with mycor­rhizal infection and high tissue levels of zinc conducive to car­bohydrate storage in crown tissues. The application of zinc to foliage after seedling emergence has no effect on the incidence or severity of sharp eyespot.

Rotation with a legume or other nonhost crops is beneficial.No effective and economical chemical controls are available.

Selected References

Clarkson, J. D. S., and Cook, R. J. 1983. Effect of sharp eyespot (Rhizoctonia cerealis) on yield loss in winter wheat. Plant Pathol. 32:421–428.

Clarkson, J. D. S., and Griffin, M. J. 1977. Sclerotia of Rhizoctonia solani in wheat stems with sharp eyespot. Plant Pathol. 26:98.

Hollins, T. W., and Scott, P. R. 1985. Differences between wheat cul­tivars in resistance to sharp eyespot caused by Rhizoctonia cere­alis. Tests of Agrochemicals and Cultivars, No. 6. Ann. Appl. Biol. 106(Suppl.):166–167.

Huber, D. M. 1981. Yield and quality of soft red winter wheat infected with Rhizoctonia spring blight. (Abstr.) Phytopathology 71:227.

Huber, D. M., Baird, R. E., and McCay­ Buis, T. S. 1992. Environmen­tal conditions associated with Rhizoctonia “winter­ kill” of wheat in Indiana. (Abstr.) Phytopathology 82:1114.

Huber, D. M., McCay­ Buis, T. S., Riegel, C., Graham, R. D., and Robinson, N. 1993. Correlation of zinc sufficiency with resistance of wheat to Rhizoctonia winter­ kill. Abstr. 115. Int. Congr. Plant Pathol., 6th.

Lipps, P. E., and Herr, L. J. 1982. Etiology of Rhizoctonia cerealis in sharp eyespot of wheat. Phytopathology 72:1574–1577.

Murray, D. I. L., and Burpee, L. L. 1984. Ceratobasidium cereale sp. nov., the teleomorph of Rhizoctonia cerealis. Trans. Br. Mycol. Soc. 82:170–172.

Ogoshi, A., and Ui, T. 1985. Anastomosis groups of Rhizoctonia so­lani and binucleate Rhizoctonia. Pages 57–58 in: Ecology and Man­agement of Soilborne Plant Pathogens. C. A. Parker, A. D. Rovira, K. J. Moore, P. T. W. Wong, and J. F. Kollmorgen, eds. American Phytopathological Society, St. Paul, Minn.

Richardson, M. J., and Cook, R. J. 1985. Rhizoctonia on small­ grain cereals in Great Britain. Pages 63–65 in: Ecology and Manage­ment of Soilborne Plant Pathogens. C. A. Parker, A. D. Rovira, K. J. Moore, P. T. W. Wong, and J. F. Kollmorgen, eds. American Phyto­pathological Society, St. Paul, Minn.

(Prepared by Don M. Huber)

Causal OrganismRhizoctonia cerealis E. P. Hoeven, a widespread soilborne

plant pathogen, causes sharp eyespot. It forms no spores and produces characteristically binucleate mycelium (Fig. 92). Its hyphae are white to gray brown and 4–15 µm wide, and they tend to branch at right angles (see Rhizoctonia Root Rot). The teleomorph of R. cerealis is the basidiomycete Ceratobasidium cereale D. Murray & L. L. Burpee. It is rare in nature and is not observed in association with sharp eyespot symptoms.

R. cerealis mycelium grows on many media and forms abun­dant sclerotia. The sclerotia are irregular in shape and light to dark brown, and they lack a distinct rind. They often occur under lesions on wheat leaf sheaths.

Disease CycleCulm infection originates from soilborne mycelium or scle­

rotia. Infection depends on cool, moist conditions near the base of the plant. After invading seedling leaf sheaths, the patho­gen spreads by mycelial growth on and within the plant during the early growing season. Spring blight starts with infection

Fig. 92. Binucleate mycelium of Rhizoctonia cerealis, the cause of sharp eyespot and spring blight. (Cour tesy R. W. Smiley and J. L. Dale, reprinted from R. W. Smiley, P. H. Dernoeden, and B. B. Clarke, 2005, Compendium of Turfgrass Diseases, 3rd ed., American Phytopathological Society, St. Paul, Minn.)

Fig. 91. Wheat killed and damaged by spring blight after the weather has become drier and warmer in the spring. (Cour tesy D. M. Huber)