The Disease Compendium Series

of The American Phytopathological Society

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Apple and Pear Diseases Potato Diseases
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Diseases Rice Diseases
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Elm Diseases Strawberry Diseases
Flowering Potted Plant Sweet Potato Diseases
Diseases
Tobacco Diseases
Grape Diseases
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Onion and Garlic Diseases
Ornamental Foliage Plant Tropical Fruit Diseases
Diseases Turfgrass Diseases, 2nd ed.
Pea Diseases Wheat Diseases, 2nd ed.

Other titles are planned for this ongoing series.

Compendium of Peanut Diseases
SECOND EDITION

Edited by
N. Kokalis-Burelle
Auburn University
Auburn, Alabama

D. M . Porter (retired')
U SDA Agricultural Research Service
Suffolk, Virginia

R. Rodriguez-Kabana
Auburn University
Auburn, Alabama

D. H. Smith (retired)
Texas A&M University
Yoakum

P. Subrahmanyam
International Crops Research Institute
for the Semi-Arid Tropics
Lilongwe, Malawi

A PS PRESS
The American Phytopathological Society
Financial Sponsors
American Cyanamid
ISK Biotech Corporation
Miles Inc.
National Peanut Council
Oklahoma Peanut Commission
Rhone-Poulenc Ag Company
South Carolina Peanut Board

Cover photographs by N. Kokalis-Burelle

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 Catalog Card Number: 96-78765

International Standard Book Number: 0-89054-218-X

1984, 1997 by The American Phytopathological Society

Published 1984. Second Edition 1997

All rights reserved.

No part of this book may be, reproduced in any form, including
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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

The American Phytopathological Society

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 Preface
This compendium was written by and for individuals^world IV, miscellaneous detrimental as well as beneficial organisms.
wide who have a direct interest in peanut production as affected Since future disease control appears to depend heavily upon
Tjy plant and seed abnormalities. The technical data on specific disease resistance, Part V, Management of Peanut Diseases,
causal organisms, etiologies, and control strategies for known contains sections on management strategies, genetic modifica
peanut disorders or abnormalities should .serve as . a .valuable tion, and disease- and insect-resistant cultivars already avail
resource for those interested in the economical production of able for use by growers and in breeding programs.
top-quality peanuts free of undesired contaminants. The authors who contributed to specific sections of this com
To further broaden the appeal of the compendium to those pendium are noted at the end of their sections. The time and
involved in extension and scientific activities and to agribusi effort put forth by each author are appreciated. These valuable
ness and crop specialists, experts from throughout the world contributions will enhance the acceptance of this compendium.
have participated in preparing this edition. In fact, authors from The editors especially thank the following individuals who
India, the Peoples Republic of China, Malawi, Australia, Israel, reviewed the entire manuscript: J. P. Damicone, Oklahoma
and South Africa have prepared sections in the areas of their State University, Stillwater; T. B. Brenneman, University of
expertise. Thus, the second edition of this compendium is truly Georgia, Tifton; and J. Fletcher, Oklahoma State University,
international in scope and should be even more useful to Stillwater.
people in all segments of the peanut industry. We also thank those who contributed photographs and illus
For reference and clarity, this compendium is divided into trations. Where possible, proper credit is given.
five parts. Part I covers biotic diseases caused by fungi, bac The editors gratefully acknowledge the contributions of the
teria;, nematodes, viruses, and phytoplasmas; Part n , abiotic secretarial staff including N. T. Whitfield and R. M. Waldo.
diseases caused by environmental stresses such as drought, Special thanks to F. S. Wright, R. A. Taber, and the Depart
herbicide injury, nutrient imbalances, and air pollution; Part in , ment of Plant Pathology at Auburn University.
diseases and injury caused by insects and arthropods; and Part

Authors
P. A. Backman T. E. Boswell A. S. Csinos
Department of Plant Pathology Plant Disease Research Station Department of Plant Pathology
Auburn University Texas A&M University, Yoakum Coastal Plain Experiment Stations*
Auburn, Alabama Tifton, Georgia
T. B. Brenneman
D. K. Bell Department of Plant Pathology A. K. Culbreath
Department of Plant Pathology Coastal Plain Experiment Station Department of Plant Pathology
Coastal Plain Experiment Station Tifton, Georgia Coastal Plain Experiment Station
Tifton, Georgia Tifton, Georgia
T. A. Coffelt
Y. Ben-Yephet USD A Agricultural Research Service J. P. Damicone
Institute of Plant Protection Water Conservation Lab Department of Plant Pathology
The Volcani Center Phoenix, AZ Oklahoma State University,
Bet Dagan, Israel Stillwater
D. L. Cole
M. K. Beute Department of Crop Science J. W. Demski
Department of Plant Pathology University of Zimbabwe Department of Plant Pathology
North Carolina State University, Mount Pleasant, Harare Georgia Experiment Station, Griffin
Raleigh
F. R. Cox G. H. Elkan
M. C. Black Department of Soil Science Department of Microbiology
Texas Agricultural Extension Service North Carolina State University, North Carolina State University,
Uvale Raleigh Raleigh

iii
 V. J. Elliott H. A. Melouk D. H. Smith (retired)
USDA Agricultural Research Service USDA Agricultural Research Service Texas Agricultural Experiment Station
Shatter, California Department of Plant Pathology Texas A&M University, Yoakum
Oklahoma State University,
Z. R. Frank Stillwater H. W. Spurr, Jr.
Institute of Plant Protection USDA Agricultural Research Service
The Volcani Center N. A. Minton Oxford Tobacco Laboratory
Bet Dagan, Israel USDA Agricultural Research Service Oxford, North Carolina
Coastal Plain Experiment Station
D. W. Gorbet Tifton, Georgia H. T. Stalker
North Florida Research Crop Science Department
and Education Center P. M. Phipps North Carolina State University,
University of Florida, Marianna Department of Plant Pathology Raleigh
Tidewater Agricultural Research
A. C. Hayward and Education Center J. L. Starr
Department of Microbiology Suffolk, Virginia Department of Plant Pathology
University of Queensland and Microbiology
St. Lucia, Brisbane, Australia J. W. Pitt Texas A&M University,
CSIRO Food Research Laboratory College Station
L. Y. He North Ryde, New South Wales,
Department of Plant Bacteriology Australia P. Subrahmanyam
and Virology SADC-Intemational Crops Research
Chinese Academy of Agricultural D. M. Porter (retired) Institute for the Semi-Arid Tropics
Science, Beijing USDA Agricultural Research Service Chitedze Agricultural Research.
Tidewater Agricultural Research Station
A. S. Heagle and Education Center Lilongwe, Malawi
USDA Agricultural Research Service Suffolk, Virginia
North Carolina State University, C. W. Swann
Raleigh N. L. Powell Department of Crop and Soil
Department of Crop and Soil Environmental Sciences
B. W. Horn Environmental Sciences Tidewater Agricultural Research
National Peanut Laboratory Tidewater Agricultural Research and Education Center
Dawson, Georgia and Education Center Suffolk, Virginia
Suffolk, Virginia
N. Kokalis-Burelle R. A. Taber (retired, emeritus)
Department of Plant Pathology G. V. Ranga Rao Texas A&M University
Auburn University International Crops Research Institute current address: La Vale, Maryland
Auburn, Alabama for the Semi-Arid Tropics
Patancheru. Andhra Pradesh, P. J. A. van der Merwe
C. M. Liddell India Grain Crops Research Institute
Department of Entomology, Plant Potchefstroom, South Africa
Pathology, and Weed Science D. V. R. Reddy
New Mexico State University, International Crops Research Institute C. Venter
Las Cruces for the Semi-Arid-Trepies Oil and-ProteinSeed Centre
Patancheru, Andhra Pradesh, Grain Crops Research Institute
R. E. Lynch India Potchefstroom, South Africa
USDA Agricultural Research Service
Insect Biology Laboratory R. Rodriguez-Kabana A. K. Weissinger
Tifton, Georgia Department of Plant Pathology Department of Crop Science
Auburn University North Carolina State University,
D. McDonald Auburn, Alabama Raleigh
International Crops Research Institute
for the Semi-Arid Tropics F. M. Shokes J. A. Wightman
Patancheru, Andhra Pradesh, North Florida Research and Education International Crops Research Institute
India Center for the Semi-Arid Tropics
University of Florida, Quincy Patancheru, Andhra Pradesh, India
V. K. Mehan
International Crops Research Institute C. E. Simpson Z. Xu
for the Semi-Aiid Tropics Texas Agricultural Experiment Department of Plant Pathology
Patancheru, Andhra Pradesh, Station Oil Crops Institute
India Stephenville Wuhan, Peoples Republic of China
 Contents

Introduction 40 Yellow Mold and Aflatoxin

1 The Peanut Plant 42 Zonate Leaf Spot
2 Origin of the Peanut 43 Diseases Caused by Bacteria
2 Taxonomy of the Genus Arachis 43 Bacterial Leaf Spot
3 Peanut Diseases 43 Bacterial Wilt
45 Diseases Caused by Nematodes
45 Root-Knot Nematodes
Part I. Biotic Diseases 48 Root-Lesion Nematodes
7 Diseases Caused by Fungi 50 Sting Nematodes
7 Altemaria Leaf Spot 50 Ring Nematodes
7 Anthracnose 52 Peanut Pod Nematodes
7 Aspergillus Crown Rot 52 Other Nematodes
8 Black Hull 53 Diseases Caused by Viruses
10 Botrytis Blight 53 Tomato Spotted Wilt and Peanut Bud Necrosis
11 Charcoal Rot 54 Peanut Clump and Indian Peanut Clump
12 Choanephora Leaf Spot 55 Groundnut Rosette
12 Cylindrocladium Black Rot 56 Peanut Mottle
15 Delimited Shell Spot 56 Peanut Stripe
16 Diplodia Collar Rot 57 Peanut Stunt
17 Early and Late Leaf Spots 57 Cowpea Mild Mottle
20 Fusarium Diseases 57 Cucumber Mosaic
22 Melanosis 58 Peanut Chlorotic Streak
23 Myrotheciurri Leaf Blight 59 Other Viruses
23 Neocosmospora Foot Rot 59 Witches-Broom
23 Olpidium Root Discoloration
23 Peanut Pod Rot Complex
24 Pepper Spot and Leaf Scorch Part II. Abiotic Diseases
26 Pestalotiopsis Leaf Spot 60 Drought Stress
26 Phanerochaete omnivora 60 Frost Injury
26 Phomopsis Blight 60 Genetic Disorders
26 Phyllosticta Leaf Spot 60 Haii Injury
27 Phymatotrichum Root Rot 60 Herbicide Injury
27 Powdery Mildew 62 Lightning Injury
27 Pythium Diseases 62 Nutrient Imbalances
30 Rhizoctonia Diseases 63 Ozone Damage
31 Rust
33 Scab
34 Sclerotinia Blight Part III. Insects and Arthropods
36 Stem Rot 65 Foliage Feeders
37 Thermophilic Fungi 66 Intracellular Feeders
37 Verticillium Wilt 67 Root and Pod Feeders
39 Web Blotch 68 Stored-Product Feeders

V
Part IV. Other Organisms Part V. Management of Peanut
70 Parasitic Flowering Plants Diseases
70 Alectra vogelii 76 Strategies
70 Striga spp. 79 Genetic Modification
71 Cuscuta campestris 81 Disease- and Insect-Resistant Cultivars
71 Beneficial Organisms
71 Mycorrhizae 85 Glossary
72 Rhizobia
73 Bacillus subtilis 91 Index
74 Leaf-Surface Epiphytes
75 Dicyma pulvinata Color Plates (following page 42)
 Introduction
The peanut (Arachis hypogaea L.) is cultivated throughout
the world; India and China are the largest producers (Table The Peanut Plant
1). The United States, the worlds third largest producer,
produces more peanuts per cultivated unit area than any other The cultivated peanut plant (A. hypogaea) (Fig. 1) is an erect
country. Production of peanut in the United States is limited or prostrate, sparsely hairy, annual legume, 15-60 cm high or
to nine states (Table 2), of which Georgia and Texas are the higher. It has a well-developed taproot with many lateral roots.
largest producers. More than 675,000 ha (1.7 million acres) Roots are usually devoid of hairs and a distinct epidermis.
were harvested in the United States in 1992 with an average
yield of 2,877 kg/ha (2,567 lb/acre) and a value approaching
$1.3 billion.
The peanut plant is unusual because it flowers above
ground and pods containing one to five edible seed are
produced below ground. Seed from the pods are eaten raw or
cooked. Peanut seed are very nutritious and high in calories
and contain 25% protein. They may be boiled, broiled,
roasted, fried, ground into peanut butter, or crushed for oil.
Peanut seed also contain fats, carbohydrates, fiber, vitamin
E, niacin, folacin, calcium, phosphorus, magnesium, zinc,
iron, riboflavin, thiamine, and potassium. Most of the peanut
crop produced in the United States is shelled and sold as
peanut butter, salted peanuts, and confections. Peanut oil is
of high quality and contains unsaturated fats .such as oleic
and linoleic acids.

TABLE 1. Peanut Production, 1992

Area Planted Production
Country (ha) (metric tons)
India 8,750,000 7.500,000
China 2,975,000 6,200,000
Senegal 872,000 724,000
United States 816,000 2,235,000
Indonesia 645,000 920,000
Burma (Myanmar) 550,000 500,000
Zaire 530,000 380,000
Sudan 530,000 400,000
Nigeria 480,000 220,000
Cameroon 320,000 140,000
Argentina 190,000 400,000
aData from Agricultural Statistics, 1992, U.S. Government Printing
Office, Washington, DC.

TABLE 2. Peanut Production in the United States, 1992a

Area Planted Yield Production
State Acres Hectares lb/acre kg/ha (metric tons)
Alabama 237,000 95,912 2,505 2,781 268,157
Florida 88,000 35,628 2,530 2,836 91,858
Georgia 675,000 273,169 2,705 3,032 825,758
New Mexico 21,000 8,498 2,760 3,094 26,416
North Carolina 153,000 61,918 2,660 2,982 184,605
Oklahoma 100,000 40,470 2,410 2,702 107,131
South Carolina 14,000 5,666 2,500 2,803 14,742
Texas 308,000 124,696 2,330 2,612 308,514
Virginia 94,000 38,041 2,755 3,088 116,218
aData from Agricultural Statistics, 1993, U.S. Government Printing Office, Washington, DC.

1
 Peanut leaves are pinnate, with two opposite pairs of leaflets America. Archeological evidence suggests that peanuts similar
2-5 cm long. The petioles are 3-7 cm long. Flowers are borne to some of todays germ plasm were cultivated by the residents
on inflorescences located in the axils of leaves but never at the of South America _3,000-3,700 years ago. In spite of its long
same nodes as vegetative branches. Nodes have one to many history of cultivation, A. hypogaea has not been found in the
flowers. Flowers have two calyx lobes, an awllike one opposite wild. A. hypogaea is an allotetraploid thought to have been
the keel and a broad, four-notched one opposite the back of the developed from chromosome doubling of a cross between two
standard. The five yellow petals consist of a yellow to orange diploid wild species. Although several proposals have been
standard, two yellow to orange wings, and two petals. The made as to which species are the progenitors of A. hypogaea,
flower has 10 monadelphous stamens. conclusive evidence has not yet been presented.
Flowers appear 4-6 weeks after planting. Self-pollination Equally important to peanut improvement is the clarification
occurs in the closed keel of the flower at sunrise. The flower of the origin of the subspecies within A. hypogaea. Whether
withers 5-6 hr after opening. the subspecies are the results of genetic divergence over a long
Within about 1 week after fertilization, a pointed, needlelike period or of different crosses among species has not been deter
structure (the carpophore), commonly called the peg, devel mined.
ops and elongates quickly. The fertilized ovaries are located Peanuts were being grown extensively, some under irriga
behind the tip of the peg. The peg grows into the soil to a depth tion, when the first European explorers came to South Amer
of 2-7 cm. The tip orients itself horizontally, the ovary en ica. These explorers were responsible for introducing peanuts
larges rapidly, and pod growth begins. into Africa, Asia, Europe, and the Pacific islands. Peanuts were
The mature pod (fruit) is an oblong, indehiscent legume (1-8 introduced into the United States from Africa, the Caribbean
x 0.5-2 cm) containing one to five seed. The dry shell (peri islands, and Spain by traders. Beginning in about 1800, pea
carp) of the mature pod is reticulate and has one to 15 nuts were planted near seacoast towns including Wilmington,
longitudinal ridges. Of the pod weight, 20-30% is shell. Ma North Carolina; Charleston, South Carolina; Norfolk, Virginia;
ture seed (incorrectly termed kernels) are cylindrical or ovoid and Savannah, Georgia. The first commercial production of
and measure 1-3.5 x 0.5-1.5 cm. The seed coat varies among peanuts in the United States is thought to have been near
cultivars in color; it can be white, pink, red, purple, shades of Waverly, Virginia, in 1844.
brown, or variegated. Seed have two large cotyledons, an epi-
cotyl with three meristems, a hypocotyl, and a primary root. Selected References
Seed weight varies from about 0.2 to 2 g.
Coffelt, T. A. 1989. Peanut. Pages 319-338 in: Oil Crops of the
Selected References World. G. Robbelen, R. K. Downey, and A. Ashri, eds. McGraw-
Hill, New York.
Gregory, W. C., Gregory, M. P., Krapovickas, A., Smith, B. W., and Fernandez, A., and Krapovickas, A. 1994. Chromosomas y evolucion
Yarbrough, J. A. 1973. Structures and genetic resources of peanuts. en Arachis (Leguminosae). Bonplandia 8:187-220.
Pages 47-113 in: Peanuts, Culture and Uses. American Peanut Simpson, C. E. 1984. Plant exploration: Planning, organization, and-
Research and Education Society, Stillwater, OK. implementation with special emphasis on Arachis. Pages 1-20 in:
Norden, A. J., Smith, O. D., and Gorbet, D. W. 1982. Breeding of the Conservation of Crop GermplasmAn International Perspective.
cultivated peanut. Pages 95-122 in: Peanut Science and Tech Spec. Publ. 8. Crop Science Society of America, Madison, WI.
nology. H. E. Pattee and C. T. Young, eds. American Peanut Re Williams, D. E. 1991. Peanuts and peanut farmers of the Rio Beni:
search and Education Society, Yoakum, TX. Traditional crop genetic resource management in the Bolivian
Amazon. Ph.D. diss. The City University of New York, New York.
(Prepared by D. M. Porter)
(Prepared by T. A. Coffelt and C. E. Simpson)

Origin of the Peanut

Taxonomy of the Genus Arachis
The peanut {Arachis spp.), indigenous to South America, is a
self-pollinating, indeterminate, herbaceous legume. Sixty-nine Carolus Linnaeus described the cultivated peanut Arachis
species have been identified (see Taxonomy of the Genus hypogaea L. in 1753. The first taxonomic treatment of the
Arachis). Of these, only six have been cultivated to any extent: genus, including five species, was published in 1841. During
A. hypogaea L., A. villosulicarpa Hoehne, and A. stenosperma the next 100 years, approximately 10 additional species de
Krapov. & W. C. Gregory for their edible seed and A. repens scriptions appeared. Much confusion was introduced into the
Handro, A. pintoi Krapov. & W. C. Gregory, and A. glabrata Arachis taxonomy during this time, and a vast increase in new
Benth. for forage and ground cover. A. villosulicarpa is culti species and accessions occurred with the 1959-1961 collec
vated only by the native people of western Brazil. The most tions. Delays in describing these materials resulted in the use
widespread cultigen of the genus A. hypogaea is found in the of several undescribed species names (nomen nudum) in the
tropical and subtropical areas on every continent except Ant literature. From 1976 to 1993, the International Board for Plant
arctica. Genetic Resources funded collection efforts in the primary cen
The genus Arachis originated in the central part of Brazil, ter of origin of Arachis. New species were collected; and by
probably predating the present Amazonian forest by several 1994, the number of species approached 70, only 23 of which
millennia. The pod, fleshy root systems, many plant forms and were officially described.
leaf structures, and an immense potential to recover from envi A summary of the taxonomy of the primary cultivated
ronmental stress have all evolved as a result of the wide range species is shown in Table 3. A. hypogaea was divided into two
of climatic changes imposed on Arachis spp. since the early subspecies and six botanical varieties. Subspecies hypogaea
origins of the genus. The ability to survive in harsh environ includes variety hypogaea, which contains the Virginia and
ments is in large part the result of the specialized root systems runner market types in the United States peanut trade. Variety
and the pods. Agents capable of physically moving soil con hirsuta also belongs to this larger-seeded, slower-maturing,
taining pods, such as water, are the most likely means of effec prostrate, plant-type group. A. hypogaea hypogaea hirsuta has
tively distributing species within regions. small hairs on both surfaces of the leaflets, stipules, petioles,
A. hypogaea was likely first domesticated in the valley of and stems. Subspecies fastigiata contains four varieties: 1)
the western Paraguay River in the Chaco region of South fastigiata, the Valencia market type (United States trade); 2)
2
 vulgaris, the United States spanish type; 3) peruviana, the future because those from the primary and secondary gene pools
deeply reticulated pod type from northern Peru; and 4) aequa- are accessible without DNA technology. Utilization in peanut-
toriana, which has a deeply reticulated pod with very hairy breeding programs of genes in the tertiary gene pool (i.e., outside
plant parts. section Arachis) will probably require DNA technology.
Sixty-eight wild Arachis species and their assignment to
nine taxonomic sections have been described. The most signifi Selected References
cant characters distinguishing Arachis species are their under
ground structures including pods (fruits), rhizomatous stems, Bentham, G. 1841. On the structure and affinities of Arachis and
root systems, and hypocotyls. These variations, coupled with Voandzeia. Trans. Linn. Soc. London 18:155-162.
autogamous reproductive systems, agametic reproduction, and Krapovickas, A., and Gregory, W. C. 1994. Taxonomia del Genero
the limited means of seed dispersal, can be attributed to the Arachis (Leguminosae). Bonplandia 8:1-186.
genetic variability that gives rise to noticeable infertility in Simpson, C. E. 1984. Plant exploration: Planning, organization, and
crosses between species within sections and near total infer implementation with special emphasis on Arachis. Pages 1-20 in:
Conservation of Crop GermplasmAn International Perspective.
tility in crosses between species from different sections.
Spec. Publ. 8. Crop Science Society of America, Madison, WI.
A few major differences between the new taxonomy and Stalker, H. T., and Simpson, C. E. 1995. Germplasm resources in
what is commonly found in the pre-1994 literature include the Arachis. Pages 14-53 in: Advances in Peanut Science. H. E. Pattee
following: arid H. T. Stalker, eds. American Peanut Research and Education
Society, Stillwater, OK.
1. Two new varieties of cultivated peanut, both in the sub
species fastigiata, have been described: var. peruviana and (Prepared by C. E. Simpson and T. A. Coffelt)
var. aequatoriana (Table 3).
2. A. chacoensis (or A. chacoense) Krap. et Greg., nom. nud.,
does not appear in the new revision. This accession (GKP-
10602), included under the name A. diogoi, was collected Peanut Diseases
downstream (Paraguay River) from accessions of A. diogoi.
Morphologically, it is difficult to distinguish between Most widespread peanut diseases of today were noted and
accessions. described during the early days of commercial peanut produc
3. A. duranensis includes all old accessions that were called A. tion. As the peanut became more economically important in
spegazzinii Krap. et Greg., nom. nud. world agriculture, emphasis in production shifted from mini
4. A. pusilla Benth. is assigned to the section Heteranthae, not mal input to intense input, which resulted in high yields and
Triseminalae. Assignments were based on very young improved seed quality. As the peanut went from a low-value to
seedlings, not mature plant parts. a high-value crop and production intensity increased, both old
and new diseases prevailed. The development and severity of
The evolutionary and phylogenetic relationships between the peanut diseases depend on complex interactions among the
nine different taxonomic sections make it evident that the host, the pathogen, and the environment (Fig. 2).
genetic distances separating the sections are far from being of Pesticides, cultural practices, and resistant cultivars have
the same magnitude. The presumably older sections (Trisemi been developed to aid in the control of specific pathogens.
nalae, Trierectoides, Erectoides, Extranervosae, and Heteran However, disease is the main factor limiting peanut production
thae), except for Erectoides, are much more isolated from the in many parts of the world. In the United States, economic
remaining sections and each other than those believed to be of losses caused by reduced yields and the preventive measures
more recent origin (Procumbensae, Caulorhizae, Rhizomato- taken to control disease cost many millions of dollars annually.
sae, and Arachis).
Section Arachis is by far the largest, containing about 39% Biotic Agents
of the species described. Species of this section appear to be Any abnormality of the peanut plant (foliage, roots, pods,
invading geographical areas occupied by species of other sec and seed) is considered to be a disease. Diseases are caused by
tions. They grow intermixed with populations of Extranervosae
in the upper Paraguay River basin, occupy common ground
with section Procumbensae in the Gran Pantanal and central
Bolivia, and grow with Heteranthae, Extranervosae, and
Rhizomatosae in eastern and northeastern Brazil. They have
reached the shores of La Plata and the southeastern coast of
Brazil and grow from Salta in northwestern Argentina to the
Tocantines in northeastern Brazil.
The 27 species of section Arachis will provide most of the
genes for the improvements in cultivated peanut in the near

TABLE 3. Taxonomic Assignment of the Cultivated

Peanut Species Arachis hypogaea L.a
U.S. Market
Subspecies Variety Type Primary Area of Origin
hypogaea hypogaea Virginia Southern Bolivia and
Runner northern Argentina
hirsuta Peru
fastigiata fastigiata Valencia Peru, Brazil, and Paraguay
peruviana Peru
aequatoriana Ecuador
vulgaris Spanish Paraguay, Uruguay, and
Brazil
Fig. 2. Interacting factors commonly associated with disease de
aSource: Krapovickas and Gregory, 1994. velopment in peanut plants.

3
infectious (biotic) agents or noninfectious (abiotic) agents. tions. Sexual spores (produced, usually in lower numbers, by
Biotic agents that cause diseases of major importance include sexual fusion) are thick walled and serve as primary overwin
fungi, bacteria, nematodes, viruses and viroids, and phyto tering propagules. These sexual spores often provide the pri
plasmas (mycoplasmalike organisms [MLOs]) (Fig. 3). mary inoculum for the initial infection of the host. Spores of
Fungi. Fungi, the most numerous of all peanut pathogens, both types are spread by air, water, animals, and machinery.
are simple, filamentous organisms lacking chlorophyll (Fig. 4). Fungi also survive by forming resting bodies: chlamydospores,
They depend on the oxidation of organic matter for food rather sclerotia, or oospores (Fig. 4C). These survival propagules can
than on energy obtained from sunlight. While most live as persist in the soil for many years. The filamentous threads
saprophytes, some fungi are parasites, obtaining their food characteristic of fungi are called hyphae or mycelia (Fig. 4D).
from other living plants, such as the peanut. Approximately 50 Bacteria. Bacteria are one-celled, prokaryotic organisms
genera of fungi are causal agents of peanut diseases. Some fun (Fig. 5). They are characterized by a single chromosome, lack
gi penetrate the host directly; others penetrate through natural mitochondria or endoplasmic reticulum, and have no organized
openings or wounds. Once inside the host tissue, fungi grow nucleus. They obtain food by saprophytic means from decaying
intercellularly and intracellularly. plant and animal material or by parasitic means from living
Many genera of fungi produce asexual spores in large num plants. Some bacteria are cocci (spheres), some are rods, and
bers on infected plant parts (Fig. 4A and B). Such spores are others are comma shaped to spiral. Some have flagella for
usually short lived and provide inoculum for secondary infec motility. Most plant-parasitic prokaryotes have rigid, distinct

Fig. 3. Shapes and sizes of certain plant pathogens in relation to the size of the plant cell. (Reprinted, by permission, from G. N. Agrios,
1988, Plant Pathology, 3rd ed., Academic Press, San Diego, CA)
cell walls. However, phytoplasmas (Fig. 6), a group of extreme distinguishing characteristic of plant-parasitic nematodes is the
ly minute prokaryotes that cause plant diseases, do not have presence in the anterior (head) region of the body of a stylet, a
distinct cell walls and are pleomorphic. needlelike organ that the nematode inserts into plant cells.
Bacteria are spread by water, insects, machinery, and hu Through it, the nematode injects enzymes that aid in cell diges
mans. Some cause local infections, and some travel throughout tion, resulting in injury to the plant.
the plant via the vascular system, causing systemic infections.
Through the activity of enzymes and/or toxins, bacteria kill
plant cells and use their contents for food. Bacteria survive in
the soil, on plant debris, and on plant hosts.
Nematodes. Nematodes are unsegmented roundworms,
sometimes referred to as eelworms (Fig. 7). They are found in
soils, in fresh and salt waters, and on plants and. animals. The
vast majority of nematode species are nonparasitic.
Most plant-parasitic nematodes are slender and vary in
length from a few tenths of a millimeter to 2 mm. Usually
males and females of the same species are alike in shape,
appearance, and size. Sometimes males are slightly smaller. A

L '

Fig. 6. Phytoplasmas (mycoplasmalike organisms) in phloem.

(Courtesy D. Errampalli and J. Fletcher)

D
Fig. 4. Representative structures of four fungal pathogens of pea
nut. A, Spores of Fusarium spp.; B, spores of Leptosphaerulina
crassiasca\ C, resting bodies of Pythium spp.; and D, hyphae of
Rhizoctonia solani. (Courtesy R. Taber)

-18#
'ft * *

Fig. 7. The sting nematode, Belonolaimus longicaudatus. A, Fe

male head; B, female anterior region; C, male head; D and E,
female tails, with intestine extending into caudal cavity, serpen
tine lateral canals, and (in D) annulation of phasmid region and
terminus; F, male doacal region, with spicules extended; and G,
male tail. (Reprinted, by permission, from C.I.H. Descriptions of
Fig. 5. Cells of the pathogenic bacterium Pseudomonas solana- Plant-Parasitic Nematodes, Commonwealth Institute of Para
cearum (20,000x). (Courtesy R. Gitaitis) sitology; 1986 C.A.B. International)

5
 Some plant-parasitic nematodes (ectoparasites) feed on the shaped, or spherical; the adult male remains slender and worm
epidermal and cortical cells of roots and never actually enter like.
the roots. Others (endoparasites) penetrate the root tissue and Viruses. Viruses are obligate parasites. They are submicro-
either become sedentary for the rest of their life cycle or mi scopic entities (Fig. 8) not differentiated into cells but com
grate after a period of feeding. Sedentary endoparasites, such posed of a nucleic acid center surrounded by a protein coat.
as root-knot nematodes, show pronounced sexual dimorphism. These particles replicate only in a living host plant or in insect
The females, once they have become established in the plant vectors. They are transmitted by insects, nematodes, fungi,
tissue, lose their slender form and become lemon shaped, pear dodder, and mechanical means; some are transmitted by seed.
Viruses may survive from one growing season to the next in
weed hosts, volunteer plants, insect vectors, or seed of the
primary host.
Phytoplasmas. A phytoplasma is a prokaryote that lacks a
firm outer wall. These organisms commonly occur in conduct
ing tissue such as phloem. Common symptoms of phytoplasma
infection include yellowing, intemode shortening, phyllody,
proliferation of axillary shoots, sterility, virescence, and reduc
tion in root growth. Phytoplasmas can be spread by insects and
seed.

Abiotic Agents
Diseases caused by abiotic agents occur wherever peanuts
are grown. Pathogens are not associated with these diseases,
which are noninfectious. Abiotic diseases interfere with the
normal physiological processes of the plant, including those
associated with the leaflets, branches, roots, pods, and seed.
These diseases may be caused by an excess or lack of a certain
substance, e.g., soil moisture (too little moisture results in
drought stress; too much moisture results in drowning). Abiotic
diseases of the peanut can also be caused by factors such as
nutritional imbalance, soil pH, pesticides (too much may cause
bum), air pollutants, radiation, and frost.

(Prepared by D. M. Porter)

6
 Part I. Biotic Diseases
Diseases Caused by Fungi
ous, continuous or septate, none to numerous, attenuate,
Alternaria Leaf Spot brown, and 62-215 pm long. Conidiophores (13.0 x 3.75 (jm)
are hyaline, cylindrical, granulose or guttulate, and continuous,
Foliar diseases of peanut caused by Alternaria arachidis and both ends are rounded.
Kulk. and A. altemata (Fr.:Fr.) Keissl. have been reported in
India. Symptoms of Alternaria leaf spot include orange brown Selected Reference
lesions in interveinal areas of leaves. These lesions often extend
to veins and veinlets (Plate 1). Jackson, C. R., and Bell, D. K. 1969. Diseases of peanut (groundnut)
caused by fungi. Ga. Agric. Exp. Stn. Res. Bull. 56.
Selected Reference
(Prepared by D. H. Smith)
Balasubramanian, R. 1979. A new type of alternariosis in Arachis
hypogaea L. Curr. Sci. 48:76-77.
Aspergillus Crown Rot
(Prepared by D. H. Smith)
Aspergillus crown rot of peanut was first reported from
Sumatra in 1926. The pathogen had been reported in 1920 to
Anthracnose cause pod and seed discoloration of peanut. Aspergillus crown
rot is now an important disease that is probably established in
Anthracnose has been reported on peanut in Argentina, India, all major peanut-growing areas of the world.
Senegal, Taiwan, Tanzania, Uganda, and the United States. Stand losses caused by the crown rot fungus are variable and
Although anthracnose has been observed in peanut-production difficult to assess. Stand losses in individual fields may be as
areas of various countries, it is a disease of minor importance. high as 50% but usually vary from trace levels to 1%.

Symptoms Symptoms
Brownish gray lesions, marginal to elongate, form on both Seedlings and young plants are very susceptible to infection^
leaf surfaces and infrequently on petioles and stems of peanut (Fig. 9). Infection of young plants usually results in high
plants infected with Colletotrichum mangenoti.
Small (1-3 mm in diameter), water-soaked, yellow spots
appear on plants infected with C. dematium. Older spots are
dark brown. Spots sometimes enlarge rapidly, become irregu
lar, and cover the entire leaf. Petioles are frequently colonized
by C. dematiuni, and plants may be killed.

Causal Organisms
C. mangenoti Chevaugeon, C. arachidis Sawada, and C.
dematium (Pers.) Grove are pathogens of Arachis spp. C.
dematium produces circular, erumpent, brown to black acer-
vuli, 75-135 pm in diameter. Setae are black with two to seven
septa and 78-146 pm long. Conidiophores (21-28 x 2-4 |im)
are hyaline, simple, and erect. Conidia (19-30 x 2.5-4.0 |jm),
which are produced in pink or creamy masses, are unicellular,
hyaline, falcate, and bluntly tapered.
C. arachidis has black, epiphyllous, sparsely scattered acer-
vuli arising from pseudoparenchymatic, dark brown stromata.
Conidiophores (13-15 x 4.5 pm) are cylindrical, unicellular,
short, and hyaline. Setae are few and black. Conidia (10-15 x
4.5-6 |im) are elliptic, rounded at the apex, rounded or obtuse
at the base, hyaline, and unicellular.
C. mangenoti has acervuli that are flattened, lenticular, or
elliptic; rose to black; 67-160 |im in diameter; and subepi- Fig. 9. Crown rot of peanut seedlings caused by Aspergillus ni-
dermal, becoming erumpent. Setae are rigid, erect to subflexu- ger. Arrows indicate fruiting structures. (Courtesy K. Garren)

7
 mortality rates (Plate 2). As plants mature, they become less Hsi, D. C. H. 1966. Observations on an outbreak of Aspergillus crown
susceptible, and the mortality rate declines. In some years, rot of Valencia peanuts in New Mexico. Plant Dis. Rep. 50:175-
plants may be killed by the fungus throughout the growing sea 177.
son. Seed rot and preemergence damping-off are common Jackson, C. R. 1962. Aspergillus crown rot of peanut in Georgia.
phases of the disease, but the most obvious symptom is sudden Plant Dis. Rep. 46:888-892.
Purss, G. S. 1962. Peanut diseases in Queensland. Queensl. J. Agric.
wilting of young plants. A dark brown discoloration of the
Sci. 88:540-553.
vascular tissues is evident in the crowns and roots of wilted Vaziri, A., and Vaughan, E. K. 1976. Aspergillus crown rot of peanut
plants. The hypocotyls of infected plants also may be swollen. in Iran. Plant Dis. Rep. 60:602.
Infection of seedlings commonly occurs in the cotyledons or
hypocotyls shortly after germination. Disease progresses rapid (Prepared by H. A. Melouk and J. P. Damicone)
ly, and infected plants often die within 30 days after planting.
Others may survive longer periods, and death of individual
limbs or entire plants may occur later in the season. Decayed
roots and hypocotyls are often covered with black masses of
mycelia, conidiophores, and conidia (Plates 3 and 4). On Black Hull
spanish cultivars, a major symptom of Aspergillus crown rot of
older plants is the dead central stem, which is often broken at Black hull is an extensive, often cosmetic, black discolor
the soil line. ation of peanut shells and pegs that was first observed in the
United States in 1960 on New Mexico Valencia peanuts (A.
Causal Organism fastigiata var. fastigiata). New Mexico peanut producers have
Aspergillus niger Tiegh., the causal organism, is ubiquitous been disproportionately affected by black hull because this
in field soils throughout the world. Sometimes A. pulverulentus state is the major United States producer of peanuts grown for
(McAlpine) Thom, a probable mutant of A. niger, is also iso in-shell marketing. Black hull can affect all commercial peanut
lated from diseased plants. Colonies of A. niger grow well at cultivars but is of economic significance during severe epi
25C on a variety of media, producing abundant large, black, demics or on peanuts marketed in-shell. The disease was first
conidial heads that reach 700-800 |im in diameter. Conidio reported from Italy in 1949 and has been reported from Argen
phores are variable, measuring 1.5-3.0 mm x 15-20 |im. Co tina, the United States, and most recently (during the 1980s)
nidia, globose at maturity, are 4.0-5.0 |im in diameter. Sclero- from South Africa, where severe outbreaks have occurred.
tia may be produced by some strains.
Symptoms
Epidemiology Symptoms and signs of this disease are most commonly
A. niger is widely distributed in soils throughout the world. found on the external parts of the peanut shell as small, dis
Growth and sporulation of the fungus are usually favored by crete, black spots that often coalesce into large, dark lesions
warm, moist conditions. Fewer propagules are found in very covering almost the whole pod (Fig. 10 and Plate 5). Dark
wet soils than in dry soils. Soil type has not been correlated lesions also may be found on the pegs and roots under severe
consistently with prevalence of crown rot, but the disease often disease pressure, causing significant yield losses in quantity as
is more prevalent in soils low in organic matter. well as quality. The dark lesions are formed by the production
A. niger is seedbome. The infestation levels of certain seed of dark chlamydospores on and in host tissue. The seed coat
lots often exceed 90%. Seedlings from such seed usually pro and seed may also become infected and discolored, leading to
duce a high percentage of infected plants. However, soilbome seed transmission of the disease.
inoculum may serve as the primary inoculum. Also, A. niger is
more prevalent in fields continually cropped to peanut than in Causal Organism
fields planted to nonhost crops. Outbreaks of Aspergillus The fungus that causes black hull produces two spore types:
crown rot are sporadic. Predisposition appears to be a major dark-walled chlamydospores and hyaline or subhyaline to pale
factor in the development of the disease. Drought stress and
high temperatures early in the season are associated with
crown rot outbreaks. Other adverse conditions such as extreme
fluctuations in soil moisture and temperature, poor seed qual
ity, seedling damage from pesticides, insect feeding on roots
and crowns, and factors that delay seedling emergence are
associated with disease.

Control
All commonly grown cultivars are susceptible to the crown
rot fungus. Cultivars that fruit in a bunch pattern usually are
more susceptible than runner types. Resistance to A. niger has
been reported, but it has not been incorporated into agronom-
ically acceptable cultivars. Fungicide seed protectants may
provide some control when used where conditions and prac
tices favor rapid germination and seedling emergence.

Selected References

Ashworth, L. J., Jr., Langley, B. C., Mian, M. A. W., and Wrenn, C. J.

1964. Epidemiology of a seedling disease of Spanish peanut caused
by Aspergillus niger. Phytopathology 54:1161-1166.
Garren, K. H., and Jackson, C. R. 1973. Peanut diseases. Pages 429-
494 in: Peanuts, Culture and Uses. American Peanut Research and Fig.L10. SymptomsjDf_black huN, caused by Chalara elegans, on
Education Society, Stillwater, OK. Valencia peanut pods. (Courtesy D. H. Smith)
brown mitospores (enteroblastic phialospores) (Fig. 11). The base is 20-40 x 6-9.5 pm, and the collarette is 25-40 x 3.5-5
classification of this fungus and the nomenclature of the two pm. The mitospores are enteroblastic phialospores: the first
spore stages has been confused since 1910 and remains con spore is holoblastic, and the following spores are delimited in a
fused today. The fungus was originally described as Torula retrogressive fashion inside the original wall of the sporog
basicola Berk. & Br. in 1850 from Pisum and Nemophila spp., enous cell, leaving a collarette at a fixed sporogenous locus.
entirely on the basis of the chlamydospores. In 1910, tie The mitospores are extruded in chains and are cylindrical to
fungus was transferred to Thielaviopsis basicola (Berk. & barrellike with truncate or obtuse ends; aseptate; and hyaline,
Broome) Ferraris, but this transfer was applicable only to the subhyaline, or pale brown (Fig. 11). The chlamydospores are
chlamydospore stage. The mitospore stage remained effec thallic (usually thallic-endoarthritic), intercalary or character
tively unnamed until 1975, when both the chlamydospore and istically terminal, usually in chains of five to seven, and often
mitospore stages were named Chalara elegans Nag Raj & in rosettes of three or more chains in culture. The terminal
Kendrick. The subsequent usage and confusion over the status chlamydospore is rounded, and the rest are short cylindrical,
of these names has led to these stages being erroneously unicellular, dark brown or amber, and 6.5-14 x 9-13 pm.
referred to as synanamorphs and the names used as synonyms. Chlamydospore chains are 24-55 pm long (Fig. 12). New
Literature on this fungus and the black hull disease is found Mexico isolates of C. elegans grow optimally at temperatures
under both names. However, the only name available for both of 15.5-19C and at pH 6.8-7.6.
the mitospore (phialospore) and chlamydospore stages is Cha
lara elegans Nag Raj & Kendrick. Confusion also has occurred Disease Cycle
in phytopathological literature because of the common occur Black hull severity varies from year to year because of cli
rence of the ascomycete Thielavia basicola Zopf with C. matic variability and changing crop-management practices. C.
elegans. Early literature reported that these fungi were genet elegans persists indefinitely as chlamydospores in host residue
ically related, and this misconception has persisted into more and soil and as a competitive saprophyte growing on soil or
recent literature. Thielavia basicola is not related to Thiela ganic matter. The black hull fungus does not have a known
viopsis basicola or to C. elegans. meiotic spore stage (perfect state) and passes through a simple
C. elegans has distinct sporogenous cells that are borne on life cycle and only slightly more complex disease cycle. The
simple, erect phialophores, which are cylindrical to sub- chlamydospores are the overwintering structures, which ger
cylindrical, three- to five-septate (occasionally aseptate), sub minate to initiate primary infections. The chlamydospore germ
hyaline to pale brown, and 70-95 pm long. The sporogenous tubes infect the peanut directly or indirectly through phialo
cells are swollen at the base with a characteristic cylindrical spores, which can be produced rapidly on susceptible tissue
barrel (collarette). The sporogenous cell is 55-80 pm long, the and therefore likely act as important sources of secondary
inoculum. The fungus penetrates by means of an infection peg
formed under a small aggregation of hyphae, although appres-
soria have also been observed. The infection peg enlarges into
a cylindrical structure, which gives rise to short, budlike cells
from which the fungus colonizes the host tissue in an inter- and
intracellular fashion. Chlamydospore and phialospore produc
tion can occur within 72 hr after infection. It is the abundance
of the dark-walled chlamydospores on the surface and within
the intercellular spaces of the sclerenchymatous mesocarp that
gives the black hull disease its name.
Initial inoculum arises from infected hulls and other plant parts
left in the field- from previous seasons. Factors increasing black
hull severity include high soil pH, low temperatures late in the
season, overly moist conditions arising from excessive irrigation
or rainfall, high-density plantings, the monoculture of peanut,
and rotation to peanuts after cotton or sweet potatoes.

Fig. 11. Chalara elegans. A, Endoconidial cells and emerging

endoconidia; B, chlamydospores; and C, chlamydospores break
ing into segments. (After W. W. Gilbert. Reprinted from Compen
dium of Alfalfa Diseases, The American Phytopathological So
ciety, 1979) Fig. 12. Chlamydospores of Chalara elegans. (Courtesy D. Hsi)
 Control
No commercial resistance to black hull is currently available.
The disease has decreased in incidence and severity in New
Mexico during the past few years because of improved rotation
and irrigation practices instigated to control web blotch, another
disease favored by cool, moist conditions. Recommendations for
control include rotation from peanuts to small grains in 3- to 4-
year cycles, use of clean seed, and wider row spacing. The
fungicides benomyl and thiophanate-methyl have been shown to
reduce black hull incidence. Moving peanut production to new
land is no more effective than a good rotation schedule.

Selected References

Corbaz, R. 1985. Pathotypes et variations du pouvoir pathogene chez

Chalara elegans Nag Raj et Kendrick (= Thielaviopsis basicola).
Phytopathol. Z. 113:289-299.
Hsi, D. C. H. 1978. Effect of crop sequence, previous peanut black-
hull severity, and time of sampling on soil populations of Thiela
viopsis basicola. Phytopathology 68:1442-1445.
Labuschagne, N., and Kotze, J. M. 1991. Incidence of Chalara ele
gans in groundnut samples and seed transmission of blackhull.
Plant Pathol. 40:639-642.
Litton, L. C. 1982. Survival of Thielaviopsis basicola in naturally
infested soil and in pure culture. Tob. Sci. 26:94-97.
Nag Raj, T. R., and Kendrick, W. B. 1975. A Monograph of Chalara
and Allied Genera. Wilfrid Laurier University Press, Waterloo,
Ontario, Canada.

(Prepared by C. M. Liddell) Fig. 13. Botrytis blight on pegs, pods, and stems. (Courtesy K.
Garren)

Botrytis Blight
Botrytis blight has been reported in most of the peanut-
producing countries of the world. However, damage is usually
slight, since environmental conditions conducive to disease de
velopment usually are not present during the growing season.
Reports of disease occurrence serious enough to-greatly reduce
yields are rare.

Symptoms
All parts of the peanut plant, above and under the ground,
are subject to attack by this_soilbomefungus. Plants~mjured~by
frost or with reduced vigor from attacks by other pathogens are
especially prone to infection, which usually begins on aerial
plant parts. Branch tips and branches in contact with the soil
surface are especially susceptible.
Peanut leaflets are sometimes infected without any evidence Fig. 14. Sclerotia of Botrytis cinerea on pods and a stem. (Cour
tesy K. Garren)
of disease on other plant parts. Infection is characterized by the
formation of one to numerous distinct leaf spots on adaxial
leaflet surfaces (Plate 6). Leaf spot size may exceed 10 mm in usually unbranched, septate, and 11-23 pm thick. Projections
diameter. Conidiophores and conidia are produced sparingly on form at the tips, and from these, conidia are formed so
both adaxial and abaxial leaflet surfaces (Plate 7). A Glio- abundantly that the infected plant parts become dustlike and gray
cladium species has been constantly associated with the leaf (Plate 11). Conidia are disseminated readily by air currents.
spot fungus and parasitizes conidia, conidiophores (Plate 8), Sclerotia (1-5 mm long) are hard, black, and irregularly shaped
and sclerotia of Botrytis. (Figs. 14 and 16). They are rounded on the upper surface and flat
Under favorable environmental conditions, the causal organ or concavely depressed on the underside when attached to in
ism colonizes plant parts rapidly, causing wilt and death of fected substrate (Fig. 14). The ascomycetous stage of B. cinerea,
individual limbs or entire plants (Fig. 13 and Plate 9). The Botryotiniafuckeliana (de Bary) Whetzel, is rarely observed.
fungus moves rapidly from aerial plant parts into underground
parts. Botrytis blight is characterized by the profuse production Disease Cycle
of conidia (Plates 10 and 11) and sclerotia (Fig. 14) on infected Temperatures below 20C accompanied by heavy dews or
plant parts. excessive rainfall are prerequisites for infection by B. cinerea.
Senescing, frost-injured, and mechanically injured plant parts
Causal Organism also are prone to colonization. Organic debris, such as defo
Botrytis cinerea Pers.:Fr. bears conidia on the tips of erect liated leaflets and abscised flower parts, on the surface of the
conidiophores that cover the surface of the host substrate (Fig. 15 soil serves as a food base and aids in the infection process. B.
and Plate 10). Conidia (9-12 x 6.5-10 pm) are ellipsoid to ovoid cinerea overwinters in the sclerotial form in the soil. Although
and one celled with almost hyaline walls. Conidiophores are apothecia have been reported, the primary inoculum source

10
Fig. 15. Conidia of Botrytis cinerea. Left and center, conidia on conidiophores. (Reprinted from Compendium of Potato Diseases, The
American Phytopathological Society, 1981)

Charcoal Rot
Charcoal rot, caused by the common soilbome fungus Macro-
phomina phaseolina, is widely distributed in most peanut-
producing countries. The fungus is distributed throughout the
world and causes diseases in a wide range of crops. In peanut,
it is responsible for seed and seedling rots, wilt, root and stem
rots, leaf spot, rotting of developing pods and seed, and con
cealed damage. The term charcoal rot is used to describe the
damage done to roots and stems of seedlings and older plants.
Charcoal rot is of only minor importance in the United States,
although occasionally it can greatly reduce plant stands. In
India, it is the most common disease of peanut seedlings.

Symptoms
The occurrence of water-soaked lesions on the hypocotyl
near the soil surface is a characteristic sign of this disease.
After the hypocotyl is girdled, the seedling dies. Similar symp
toms are observed on older plants at the soil line, although all
plant parts at all stages of growth are susceptible. Stem and
root lesions appear water soaked at first, but infected tissues
Fig. 16. Culture of Botrytis cinerea on potato-dextrose agar show
ing sclerotia.
later become a dull light brown (Plates 12 and 13). The infec
tion extends down into the taproot and up into the stem and
branches (Plate 14). When lesions girdle the stem, the plant
appears to be mycelium originating from germinating sclerotia or wilts, and the fungus rapidly colonizes the branches, which
omnipresent conidia. Conidia are dispersed by wind and rain. turn brown and die. The dead tissues rot and turn black as
sclerotia of the fungus develop profusely. Roots, pegs, and
Control pods also rot and become covered with sclerotia. In some
Foliar sprays with fungicides such as benomyl and chloro- cases, the disease is at first restricted mainly to the roots,
thalonil offer some protection against B. cinerea. The use of which become rotted and blackened and the taproot shreds.
early-maturing peanut cultivars might lessen frost damage and The foliage of such plants turns yellow and wilts, and the
thereby reduce disease severity. typical symptoms of stem blight and charcoal rot appear.

Selected References
Causal Organism
Orellana, R. G., and Bailey, W. K. 1964. Blight of peanuts in Mary M. phaseolina (Tassi) Goidanich, the pycnidial state of Rhi-
land and Virginia in 1963. Plant Dis. Rep. 48:519-521. zoctonia bataticola (Taubenhaus) E. J. Butler or Sclerotium
Porter, D. M., Smith, D. H., and Rodnguez-Kabana, R. 1982. Peanut bataticola Taubenhaus, was derived from Macrophoma phas
diseases. Pages 326-410 in: Peanut Science and Technology. H. E. eolina by Tassi in 1901. The sterile mycelial phase of M.
Pattee and C. T. Young, eds. American Peanut Research and Edu phaseolina was first named S. bataticola by Taubenhaus but
cation Society, Yoakum, TX.
was later transferred to the genus Rhizoctonia.
Rothwell, A. 1962. Diseases of groundnuts in Southern Rhodesia.
Pycnidia of M. phaseolina (100-200 (im in diameter) are
. Rhod. Agric. J. 59:199-201.
membranous to subcarbonaceous, first immersed and then at
(Prepared by D. M. Porter) least partially erumpent, and globose or flattened globose with
11
inconspicuous truncate ostioles. Their walls are composed of Selected References
several layers of dark, thin-walled, angular cells, 9 jam in
diameter, and are lined with a hyaline layer two or three cells Goidanich, G. 1947. Revisione del genere Macrophomina Petrak.
thick bearing simple, rod-shaped conidiophores, 10-15 |im Specie tipica: Macrophomina phaseolina (Tassi) G. Goid. n. comb,
long. Conidia (14-33 x 6-12 |im) are single celled, hyaline, nec M. phaseoli (Maubl.) Ashby. Ann. 1st. Sper. Mecc. Agric.
and elliptic or oval. 1:449-461.
Jackson, C. R., and Bell, D. K. 1969. Diseases of peanut (groundnut)
caused by fungi. Ga. Agric. Exp. Stn. Res. Bull. 56.
Disease Cycle Shokes, F. M., Lyda, S. D., and Jordan, W. R. 1977. Effect of water
Charcoal rot is both seedbome and soilbome. Mycelium in potential on the growth and survival of Macrophomina phaseolina.
seed and mycelium and sclerotia in plant debris in the soil are Phytopathology 67:239-241.
the primary sources of inoculum (Fig. 17). The sclerotia can Singh, S. K., Nene, Y. L., and Reddy, M. V. 1990. Influence of crop
remain viable in dry soil for many years but rapidly lose via ping systems on Macrophomina phaseolina in soil. Plant Dis.
bility in very wet soils. 74:812-814.
M. phaseolina is commonly present in peanut seed and
pods and can readily be disseminated by their movement. (Prepared by V. K. Mehan and D. McDonald)
High soil temperatures (about 35C) and low soil osmotic
potential reduce plant vigor and favor growth of the fungus
and development of charcoal rot. Fungal growth in pods is
increased by rain after harvest. Damage during harvesting Choanephora Leaf Spot
and shelling predisposes pods and kernels to injury from this
pathogen. Choanephora sp. has been observed on peanut leaves in the
Philippines, Thailand, Senegal, and Uganda. Brown lesions
Control originate at the leaflet margin and spread over the entire leaflet.
Crop rotation is generally ineffective in reducing soil inocu Abundant sporulation occurs on both leaflet surfaces and down
lum because the fungus can grow saprophytically and has a the petioles. Defoliation of infected leaflets may occur.
wide host range. However, rotation of peanut with rice for 2-3
years may reduce the soilbome inoculum of M. phaseolina. Selected Reference
Crop sanitation (e.g., burning crop residues) may help reduce
disease levels. Providing adequate fertilizer and soil water to Mukiibi, J. 1975. Minor diseases of groundnut in Uganda. East Afr.
ensure good crop growth should reduce charcoal rot develop For. J. 41:87-94.
ment. Frequent irrigation to keep the soil wet reduces the via
bility of sclerotia. (Prepared by R. A. Taber)
Seed treatment with fungicides such as captan and thiram
can reduce seedbome infection and provide the germinating
seed some protection from invasion by the fungus from soil Cylindrocladium Black Rot
bome inoculum. Soil drenching with pentachloronitrobenzene
(PCNB) can give some control of the disease. No immune or Cylindrocladium black rot (CBR) of peanut was first ob
highly resistant peanut genotypes are-available. served in Georgia in 1965. Soon thereafter, CBR was recog

Fig. 17. Sclerotial development of Macrophomina phaseolina. A, Proliferation of a single hypha; B, aggregation of several hyphae; arid
C, mature sclerotium. (Reprinted, by permission, from Jackson and Bell, 1969)

12
nized in other peanut-producing areas of the United States and A diagnostic sign of CBR is the occurrence of small, reddish
in Japan, India, and Australia. The disease has been a cause of orange perithecia of the pathogen in dense clusters on stems
major concern, particularly in Virginia and North Carolina (Plate 17), pegs, and occasionally pods. These fruiting bodies
because of its widespread occurrence and chronic threat to develop on tissues just above and below the soil surface during
peanut production in these states. In other parts of the United periods of wet, humid weather. If perithecia are not found on
States, outbreaks of CBR have remained static, and yield losses diseased plants, tissue samples must be assayed in a laboratory
are generally secondary in importance to those caused by other to positively identify the disease as CBR. These structures are
soilbome diseases. sometimes confused in the field with the somewhat smaller
rounder perithecia of Neocosmospora sp., a common sapro
Symptoms phyte that colonizes dead plant parts that are in contact with
The first visible symptoms of CBR are chlorosis and wilting soil.
of leaves on the erect, primary stem of a plant. Entire plants
may wilt and die at an alarming rate when prolonged periods of Causal Organism
high soil moisture are followed by a period of moisture stress. Numerous publications since 1966 have referred to the
In the absence of ideal conditions for disease development, causal organism as Cylindrocladium crotalariae (C. A. Loos)
plants may develop only a chlorotic, stunted appearance. When D. K. Bell & Sobers (teleomorph Calonectria crotalariae (C.
CBR is seen for the first time in a field, the diseased plants are A. Loos) D. K. Bell & Sobers). Recently, the name was
usually observed in one or more localized spots (Plate 15). changed to Cylindrocladium parasiticum Crous, Wingfield, &
Aboveground symptoms commonly include chlorosis, wilt, Alfenas (teleomorph Calonectria ilicicola Boedijin & Reits-
stunted growth, and death. ma). The fungus grows well on potato-dextrose agar, producing
All below-ground plant parts may develop symptoms of light yellow to white weblike aerial mycelium and a burnt
CBR. Hyppcotyls, primary and secondary roots, and pods be orange to dark brown submerged growth. Conidiophores are
come black and necrotic (Plate 16). The taproot is often borne laterally on a main axis or stipe that terminates in a hya
necrotic and severely decayed in plants with aboveground line,! globose swelling (vesicle) measuring 6-13 pm in diam
symptoms. eter (Fig. 18). Conidiophores develop reniform or sometimes

r i V ' ,^ * 1 iM M Im iM aM -'.h fc } *. ------ .. * .... .

I*

W-

*1
W 'u //

- * tl I

r h ih b Bh 4 a
\-r Hr: " , < v
A ls -
- 1* *1 - i
Vi ! i V
- IIP
* ^ S " Xr
llliilifl 1PPII111I WSMwm
f, ** *

D
8

IT v*"*-*- - * ' m

-4*..
F V " , * . * ' E
Fig. 18. A, Conidiophore, B, immature stipe, C, vesicles, and D, conidia of Cylindrocladium parasiticum; E, asci and ascospores and F,
ascospores of Calonectria ilicicola. (Reprinted from Bell and Sobers, 1966)

13
 doliform phialides on tertiary branches. Conidia (58-107 x Field studies have shown that microsclerotia of C. parasiticum
4.8-7.1 |im) arise by budding from the apexes of phialides and occur in clumps or clusters in the field rather than in a random or
are hyaline, cylindrical, and rounded at both ends and most uniform distribution. Studies relating inoculum density and
often have three septa. disease incidence have demonstrated that the number of observed
Perithecia (Fig. 19) (320-465 x 290-370 nm) form on host infections on roots and the level of symptom expression by
tissues and in axenic cultures incubated under lights and are plants are directly proportional to microsclerotial densities in
subglobose to oval or obovate and orange to red. Asci are hya soil. Soil temperatures of 20-25C and moisture levels near field
line and contain eight fusoid to falcate, mostly one-septate capacity are most conducive to infection and rot of peanut roots
ascospores (34-58 x 6.3-7.8 j^m). by C. parasiticum. Root infection is suppressed markedly at low
Microsclerotia of C. parasiticum are readily visible in cor soil moisture levels and soil temperatures of 30C and above.
tical tissues and Rhizobium nodules of infected peanut roots The primary infection court for C. parasiticum on peanut is
with the use of histochemical clearing agents (Fig. 20). believed to be near the root tips. Root exudates in this region
These propagules are burnt orange to dark brown and are probably trigger microsclerotial germination and subsequent
composed of a dense cluster of cells that resemble chlamyd infection processes. After germination, intercellular penetration
ospores. Microsclerotia develop abundantly in axenic cul of the cortex occurs within 12-24 hr and penetration of the root
tures of C. parasiticum on media with high carbon-nitrogen stele may occur within 48 hr. As necrosis develops in infected
ratios. roots, hyphae of the fungus begin to produce microsclerotia.
Perithecia of C. parasiticum may develop on the surfaces of
Disease Cycle diseased roots and basal stems near the soil surface during
Microsclerotia of C. parasiticum are responsible for over moist periods. Ascospores are forcibly discharged into the air
wintering and long-term survival of the fungus in soil. Micro when perithecia first mature. In the final phase of development,
sclerotia in crop debris expelled from peanut combines may be ascospores exude in a viscous ooze from the ostiole, which
carried long distances by prevailing winds (Fig. 21). As in may facilitate dispersal by rain or possibly insects. Because of
fected tissues decompose, microsclerotia are released into the the late-season development of ascospores and the rapid loss of
soil and disseminated by tillage equipment. Of the crops com viability with desiccation, their epidemiological importance is
monly grown in rotation with peanut (i.e., soybean, tobacco, believed to be of minor significance.
cotton, com, and small grains), only soybean serves as a host Although C. parasiticum is easily isolated from freshly dug
of C. parasiticum and thereby can further increase populations peanut seed, the frequency of its detection in commercially
of microsclerotia in field soil. Soil temperatures have a pro harvested seed is usually quite low. The viability of the fungus
found influence on survival of microsclerotia. Cold winters in seed is reduced by curing and storage practices and by fun
that freeze soil water in the plow layer and sustained periods of gicide seed treatments. The risk for seedbome spread of CBR
cold at or below 5C can result in a marked reductions in popu has been difficult to measure quantitatively but should not be
lations of viable microsclerotia in infested fields. discounted as a factor in pathogen dispersal;

Fig. 19. Perithecium of Calonectria ilicicola containing asci and Fig. 20. Microsclerotium of Cylindrocladium parasiticum in the
ascospores. (Courtesy R. Rowe) cortex of a peanut root. (Courtesy R. Rowe)

14
Control progress from these points of infection generally fails to result
The development and release of disease-resistant cultivars of in plant destruction or significant loss of yield.
peanut continue to make a significant contribution to CBR
management. In general, spanish cultivars are most resistant to Selected References
CBR, Valencia cultivars are the most susceptible, and Virginia
cultivars are moderately susceptible. Although CBR-resistant Bell, D. K., and Sobers, E. K. 1966. A peg, pod, and root necrosis of
lines of each type have been described and released, only one peanuts caused by a species of Calonectria. Phytopathology
56:1361-1364.
commercial cultivar (NC IOC) of the Virginia type offers par
Crous, P. W., Wingfield, M. J., and Alfenas, A. C. 1993. Cylindro
tial resistance at this time. Carefully planned crop rotation and
cladium parasiticum sp. nov., a new name for C. crotalariae.
cultural practices are necessary in deploying a CBR-resistant Mycol. Res. 97:889-896.
cultivar. The severity of CBR increases when roots are para Diomande, M., and Beute, M. K. 1981. Effects of Meloidogyne hapla
sitized by the northern root-knot nematode (Meloidogyne hap- and Macroposthonia ornata on Cylindrocladium black rot of pea
la) and the ring nematode (Criconemella ornata). An increase nut. Phytopathology 71:491-496.
in the severity of CBR on peanut may also result from root Phipps, P. M. 1990. Control of Cylindrocladium black rot of peanut
injury caused by certain preplant herbicides. Soils relatively with soil fumigants having methyl isothiocyanate as the active
high in organic matter and with a greater capacity for moisture ingredient. Plant Dis. 74:438-441.
retention generally favor disease development. Low soil tem Phipps, P. M., and Beute, M. K. 1979. Population dynamics of Cylin
peratures and high levels of soil moisture early in the growing drocladium crotalariae microsclerotia in naturally infested soil.
season are most conducive to CBR. Warm soil and low soil Phytopathology 69:240-243.
moisture are generally unfavorable for root infection. Rowe, R. C., Johnston, S. A., and Beute, M. K. 1974. Formation and
Because of cooler soil conditions and the probability for dispersal of Cylindrocladium crotalariae microsclerotia in infected
peanut roots. Phytopathology 64:1294-1297.
higher levels of soil moisture, peanuts planted early are more
vulnerable to CBR damage than those planted late. Crop rota
(Prepared by P. M. Phipps and M. K. Beute)
tion with nonhosts such as com, small grains, cotton, or tobac
co may help reduce the incidence of CBR, whereas rotations
with leguminous crops such as soybean can result in increased
populations of C. parasiticum in the soil. Tillage practices that Delimited Shell Spot
maximize exposure of microsclerotia to winter temperatures
may reduce populations significantly. Such practices include Delimited shell spot (DSS), a blemish of peanut pods, is
removal and destruction of peanut haulm (hay), omission of a limited to the Mediterranean region. Affected peanut crops are
winter cover crop, and no soil tillage until spring. Movement frequent in poorly aerated soils. Spots are abundant when a
of the pathogen from field to field can be minimized by clean legume is included in the crop rotation. DSS greatly reduces the
ing field implements and combines to remove adhering soil quality of the pods. Also, various fungi frequently invade the pod
and plant debris. cavity through the necrotic lesions and cause seed decay.
An early spring application of metham sodium at 36 kg/ha
(Vapam, 10 gallons per acre) is widely used for CBR control in Symptoms
heavily infested fields in Virginia and North Carolina. The A spot originating as a transitory and inconspicuous tiny
fumigant is applied through chisel shanks under each row (8- depression occurs in or on the surface of the fleshy, lignifying
10 in. deep) at least 2 weeks prior to planting and when soil pod shell. A typical spot (approximately 5 mm in diameter)
temperatures are at or above 15C. At the time of application, develops as lignification proceeds. The spot becomes necrotic,
rows are bedded to facilitate the alignment of planters over dry, and light beige to pale grayish beige and is delineated from
sites of fumigant placement. Control is achieved by killing the the unspotted areas of the shell by a distinct, dark tan margin.
fungus in the zone of taproot growth. Lateral roots outside the Cells below the spot are rich in starch granules and are thin
zone of fumigant activity may become infected, but disease walled, whereas in unaffected cells, starch granules gradually
disappear and the cell walls thicken. Spots frequently are
aggregated in clusters (Plate 18). Secondary invaders often
alter spot appearance: it may darken in the center, become
necrotic, or expand concentrically (Plate 19 and Fig. 22).

Fig. 21. Microsclerotia (arrows) in windblown debris from a com

bine. (Courtesy R. Rowe) Fig. 22. Pods with delimited shell spots.

15
 Causal Agents lateral branch or the entire plant is usually the first symptom of
The etiology of DSS is, for the most part, uncertain. That the disease in older plants. Wilt develops rapidly, and the plant
causal agent, or group of agents, is biotic can be demonstrated usually dies within a few days. Lesions that develop on above
by control with physical and chemical, broad-spectrum soil ground stems are characterized by elongated necrotic areas
treatments. Nematodes are not involved in the DSS complex. with light brown centers and dark brown margins. Infected
Inoculation of peanut plants with microorganisms that were roots become slate gray to black and shred easily. Pycnidia
isolated from plants with DSS symptoms (at different develop embedded in the infected host tissue resemble small, erumpent,
mental phases of pods and lesions) did not cause DSS. Statis black dots (Plate 22). The fungus also causes concealed dam
tical analysis of spot distribution on individual pods proved age of peanut seed that is not visible on the external surface.
that the causal factor does not attack the shell randomly. More Originally, the term concealed damage was restricted to
over, the clustering of spots is reminiscent of an arthropod damage caused by quiescent, natural, pod mycoflora. However,
feeding around its first probe. Indeed, when various selective it now encompasses mechanical damage, damage associated
biocides were applied to soils with a history of DSS, several with calcium and boron deficiencies, and damage caused by
insecticides and acaricides reduced spot numbers significantly. some pathogenic fungi such as Diplodia gossypina.
Small populations of Rhizoglyphus mites were consistently
associated with DSS. However, infestation of pods with labo Causal Organism
ratory-grown gnotobiotic populations of Rhizoglyphus sp. did not Although Lasiodiplodia theobromae (Pat.) Griffon & Maubl.
induce DSS development. The following is hypothesized: 1) in and Botryodiplodia theobromae Pat. have been associated with
nature, Rhizoglyphus sp., or another microarthropod, may serve peanuts exhibiting symptoms of collar rot, Diplodia gossypind
as a vector for a submicroscopic parasite of endemic legumes (Cooke) probably is the causal agent of collar rot of peanut.
that causes local lesions to the pod shell of the Arachis plant; 2) Simple or compound pycnidia occur either singly or in groups
in cryptoaerobic microsites that prevail at pod-to-soil interfaces on the surfaces of necrotic tissues. They may appear immersed
in poorly aerated soil, even tiny wounds do not heal immediately, or erumpent, and they possess a prominent ostiole. Pycnidia
and each spot expands until arrested by the surrounding tissue; range in diameter up to 400 (jm. Conidia (Plate 23) are bome
therefore, the number of spots increases with time. on short conidiophores. Mature pycnidiospores (17-34 x 10-
18 (jm) are elliptic with one septum. Mature, two-celled co-
Control nidia are brown and lack longitudinal striations.
To reduce the risk of DSS development, poorly aerated soils
should be avoided and crop rotation should exclude legu Disease Cycle
minous crops or weeds. Winter cereals cut green (for fodder) Mycelium and mature conidia of D. gossypina can remain
preceding peanuts reduce DSS abundance significantly. Deep dormant in soil and plant debris for long periods. Germination
plowing improves soil aeration and further reduces DSS. and infection occur when a suitable substrate becomes avail
Mechanized formalin applications to the seedbed (3,000 liters able. Peanut plant tissue predisposed by heat stress-is more-
per hectare of a 37% formaldehyde solution) were found to be subject to colonization by D. gossypina than is similar tissue
cost effective and reduced DSS. Experimentally, seedbed solar- not so predisposed. However, predisposition is not a prerequi
ization of metham-treated soil was highly effective in reducing site for infection. Primary infection may be caused by myce
DSS, but it is not cost effective. Nevertheless, in severely af lium originating from germinating, mature conidia or mycelial
fected sites, all these measures do not eliminate DSS unless fragments. Upon penetration, the fungus grows from one cell
they are used in combination with-resistant-genotypes.-These to another throughout the cortical parenchyma. Hot, dry weath
genotypes combine shallow fruiting (thus partially escaping er favors disease development.
cryptoaerobic conditions) with a hardy pod shell and bear few D. gossypina can be isolated from up to 10% of seed from
spots. Unfortunately, yield of these genotypes is low, but they fields exhibiting severe disease symptoms. Seed-treatment fun
have potential as sources of resistance in breeding programs. gicides reduce the incidence of D. gossypina but do not eradi-
cate it; dius_implying the possibility of seed transmission. The
Selected Reference causal organism also can be isolated from seed from apparently
healthy plants not exhibiting aboveground disease symptoms.
Frank, Z. R., Ben-Yephet, Y., and Katan, J. 1986. Synergistic effect of
metham and solarization in controlling delimited shell spots of Control
peanut pods. Crop Prot. 5:199-202. Rotations with nonhost crops can reduce disease incidence.
Although resistance to D. gossypina is not available in com
(Prepared by Z. R. Frank) mercial cultivars, some breeding lines, including F 334 AB-14
and Florispan Runner, possess high degrees of tolerance to this
disease and are available for use in breeding programs. By
manipulating row orientation and controlling foliage diseases
Diplodia Collar Rot so that foliage is maintained to provide shade throughout the
growing season, one can minimize heat injury to plant basal
Diplodia collar rot usually occurs sporadically throughout stems and perhaps reduce disease incidence.
the world, rarely causing economically important losses. In 1993,
however, collar rot was severe on several farms in Virginia (Plate
20). Diseased areas often exceeded one acre in size. In such Selected References
areas, almost all plants exhibited typical collar rot symptoms.
Yield reductions caused by collar rot usually are less than 1%, Boyle, L. W. 1953. Heat canker: A primary phase of collar rot on
but reductions of 25% or more have been reported. In Virginia in peanuts. Phytopathology 43:571-576.
Jackson, C. R., and Bell, D. K. 1969. Diseases of peanut (groundnut)
1993, yield losses in severely diseased fields exceeded 75%.
caused by fungi. Ga. Agric. Exp. Stn. Res. Bull. 56.
Symptoms McGuire, J. M., and Cooper, W. E. 1965. Interaction of heat injury
and Diplodia gossypina and other etiological aspects of collar rot
The causal agent, a common soilbome saprophyte, is usually of peanut. Phytopathology 55:231-236.
associated with the peanut plant only as a wound parasite or as Phipps, P. M., and Porter, D. M. 1995. Susceptibility of peanut
a secondary pathogen. Peanut seedlings and older plants, cultivars to Diplodia collar rot in Virginia. Biol. Cult. Tests Control
including pods, are subject to attack (Plate 21). Wilting of a Plant Dis. 10.73.

16
Porter, D. M., and Phipps, P. My 1994. Diplodia collar rot of peanut, a typically light tan to reddish brown on the undersides (abaxial
reoccurrence. Proc. Am. Peanut Res. Educ. Soc. 26:58. surfaces) of leaflets, whereas late leaf spot lesions will usually
Porter, D. M., Smith, D. H., and Rodnguez-Kdbana, R. 1982. Peanut be dark brown to black. This characteristic also may be unre
diseases. Pages 326-410 in: Peanut Science and Technology. H. E. liable on many cultivars because lesions often differ in color on
Pattee and C. T. Young, eds. American Peanut Research and Edu the abaxial surface. The most reliable method of distinguishing
cation Society, Yoakum, TX.
between the two leaf spots is identification of conidia by
microscopic examination. Sporulation of the early leaf spot
(Prepared by D. M. Porter and P. M. Phipps)
fungus is more prevalent on the adaxial surfaces of leaflets,
whereas sporulation of the late leaf spot fungus occurs more
often on the abaxial surfaces. Conidia are sometimes absent
from early leaf spot lesions but are generally present on late
Early and Late Leaf Spots leaf spot lesions. When present, conidia are often sparse and
light in color on early leaf spot lesions, but conidia on late leaf
Many of the diseases of peanut have a limited geographic spot lesions will usually be dark and borne in tight clusters
range, but the two major foliar diseases, early and late leaf arranged in concentric rings. If leaf spots are actively sporu
spots, occur wherever peanut is grown. Other common names lating, distinction between early and late leaf spot is often
for these diseases include Cercospora leaf spots, tikka leaf possible with a lOx hand lens.
spots, peanut cercosporosis, Mycosphaerella leaf spot, and Neither early nor late leaf spot is likely to be confused with
brown leaf spot. In some areas, early leaf spot is the pre other foliar diseases, but symptoms caused by certain phyto
dominant disease, and in others, late leaf spot is predominant. toxic pesticides are very similar to leaf spot symptoms. This is
For example, early leaf spot was the predominant foliar disease particularly a problem where early-season herbicides are used
of peanut in the southeastern United States during the 1960s for management of weeds or where systemic insecticides are
and 1970s, but late leaf spot predominated there during the used for thrips control. Spots caused by pesticide injury are
1980s. Recently, early leaf spot has again become predominant usually slightly lighter in color in the center, and there is no
in some areas of this region. Similar changes in the relative sporulation on the spots. Leaf spots caused by pesticide injury
incidence and importance of early and late leaf spots have been are also less clearly defined on the abaxial leaf surface.
observed in other areas of the world.
When fungicide sprays are not used, pod yield losses of up Causal Organisms
to 50% are common. Losses to late leaf spot as high as 70% Early leaf spot. The anamorph of early leaf spot, Cercos
have been recorded in research plots where the disease was not pora arachidicola S. Hori, is commonly present on lesions.
controlled. The quantitative relationship between these foliar Fruiting of C. arachidicola is amphigenous; however, conidia
diseases and pod yield loss is related to defoliation and time of form primarily on the adaxial surfaces of lesions. Stromata are
harvest, as shown in Figure 23. For a given level of defoliation, dark brown and up to 100 (im in diameter. Pale olivaceous or
pod yield loss increases with delays in harvest. yellowish brown conidiophores (15-45 x 3-6 |im) form in
dense fascicles (Fig. 24), five to many in number. Conidio
Symptoms and Signs phores are darker at the base, mostly once geniculate, un
Although the diseases are called leaf spots, the symptoms of branched, and septate. Subhyaline conidia (35-110 x 3-6 pm)
both diseases develop on petioles, stipules, stems, and even are olivaceous, obclavate, and often curved. Each has three to
pegs during the later stages of an epidemic. Lesions are first 12 septa, a truncate base, and a subacute tip (Fig. 25). The
visible about 10 days after spore deposition as small, chlorotic teleomorph of the early leaf spot pathogen, Mycosphaerella
flecks. These flecks become darker lesions, enlarging to 1-10 arachidis Deighton, as described by Jenkins, is rarely observed
mm in diameter (Plates 24 and 25). Mature, sporulating lesions on peanut.
may be apparent by about 15 days after spores are deposited.
Early and late leaf spots often look very similar on the upper
(adaxial) surfaces of leaflets, but early leaf spot usually has a
prominent yellow halo (Plate 25) that is often less conspicuous
or absent from late leaf spot lesions. The presence, absence, or
distinctiveness of a halo, however, is not a reliable character
istic for distinguishing between early and late leaf spot. On
some cultivars (e.g., Florunner) early leaf spot lesions are

% Defoliation
Fig. 23. Effects of defoliation caused by leaf spot diseases on Fig. 24. Conidiophores of Cercospora arachidicola, the cause of
yield of peanut. Note that yield loss is greater for a given level of early leaf spot, erupting from the surface of a peanut leaf. (Cour
defoliation when harvest is delayed. tesy N. Kokalis-Burelle)

17
 Late leaf spot. The anamorph Cercosporidium personation Disease Cycle
(Berk. & M. A. Curtis) Deighton is known by several other Disease cycles for early and late leaf spots are presented in
names in the literature. The most recent is Phaeoisariopsis Figure 28. Conidia produced on crop residue in the soil are the
per sonata, proposed by von Arx in 1983 on the basis of small main source of initial inoculum. However, ascospores, chla
synnemata or long conidiophores and less thickened and dark mydospores, and mycelial fragments are potential inoculum
ened, bulging scars. This name change has not been widely sources. Mycelium in lesions on stems, petioles, and pegs is
accepted, and Cercosporidium personatum is preferred. The more likely to overseason than that on leaflets and is therefore
anamorph as commonly observed on late leaf spot lesions is a probable means of survival of the leaf spot pathogens from
amphigenous with fruiting on both sides of the leaflet, but one season to the next.
sporulation is more common on the lower surface. Dense, Release of conidia of C. arachidicola is favored by temper
pseudoparenchymatous stromata are up to 130 pm in diameter atures of 20-24C when relative humidity is greater Ilian 90%.
(Fig. 26). Conidiophores (10-100 x 3.0-6.5 |jm) are numerous, Spore production is favored by long periods of leaf wetness,
pale to olivaceous brown, smooth, and one to three geniculate and epidemics are favored by temperatures greater than 19C
and have conspicuous conidial scars 2-3 fim wide. Conidia and relative humidity that exceeds 95% for extended periods.
(20-70 x 4-9 nm) are medium olivaceous, cylindrical, obcla- Conidia germinate, forming one to several germ tubes, which
vate, usually straight or only slightly curved, rounded at the enter open stomata or penetrate the epidermal cells directly.
apex, and not constricted; they have one to nine (mostly three Under favorable conditions, lesions may develop within 6-8
or four) septa, a wall that is usually finely roughened, and a days. Cercosporidium personatum produces intercellular, bo-
base shortly tapered with a conspicuous hilum (Figs. 25 and tryose haustoria, but C. arachidicola does not produce haus-
27). Conidiophores commonly form dense fascicles in con toria. Maximum late leaf spot infection occurs when temper
centric rings. The teleomorph, Mycosphaerella berkeleyi Jenk., atures are about 20C and relative humidity exceeds 93% for
like that of the early leaf spot pathogen, is rarely observed on more than 12 hr or with continuous leaf wetness periods of 10
peanut. hr. Few infections occur if temperatures are above 28 C, if
relative humidity is high for less than 12 hr, or if leaf wetness
periods are less than 10 hr. Late leaf spot lesions occur about
10-14 days after infection. Although late leaf spot usually has
a longer incubation period than early leaf spot, it may cause
more severe damage over a shorter period of time because of
the capacity of Cercosporidium personatum to produce more
spores per lesion than C. arachidicola.
Conidia are dispersed by wind, splashing water, and insects.
Peak dispersal periods for conidia occur at dew dry-off in the
morning and at the onset of rainfall. Although vertical dis
persal of C. arachidicola conidia to 2.7 m above the soil sur
face has been reported, long-distance dispersal of C. arachid
icola and Cercosporidium personatum conidia has not been
well documented.

Management
Two management strategies are employed to reduce the
threat of leaf spot epidemics. The first is to reduce initial
inoculum by crop rotation and burial of peanut crop residue
with a moldboard plow. Crop rotation for 2-3 years out of
peanut is preferred, and this alone may provide as much as a 2-
to 3-week delay in development of a leaf spot epidemic (Fig.
Fig. 25. Conidiophores and conidia of Cercospora arachidicola 29). Volunteer peanut plants in the nonhost crop should be
(top) and Cercosporidium personatum (bottom). (Reprinted, by destroyed to prevent inoculum buildup and carryover. Because
permission, from Subrahmanyam et al., 1982) of the potential for a rapid rate of increase of leaf spot diseases,
crop rotation alone is insufficient for their control.

Fig. 26. Conidiophores of Cercosporidium personatum, the cause

of late leaf spot, erupting from the surface of a peanut leaf. Fig. 27. Conidia of Cercosporidium personatum germinating on
(Courtesy N. Kokalis-Burelle) the surface of a peanut leaf. (Courtesy N. Kokalis-Burelle)

18
 The primary management strategy involves the use of tactics zole, and tebuconazole are examples of fungicides that either
that reduce the rate of spread of leaf spot diseases. Multiple have been used or are being used for management of early and
applications of fungicidal sprays (Plate 26) are usually required late leaf spots.
to keep leaf spot diseases below damaging levels. Benomyl, Fungicides are applied with tractor-mounted boom sprayers,
chlorothalonil, copper hydroxide, mancozeb, sulfur, propicona- fixed-wing aircraft, helicopters, sprinkler irrigation systems,
Sp ore s d i s s e m i n a t e d by
A w in d , s p la s h i n g w a t e r , and i ns e c ts

In fe c ti o n o f
ho s t tis su e

C o n i d io p h o r e s
on l e a f s u r f a c e

U pp e r l e a f s u r fa c e

Spores d is s e m i n a t e d by
B w in d , s p l a s h i n g w a t e r , and in s e c ts

Infection of
hos t ti s su e

C o n i d io p h o r e s on
lower l e a f s u r f a c e

I n t e r c e l l u l a r m y ce liu m
w ith h austoria y

O v e r w in t e r i n g
s ta g e s on
cr o p re s id u e

L ow er lea f s u r fa c e

Fig. 28. Disease cycles of A, early leaf spot, caused by Cercospora arachidicola, and B, late leaf spot, caused by Cercosporidium
personatum. (Prepared by Nancy Browning)

19
 and underslung spray booms on pivot irrigation systems. Gener and desirable agronomic traits have been developed, but this
ally, application volumes of 5 gallons per acre are recom resistance is nOt complete. Components of resistance to leaf
mended for aircraft and 15 or more gallons per acre for ground spot diseases that may delay disease progress under field con
sprayers. Chemigation is the least effective method because ditions include extended latent period, decreased sporulation,
less fungicide is deposited on foliage than with other methods. smaller lesions, reduced infection frequency, reduced necrotic
Disease-forecasting systems based on temperature and rela area of leaves, reduced defoliation, and fewer lesions on stems.
tive humidity, temperature and leaf wetness, or simply the The best disease-management strategy for leaf spot diseases
number of rain events and rainfall probabilities are in use in should integrate several of the above tactics into a program
some peanut-production areas. Requirements of the systems adapted to the cultivars and cultural practices of a given area.
vary from the use of an in-field, computer-controlled weather
station to a simple rain gauge. Scheduling fungicide applica Selected References
tions with a forecasting system allows applications on an as-
needed basis when environmental conditions are favorable for Nutter, F. W., Jr., and Shokes, F. M. 1995. Management of foliar dis
rapid disease development. Such methods are in contrast to the eases caused by fungi. Pages 65-73 in: Peanut Health Management.
traditional application of fungicides on a calendar schedule, H. A. Melouk and F. M. Shokes, eds. American Phytopathological
beginning at 30-40 days after planting and continuing at 10- to Society, St. Paul, MN.
Porter, D. M., Smith, D. H., and Rodriguez-Kabana, R. 1982. Peanut
14-day intervals until 14-21 days before the anticipated date of
diseases. Pages 326-410 in: Peanut Science and Technology. H. E.
harvest. Pattee and C. T. Young, eds. American Peanut Research and Edu
Indiscriminate application of fungicides for control of early cation Society, Yoakum, TX.
and late leaf spots may result in undesirable effects. For exam Shokes, F. M., and Smith, D. H. 1990. Integrated systems for man
ple, benomyl-tolerant strains of C. arachidicola and Cerco agement of peanut diseases. Pages 229-238 in: Handbook of Pest
sporidium personatum developed in the southeastern United Management in Agriculture, vol. 3. D. Pimentel, ed. CRC Press,
States within 3 years after benomyl was registered for use in Boca Raton, FL.
the United States. The use of chlorothalonil for control of foliar Smith, D. H., and Littrell, R. H. 1980. Management of peanut foliar
diseases may also increase the severity of Sclerotinia blight diseases with fungicides. Plant Dis. 64:356-361.
where that disease is a problem. In addition, some fungicides Smith, D. H., Pauer, G. D. C., and Shokes, F. M. 1992. Cerco
suppress development of twospotted spider mites, while other sporidium and Cercospora leafspots of peanut (groundnut). Pages
fungicides contribute to increased populations. 285-304 in: Plant Diseases of International Importance. Vol. 2,
New fungicides with systemic activity have been developed. Diseases of Oilseeds and Vegetable Crops. H. S. Chaube, J. Kumar,
A. N. Mukhopadhyay, and U. S. Singh, eds. Prentice Hall, Engle
In particular, the ergosterol-biosynthesis-inhibiting (EBI) fun
wood Cliffs, NJ.
gicides work well against leaf spot diseases. Propiconazole has Subrahmanyam, P., McDonald, D., and Gillons, R. W. 1982. Variation
good efficacy against early leaf spot, a little less against late in Cercosporidium personatum symptoms on certain cultivars of
leaf spot, very little against stem rot (Sclerotium rolfsii), and Arachis hypogaea. Oleagineux 37:63-67.
none against peanut rust (Puccinia arachidis). Therefore, pro
piconazole is not recommended late in the season where late (Prepared by F. M. Shokes and A. K. Culbreath)
leaf spot and/or rust is prevalent. In contrast, tebuconazole has
good efficacy against this entire spectrum of diseases. It is pos
sible to substitute an EBI for a protective fungicide for several
applications during the season and thereby control a broader
spectrum of diseases or to use lower rates of the protective
Fusarium Diseases
fungicide mixed with an EBI full-season to attain control of
foliar and some soilbome diseases of peanut. Systemic EBI Fusarium spp. are ubiquitous in the soil of peanut-growing
fungicides are not recommended_ior__.full-season_use.alojQe areas. They are commonly isolated from roots (even those of
because they may increase the risk that resistant populations of nonsusceptible plants), seed, and the hypocotyls and cotyle
the leaf spot pathogens will develop. dons of germinating seed. Fusarium spp. affect peanut plants
Partially resistant cultivars may also be used to reduce the sporadically; and until recently, Fusarium-ie.la.ted epidemics
rate of spread of leaf spot epidemics. A few high-yielding cul were rare, except for pod rots, in which Fusarium spp. are part
tivars with moderate resistance to early and/or late leaf spots of the complex of causal pathogens. Fusarium spp. of soil
bome origin frequently penetrate the pod and colonize the seed
coat.

Symptoms
In seedlings, preemergence damping-off caused by Fusarium
spp. results in the young plant roots and hypocotyls becoming
gray, water soaked, and frequently overrun by mycelium. Chla
mydospores of F. oxysporum can germinate in the rhizosphere
of young roots.
An infected seedling is stunted, the taproot becomes brown,
and the hypocotyl is quickly invaded. In an older seedling, up
to the age of about 1 month, dry rot of the taproot, caused by F.
solani, may occur and spread to secondary roots.
A syndrome of Fusarium root rot and slow wilting may
appear in adult plants. Symptoms include the folding of leaflets
against each other during dry periods, chlorosis of leaflets, and
DAYS AFTER PLANTING slight wilting. At this stage, elongate, slightly sunken, brown
lesions are found on the taproot near the crown. As the lesions
Fig. 29. Effect of crop rotation on defoliation caused by late leaf
spot. Note that when peanut follows peanut, defoliation reaches
enlarge to girdle the taproot, wilting progresses. Leaves turn,
damaging levels (about 30%) 3 -4 weeks sooner than when pea brown and die gradually. In moist soil, plants may form adven
nut is in the first year or when it follows several years of nonhost titious roots around the crown early enough to escape terminal
crops. wilting, but plant development and pod yield are impaired. In
20
 the advanced stage of the disease, all tissues near the lesions five septa and pointed ends. They are produced on phialides
are invaded by F. solani. Hyphae of this fungus are sometimes arranged sparsely or in sporodochia.
observed in vessels of the root, even at the earliest phase of
disease expression. At this stage, no other organisms can be Disease Cycle
isolated, but some appear later. Thus, F. solani has been impli Fusarium spp. live saprophytically in soil and reproduce on
cated in the cause of the disease, although inoculation tests plant debris. Conidia are abundant but short lived. Chlam'ydo-
have been inconsistent in verifying the pathogenicity of this spores are the persistent survival structures. Symptomless car
fungus. riers actively maintain Fusarium spp. during seasons when
Fusarium wilt appears sporadically in peanut fields. During nonhost crops are planted. Seedbome inoculum and hyphae
sudden wilting (Plate 27), leaves of an entire plant turn grayish sheltered in slowly disintegrating debris also carry the path
green, and during dry weather, the canopy becomes dry, brittle, ogen over from one season to another. Seedbome inoculum is
and bleached. If the wilt is less sudden, leaves turn yellow, and frequent, even on the seed coats of sound seed from sound pods.
sometimes plants are defoliated before death. In both cases, Injury to seed predisposes seedlings to Fusarium spp. that
taproots show vascular browning; however, secondary roots are in soil and carried on the seed coat. Epidemics of seedling
and rootlets appear healthy. These symptoms, in particular the damping-off, and the resulting poor stands, occur when soil
sudden wilting, implicate F. oxysporum in the peanut wilt temperatures are too low for rapid emergence. If in addition
complex. soils are wet and insufficiently drained, seed may decay at the
Peg lesions usually develop on the underground part of the beginning of germination.
peg, mainly near the soil line, where the high soil temperatures Injury to roots predisposes seedlings to infection by Fusar
that often prevail can injure the epidermal cells of the pegs and ium i spp. Slow wilting most seriously affects young plants
predispose them to soil-inhabiting fungi. Wound parasites, in during hot, dry weather. Without water stress, damage levels
cluding some Fusarium spp., can be isolated from the lesions, are low.
which may girdle and rot the peg. As a result, the peg tissues Fusarium spp. are facultative xerophytes that can grow ac
weaken and pods separate from the plant at harvest and are tively under dry conditions. Nevertheless, moist soil enhances
lost.
Pod diseases may take the form of pod blight, pod rots, or
external blemishes. Pod blight affects primordial, (i.e., very
young) pods. F. solani and F. scirpi are two of a series of fungi
that have been isolated from blighted pods soon after peg
penetration of the soil. Both species are pathogenic to young
pods. Pod blight is considered a cause of death of many pri
mordial pods that die early in their development.
Maturing pods affected by a dry rot attributed to various
Fusarium spp. may show grayish, pinkish, or whitish violet
coloration (Plate 28). However, these visible symptoms are not
proof of the presence of Fusarium spp., nor are they proof that
a Fusarium sp. is the major causal organism. In Libya, F.
solani and F. scirpi have been reported as the causes of a simi
lar pod rot.
External blemishes of the shell and seed coat on whole, ma
ture pods may be caused by a variety of fungi, including F.
solani and F. oxysporum. Under controlled conditions, only F.
oxysporum incited this symptom.
A common and. devastating pod rot, commonly referred to as
peanut pod rot complex, is thought to be caused by several Fig. 30. Chlamydospores of Fusarium solani. (Courtesy Fusarium
pathogens including Rhizoctonia spp. (see Peanut Pod Rot Research Center, Department of Plant Pathology, The Pennsyl
Complex) and the Pythium disease complex (see Pythium Dis vania State University, University Park)
eases). F. solani plays a role in the development of this rot,
both as a predisposing factor and as one of the saprophytic
microflora that aggravate the final breakdown of the pod. F.
solani alone is unable to cause an epidemic. Pods affected by
the pod rot complex typically have coalescing (confluent)
chocolate brown dots and spots.

Causal Organisms
About 17 species and varieties of Fusarium have been iso
lated from the soil around peanut roots or pods and from the
root, collar, pegs, and pods, including shells and seed. Of
these, only members or close relatives of the following species
have been reported as responsible for peanut diseases: 1) F.
solani (Mart.) Sacc., in particular F. solani f. sp. phaseoli
(Burkholder) W. C. Snyder & H. N. Hans.; 2) F. oxysporum
Schlechtend.:Fr.; 3) F. equiseti (Corda) Sacc. and F. scirpi
Lambotta & Fautrey; 4) F. tricinctum (Corda) Sacc.; 5) F.
moniliforme J. Sheld.; and 6) F. avenaceum (Fr.:Fr.) Sacc.
All Fusarium spp. produce microconidia, macroconidia, and
chlamydospores. Chlamydospores (7-11 |jm in diameter) are
borne singly or in chains (Fig. 30). Microconidia (5-12 x 2-3.5 Fig. 31. Macroconidia and microconidia of Fusarium solani. (Cour
pm) are hyaline, nonseptate, and oval to ellipsoid or cylindrical tesy Fusarium Research Center, Department of Plant Pathology,
(Fig. 31). Macroconidia (Figs. 31-33) are hyaline with three to The Pennsylvania State University, University Park)

21
 duration and of subsequent drainage and drying of the topsoil
than do other irrigation methods. Infrequent irrigation with
adequate amounts of water are preferable to frequent irrigation
with smaller amounts because the former regime allows the
topsoil, which contains the pods, to dry.
Soil treatments with sublethal doses of the biocide metham
sodium and solarization (solar pasteurization beneath trans
parent tarps) selectively reduce soil fungal populations. These
treatments reduce Fusarium populations and increase total pod
yield, apparently by reducing the incidence of peg blight and
pod rot.
Breeding for resistance to peanut diseases caused by Fusar
ium spp. has not been systematically pursued. However, the
rarity of epidemics caused by Fusarium spp. in peanut suggests
that in field nurseries, Fusarium-diseased plants either die or
are discarded; thus, lines selected on the basis of other char
acteristics have incidentally been given field resistance to
several Fusarium spp.

Fig. 32. Macroconida of Fusarium roseum. (Courtesy Fusarium

Research Center, Department of Plant Pathology, The Pennsyl Selected References
vania State University, University Park)
Frank, Z. R. 1972. Pythium myriotylum and Fusarium solani as
cofactors in a pod-rot complex of peanut. Phytopathology 62:1331-
1334.
Garcia, R., and Mitchell, D. J. 1975. Interactions of Pythium myrio
tylum with Fusarium solani, Rhizoctonia solani, and Meloidogyne
arenaria in pre-emergence damping-off of peanut. Plant Dis. Rep.
59:665-669.
Jackson, C. R.. and Bell, D. K. 1969. Diseases of peanut (groundnut)
caused by fungi. Ga. Agric. Exp. Stn. Res. Bull. 56.
Joffe, A. Z. 1973. Fusarium species on groundnut kernels and in
groundnut soils. Plant Soil 38:439-446.
Porter, D. M., Smith, D. H., and Rodriguez-Kabana, R. 1982. Peanut
diseases. Pages 326-410 in: Peanut Science and Technology. H. E.
Pattee and C. T. Young, eds. American Peanut Research and Edu
cation Society, Yoakum, TX.

(Prepared by Z. R. Frank and Y. Ben-Yephet)

Melanosis
Fig. 33. Macroconidia of Fusarium oxysporum. (Courtesy Fusar
ium Research Center, Department of Plant Pathology, The Penn Melanosis of peanut leaves has been reported in Argentina
sylvania State University, University Park) and is referred to as Stemphylium leaf spot in the United
States.

pod rot, possibly because of poor soil aeration (the shortage of Symptoms
oxygen predisposes the pod to pathogens, including Fusarium Lesions are dark brown, 0.5-1.0 mm in diameter, and usual
spp.). ly circular. Solitary or confluent, they appear only on the abax
Under continuous peanut cultivation, the population densi ial leaflet surface and are at first slightly submerged but later
ties of Fusarium spp. in the soil increase considerably. This become raised and crustlike.
abundance in the soil is rarely accompanied by a disease epi
demic, with the exception of pod rots. Causal Organism
The causal organism, Stemphylium botryosum Wallr., pro
Control
duces spores that are terminal, solitary, muriform, pale to dark
Fusarium spp. have been isolated from hypocotyls and brown to olivaceous, and sometimes minutely verruculose or
cotyledons of fimgicide-treated seed. Seed dressings are not echinulate. They are borne on conidiophores with terminal
highly efficient against Fusarium spp., but they significantly swellings, which become, through percurrent proliferation,
reduce damping-off diseases because of their effect on other intercalary.
pathogens.
Crop rotation may retard a quick buildup of Fusarium propa
gules; nevertheless, it does not efficiently reduce populations Selected Reference
of the fungus enough to avert Fusarium-incited diseases.
Avoiding peanut cultivation in poor, acid soils and improv Farr, D. F., Bills, G. F., Chamuris, G. P., and Rossman, A. Y. 1989.
ing general soil fertility by organic amendments (manure) may Fungi on Plants and Plant Products in the United States. American
reduce incidence of Fusarium-incited root rot. Phytopathological Society, St. Paul, MN. p. 976.
Cultivation in well-drained soil will minimize pod rots. Over
head irrigation permits better control of irrigation intensity and (Prepared by R. A. Taber and D. H. Smith)

22
 Myrothecium Leaf Blight
A leaf blight of peanut caused by Myrothecium roridum has
been observed in Lidia and Thailand. M. gramineum has also
been reported as a leaf blight pathogen in India. Both patho
gens infect a wide range of host plants.

Symptoms
The two pathogens produce similar symptoms on infected
peanut leaves. Lesions are round to irregular, 5-10 mm in
diameter, with tan centers and brown margins surrounded by
chlorotic halos. The centers of these lesions become thin,
papery, and light tan. Lesions coalesce to give affected leaves a
blighted appearance. Abundant olive green to black fruiting
bodies, often arranged in circular rings, are formed on necrotic
areas of both leaf surfaces (Plate 29).

Causal Organisms
The conidia of M. roridum Tode:Fr. are hyaline, one celled, Fig: 34. Endospores of Olpidium brassicae with typical stellate
elongated, and 4.7-11.7 x 1.2-3.5 pm. Conidia of M. gramin wall surfaces.
eum lib . are 5.5-14.0 x 3.0-5.0 |im with stiff, acute setae
mixed with smaller, torsive ones.
in size (8-32 |im in diameter) with a single exit tube. Resting
Selected Reference spores are spherical (10-27 |jm in diameter) and consist of
thick, stellate exospores and thin, smooth endospores (Fig. 34).
Mahrshi, R. P. 1983. Myrothecium gramineumA new report on Zoospores are spherical and have a single posterior, whiplash
groundnut from Rajasthan. Indian Phytopathol. 36:728. flagellum.
O. brassicae is widely distributed, particularly in temperate
(Prepared by P. Subrahmanyam) regions. It is parasitic on roots of several phanerogams and is a
vector of several soilbome plant viruses.

Neocosmospora Foot Rot Selected Reference

Subrahmanyam, P., and McDonald, D. 1980. Occurrence of Olpidium

Foot rot has been observed in peanuts in Taiwan and South brassicae on groundnut. Trans. Br. Mycol. Soc. 75:506-509.
Africa, The causal organism, Neocosmospora vasinfecta E. F.
Sm., has been observed colonizing aboveground plant parts and (Prepared by P. Subrahmanyam)
is also pathogenic to pod hulls and seed. Pods exhibit discolored
internal tissues and later decompose. Diseased plants are stunted
with yellow lower leaves and frequently defoliate and senesce
prematurely. There are no control measures available. Peanut Pod Rot Complex
Selected References Peanut pod rot (pod breakdown) is a sporadic but common
disease of peanut that causes serious losses throughout all pea
Baard, S. W., and Van Wyk, P. S. 1985. Neocosmospora vasinfecta
nut-growing regions of the world. In 1954, the condition was
pathogenic to groundnuts in South Africa. Phytophylactica 17:49-
described in Georgia as black pod, and it has been prevalent in
50.
Huang, J. W., Chen, S. S., and Chung, W. C. 1992. Neocosmospora Israel since 1959. In 1964, a preharvest pod (fruit) rot of pea
foot rot of peanut in Taiwan. Plant Pathol. Bull. 1:203-205. nut in Virginia was described and referred to as pod break
down. Others have since referred to what appears to be the
(Prepared by D. M. Porter) same malady as the peanut pod rot complex. Losses are varia
ble and appear to be related to cultivar, the pathogen involved,
and nutrition.
Olpidium Root Discoloration Symptoms
Symptoms of the pod rot disease complex vary depending on
Root discoloration of peanut caused by Olpidium brassicae the location, season, and pathogens involved. Deterioration or rot
has been reported in the Indian states of Andhra Pradesh, of fully developed pods is the first sign of disease. Pods develop
Gujarat, and Punjab and in Texas in the United States. either a tan to brown, dry decay or a greasy, black, wet decay,
depending on the pathogens and environmental conditions (Plate
Symptoms 30). Many pods, both sound and rotted, may remain in the soil
Lightly infected roots remain apparently healthy, but when after digging, the result of weakened or decayed pegs.
infection is advanced, the root cortex becomes brown to black. There are no aboveground symptoms of pod rot, except that
The pathogen is restricted to the peripheral layers of the cortex severely affected plants may be darker green and exhibit pro
of infected roots. longed flowering. The root system generally is not infected,
and the reduced demand for carbohydrate from the loss of the
Causal Organism fruit usually increases the vigor of the foliage. Plants with the
Plasmodia of O. brassicae (Woronin) P. A. Dang, are thin greatest degree of pod rot at or near harvest will appear to be
walled, cylindrical to rounded, and 10-22 x 15^45 |im and the most vigorous and provide no indication of serious disease
have densely granulated protoplasm. Zoosporangia are variable losses below the soil surface.
23
Causal Organisms were found among treatments for soil populations or isolation
This overview of the peanut pod rot disease complex focuses frequency from decaying pods. Plots treated with a calcium
on Pythium myriotylum Drechs., Rhizoctonia solani Kuhn, and source were generally higher in pod yield and grade and
Fusarium solani (Mart.) Sacc., since there is considerable evi exhibited a lower incidence of pod rot. There was a positive
dence indicating that the complex involves these three fungal correlation between the concentrations of most elements in
species. In Libya, pod rot is caused mainly by F. solani and pods and pod rot, except in the case of calcium, for which con
other Fusarium spp. Fusarium spp. have been implicated in centration was negatively correlated with amount of pod rot.
Pythium-Rhizoctonia pod rot in the United States. In Virginia, The key factor in the reduction of peanut pod rot (pod
Fusarium spp. have been reported to precede P. myriotylum. A breakdown) in the studies conducted in Virginia and Georgia
three-step progression of the pod rot complex has been was the increased concentration of calcium in the pods. In
described in Israel. In step 1, F. solani predisposes pods to Texas, where high sodium levels exist in the water, pod rot of
sporadic infection by P. myriotylum. Step 2 involves pod peanut can be reduced with applications of gypsum. Although
colonization by P. myriotylum and a rapid increase in pod rot. water relations in the peanut pod rot system have not been
In step 3, F. solani and saprophytic organisms cause the dis studied extensively, it is well accepted that calcium must be in
integration of pods and there is a sharp reduction or disap an aqueous form to be absorbed by the fruit. Since peanut pods
pearance of P. myriotylum. develop in the soil, they could be very susceptible to coloniza
Soil fauna often plays an important role in the pod rot com tion by microorganisms after predisposition by a nutrient im
plex. The feeding of insects and nematodes impacts the severity balance or deficiency. Striking similarities between the peanut
of pod rot caused by P. myriotylum, R. solani, and F. solani. In pod rot complex and blossom-end rot of tomato and pepper are
studies conducted in Texas, pod damage was influenced by the evident.
feeding of insect larvae. In Virginia, pods injured by larvae of
the southern com rootworm (Diabrotica undecimpunctata how- Control
ardi Barber) were more susceptible than uninjured pods to in Current recommendations for control of the pod rot com
fection by various fungi. In Florida, pods exposed to moderate, plex in the eastern United States include high rates of gyp
combined inoculum levels of the peanut root-knot nematode sum applied at flowering time. Nutritional imbalances in the
(Meloidogyne arenaria (Neal) Chitwood) and P. myriotylum pod-development zone are discouraged. Large-seed peanuts
sustained 31% more decay than those exposed to P. myriotylum tend to be more susceptible than small-seed cultivars. Pesti
alone. In North Carolina, soil mites (Caloglyphus spp.) were cides such as pentachloronitrobenzene (PCNB) and metal-
associated with more than 50% of decaying pods where P. axyl, which have activity on Rhizoctonia and Pythium spp.,
myriotylum was the primary fungal pathogen. respectively, are being used. Although chemicals such as
PCNB and metalaxyl have sometimes been recommended for
Nutrition the management of pod rot, little or no economic gain has
The severity of pod rot associated with the pod rot complex been demonstrated.
appears to be related to the presence of a specific pathogen or
multiple pathogens and a wide range of environmental factors, Selected References
such as the presence or absence of a specific plant nutrient.
The first symptoms of peanut pod rot complex include a col Alva, A. K., Gascho, G. J., and Yang Guang. 1989. Gypsum material
lapse of pod tissues, which are usually attacked by various soil effects on peanut and soil calcium. Commun. Soil Sci. Plant Anal.
fungi causing the characteristic dark discoloration of the pod. 20:1727-1744.
The pod rot complex appears to be more common on large- Csinos, A. S., and Gaines, T. P. 1986. Peanut pod rot complex: A
geocarposphere nutrient imbalance. Plant Dis. 70:525-529.
seeded Virginia peanuts than on the smaller-seeded runner and
Csinos, A. S., Gaines, T. P., and Walker, M. E. 1984. Involvement of
spanish types. Large amounts (2 t/ha) of gypsum (CaS04- nutrition and fungi in the peanut pod rot complex. Plant Dis. 68:61-
2H20 ) applied to peanuts at bloom significantly reduces the 65.
severity of pod breakdown and maximizes pod yield. High Filonow, A. B., Melouk, H. A., Martin, M., and Sherwood, J. 1988.
rates of gypsum (1-3 t/ha) applied to Virginia Bunch 46-2 also Effect of calcium sulfate on pod rot of peanut. Plant Dis. 72:589-
reduced pod breakdown in 2 of 3 years and increased pod 593.
yields and the percentage of sound, mature seed. Gypsum in Frank, Z. R. 1972. Pythium myriotylum and Fusarium solani as cofac
creases the amount of calcium and decreases the amount of tors in a pod-rot complex of peanut. Phytopathology 62:1331-1334.
potassium in pods. Applications of M gS04 (1.3 t/ha) and Garcia, R., and Mitchell, D. J. 1975. Interactions of Pythium myrio
K2S 0 4 (1-2 t/ha) increase pod breakdown and the amount of tylum with several fungi in peanut pod rot. Phytopathology 65:
potassium in pods but decrease or tend to decrease pod yield 1375-1381.
and calcium levels in pods. The vulnerability to pod-break- Garren, K. H. 1964. Landplaster and soil rot of peanut pods in
down pathogens is reduced in pods containing 0.20% or more Virginia. Plant Dis. Rep. 48:349-352.
Garren, K. H. 1970. Rhizoctonia solani versus Pythium myriotylum as
calcium. However, similar treatments of gypsum did not sup
pathogens of peanut pod breakdown. Plant Dis. Rep. 54:840-843:
press pod rot in Oklahoma.
Hallock, D. L. 1962. Effect of time and rate of fertilizer application
Studies have been conducted in Georgia to determine the on yield and seed-size of jumbo runner peanuts. Agron. J. 54:428-
effects of peanut cultivar and rate of gypsum on pod rot in soils 430.
naturally low and naturally high in calcium. Pod rot did not Porter, D. M., Smith, D. H., and Rodriguez-Kabana, R. 1982. Peanut
occur on any cultivar in any treatment in the high-calcium soil. plant diseases: Soilborne diseases. Pages 348-378 in: Peanut Sci
In the low-calcium soil, severe pod rot occurred on plots receiv ence and Technology. H. E. Pattee and C. T. Young, eds. American
ing no gypsum, but the severity decreased for all cultivars as Peanut Research and Education Society, Yoakum, TX.
the rate of gypsum increased. Cultivars with high calcium
requirements (e.g., Early Bunch) were more susceptible to pod (Prepared by A. S. Csinos and D. K. Bell)
rot than cultivars less dependent on calcium fertilization (e.g.,
Florunner).
An evaluation of pathogen-specific fungicides for the control
of the pod rot complex pathogens failed to distinguish which Pepper Spot and Leaf Scorch
pathogen was involved. Although Pythium, Rhizoctonia, and
Fusarium spp. were isolated from soil and decaying pods and Pepper spot and leaf scorch have been reported in Angola,
pegs throughout the growing season, no consistent differences Argentina, Burkina Faso, India, Madagascar, Malawi, Maur
24
itius, Mozambique, Niger, Senegal, Swaziland, Thailand, Selected References
Taiwan, Uganda, the United States, Vietnam, Zambia, and Zim
babwe. The diseases do not usually contribute to pod yield Graham, J. H., and Luttrell, E. S. 1961. Species of Leptosphaerulina
losses. on forage plants. Phytopathology 51:680-693.
Jackson, C. R., and Bell, D. K. 1968. Leptosphaerulina crassiasca
(Sechet) Comb. Nov., the cause of leaf scorch and pepper sppt of
Symptoms peanut. Oleagineux 23:387-388.
Pepper spot lesions are dark brown or black (Plate 31), less Pettit, R. E., Taber, R. A., and Harrison, A. L. 1968. Leptdsphaeru-
than 1.0 mm in diameter, and irregular to circular and may be lina-Cercospora complex on peanuts in Texas. (Abstr.) Phyto
depressed. They form on the adaxial leaf surface and slowly pathology 58:1063.
enlarge. Porter, D. M., Garren, K. H., Mozingo, R. W., and van Schaik, P. H.
Leaf scorch (Plate 32) usually appears at the leaflet apex, 1971. Susceptibility of peanuts to Leptosphaerulina crassiasca
followed by the development of a wedge-shaped lesion with under field conditions. Plant Dis. Rep. 55:530-532.
Subrahmanyam, P., and Smith, D. H. 1991. Variability in patho
a vivid yellow zone adjacent to its advancing margin. Le
genicity and symptomatology of Leptosphaerulina crassiasca on
sions caused by Cercospora arachidicola or Cercosporidium peanut. Plant Dis. 75:1266-1269.
personatum are sometimes observed in necrotic areas of
tissue. Therefore, it appears that Leptosphaerulina crassiasca (Prepared by D. H. Smith and R. A. Taber)
is well adapted to secondary colonization of peanut leaf
tissue.

Causal Organism
L. crassiasca (Sechet) C. R. Jackson & D. K. Bell is the
causal pathogen of both conditions. Only the teleomorphic
state of this homothallic fungus has been reported. Mycelial
hyphae are septate with uninucleate cells that give rise to fer
tile hyphae with binucleate or multinucleate cells. Asci contain
eight ascospores, which are initially uninucleate. Mature asco
spores are multinucleate with three to five transverse septa and
zero to two longitudinal septa. The asComa is a uniloculate
pseudothecium with a papillate, ostiolar neck. Asci are bituni-
cate, and ascoma ontogeny is typical of the Dothidea type of
development.
Pseudothecia (Fig. 35) contain eight to 20 asci, each 50-80 x
25-55 |om. Ascospores (23-40 x, 11-17 |im) are oblong to
ellipsoidal, hyaline, and pale yellow to light brown at maturity
(Figs. 36 and 37)

Disease Cycle '

Pseudothecia form abundantly in necrotic leaf tissue. Peak
dispersal periods of forcibly ejected ascospores occur at the
end of the dew period and at the Onset of rainfall. Germ tubes
form appressoria with subsequent direct penetration of epi
dermal cells.

Control
Leaf scorch and pepper spot are controlled quite effectively
with fungicides such as chlorothalonil.
Fig. 36. Ascospores of Leptosphaerulina crassiasca. (Reprinted
from Graham and Luttrell, 1961)

Fig. 35. Pseudothecia of Leptosphaerulina crassiasca. Fig. 37. Germinating ascospores of Leptosphaerulina crassiasca.

25
 Sympitoms
Pestalotiopsis Leaf Spot Parallel rows of pycnidia develop on dead peanut stems
infected with Phomopsis sp. The stems become blackened. A
Pestalotiopsis leaf spot has been observed on peanut leaves scorch symptom similar to that of Leptosphaerulina leaf scorch is
in India. often observed on the leaflets. Phomopsis spp. are often isolated
from lesions caused by other fungi such as Colletotrichum sp.,
Symptoms Cercospora arachidicola, and Cercosporidium personata.
Lesions are dark brown and circular. They are surrounded by
yellow halos and are commonly restricted to either side of the Causal Organism
midrib. Acervuli containing the dark conidia form near the Phomopsis sojae Lehman is the causal organism. Conidio-
center of diseased tissue. mata are eustromatic and separate or aggregated to confluent
and have short, ostiolate beaks. Two forms of conidia are pro
Causal Organisms duced. Alpha conidia (4.5-9.8 x 1.1-3.9 |im) are one celled,
Two species, Pestalotiopsis arachidis Satya and P. neglecta hyaline, rounded at both ends, and usually biguttulate. Beta
Thuem., have been reported in India. The distinction between conidia (9-27 x 0.8-1.8 (im) are long, filiform, nonseptate, and
these species and the genus description are incomplete. Co straight or more often hamate.
nidia have four septa and are fusiform, tapering to the base,
with hyaline appendages. Selected References

Frezzi, M. J. 1955. Quemadura de las hojas causada por Lepto

Selected Reference
sphaerulina arachidicola y otros hongos, en manies silvestres
(grupo rizomatoso) de distinta procedencia. Rev. Invest. Agropecu.
Gupta, D. K. 1988. New host records from India. Indian Phytopathol. Ser. 5. 2:13-24.
41:506. Jackson, C. R., and Bell, D. K. 1969. Diseases of peanut (groundnut)
caused by fungi. Ga. Agric. Exp. Stn. Bull. 56.
(Prepared by R. A. Taber and D. H. Smith)
(Prepared by R. A. Taber and D. H. Smith)

Phanerochaete omnivora
Phyllosticta Leaf Spot
A yellow orange, resupinate, hydnaceous basidiomycete has
been observed on peanut plants and soil in several counties in Phyllosticta leaf spot occurs in many countries, including the
Texas. Basidiocarps were commonly effused and poorly devel United States, Pakistan, India, China, Niger, Burkina Faso,
oped in patches; however, weather conditions during the 1989 Thailand, and the Philippines. Occasionally, it is destructive in
growing season were favorable for extensive development of Argentina and Zimbabwe.
the fungus. It sporulated profusely on plants diagnosed to be
infected with cotton root rot as well as plants not exhibiting Symptoms
symptoms of this disease. It was identified as Phanerochaete Lesions (0.5-5 mm) are usually circular and have reddish
omnivora (Shear) Burdsall & Nakasone, a fungus that is sapro brown borders with light brown to tan centers (Plate 33). The
phytic on wood in the forests and desert areas of the southwest light center often drops out with age, and then the lesion appears
and is associated with a white rot of hardwoods. This is the as a shot-hole.
first report of its being associated with. an_berbaceous_plant.
Although the orange teeth and rhizomorphs of the south Texas Causal Organisms
isolates resemble those of P. chrysorhiza (Torr.) Budington & Phyllosticta arachidis-hypogaea V. G. Rao forms scattered,
R. L. Gilbertson, an eastern species, the micromorphology dark brown pycnidia (Plate 34), which are spherical, thick
(including basidiospore size and ability to grow at 36C) is walled, and 69.3-172.3 |_im in diameter. Conidiospores (5.2-
characteristic of P. omnivora. Rhizomorphs of the fungus ex 6.9 x 2.2-3.2 |im) are elongate, hyaline, and nonseptate.
tend down into the soil for several feet. The fungus appears to P. sojaecola C. Massal. forms numerous pycnidia (105-175
be superficial on the surface of the plant, although pathoge (jm) in concentric circles. Conidiospores (7.1-9.8 x 2.1-3.2
nicity studies are incomplete. |im) are hyaline and ellipsoid or claviform.

Selected References
Control
Fungicides applied for early and late leaf spot control often
Burdsall, H. H. 1985. A contribution to the taxonomy of the genus control Phyllosticta leaf spot.
Phanerochaete. Mycol. Mem. 10.
Taber, R. A., Smith, D. H., Burdsall, H. H., Jr., Black, M. C., and Selected References
Crumley, C. R. 1990. Association of Phanerochaete with peanut in
Texas. (Abstr.) Phytopathology 80:438. Jackson, C. R., and Bell, D. K. 1969. Diseases of peanut (groundnut)
caused by fungi. Ga. Agric. Exp. Stn. Bull. 56.
(Prepared by R. A. Taber) Patil, A. S, 1987. Leaf spot of groundnut caused by Phyllosticta
arachidis-hypogaea Rao in Maharashtra state, India. J. Maharash
tra Agric. Univ. 12:205-209.
Subrahmanyam, P., Bose, J., Hassane, H., Smith, D. H., Mounkaila,
A., Ndunguru, B. J., and Sankara, P. 1992. Groundnut diseases in
Phomopsis Blight Niger and Burkina Faso. Oleagineux 47:119-133.
Zhang, M., and Wang, Y. X. 1991. Effect of agricultural antibiotic
120 against peanut Phoma blight (caused by Phyllosticta sp.). Chin.
Phomopsis leaf and stem diseases have been reported in the J. Biol. Control 7:175-176.
United States, and a leaf scorch caused by a Phomopsis sp. has
been reported in Argentina. (Prepared by R. A. Taber and D. H. Smith)

26
 Phymatotrichum Root Rot Pythium Diseases
Phymatotrichum root rot of peanut, which occurs in the cal Several species of Pythium may cause pod breakdown (pod
careous soils of the southwestern United States and Mexico, is rot), preemergence and postemergence damping-off, vascular
reported under the names Phymatotrichum root rot, cotton root wilt, and root rot diseases of peanut. All species are cosmo
rot, and Ozonium root rot. It is not widespread in the South politan in soils and attack a wide range of crop plants.
west because peanut is not often cultivated in calcareous soils. Pod breakdown (Plate 37), a term used to describe an in-soil
rot of pods, is usually called pod rot. The disease is widespread
Symptoms in peanut-growing areas of the world, often causing economic
Wilted plants with attached leaves first occur in small, losses. Such losses caused by Pythium spp. may be 0-80% but
scattered patches. Patches enlarge, with newly wilted plants are difficult to define, since infection by these pathogens usu
occurring at the leading edges of diseased areas. The taproots ally does not result in well-defined, aboveground symptoms. P.
of affected plants are severely decayed. The surfaces of de myriotylum is considered the major pod-rotting pathogen in
cayed roots are frequently covered with tan to light brown North Carolina, Virginia, and other peanut-growing areas.
mycelial strands (rhizomorphs). Diseased areas may expand to However, several pathogens, including Pythium spp., Rhizoc-
up to an acre in size. Tan to buff-colored spore mats often toriia solani, and Fusarium solani, can cause pod breakdown
appear on the soil surface at the edges of diseased areas after singly or in combination, i.e., in a pod breakdown complex. A
rain, but these are transient and dissipate after 2-3 days. complex involving P. myriotylum and F. solani is necessary for
pod rotting to occur in Israel. Similar synergistic interactions
Causal Organism also were noted with pathogens isolated from peanuts in
Phymatotrichum omnivorum Duggar (syn. Phymatotrichop- Florida. In Israel, Pythium spp. are thought to precede Fusar
sis omnivora (Duggar) Hennebert) produces rhizomorphs on ium spp. in the pod rot complex, whereas in the United States,
infected roots and conidia in spore mats. Rhizomorphs and Fusarium spp. reportedly precede Pythium spp. A more com
acicular (cruciform) hyphae are useful for identification of this plete discussion of the etiology of pod rot is found in the
fungal pathogen (Plate 35). Globose, single-celled conidia are section Peanut Pod Rot Complex.
45-55 (jm in diameter (Plate 36). Hydnum omnivorum Shear Environmental conditions are frequently important, in deter
and Sistotrema brinkmannii (Bres.) J. Eriksson are reported to mining the severity of preemergence and postemergence
be teleomorphs of this fungus. P. omnivorum sclerotia are damping-off, vascular wilt, and root rot alone or in combina
present in soil at depths of 30-75 cm. tion. P. myriotylum isolates vary widely in virulence as well as
in differential pathogenicity to seedlings, roots, and pods of
Disease Cycle peanut cultivars. P. myriotylum is generally considered a
P. omnivorum survives in soil as sclerotia for many years warm-soil pathogen that is favored by constantly moist soil
and is well adapted for survival in alkaline, poorly aerated, conditions; however, pod rot epidemics have been observed in
black clay soil. It survives also on weed hosts. However, it soil drier than the wilting range for mesophytes.
does not survive at temperatures below 0C. Propagules of this
pathogen can be disseminated with farm equipment. Symptoms
In preemergence or early postemergence rot of peanut seed
Control lings caused by P. myriotylum, the predominant symptoms
Partial disease management is possible with deep plowing include a black root rot, in which the roots are rapidly decayed,
and crop rotation with grain sorghum. Fungicides are not effec and the collapse of the top of the plant, generally without
tive for management of Phymatotrichum root rot. Peanut and apparent invasion of the stem above the ground. The* cotyle
other susceptible crops such as alfalfa and cotton should not be dons and primary roots are often covered with a loose, white
planted in infested fields. mycelial mat if moisture is available. Seedlings that emerge are
stunted; leaves are light green and rapidly become necrotic.
Selected Reference Root systems are water soaked and clumped. Cortical tissues
Lyda, S. D. 1978. Ecology of Phymatotrichum omnivorum. Annu.
Rev. Phytopathol. 16:193-209.
(Prepared by D. H. Smith)

Powdery Mildew
Powdery mildew (Fig. 38) has been observed on peanut in
India, Israel, Mauritius, Portugal, and Tanzania. The causal
pathogen, Oidium arachidis Chorin, is limited mainly to the
adaxial leaf surface. Oidia are 3 1 ^ 4 x 13-15 (im. Conidio
phores produce one to two oidia under drought stress condi
tions, but chains of three or four oidia develop under humid
and calm conditions. Subspherical, pyriform haustoria form in
epidermal cells. Rapid development of powdery mildew at
25C has been reported in Israel.

Selected Reference

Chorin, M., and Frank, Z. 1966. Oidium arachidis Chorin, powdery

mildew of groundnut foliage. Isr. J. Bot. 15:133-137.
Fig. 38. Powdery mildew on an upper leaf surface. (Reprinted, by
(Prepared by D. H. Smith) permission, from Chorin and Frank, 1966)

27
rapidly become brown and disintegrate, leaving a nonfunc range, including grass crops used in rotation with peanut. The
tional vascular skeleton. incidence of pod rot and the population density of Pythium spp.
Fibrous roots are especially susceptible to decay by P. in soil, however, are significantly higher in fields in which
myriotylum.-, however, all root tissues and nodules can be peanut is grown successively than in fields in which crops are
infected and ultimately turn dark brown to black during decay rotated.
(Fig. 39). The total root system usually is greatly reduced by Oospores are the primary survival structures of P. myrio
deterioration of lateral and branch roots. Cortical tissues dis tylum in soil. Zoospores and sporangia are short lived. Mycelia
integrate and slough off readily, leaving a fragmented, non of P. myriotylum, produced by zoospores or germination of
functional vascular system. Plants with root rot generally are oospores, form appressoria and directly penetrate epidermal
stunted and readily wilt during moisture stress. Wilted plants cells of peanut pods (Fig. 41). Penetration occurs in 2 hr at 30-
may recover turgidity and outgrow the disease if conditions are 34C, but no penetration occurs below 25C.
conducive to growth. Pythium spp. are not restricted in their ability to infect
Occasionally, peanut plants without obvious Pythium root peanut tissues but vary in pathogenic ability when infecting
rot symptoms wilt suddenly (Plate 38) and quickly die. Shortly diverse tissues. Pathogenic ability is also variable within
after the appearance of wilt symptoms, leaflets become chlo- species. Infection of plant tissue by Pythium spp. is influenced
rotic or light green. Leaflet margins pucker, and adaxial curling by soil moisture, soil temperature, pH, cation composition,
or rolling occurs, starting at the apical end of the leaflet. Some light, the presence of other organisms, and inoculum density.
leaflets eventually fold, turn brown gradually, and shed pre The optimum temperature for mycelial growth of P. myrio
maturely. Plants with these symptoms usually have some evi tylum is 35C. In Florida, inoculum densities of 1543 oo
dence of root deterioration. In addition, in advanced stages of spores per gram of soil resulted in 50% infection of peanut
infection, the vascular tissue of the taproot is dark brown from roots by P. myriotylum. In Oklahoma, preplant densities of
the tip to several centimeters into the stem. The discoloration three to 20 oospores per gram of soil were reported to have
extends into the primary and lateral branches of the stem and, increased approximately 100-fold after 67 days; populations
in some cases, may be found in the vascular tissue of the then declined to approximately 30 oospores per gram of soil at
petioles. Pods usually rot on plants that wilt early in the season harvest time. Although seven cultivars tested in Oklahoma
but not on plants that wilt later. varied in their susceptibility to infection by Pythium spp., no
effect was noted when cultivars and mean pathogen population
Causal Organisms were compared over a whole season. Use of the soil fungicide
Although P. myriotylum Drechs. is the dominant pathogen metalaxyl was reported to suppress Pythium population peaks
associated with peanut disorders caused by Pythium, other at midseason, but disease incidence and final inoculum density
species, including P. aphanidermatum (Edson) Fitzp., P. debary- were nOt significantly reduced at harvest
anum Auct. non R. Hesse, P. irregulare Buisman, and P. A significant positive correlation between increasing soil
ultimum Trow, also are pathogenic to the peanut. moisture and incidence of Pythium pod rot has been demon-
Pythium spp. are characterized by the presence of coenocytic
mycelium, from which develop asexual reproductive structures
(sporangia) that differ in size and shape among species (Fig.
40). The sporangia of P. myriotylum may be terminal or inter
calary and may consist of simple or branched portions of my-
celia. Sporangia germinate by producing either a germ tube or
zoospores. Smooth-walled oogonia (average diameter 26.5 |im)
are produced abundantly and borne most often on hyphal tips.
Antheridia, usually three to six per oogonium, are declinous
and crook necked. Oospores (12-37 |j.m in diameter) do not fill
the oogonium. Each has a single reserve globule, a wall up to
2 pm thick, and pale golden contents.

Disease Cycle
Species of Pythium naturally inhabit the soil and can subsist
indefinitely as saprophytes. P. myriotylum has a wide host

Fig. 40. Pythium sex organs, a -g , Different types of antheridia;

Fig. 39. Roots affected by Pythium myriotylum (left) and healthy h, i, k, and I, oogonia; and j and m, oospores in oogonia. (Re
roots (right). (Courtesy D. M. Porter) printed, by permission, from Robertson, 1980)

28
strated in Israel. Frequent irrigation of sandy soils increased to P. myriotylum has shown that equally susceptible cultivars
the severity of pod rot caused by a combination of P. myrio differ in disease incidence and that a low disease incidence
tylum and F. solani, whereas less frequent and heavier irriga does not necessarily mean a high degree of resistance but could
tions reduced pod rot severity. Pod rot incidence and/or sever imply the existence of an escape mechanism.
ity also may increase after injury resulting from feeding by Wide-spectrum fungicides or combinations of fungicides
diverse soil fauna. Soilbome mites and springtails have been often are needed to control pod rot. Use of effective nemati-
implicated in the spread of P. myriotylum from infected to cides can be important, since some types of nematodes inten
healthy peanut pods in North Carolina. Wounds created by sify pod rot in certain locations. Soil fumigants containing
southern com rootworm feeding were involved in increased methyl isothiocyanate and a nematicide have provided some
pod rot incidence in Virginia. The peanut root-knot nematode, . control. Metham sodium applied in irrigation water controls
Meloidogyne arenaria, may increase the incidence of both pod pod rot in Israel.
rot and preemergence damping-off of peanut caused by P. Pod rot caused by P. myriotylum can be significantly sup
myriotylum in Florida. pressed in some areas by the application of high dosages of
gypsum. However, the addition of gypsum to peanut plants did
Control not reduce the severity of pod rot caused by P. myriotylum or F.
Some resistance to pod rot caused by P. myriotylum has been solani in Israel. Application of K2S 0 4 or M gS04 to peanut
reported. The most widely planted peanut cultivars in Virginia plants at blooming increased pod rot.
are the most resistant to P. myriotylum. High yield potential Control of Pythium diseases of peanut through field man
and moderate levels of resistance to Pythium spp. have been re agement has been difficult. Traditional crop rotations are re
ported in certain peanut lines grown in Pythium-infested soil in ported to have little effect on controlling pod rot in peanuts;
Texas. The spanish variety Toalson has resistance to both P. however, fields in which peanut has been grown for several
myriotylum and R. solani. In Israel, spanish and Valencia pea seasons in succession have significantly more pod rot caused
nuts resistant to pod rot caused by P. myriotylum and F. solani by Pythium spp. than fields that are fallow for two growing
have been developed. Evaluation of components of resistance seasons.

Germ,tube
Encysted zoospore
Soil line

Zoospores,

Oospore!1.

Overwinter Sporangia
ing oospore

Fertilization
of oogonium 'IH /n u T i'll I T

Dead plants Dying seedling

Rotted pod
Fig. 41. Life cycle of Pythium. (Modified and reprinted, by permission, from G. N. Agrios, 1978, Plant Pathology, 2nd ed., Academic
Press, New York. Prepared by A. J. Jaks)

29
 Selected References traffic (Plate 42). These lesions may expand inward toward the
crown of the plant Additional lesions may form on stems,
Csinos, A. S., Gaines, T. P., and Walker, M. E. 1982. Influence of either from direct infection or from fungal growth up infected
calcium source on peanut peg and pod rot complex. Proc. Am. pegs or leaves (Plate 43). Girdling of the stem is sufficient to
Peanut Res. Educ. Soc. 14:105. cause the loss of any pods between the lesion and the stem
Filonow, A. B., and Jackson, K. E. 1989. Effect of metalaxyl plus terminal. Pods formed on the outer limbs are more likely to rot
PCNB or metalaxyl plus tolclofos-methyl on peanut pod rot and or be shed at harvest, but the pathogen can also damage the
soil populations of Pythium spp. and Rhizoctonia solani. Peanut
primary pod crop (Plate 44).
Sci. 16:25-32.
R. solani frequently destroys the tips of pegs or colonizes
Frank, Z. R. 1972. Pythium myriotylum and Fusarium solani as
cofactors in a pod-rot complex of peanut. Phytopathology 62:1331-
pegs near the soil line (Plate 45). The fungus may subsequently
1334. colonize attached pods at any time or simply cause their loss at
Garcia, R., and Mitchell, D. J. 1975. Synergistic interactions of Pyth harvest by severing the peg. Rhizoctonia is a major component
ium myriotylum with Fusarium solani and Meloidogyne arenaria in of the peanut shell mycobiota, and shed pods remaining in the
pod rot of peanut. Phytopathology 65:832-833. soil have higher populations of Rhizoctonia spp. than those
Garren, K. H. 1967. Relation of several pathogenic organisms, and harvested successfully. Infected pods have dry, dull-colored,
the competition of Trichoderma viride to peanut pod breakdown. light to dark brown lesions (Plate 46) in contrast to the dark,
Plant Dis. Rep. 51:601-605. greasy-appearing lesions characteristic of Pythium myriotylum
Garren, K. H. 1970. Rhizoctonia solani versus Pythium myriotylum as infections. In fact, Rhizoctonia spp. may play a vital role in
pathogens of peanut pod breakdown. Plant Dis. Rep. 54:840-843. peanut pod rot (see Peanut Pod Rot Complex).
Porter, D. M. 1970. Peanut wilt caused by Pythium myriotylum. Phy
topathology 60:393-394.
Robertson, G. I. 1980. The genus Pythium in New Zealand. N. Z. Causal Organism
J. Bot. 18:73-102. R. solani Kuhn (teleomorph Thanatephorus cucumeris
Soufi, R. K., and Filonow, A. B. 1992. Population dynamics of Pyth (A. B. Frank) Donk) is found wherever peanut is cultivated and
ium spp. in soil planted with peanut. Plant Dis. 76:1203-1209. can be readily isolated from plants or soil. A severe foliar
blight caused by R. solani anastomosis group 1 (AG-1) has
(Prepared by M. K. Beute) been reported, and AG-2 isolates are sometimes weakly viru
lent. However, AG-4 is the most common pathogen of peanut
(Fig. 42). R. solani AG-4 is highly virulent on seed and seed
lings as well as on stems and foliage of mature plants.
Rhizoctonia Diseases
Disease Cycle
The peanut plant is susceptible to diseases caused by Rhi R. solani is well adapted for long-term survival in the soil
zoctonia solani from planting until harvest. The fungus is because of its ability to survive saprophytically on plant debris
responsible for rotting pods and any aboveground portions of and form abundant sclerotia in infected plant parts. Large
the plant in close proximity to the soil as well as for seed amounts of pods (630-778 kg/ha) are often left in the soil after
decay, preemergence and postemergence damping-off of seed harvest. Isolates of R. solani AG-4 have been recovered from
lings, and root and hypocotyl rot. Seed decay and damping-off peanut pods after 2 years in the soil, but populations fall sharp
can be serious, especially in fields not involved in crop rotation ly during the first year. The pathogen also has an extremely
or when conditions are not favorable for seedling development. wide host range consisting of approximately 500 plant genera,
Replanting occasionally may be necessary. Root and hypocotyl although AG-4 is found primarily on members of Chenopo-
rot can reduce yields. In the southeastern United States, Rhi diaceae, Leguminosae, and Solanaceae. This enables the fun
zoctonia limb rot has become a major problem, particularly in gus to infect and reproduce not only on various rotated crops,
irrigated fields. Annual losses in Georgia exeeed several-million but also on a multitude of weed species (Plate 47). The addi
dollars. tion of organic matter to the soil or exudates from a susceptible
host will stimulate sclerotia to germinate. The fungus can
Symptoms penetrate the plant directly through the intact cuticle and epi
Peanut seed are sometimes decayed prior to emergence by dermis, by infection cushions, or may enter through natural
seedbome or soilbome Rhizoctonia spp. Such decay may be openings or wounds. Colonization of the plant is aided by
difficult to distinguish from that caused by other seed-rotting production of cellulolytic and pectic enzymes. Mechanical
pathogens. Symptoms on emerged seedlings are more distinct injury to stems has been clearly linked to increased limb rot
tive and include dark, sunken, sore-shin lesions just below severity. Therefore, tractor traffic should be kept to a mini
the soil line (Plate 39). As the fungus colonizes the hypocotyl, mum, especially after the plants have closed the row middles.
the lesions become darker and larger. Under optimum condi Also, overhead irrigation and excessive fertilization have been
tions for disease development, the fungus will cause enough shown to increase limb rot severity. Disease severity is
damage to the hypocotyl and roots to cause plant death (Plate probably most damaging either early season, when it promotes
40). Under less favorable conditions, lesions will be more excessive foliar growth, or late season, when the disease pro
restricted and the plants will survive. Colonization of roots by gresses most rapidly because of prolonged moisture under the
Rhizoctonia spp. may cause small, brown lesions on secondary dense plant canopy.
or tertiary roots or involve severe necrosis of the entire root
system. Older plants tend to have sunken, brown or black Control
lesions on the upper taproots. Rotation with grass crops reduces severity of many peanut
Symptoms of Rhizoctonia infection on aboveground plant diseases, including those caused by R. solani AG-4, although
parts can be dramatic. Although the disease is commonly re brace roots of com are reported to be symptomless carriers of
ferred to as Rhizoctonia limb rot, symptoms may be evident on AG-4. Other cultural practices such as deep plowing and
stems, leaves, or pegs. Lower branches in contact with the soil nondirting cultivation (i.e., dirt is not thrown into the crown
are usually the first to become infected. Lesions are initially of the plant) are helpful in managing Rhizoctonia-induced
small and light to dark brown with a distinctly zonate or target diseases.
pattern (Plate 41). They often form near the terminal end of The recent registration of tebuconazole offers an effective
stems, particularly when stems have been injured by tractor chemical control for Rhizoctonia limb rot. Other fungicides
30
such as flutolanil or fluazinam may be registered also. These
treatments will also reduce losses to Rhizoctonia-induced pod
Rust
rots but may not be active against other pod-rotting organisms
such as Pythium myriotylum and Fusarium solani. Foliar Rust is an economically important disease in most peanut-
sprays of flutolanil have been shown to reduce the incidence of producing countries of the world and causes substantial yield
R. solani in peanut pods left in the soil. Adequate calcium losses, particularly if the crop is also attacked by the leaf spot
nutrition is known to be essential for pod rot management. pathogens Cercospora arachidicola and Cercosporidium per-
Combination chemical treatments containing carboxin, PCNB, sonatum. During recent years, combined attacks by rust and
and captan provide some control of R. solani on seed and leaf spot have caused severe crop losses in many countries of
seedlings, although stand reductions can still be significant in Asia and Africa and have all but eliminated commercial peanut
cold, wet soils. Resistance to limb rot has not been available in production in the Caribbean region and Central America. In the
large-seeded peanut cultivars. Some resistance has been Peoples Republic of China, rust caused a 49% reduction in
reported in spanish-type peanuts. The recently released runner pod yield and lowered the 100-kemel weight by 19%. Artifi
cultivar, Georgia Browne, has good partial resistance to limb cially induced rust epidemics caused up to 79% reduction in
rot. pod yield in India. The disease is not a major limiting factor in
peanut production in the United States, with the exception of
southern Texas, where rust causes severe economic losses dur
Selected References
ing some years. Losses measured at two locations in Texas
were 77 and 86% from foliar diseases and 50 and 70% from
Barnes, J. S., Csinos, A. S., and Hook, J. E. 1990. Effects of fungi rust alone. Establishment of the disease early in the growing
cides, cultivars, irrigation, and environment on Rhizoctonia limb season causes reduced pod fill and necessitates early harvest
rot of peanut. Plant Dis. 74:671-676. ing. In addition, hay yields are drastically reduced.
Branch, W. D., and Brenneman, T. B. 1993. White mold and Rhizoc
tonia limb rot resistance among advanced Georgia peanut breeding
lines. Peanut Sci. 20:124-126. Symptoms
Brenneman, T. B., Murphy, A. P., and Csinos, A. S. 1991. Activity of Rust can be easily recognized when the orange pustules
tebuconazole on Sclerotium rolfsii and Rhizoctonia solani, two (uredinia) appear on the lower surfaces of peanut leaves and
soilborne pathogens of peanut. Plant Dis. 75:744-747. then rupture to expose masses of reddish brown urediniospores
Turner, J. T., and Backman, P. A. 1988. Severity, distribution, and (Plates 48 and 49). In highly susceptible cultivars, the original
yield losses from taproot cankers caused by Rhizoctonia solani in pustules may later be surrounded by colonies of secondary
peanuts. Peanut Sci. 15:73-75. pustules. Pustules may later be formed on the upper surfaces of
the leaflets opposite those on the lower surfaces. The pustules,
(Prepared by T. B. Brenneman) which develop on all aerial plant parts except flowers, are
usually circular and 0.5-1.4 mm in diameter. Pustules may also Spermagonia, aecia, metabasidia, and basidiospores have not
form on shells of developing pods. Unlike the rapid defoliation been reported for P. arachidis.
associated with leaf spots, leaves infected with rust become Because there is no knowledge of spermagonia, aecia, and
necrotic but remain attached to the plant. Heavily infected hosts that basidiospores will infect, the life cycle of peanut rust
plants often appear pale green. is unknown and the taxonomic position of the fungus is
obscure.
Causal Organism
Puccinia arachidis Speg. is the causal organism of peanut Disease Cycle and Epidemiology
rust. The uredinial stage is the predominant and most com Urediniospores are the main, if not the only, means of dis
monly observed. The uredinia are pustular, scattered or irregu semination of this pathogen. There are a few authentic records
larly grouped, and round, ellipsoid, or oblong. They are subepi- of the occurrence of teliospores in South America but none
dermal in origin; covered by a thin, membranous, netlike from other countries. The pathogen is highly host specific.
peridium; and blisterlike when immature, becoming erumpent, There are no records of any collateral hosts of peanut rust
powdery, and dark cinnamon brown when mature. The ruptured outside the genus Arachis. Urediniospores are short lived in
epidermis is conspicuous. Urediniospores (Fig. 43) are broadly infected crop debris in the tropics, and the fungus is unlikely to
ellipsoid or obovoid (23-29 x 16-22 |jm), have brown walls 1- survive from season to season under postharvest conditions
2.2 nm thick, and are finely echinulate, with echinulae 2-3 |jm that include a fallow period of more than 1 month between
apart (Fig. 44). Urediniospores usually have two germ pores, successive peanut crops. The pathogen may survive from
which are nearly equatorial, often forming in flattened areas. season to season on volunteer peanut plants. Long-distance dis
Telia, chiefly occurring on the lower sides of peanut leaves, semination of the pathogen may be by airborne urediniospores,
are scattered, prominent, naked, pulvinate, and chestnut brown movement of infected crop debris, or movement of pods or
or cinnamon brown, becoming grayish from the germination of seed, the surfaces of which are contaminated with viable
spores. A ruptured epidermis is prominent. Teliospores (Fig. urediniospores. There is no reliable evidence of peanut rust
45) are oblong, obovate, ellipsoid, or ovate with a rounded to being internally seedbome, and there is no authenticated report
acute and thickened apex. They are constricted in the middle, of rust being spread by germ plasm exchange. Spread of the
tapering gradually at the base or tapered and rounded at both organism within fields is facilitated by wind, rain splash, and
ends; smooth walled; predominantly two celled but sometimes insects. Urediniospores can remain viable for several months
have one, three, or four cells; 38-42 x 14-16 |im; light or when stored at a low temperature (-16C), but at a high tem
golden yellow or chestnut brown; 0.7-0.8 jjm thick at the perature (40C), they lose viability within 5 days. The thermal
sides; and 2.5-4.0 nm thick at the top. The apical thickening is death point of urediniospores is 50C for 10 min. The optimum
almost hyaline. The pedicel is thin walled, hyaline, usually conditions for germination of urediniospores include tempera
collapsing laterally, and up to 35-65 |jm long but is usually de tures of 20-25C and low light. Temperatures of 20-30C and
tached at the spore base. Teliospores germinate at maturity free water on the leaf surfaces favor infection and subsequent
without a dormancy requirement. disease spread. Plants of all ages are susceptible. The incuba
tion period varies from 7 to 20 days, depending on environ
mental conditions and host genotype. Intermittent rains with
mean relative humidity above 87% and temperatures between
23 and 24C for several days favor disease initiation. Continu
ous dry periods with temperatures greater than 26C and rela
tive humidity below 75% delay rust infection and reduce dis
ease severity.

Control
vVherever possible, field management should include a
fallow period of at least 1 month between successive peanut

Fig. 44. Urediniospores of Puccinia arachidis with echinulation.

Fig. 43. Urediniospores of Puccinia arachidis. Bar = 15 urn. (Courtesy R. A. Taber)

32
crops. Eradication of volunteer peanut plants during this period stable, tetraploid or near-tetraploid lines derived from crosses
is important in reducing the primary source of inoculum. If between the cultivated peanut and wild species have been
cropping systems permit, time of sowing should be adjusted to developed.
avoid infection from outside sources and to avoid environ The rust resistance available in the cultivated peanut is the
mental conditions conducive to the onset of an epidemic. slow-rusting type, i.e., resistant genotypes have an increased
Existing plant-quarantine procedures should suffice to prevent incubation period, decreased infection frequency, and reduced
spread of the pathogen on pods or seed externally contami pustule size, spore production, and spore viability. On the basis
nated with rust spores to areas where the disease is absent. of field scores, rust resistance in cultivated peanut is reported
Several fungicides and mixtures of fungicides have been to be governed by two or three duplicate recessive genes. On
tested for control of rust or, more often, for control of rust and the contrary, in diploid Arachis spp., rust resistance appears to
leaf spot together. The dust formulations (copper, sulfur, and be partially dominant. In crosses involving both cultivated and
copper plus sulfur) that were commonly, used for control of leaf interspecific derivatives, rust resistance was found to be con
spot in the United States up to the 1960s also controlled rust, trolled by both additive and nonadditive gene action. Rust
but sprays of Bordeaux mixture and dithiocarbamates were resistance in most genotypes is stable over a wide range of
even more effective. The structurally related fungicides beno- geographical locations except in a few locations, indicating
myl and carbendazim are effective against leaf spot but inef possible variation in the pathogen.
fective against rust. Tridemorph is effective against rust but not Several mycoparasites of the peanut rust pathogen have been
against leaf spot. Chlorothalonil and tebuconazole are effective. reported, and mycophagous insects may feed on urediniospores
against both rust and leaf spot. It is obvious that any fungicide of peanut rust. However, no serious attempts have been made
treatment applied for control of rust must also be effective to use any of these organisms in biological control of peanut
against leaf spot, because the diseases frequently occur to rust at the field level.
gether.
Prior to 1977, there were only a few reports of research on Selected References
genetic resistance to peanut rust, but the rapid spread of rust
during the early 1970s and the increasing cost of disease man Butler, D. R., and Jadhav, D. R. 1991. Requirements of leaf wetness
agement with fungicides have resulted in increased research on and temperature for infection of groundnut by rust. Plant Pathol.
genetic resistance to peanut rust. At the ICRISAT (Interna 40:395-400.
Hennen, J. F., Subrahmanyam, P., and Figueredo, M. B. 1987. The
tional Crops Research Institute for the Semi-Arid Tropics)
taxonomy, life history, and evolution of Puccinia arachidis. Pages
Asia Center in India, the world collection of more than 13,000 145-155 in: Proc. Int. Group Discuss. Meet. Rust Dis. Groundnut.
germ plasm accessions was screened for resistance to rust International Crops Research Institute for the Semi-Arid Tropics,
during the period from 1977 to 1992, and more than 120 rust- Patancheru, India.
resistant germ plasm lines have been identified. Most of the McDonald, D., and Subrahmanyam, P. 1992. Rust of groundnut.
currently available rust-resistant genotypes originated in Peru, Pages 272-284 in: Diseases of International Importance. Vol. 2,
which is believed to be one of the secondary gene centers of Diseases of Vegetables and Oilseed Crops. H. S. Chaube, J. Kumar,
cultivated peanut. A. N. Mukhopadhyay, and U. S. Singh, eds. Prentice Hall, Engle
Most of the rust-resistant germ plasm lines are primitive wood Cliffs, NJ.
land races and have undesirable pod and seed characters. In Subrahmanyam, P., and McDonald, D. 1983. Rust disease of ground
recent years, several high-yielding, agronomically superior nut. Int. Crops Res. Inst. Semi-Arid Trop. Bull. 13.
lines, with high levels of resistance to rust and moderate levels Subrahmanyam, P., Reddy, L. J., Gibbons, R. W., and McDonald, D.
of resistance to late leaf spot, have been developed and re 1985. Peanut rust: A major threat to peanut production in the semi-
arid tropics. Plant Dis. 69:813-819.
leased for cultivation in India (e.g., ICGVs 86590, 87157,
Zhou, L., Huo, C., Liu, J., and Liu, Z. 1980. Studies on peanut rust in
87160, Gimar 1, and ALR 1). ICGV 87160 has also been
Guangdong Province. Acta Phytophylacica Sin. 7:65-74.
released in Myanmar (Burma). High levels of resistance and
immunity to peanut-rust have been found in wild Arachis spp. (Prepared by P. Subrahmanyam)
Cytogenetic research aimed at incorporating the rust resistance
from wild Arachis spp. into the cultivated peanut is in progress
in various countries. At the ICRISAT Asia Center, several
Scab
Peanut scab was first observed in Sao Paulo, Brazil, in 1937
with subsequent reports in Brazil during 1941 and 1961 and in
the Argentinian provinces of Corrientes (1966) and Cordoba
(1975). Cordoba produces 99% of the peanut crop in Argen
tina. Scab has also been reported in the Chiba prefecture of
Japan and in Swaziland. The mode of distribution of the scab
pathogen to Africa, Asia, and South America has not been
determined.

Symptoms
Symptoms first appear on leaves and petioles near the top of
the plant. Numerous small, chlorotic spots, usually less than 1
mm in diameter, often form on the adaxial and abaxial leaf
surfaces and are either uniformly distributed or clustered near
the midvein. Spots on the adaxial leaf surface are light tan with
raised margins and sunken centers, while spots on the abaxial
surface are darker and not raised. Spots have a maximum
diameter of 2 mm and coalesce near the midvein. Plant tissue
becomes necrotic and tom, and leaf margins curl upward,
Fig. 45. Teliospores of Puccinia arachidis. (Courtesy J. F. Hennen) resulting in additional tearing of tissue.
33
 Spots on petioles and stems are larger and more irregular
than spots on leaves and lead to development of cankers (Plate Sclerotinia Blight
50). As the disease progresses, lesions coalesce, plants are
stunted, petioles and stems are sinuous, and lesions become Sclerotinia blight, first observed on peanut plants in Argen
corky and cover nearly all plant parts (Fig. 46 and Plate 51). tina in 1922, is now present in most peanut-producing coun
Plants with numerous cankers appear to be burned. tries of the world. It was first observed in the United States in
Virginia in 1971, thereafter spreading to North Carolina, Okla
Causal Organism homa, and Texas. By 1982, Sclerotinia blight was considered
Sphaceloma arachidis Bit. & Jenk. is the causal pathogen of the most important disease of the peanut in Virginia and Okla
peanut scab. Acervuli (300 x 45 |jm) are amphigenous, numer homa (Plate 52). Yield losses of 10% are common, In areas of
ous, effuse, and sometimes pulvinate and erumpent. Conidio fields showing severe symptoms of disease, 1,500-2,000 kg of
phores (8-11 x 3-5 |im) are hyaline, globose, and conical and pods per hectare often remain in the soil after harvest. In such
arranged in aggregations resembling a palisade. Conidia (9-17 fields, pod losses often exceed 50% of expected yield.
x 2.5-3 |im) are hyaline and mainly unicellular. Microconidia
are approximately 1 |im in diameter. Growth of S. arachidis on Symptoms
potato-dextrose agar is slow at 22C and occurs in convoluted The first obvious symptom of Sclerotinia blight is the rapid
colonies with dark red areas. On host tissue, lesions are dark wilting or flagging of the tips of infected branches. Initial
olive with a velvet appearance. infections are characterized by small, light green, water-soaked
lesions on stems near the soil line. Older lesions appear
Control bleached or straw colored with a distinct demarcation zone
Several cultivars including Colorado Manfredi, Colorado between infected and healthy tissues. Foliage of infected
Commun, and Colorado Irradialis INTA have partial resistance to branches becomes chlorotic, turns dark brown, and withers.
S. arachidis. In Brazil, 15 of 639 breeding lines were resistant. Once the stem is girdled, the branch dies. These symptoms
Because the pathogen survives in crop residue, crop rotation result in the blight appearance for which the disease is named.
may reduce disease progress. Effective disease management White, fluffy mycelium develops on diseased tissue (Plate
can be obtained with benomyl. 53), especially during periods of high humidity. Another symp
tom characteristic of Sclerotinia blight is the shredding of in
Selected References fected branch and peg tissue (Plate 54). Severe peg infection
results in significant pod losses at harvest.
Giorda, L. M., and Munoz, J. O. 1979. Sphaceloma arachidis Bit. and Sclerotial production on and in infected plant parts is a
Jenk., causa de la sarna del manf {Arachis hypogaea L.) en characteristic sign of this disease. Sclerotia form on infected
Cordoba. Pages 284-288 in: Actas Jorn. Argent. Micol. Resist. branches (Plate 55), leaflets, pegs, and pods and inside
Ojeda, H. R. 1966. La Sarna o Verrugosis del mam, enfermedad branches, pegs, pods, and roots (Plate 56).
observada por primera vez en Argentina. Bol. Catedra Genet.
Fitotec. 2:1-6. Causal Organism
Subrahmanyam, P., Wongkaew, S., Reddy, D. V. R., Demski, J. W.,
McDonald, D., Sharma, S. B., and Smith, D. H. 1992. Field diag
Sclerotinia minor Jagger is the causal agent; however, on
nosis of groundnut diseases. Int. Crops Res. Inst. Semi-Arid Trop. rare occasions S. sclerotiorum (Lib.) de Bary also is found
Bull. 36. (Fig. 47). In artificial inoculations, either species can produce
typical blight symptoms. Apothecia of S. minor are rarely
(Prepared by D. H. Smith) observed in soils during the growing season (Plate 57) but
appear during February and March or midfall on the soil sur
face. Apothecia are pale orange to white and have concave or
flat tops. A single sclerotium can produce one to several apo-
theciarwhiclrrange up to 6 mm or more in diameter. Asci con
tain eight hyaline ascospores measuring 8-17 x 5-7 (im.
The mycelium of S. minor is white and fluffy. Sclerotia have
a black outer rind and a white inner cortex. They are small
(0.5-3 mm), black, and irregularly shaped. Spermatia, pro
duced on phialides, are globose, hyaline, and 3-4 (am in diam
eter. Their role in disease development is not known.

Fig. 46. Symptoms of scab caused by Sphaceloma arachidis. Fig. 47. Cultures of Sclerotinia minor (left) and S. sclerotiorum
Note characteristic sinuous stem. (Courtesy L. Giorda) (right) growing on potato-dextrose agar.

34
Disease Cycle Control
S. minor overwinters as sclerotia. Viable sclerotia have been High-quality peanut seed treated with chemical protectants
found in soil throughout the plow layer (the top 20 cm) of should be planted to ensure against the low possibility of seed
fields with a previous history of Sclerotinia blight but not transmission of S. minor. Minimizing the injury of peanut
planted to peanuts for 4 years. Under favorable environmental vines by machinery is highly recommended. The use of resis
conditions (17-21 C, high soil moisture, and relative humidity tant cultivars is highly desirable and profitable. Recently
above 95%), sclerotia of S. minor germinate myceliogenically. released peanut cultivars including Virginia 8 IB, Virginia 93B,
The life cycle of S. minor is provided in Figure 48. Plant tis Tamspan-90, and Southwest Runner possess resistance to S.
sues, branches, pegs, pods, and leaflets near or in contact with minor. The use of fungicides can also aid in reducing losses.
the soil and lying adjacent to a germinating sclerotium are Excessive irrigation is not advised at any time during the
infected by fast-growing, white mycelia. Before it penetrates growing season when cool conditions prevail. Some fungicides
the peanut stem, S. minor produces infection cushions (Plate applied for the control of leaf spot (Cercospora arachidicola
58). As disease progresses, infections occur in the plant canopy and Cercosporidium personatum) may increase the severity of
above the soil surface. Senescing or mechanically injured leaf Sclerotinia blight. Sclerotia are often colonized and destroyed
lets and stems can be colonized readily by S. minor. However, by an array of soilbome fungi. Trichoderma spp., Gliocladium
this is not a prerequisite for infection, since disease can be spp., and Penicillium spp. can be easily isolated from sound
come severe in healthy, vigorously growing plants. sclerotia and might be used as biocontrol agents (Plate 59).
Infection by S. minor is favored by cool conditions (18C),
moist soils, and high relative humidity (95-100%). Optimum Selected References
sclerotial germination occurs at a pH of 6.5. Under favorable
environmental conditions, white, fluffy mycelia can be seen on Akem, C. N., Melouk, H. A., and Smith, O. D. 1992. Field evaluation
infected plant parts as well as on the soil surface. Sclerotia are of peanut genotypes for resistance to Sclerotinia blight. Crop Prot.
produced abundantly on infected plant parts. The number of 11:345-348.
sclerotia at harvest often exceeds one sclerotium per 4 g of soil Kohn, L. M. 1979. A monographic revision of the genus Sclerotinia.
Mycotaxon 9:365-444.
in areas exhibiting severe symptoms of Sclerotinia blight.
Melouk, H. A., Singleton, L. L., Owens, F. N., and Akem, C. N. 1989.
Although sclerotial counts decline throughout the winter, more
Viability of sclerotia of Sclerotinia minor after passage through the
than enough viable sclerotia survive to propagate the disease digestive tract of a crossbred heifer. Plant Dis. 73:68-69.
during the following year. One sclerotium per 100 g of soil is- Porter, D. M. 1980. Increased severity of Sclerotinia blight in peanuts
sufficient to cause severe disease. Transmission of S. minor treated with captafol or chlorothalonil. Plant Dis. 64:394-395.
through peanut seeds is considered negligible, provided seeds -- Porter, D. M., Taber, R. A., and Smith, D. H. 1989. The incidence and
are properly picked (which includes removal of damaged , survival of Sclerotinia minor in peanut seed. Peanut Sci. 16:113-115.
seed), screened (15/64-in. screen), and treated with a recom Porter, D. M., Wright, F. S., and Powell, N. L. 1987. Effects of sprinkler
mended seed treatment. irrigation on peanut diseases in Virginia. Plant Dis. 71:512-515.

DQ
M yc e liu m a t t a c k s W h i t e , f l u f f y m y c e li u m
lower b r an ch e s and g row s on s u r f a c e o f
in va d e s s u c c u l e n t i nv ad ed t i s s u e . M yc eliu m
tissues ra p id ly . In fe c tio n site c o n t in u e s to invad e \
t Ascospore Cells c o lla p s e p la n t t i s s u e s ^
A l ands and
\germinates In fe c te d p la n t
' o n plant
X

Sclerotia form on o r in i n f e c t e d ti s s u es

Apothecium B ra n c h e s Pegs

S. sclerotiorum

Carpogenic
I n f e c t e d b r a n c h and
germination
(of minor importance) p eg t i s s u e s become
shredded
S. m i n o r

M y c e lio g e n ic
g e rm in a tion
Fungus o v e r w i n t e r s as H f
\ S clero tia germ inate
s c l e r o t i a in dead p la n t
S c l e r o t i a shed
in to so il
t i s s u e s and in o r on
so i i

Fig. 48. Disease cycle of Sclerotinia minor. (Modified and reprinted, by permission, from G. N. Agrios, 1978, Plant Pathology, 2nd ed.,
Academic Press, New York. Prepared by Nancy Browning)

35
Wadsworth, D. F., and Melouk, H. A. 1985. Potential for transmission Disease Cycle
and spread of Sclerotinia minor by infested peanut seed. Plant Dis. S. rolfsii has a broad host range of more than 200 plant
69:379-381. species. The pathogen can colonize either the living plant or
Woodard, K. E., and Simpson, C. E. 1993. Characterization of growth plant debris. Disease severity in sugar beets (Beta vulgaris L.)
and sclerotial production of Sclerotinia minor isolated from peanut is a function of sclerotial population size; but in peanuts, the
in Texas. Plant Dis. 77:576-579. populations required to produce severe disease are so low that
current quantification methods are insufficient to measure
(Prepared by D. M. Porter and H. A. Melouk) them. Deeply buried sclerotia survive a year or less, while
those near the soil surface remain viable for many years.
Because S. rolfsii has a high demand for oxygen, over
wintering sclerotia are activated only when they occur in the
Stem Rot upper regions of the soil. In soils that crack deeply when dry
(e.g., vertisols), oxygen can penetrate deep into the soil profile
Stem rot of peanut, also known as white mold, southern stem allowing pod and root rots that would not occur if the same
rot, southern blight, and Sclerotium rot, is found in virtually all soils were wet. Sclerotia also germinate in response to alcohols
major peanut-growing areas of the world. Damage is easily and other volatiles released from decomposing leaves. Shed
seen during warm, wet weather, since a single infection site leaves can also serve as a bridge to facilitate plant-to-plant
will often kill several adjacent plants. Disease incidence is spread.
often determined by counting the number of disease loci (30 Control of peanut leaf spot can indirectly increase stem rot
cm or less of row length with dead or diseased plants). There is severity. Maintaining a complete canopy creates a moist sub
a strong negative correlation between numbers of disease loci canopy environment that is conducive to disease development
per unit row length and yield, but the slope of the line varies and may also intercept fungicides, directly or indirectly affect
from year to year, primarily because damage to pods and stems ing S. rolfsii.
is environmentally driven. Yield losses typically do not exceed
25% but may be as great as 80%. This disease causes the Control
greatest yield losses of all diseases of peanut in the United Control of stem rot begins with prevention of inoculum
States. Losses to stem rot average 7-10% annually in the buildup. Deep plowing serves to bury crop debris, which
southeastern United States but are usually much lower in the serves as a saprophytic food base, and sclerotia, which do not
southwest and Atlantic states. survive as well deeper in the soil. Cultivation for weed control
will reduce disease buildup if growers are careful to prevent
Symptoms the movement of soil onto the plant crown or lateral stems.
Stem rot does not usually occur until midseason when the Crop rotation is a very effective practice, but long rotations (3-
foliage has covered the row middles. The first obvious symp 4 years) are required if a severe infestation has already devel
tom of the disease is the yellowing and wilting of a lateral oped. Grass crops such as com, grain sorghum, or pasture
branch, the main stem, or the entire plant. Sclerotium rolfsii grasses are particularly effective. Weed control is essential in
produces large amounts of oxalic acid, a phytotoxin that any rotation, including fallow, because of the wide host range
produces a purple stain on seed and is responsible for chlorosis of the fungus.
and necrosis of foliage during the early stages of disease Pesticides can influence the development of stem rot. Beno-
development. Sheaths of white" mycelium can be seen at or myl can actually increase the severity of stem rot by reducing
near the soil line around affected plant parts (Plate 60). The levels of Trichoderma spp., a natural biological control agent.
mycelium grows rapidly under favorable environmental condi The dinitro herbicides and the insecticides ethoprop, fensulfo-
tions and quickly spreads to other branches and plants. Spheri thion, and chlorpyrifos are all reported to suppress the severity
cal sclerotia (0.5-2.0 mm in diameter), produced abundantly of stem rot. Chlorpyrifos has been used extensively for this
on affected plant parts and the soil surface, are initially white purpose and also provides control of the lesser cornstalk borer,
but later turn dark brown (Plates 61 and 62). Lesions produced Elasmopalpus lignosellus (Zeller).
on the basal areas of branches and on pegs are initially light
brown, become dark brown as disease develops, and do not ex
tend more than 2-4 cm above the soil surface. Infected pods
are usually rotted and tan to brown with a wet, spongy texture
and may occur on plants without any visible aboveground
symptoms (Plate 63). Infected pods often will be covered with
soil clinging to mycelium on the pod surface (Plate 64).

Causal Organism
Stem rot is caused by S. rolfsii Sacc. The fungus grows well
on a wide range of culture media and is characterized by the
:ii
presence of white mycelium and hard, round, brown sclerotia,
which are larger when produced in potato-dextrose agar cul *1*
tures than in the field (Fig. 49). The fungus does not produce r .
asexual spores. The basidial stage, Athelia rolfsii (Curzi) Tu &
Kimbrough, is rarely seen in the field or in culture. When it V *
m
does develop, A. rolfsii produces an exposed hymenium bear
ing clavate basidia and hyaline, pyriform basidiospores (1.0-
...
1.7 x 6-12 (jm). Considerable diversity in traits such as growth
rate, virulence, and sclerotial production have been found, even
among single-basidiospore strains (presumed homokaryons)
from one parental isolate. At least 42 different mycelial com
patibility groups have been used to classify S. rolfsii, although
recent studies of peanut isolates from Texas, indicate the pres Fig. 49. Culture of Sclerotium rolfsii on potato-dextrose agar with
ence of many more. characteristic sclerotia. (Courtesy D. M. Porter)

36
 PCNB and carboxin have been used for many years in the son, Aspergillus fumigatus Fresen. (considered to be thermo-
United States to suppress stem rot. They offer no more than tolerant), Thielavia albomyces (Cooney & Emerson) Malloch
50% control and are used as either granules or liquid delivered & Cain, Sporotrichum sp., and Chaetomium sp. as well as
via irrigation water. Tebuconazole, registered for use on pea numerous actinomycetes and bacteria. Discoloration of shells
nuts in the United States in 1994, provides a level of control and seed is associated with several of these f ungi
superior to that achieved with previously registered products.
Tebuconazole and several other triazole-type, sterol-inhibiting Selected Reference
fungicides have given greater than 80% control of stem rot at
seasonal use rates of less than 1.0 kg/ha. These treatments are Taber, R. A., and Pettit, R. E. 1975. Occurrence of thermophilic
applied either in a block at midseason or as full-season tank microorganisms in peanuts and peanut soil. Mycologia 67:157-161.
mixes with chlorothalonil. The triazoles generally have excel
lent activity against foliar pathogens as well, and propicona- (Prepared by R. A. Taber)
zole was registered for that purpose in 1994. Propiconazole has
been shown to be most active against stem rot when applied
via chemigation, but control is still moderate at best. Flutolanil
is a systemic fungicide that is not a triazole but also offers Verticilliiim Wilt
excellent control of stem rot. This experimental fungicide is
usually applied as a tank mix with chlorothalonil once or twice The first report of Verticillium wilt in peanut was from Asia
during midseason. It has little activity against leaf spot, and in 1937. The disease was reported in Australia in 1945 and in
therefore full rates of chlorothalonil are required. Several other the United States (New Mexico) in 1985. It occurs in other
new fungicides have shown promise for stem rot control but peanut-growing countries, and although yield reductions of
are not yet registered. Both disease control and the related 60% have been reported in Argentina, it is not considered a
yield increases can be dramatic with these products where serious worldwide production constraint. Verticillium wilt of
disease incidence is high (Plate 65). peanut is found in all peanut-producing areas of the United
Biological control with the antagonistic fungus Trichoderma States and has increased since 1970, but the disease is of
harzianum Rifai has successfully suppressed stem rot severity, economic importance only in New Mexico and Oklahoma. The
with control levels similar to those of PCNB. Commercializa occurrence of Verticillium wilt in Oklahoma in 1994 was
tion of this agent has not been successful because of the diffi widespread and severe in some fields. Data on yield losses in
culty of delivering a viable formulation to the field. peanut in the United States caused by Verticillium wilt are not
Until recently, only low levels of tolerance to stem rot had yet available.
been reported in peanut germ plasm. Generally, genotypes with
a more erect growth habit had less disease than cultivars with a Symptoms
spreading growth habit. However, Southern Runner produces a The first symptoms of Verticillium wilt may appear as
heavy, spreading canopy, and its disease incidence is about early as flowering but generally occur during pod fill (Plate
one-half that of Florunner, the current predominant cultivar. 66). Early symptoms appear on leaves and consist of mar
Georgia Browne has resistance comparable to that of Southern ginal chlorosis, loss of turgidity, and curling. As foliar symp
Runner, and recent studies have identified germ plasm with toms progress, general yellowing, marginal leaf necrosis
even higher levels of resistance. (Plate 67), wilting, defoliation, stunting, and dehydration of
infected plants precede plant death. Symptoms intensify most
Selected References rapidly under conditions of moisture stress and daytime air
temperatures above 26C. With adequate moisture, infected
Backman, P. A., Rodnguez-Kabana, R., and Williams, J. C. 1975. The plants may exhibit moderate wilt symptoms and live to matur
effect of peanut leafspot fungicides on the nontarget pathogen, ity. Infected plants usually mature earlier than noninfected
Sclerotium rolfsii. Phytopathology 65:773-776. plants.
Branch, W. D., and Brenneman, T. B. 1993. White mold and limb rot Internal symptoms consist of light brown to tan vascular
resistance among advanced Georgia peanut breeding lines. Peanut discoloration in crowns and stems (Plate 68). When wilt symp
Sci. 20:124-126. toms are severe, vascular discoloration also occurs in the roots
Csinos, A. S. 1989. Targeting fungicides for control of southern stem
and petioles (Plate 69). In a greenhouse study, the root mass of
rot on peanut. Plant Dis. 73:723-726.
Garren, K. H. 1959. The stem rot of peanuts and its control. Va. Verticillium-infected plants of the spanish cultivar Tamnut-74
Agric. Exp. Stn. Bull. 144. was reduced by 50%.
Rodnguez-Kabana, R., Backman, P. A., and Williams, J. C. 1975.
Determination of yield losses to Sclerotium rolfsii in peanut fields. Causal Organisms
Plant Dis. Rep. 59:855-858. Verticillium dahliae Kleb., a soilbome fungus, is considered
the primary causal agent of Verticillium wilt of peanut. How
(Prepared by P. A. Backman and T. B. Brenneman) ever, V. albo-atrum Reinke & Berthier has also been implicated
as a pathogen. Both species are widespread and are the two
most important vascular wilt pathogens within this genus. They
attack a wide range of hosts in more than 36 plant families,
Thermophilic Fungi including many important herbaceous and woody plants. The
two species have different temperature requirements and mor
Thermophilic fungi have been isolated from peanut and pea phology. V. dahliae grows at 32C and forms melanized micro
nut field soils in nine counties in Texas and three counties in sclerotia that range in size from 50 to 200 pm (Fig. 50A). V.
Oklahoma. Thermophiles are defined as those fungi that have a albo-atrum grows better at temperatures below 32C and does
maximum temperature for growth at or above 50C and a mini not produce microsclerotia but does form thick-walled, dark
mum temperature at or above 20C. Species isolated include mycelium (Fig. 50B).
Mucorpusillus Lindt, Humicola lanuginosa (Griffon & Maubl.) The conidial stages of V. dahliae and V. albo-atrum are
Bunce (syn. Thermomyces lanuginosus Tsiklinsky), Talaro- similar. When grown on potato-dextrose agar, V. dahliae
myces (Penicillium) dupontii (Griffon & Maubl.) Emerson produces white, fluffy, aerial mycelium with slender, often-
Apinis, Thermoascus aurantiacus Miehe, Malbranchea pul- branched conidiophores, which are usually arranged in
chella Sacc. & Penzig var. sulfurea (Miehe) Cooney & Emer whorls. Conidia (3 x 6.5 pm) are hyaline, unicellular, ovoid
37
to ellipsoid, and bome singly or in small clusters apically soil, either freely or embedded in debris pieces, and remain
(Figs. 51 and 52). Microsclerotia form in 1 week at 20C. dormant until peanut or other host root exudates stimulate them
White mycelial sectors, often devoid of microsclerotia, some to germinate. Infection occurs through the roots, and the fun
times develop. gus spreads throughout the vascular system. A recent field
observation in Oklahoma on a runner-type cultivar suggests
Disease Cycle that the interaction of the northern root-knot nematode and
V. dahliae survives in soil mainly as pigmented micro- the Verticillium wilt pathogen can produce severe wilt
sclerotia capable of withstanding environmental stress over symptoms.
prolonged periods, sometimes for several years. Microsclerotia V. dahliae spreads within and between fields by movement
are formed abundantly on or in all infected plant parts, includ of soil or infested debris carrying microsclerotia on farm
ing stems, pegs, pods, and roots (Plate 70). When infested machinery from infested to noninfested areas. The pathogen
peanut debris decomposes, microsclerotia are released into the can also be spread by wind and water movement of infested
soil and infected tissue. Another possible means of dissemina
tion of V. dahliae is by infected peanut seed. One to four
percent of peanut seed harvested from field-grown plants that
exhibited 50% wilt incidence carry V. dahliae. However, seed
transmission of Verticillium in peanut has never been docu
mented.

Control
Severity of Verticillium wilt is increased by high temper
atures and moisture stress. Infested fields should be irrigated
more frequently to reduce wilt symptoms and allow plants to
mature. Use of Verticillium-free seed also is recommended.
Weed control might aid in alleviating the incidence of Verti
cillium wilt, since some weeds are also susceptible to V.
dahliae.
Peanut following nonhost crops such as grain sorghum or
B Sudan grass develop less wilt than peanut following susceptible
crops such as cotton, okra, or peanut. Control of root-knot
nematodes may reduce severity of wilt symptoms. Removing
and burning infected crop residues reduces th ein ocu ln m den
sity of the pathogen in field soil.

Fig. 50. Formation of resting structures. A, Microsclerotia of Verti

cillium dahliae and B, dark mycelium of V. albo-atrum.

A B
Fig. 51. Verticillate branching of Verticillium conidiophores in Fig. 52. Clusters of conidia on conidiophores of Verticillium albo-
water mount (A) and bearing clusters of conidia (B). atrum. (415x) (Courtesy F. Uecker)

38
 Chemical control of Verticillium wilt of peanut has not been Schoschiaschvili). The teleomorph has also been assigned to
effective in the United States. In Israel, the disease has been various taxa, including the genera Mycosphaerella (M. arach
effectively controlled in sandy soil with metham sodium ap idicola Jenk. non Chochrjakov and M. argentinensis Frezzi),
plied by sprinkler irrigation. Didymosphaeria (D. arachidicola (Choch.) Alcorn, Punith., &
No cultivars of peanut are resistant to Verticillium wilt. McCarthy), and Didymella (D. arachidicola (Choch.) Taber,
Valencia and spanish peanuts are more susceptible to Verti Pettit, & Philley), or considered to be none of these. Confusion
cillium wilt than bunch or runner types. In Israel, where over placement of the teleomorph centers around interpretation
Verticillium wilt is a problem, several breeding lines resistant of the identity of sterile elements in the pseudothecium (Fig.
to Verticillium. have been developed. 53) and differences in opinions on development of pigmenta
tion of the ascospores. Didymella arachidicola is the most
commonly used holomorph classification.
Selected References Pycnidia of P. arachidicola are pale to dark brown, separate,
globose to flask shaped, ostiolate, amphigenous, and immersed
Frank, Z. R., and Krikun, J. 1969. Evaluation of peanut (Arachis in the necrotic leaf spots. Pycnidiospores are not readily visible
hypogaea) varieties for Verticillium wilt resistance. Plant Dis. Rep.
but can be seen distinctly in cleared (in KOH) and stained leaf
53:744-746.
tissue (Fig. 54). Size varies with the substrate and isolate, but
Krikun, J., and Frank, Z. R. 1982. Metam sodium applied by sprinkler
irrigation to control pod rot and Verticillium wilt on peanut. Plant in general, they are 85-240 pm in diameter. Conidia are formed
Dis. 66:128-130. in basipetal succession on short, conidiogenous cells and,
Melouk, H. A., and Wadsworth, D. F. 1990. Infection of peanut seed under humid conditions, are exuded through the ostiole as
with Verticillium dahliae. Page 15 in: Proc. Int. Verticillium Symp., light-colored droplets. Conidial sizes vary with the substrate
5th. and septation. One-celled, obovoid conidia (49 x 2.5-4 pm)
Purss, G. S. 1961. Wilt of peanut (Arachis hypogaea L.) in Queens are produced in culture, while on host material, spores may be
land, with particular reference to Verticillium wilt. Queensl. J. larger (7-18 x 3-6 pm ) and a large proportion of them are
Agric. Sci. 18:453-462. septate. Conidial sizes are also influenced by temperaturethe
lower the temperature the larger the conidia. Colonies of P.
(Prepared by H. A. Melouk and J. P. Damicone) arachidicola on malt agar at 25C are dark grayish olive. They
may be loose and felty or closely appressed at the periphery.
The hyphae are 2-8 pm in diameter, olivaceous to brown, and

Web Blotch
Web blotch of peanut occurs in many peanut-growing areas
throughout the world, although its economic importance varies
from country to country. It has been reported from Angola,
Argentina, Australia, Brazil, Canada, China, Japan, Lesotho,
Malawi, Mauritius, Nigeria, South Africa, Swaziland, Zambia,
Zimbabwe, the United States (initially in Texas and subse
quently in Florida, Georgia, New Mexico, Oklahoma, and Vir
ginia), and the former Soviet Union. It is one of the most
important foliar diseases of peanut in the Vaalharts and Natal
regions of South Africa; in Zimbabwe, especially at high ele
vations and on irrigated, long-seasoh cultivars; and in the United
States on valencia-type peanuts in western Texas and New
Mexico. In Zimbabwe, losses of approximately 10% of yield can
Fig. 53. Pseudothecia of the web blotch fungus, Phoma arachidi
be directly attributed to web blotch. Losses in New Mexico reach cola. (Courtesy R. Taber)
50% in some years, and the disease can have a heavy impact on
the quality of Valencia peanuts marketed in-shell.
Web blotch is often referred tO as net blotch because of the
netlike appearance of the lesions. It is also known as Phoma
leaf spot, Ascochyta leaf spot, and muddy spot.

Symptoms
The first signs of web blotch are small, dark brown or tan
blotches (the color depends on the type of peanut) or netlike
brown lesions (Plate 71) on the adaxial surfaces of leaves
under a dense canopy or under conditions of high humidity.
These blotches become more numerous and enlarge to form
dark brown, roughly circular lesions with irregular margins
(Plate 72). As lesions mature, they become darker with dull,
rough surfaces and may completely cover the upper surface of
the leaf. At this stage, small blotches may be visible on the
lower surface. The leaf becomes brittle and is liable to dis
integrate and detach from the plant (Plate 73).

Causal Organism
Web blotch is caused by Phoma arachidicola Marasas, G. D.
Pauer, & Boerema. The nomenclature of the anamorph is
confusing, because the fungus was previously assigned to the Fig. 54. Pycnidiospores (arrows) of Phoma arachidicola. (Cour
genus Ascochyta (A. arachidis Woronichin and A. adzamethica tesy R. Taber)

39
septate. Some isolates form dark, one- to multicelled chla Woodard, J. A., and Liddell, C. M. 1993. Practical implementation of
mydospores (7-19 x 8-20 |om) both on aerial and submerged BLOTCHCAST, a weather-driven predictive model of web blotch in
mycelia. Colonies on potato-dextrose agar are appressed and New Mexico Valencia peanuts. (Abstr.) Phytopathology 83:1362.
creamy white. A dark brown color develops as the fungus pro
duces pigmented chlamydospores either in clusters or in chains. (Prepared by D. L. Cole and C. Liddell)
If the temperature is lowered to 18C under near-ultraviolet light,
concentric rings of pycnidia appear after 5 days in cultures on
either medium. The teleomorph is not common in naturally
infected tissue or in culture but can be induced to form on
Yellow Mold and Aflatoxin
detached leaflets under high humidity by some isolates.
Pseudothecia (65-154 |_im in diameter) are dark brown, sub- Invasion of plant products by the yellow green molds Asper
globose to globose, short beaked or unbeaked, and usually gillus flavus and A. parasiticus is a worldwide problem, espe
immersed in the substratum. Cell walls are mostly isodiametric cially in tropical and subtropical latitudes. Peanuts, com, cot
and angular to round. Asci are hyaline, cylindric to somewhat ton seed, and tree nuts are particularly susceptible to invasion,
clavate, mostly with a differentiated foot, eight spored, and both in the field and during storage. The toxicity of these fungi
distichous. Ascospores (13-17 x 4.5-6.5 |im) have one septum was first recognized in Great Britain in 1960 when turkey
and are smooth and at first hyaline, becoming dark with poults fed a protein supplement containing Brazilian peanut
maturity. The upper cell of the ascospore is broader and more meal developed a syndrome originally called turkey X-disease.
sharply tapered than the lower. Investigations of the symptoms led to the discovery of the
highly carcinogenic aflatoxins B 1; B2, Gi, and G2; Bj is the
Disease Cycle most toxic to mammals. It has subsequently been postulated
Web blotch development is generally more severe under that cyclopiazonic acid, another mycotoxin produced by A.
cool, moist conditions and is more common on irrigated than flavus, may have been responsible for several of the symptoms
on rain-fed crops. Prolonged leaf wetness periods at temper in the early reports of turkey X-disease not characteristic of
atures of 15-21C favor disease development. P. arachidicola aflatoxin poisoning.
survives in infected crop residues or on volunteer peanut The International Agency for Research on Cancer has classi
plants. Pycnidia and, in some cases, pseudothecia develop on fied aflatoxin as a probable human carcinogen. The U.S. Food
fallen leaves and provide the initial inoculum to infect sub and Drag Administration permits maximum aflatoxin levels of
sequent peanut crops. Germ tubes penetrate the cuticle directly, 20-300 and 20 ppb in peanut products destined for animal and
and small infection pegs form near the germinated spores. Net human consumption, respectively. In other countries, accept
works of individual hyphae ramify between the cuticle and the able maximum aflatoxin levels for foods range from 0 to 50
epidermis and kill adjacent cells, resulting in the web symp ppb (5 ppb is the most common) and maximum levels for
tom. Hyphae can also penetrate subepidermal tissue, and pro animalfeeds from 10 to 200 ppb.
liferation of hyphae and subsequent extensive cell necrosis Peanut seed and their products are assayed for aflatoxin by
produce typical blotch symptoms. grinding a sample and using a solvent mixture such as
methanol and water for extraction. Aflatoxin is then directly
Control measured by use of an immunoassay; or the extract is passed
Crop rotation and management of infected crop debris and through a column, and aflatoxin is quantified by thin-layer
volunteer peanut plants assist in eliminating primary sources of chromatography or high-performance liquid chromatography.
inoculum. Under conditions that favor severe web blotch infec
tion, foliar fungicide sprays are very effective. A computer Symptoms
model to predict disease onset for efficient fungicide applica Symptoms of severe drought stress in peanut plants, includ
tion has been developed. When present, early leaf spot, which ing permanent wilting of the foliage, receding of the canopy
usually appears before web~51otch, provides some controFof between rows, and shedding of leaves, indicate conditions
web blotch because it induces the production of phytoalexins favorable for preharvest aflatoxin contamination of the seed.
in peanut leaves. Germ plasm resistant to web blotch is being Harvested pods may reveal extensive insect damage, some
included in breeding programs, but no commercial cultivars are times with visible yellow green sporulation of the causal fun
yet available. gus at the points of injury. Infected seed often exhibit areas of
brown or yellow discoloration that may also be associated with
Selected References external sporulation of the fungus (Plate 74). However, consid
erable invasion and aflatoxin contamination commonly occur
Blarney, F. P. C., Chapman, J., and Young, B. W. 1977. Epiphytology without visible sporulation. Concealed damage, in which the
of Phoma web blotch and Cercospora leafspot on Spanish ground inner lumen between the cotyledons is filled with conidial
nuts. Phytophylactica 9:63-64. heads, can be detected only by splitting the seed in half (Plate
Cole, D. L. 1982. Interactions between Cercospora arachidicola and 75).
Phoma arachidicola and their effects on defoliation and kernel High levels of infection by A. flavus in peanut seed may
yield of groundnut. Plant Pathol. 31:355-362. result in preemergence rotting of the seed and seedlings, a
Pettit, R. E., Philley, G. L., Smith, D. H., and Taber, R. A. 1986. Pea condition known as yellow mold. Brown, necrotic lesions with
nut web blotch. II. Symptoms and host range of the pathogen. sporulating A. flavus are present on the cotyledons, radicles,
Peanut Sci. 13:29-30. and hypocotyls of ungerminated and germinated seed.
Phipps, P. M. 1985. Web blotch of peanut in Virginia. Plant Dis. Emerged seedlings also exhibit necrotic lesions on the cotyle
69:1097-1099.
dons, and the plants are stunted and chlorotic and have poorly
Smith, O. D., Smith, D. H., and Simpson, C. E. 1979. Web blotch
developed root systems.
(caused by Phoma arachidicola) resistance in Arachis hypogaea.
Peanut Sci. 6:99-101.
Subrahmanyam, P., and Smith, D. H. 1989. Influence of temperature,
Causal Organisms
leaf wetness period, leaf maturity, and host genotype on web blotch Conidia-bearing structures (conidiophores) of A. flavus
of peanut. Oleagineux 44:27-34. Link:Fr. and A. parasiticus Speare arise from septate, vege
Taber, R. A., Pettit, R. E., and Philley, G. L. 1984. Peanut web blotch. tative hyphae. The nonseptate, rough-walled stipe is swollen
I. Cultural characteristics and identity of causal fungus. Peanut Sci. terminally to form a globose to subglobose vesicle. Phialides
11:109-114. may be borne directly on the vesicle (uniseriate condition) or
40
may arise from metulae that cover the vesicle surface (biseriate Peanut seed that become contaminated under conditions of
condition). The vesicle, metulae when present, phialides, and drought stress may show an increase in aflatoxin when plants
chains of conidia comprise the head (Fig. 55). The heads of A. are dug and inverted in the windrow for drying if the seed
parasiticus are predominantly uniseriate. In A. flavus, seriation become rehydrated by rainfall for an extended period. Other
is more variable; usually at least 20% of the heads are bi- wise, noncontaminated seed from sound pods do not appear to
seiiate, but a small percentage of isolates are almost entirely be invaded during windrow drying. Improper storage of the
uniseriate. Conidia are globose to ellipsoidal and 3-6 pm in seed may further increase the risk for aflatoxin production.
diameter. The texture of the conidial wall is the best means of Conditions important for aflatoxin formation during storage
distinguishing the two species: conidia of A. flavus are nearly include moisture, temperature, and the condition of the seed. In
smooth to finely roughened while those of A. parasiticus are general, aflatoxin is produced at relative humidities greater
distinctly roughened. In addition, when colonies are grown on than 83% (seed moisture content of 10.5-11.0%) and at tem
Czapeks agar medium, conidia of A. flavus are yellow green to peratures of 12-42C (optimum 20-35C).
gray green en masse whereas those of A. parasiticus are dark
green (Plate 76). Isolates of either species may produce dark Control
brown to black sclerotia. A third, related aflatoxin-producing Irrigation alleviates drought stress of plants and is the best
species, A. nomius Kurtzman, Horn, & Hesseltine, has been control measure for minimizing aflatoxin contamination in the
reported only rarely from peanut commodities. Morpho field. Where irrigation is not available, the problem may be
logically, A. nomius resembles A. flavus, differing primarily in reduced by early harvest during drought before contamination
the formation of elongate sclerotia. becomes extensive. Control of insects also lowers the inci
A. flavus typically produces aflatoxins Bi and B2 in 40-80% dence of damaged seed that contain high levels of aflatoxin,
of isolates, whereas nearly all isolates of A. parasiticus pro but drought conditions limit the use of most insecticides, which
duce aflatoxins B 1; B2, Gi, and G2. Furthermore, A. flavus often require moisture to be effective. Preemergence rotting of seed
produces cyclopiazonic acid, which has not been reported from and seedlings caused by A. flavus is best avoided by planting
A. parasiticus. noninfected, high-quality seed.
Proper storage in the warehouse will prevent further con
Disease Cycle tamination of peanut seed with aflatoxin. Seed should be pro
Inocula of A. flavus and A. parasiticus are present in soil as tected from rehydration caused by intense insect activity, leaky
conidia and sclerotia and in plant clebris as mycelium. Popula roofs, or moisture condensation resulting from temperature
tions of the two species together in fields under peanut culti fluctuations. Good ventilation and adequate roof and wall insu
vation may exceed 5,000 colony-forming units per gram of lation will limit condensation in the warehouse.
soil. These fungi are saprophytic on plant debris in soil and are
potential facultative parasites of peanut seed. A. flavus appears
to be more aggressive than A. parasiticus in the preharvest
invasion of seed, although more aflatoxin may be attributed to
A. parasiticus (on the basis of the presence of G aflatoxins) in
peanut seed than in aboveground crops such as com and cotton
seed.
The two most, important conditions that favor preharvest
invasion and aflatoxin contamination of peanut seed are exces
sive heat (a mean soil temperature of 27-30C) and prolonged
drought stress during the last 3-6 weeks of the growing season.
The leaf canopy of the peanut plants recedes during drought,
which further increases soil temperatures and evaporation of
soil moisture. As the peanut seed lose moisture and eventually
attain a water activity of approximately 0.95, phytoalexin syn
thesis ceases and fungal growth is no longer inhibited. Hence,
preharvest peanut seed are most susceptible to invasion and
aflatoxin contamination at water activities of 0.90-0.95. Below
a water activity of 0.90, fungal growth is greatly restricted
because of the reduced availability of moisture but ceases only
when the water activity is less than 0.80. Mature peanut seed
apparently have an additional resistance factor, which may
account for the greater invasion by A. flavus and A. parasiticus
as well as the higher levels of aflatoxin in smaller, immature
seed.
Much of the aflatoxin in preharvest peanut seed can be
attributed to insect damage, particularly the activities of ter
mites in Asia and Africa and the lesser cornstalk borer, Elas-
mopalpus lignosellus (Zeller), in the United States. Damage by
lesser cornstalk borers is favored by the hot, dry conditions that
also promote aflatoxin contamination. Wounding of pods
involves either direct penetration, in which the seed is often
damaged, or external scarification. Insects transmit A. flavus
and A. parasiticus to the wound sites, and damage to the seed
by their feeding encourages rapid colonization by aflatoxigenic
fungi. Seed may also become infected without visible damage
to the pod. In such instances, the route of invasion is not
understood, although it has been suggested that invasion first
occurs in the ovary of the aerial peg or, alternatively, by way of
the funiculus of the developing pod. Fig. 55. Conidiophore of Aspergillus flavus.

41
 Aflatoxin is not uniformly distributed in a contaminated seed
lot, and early removal of high-risk seed, such as those that are
damaged, immature, or loose (shelled during combining opera
tions), can eliminate more than 95% of the aflatoxin during
processing. Methods of removing high-risk seed include 1) re
moval of loose seed and small pods with a high-capacity belt
screen; 2) separation of small, immature seed after shelling by
use of vibratory screens; 3) density separation, in which,
lighter, aflatoxin-contaminated seed are separated on gravity
tables; 4) electronic color sorting, which removes seed dis
colored by fungal colonization; and 5) blanching, in which the
outer seed coat, or skin, is removed to further expose discolor
ations that can be detected by electronic color sorters. Seed
from these high-risk categories are then diverted from the
edible market to oil stock.

Selected References

Dorner, J. W., Cole, R. J., and Diener, U. L. 1984. The relationship of

Aspergillus flavus and Aspergillus parasiticus with reference to
production of aflatoxins and cyclopiazonic acid. Mycopathologia
87:13-15.
Dorner, J. W., Cole, R. J., Sanders, T. H., and Blankenship, P. D.
1989. Interrelationship of kernel water activity, soil temperature,
maturity, and phytoalexin production in preharvest aflatoxin con
tamination of drought-stressed peanuts. Mycopathologia 105:117- Fig. 56. Zonate leaf spot on the upper surface of a peanut leaflet
128.
Horn, B. W., Dorner, J. W., Greene, R. L., Blankenship, P. D., and
Cole, R. J. 1994. Effect of Aspergillus parasiticus soil inoculum on
invasion of peanut seeds. Mycopathologia 125:179-191.
Klich, M. A., and Pitt, J. I. 1988. Differentiation of Aspergillus flavus
from A. parasiticus and other closely related species. Trans. Br.
Mycol. Soc. 91:99-108.
Sanders, T. H., Cole, R. J., Blankenship, P. D., and Hill, R. A. 1985.
Relation of environmental stress duration to Aspergillus flavus
invasion and aflatoxin production in preharvest peanuts. Peanut
Sci. 12:90-93.
Subrahmanyam, P., Smith, D. H., Taber, R. A., and Shepherd, E.
1987. An outbreak of yellow mold of peanut seedlings in Texas.
Mycopathologia 100:97-102.

(Prepared by B. W. Horn and J. I. Pitt)

Zonate Leaf Spot

Zonate leaf spot, a foliar disease of minor importance, has
been observed in India, Thailand, and the United States. Cris
tulariella moricola (Hino) Redhead (syn. C. pyramidalis A. M.
Waterman & R. P. Marshall) is the causal agent. The sclerotial
state is Sclerotium cinnamomi Sawada. Necrotic lesions on
leaves are 2-12 mm in diameter (Fig. 56). Small lesions have
light brown centers surrounded by a ring of necrotic tissue. A
zonate pattern is visible on both leaf surfaces (Plate 77).
Pyramidal heads (conidia) (Fig. 57) form on both surfaces of
necrotic leaves. There may be many pyramidal heads per
lesion.

f X
Selected References

Niedbalski, M., Crane, J. L., and Neely, D. 1979. Illinois fungi. 10.
Development, morphology, and taxonomy of -Cristulariella pyra
midalis. Mycologia 71:722-730.
Smith, D. H. 1972. Arachis hypogaea: A new host of Cristulariella
/
pyramidalis. Plant Dis. Rep. 56:796-797.
Fig. 57. Pyramidal head of Cristulariella pyramidalis. (Courtesy
(Prepared by D. H. Smith) A. Latham)

42
Color Plates
 1. Alternaria leaf spot. (Courtesy D. H. Smith) 2. Early stages of Aspergillus crown rot. (Courtesy D. M.
Porter)

4. Subterranean sporulation of Aspergillus niger, (Courtesy 5. Sym ptom s of black hull, caused by
P Phipps) Chalara elegans. (Courtesy D. Hsi)

3. Sporulation of Aspergillus niger on a

shredded taproot. (C ourtesy D. M.
Porter)

6. Leaf spot sym ptom s caused by Botrytis cinerea. (Cour

tesy D. M. Porter)

7. Conidia and conidiophores of Botrytis cinerea. (Courtesy 8. G liocladium roseum associated with m ycelium of
D. M. Porter) Botrytis spp. (Courtesy D. M. Porter)

COLOR PLATES
 9. Field sym ptom s of Botrytis blight. (Courtesy D. M. Porter) 10. Botrytis cinerea sporulating on a stem, petiole, and
stipule. (Courtesy D. M. Porter)

11. Botrytis cinerea fruiting structures on a stem. (Courtesy 12. Foliar sym ptom s of charcoal rot. (Courtesy J. Dam i
D. M. Porter) cone)

13. Foliar sym ptom s of charcoal rot. (Courtesy J. Dam i 14. Taproot sym ptom s of charcoal rot. (Courtesy J. Dam i
cone) cone)

15. Field sym ptom s of Cylindrocladium black rot. (Courtesy 16. Roots, pegs, and pods infected with Cylindrocladium
P. Phipps) parasiticum . (Courtesy P. Phipps)

COLOR PLATES
*
17. Reddish orange perithecia of Calonectria ilicicola in a 18. A cluster of delim ited shell spots. (Courtesy Z. R.
plant crown at the soil surface. (Courtesy P. Phipps) Frank)

19. Pods with primary spots and spots with concentric 20. Field sym ptom s of Diplodia collar rot. (Courtesy D. M.
rings caused by secondary invaders. (Courtesy Z. R. Frank) Porter)

21. Sym ptoms of Diplodia gossypina on pods. (Courtesy 22. Pycnidia of Diplodia gossypina embedded in host tis
D. M. Porter) sue. (Courtesy D. M. Porter)

23. Conidia and conidiophores of Diplodia gossypina. 24. Early (brown lesions) and late (black lesions) leaf spots
(Courtesy D. M. Porter) on a lower leaf surface. (Courtesy D. H. Smith)

COLOR PLATES
 25. Early (left) and late (right) leaf spot. (Courtesy D. H. 26. Aerial infrared photograph of fields with good leaf spot
Smith) control (dark red, right) and defoliation caused by poor or
no leaf spot control (brown, left). (Courtesy F. M. Shokes)

v .f.f/ -*

I-- '
. ,v

\y r^v . -

- N .

27. Sudden wilt caused by Fusarium sp. (Courtesy Z. 28. Pink pods caused by Fusarium solani. (Courtesy D.
Frank) Smith)

29. Leaf blight of peanut caused by M yrothecium roridum. 30. Sym ptoms caused by the pod rot complex. Several
(Courtesy P. Subrahm anyam) pathogens can be isolated from a single pod. (Courtesy A. S.
Csinos)

31. Pepper spot caused by Leptosphaerulina crassiasca. 32. Leaf scorch caused by Leptosphaerulina crassiasca.
(Courtesy D. M. Porter) (Courtesy D. H. Smith)

COLOR PLATES
33. Phyllosticta leaf spot. (Courtesy D. H. Smith) 34. Phyllosticta leaf spot with pycnidia. (Courtesy D. H.
Smith)

35. Acicular branching and hyphal strands of P hym ato 36. Spores of Phym atotrichum omnivorum. (Courtesy R.
trichum omnivorum. (Courtesy R. Taber) Taber)

37. Pythium pod rot sym ptom s on Virginia peanuts. 38. W ilt caused by Pythium m yriotylum. (Courtesy D. M.
(Courtesy D. M. Porter) Porter)

39. Young seedlings with sore shin caused by Rhizoctonia 40. R hizoctonia lesions on young plants. (Courtesy D. M.
solani (right) and control (left). (Courtesy D. Bell) Porter)

COLOR PLATES
 41. Stem lesions caused by Rhizoctonia solani AG-4.
(Courtesy T. B. Brenneman)

42. Rhizoctonia limb rot sym ptom s on

43. Stem lesion caused by Rhizoctonia solani AG-4. plants dam aged by tracto r tires.
(Courtesy T. B. Brenneman) (Courtesy T. B. Brenneman)

,
H | 1\ V-
4 Ii J!1 /
t
f , #' j
' 11 \\ /
. ' t i . ,* r-m|
-.4. V,,v 1 ,H
*..*,f rt^*4*rf..iv. '*'#* H
i-'vi..' i i
i i
44. Severe Rhizoctonia limb rot sym ptom s and loss of pods 45. Peg dam age on plants infected with Rhizoctonia solani.
near the taproot. (Courtesy T. B. Brenneman) (Courtesy D. M. Porter)

46. Pod rot caused by Rhizoctonia solani. (Courtesy D. M 47. Sym ptom s of Rhizoctonia solani AG -4 infection of pig
Porter) weed, a comm on weed. (Courtesy T. B. Brenneman)

COLOR PLATES
48. Rust pustules on a lower leaf surface. (Courtesy P. 49. Rust pustules on a lower leaf surface. (Courtesy P.
Subrahm anyam) Subrahm anyam)

50. Sym ptom s caused by Sphaceloma arachidis on a 51. Scab sym ptom s caused by Sphacelom a arachidis.
stem. (Courtesy L. Giorda) (Courtesy L. Giorda)

52. Field sym ptom s of Sclerotinia blight. (Courtesy D. M. 53. Fluffy, white mycelium of Sclerotinia minor. (Courtesy
Porter) D. M. Porter)

54. Shredding of plant tissues caused by Sclerotinia minor. 55. Sclerotia of Sclerotinia m inor on infected branches.
(Courtesy D. M. Porter) (Courtesy D. M. Porter)

COLOR PLATES
 56. Sclerotia of Sclerotinia m inor in pods. (Courtesy D. M. 57. Apothecia from germ inating sclerotia of Sclerotinia
Porter) minor. (Courtesy D. M. Porter)

58. Infection cushion of Sclerotinia m inor on peanut stems

18 hr after inoculation. (Courtesy H. A. Melouk)

59. Sclerotia of Sclerotinia m inor colo

nized by Trichoderma sp. (Courtesy
D. M. Porter)

60. Stem rot caused by Sclerotium rolfsii with actively

growing, white mycelium. (Courtesy T. B. Brenneman)

61. Sclerotia of Sclerotium rolfsii on peanut stems and 62. Active mycelium and young sclerotia of Sclerotium rolf-
debris. (Courtesy D. M. Porter) s/7 on a single peanut peg. (Courtesy T. B. Brennem an)

COLOR PLATES
63. Sclerotial initials on pods colonized by Sclerotium rolf- 64. Right, plants killed by early Sclerotium rolfsii infection
sii. (Courtesy T. B. Brennem an) and left, plants with active stem and pod rot. (Courtesy
T. B. Brenneman)

65. Inverted peanuts treated for stem rot with a fungicide 66. Chlorosis and marginal leaf necrosis in Verticillium-
(right) and untreated peanuts (left). (Courtesy T. B. Brenneman) infected peanut plants. (Courtesy J. P. Damicone)

67. Marginal necrosis on leaves of plants infected with

Verticillium dahliae. (Courtesy D. M. Porter)

68. Vascular discoloration of the taproot

of a plant infected with Verticillium
dahliae. (Courtesy D. M. Porter)

69. Brown discoloration of the vascular elem ents in leaf

petioles from Verticillium-infected plants. (Courtesy J. P.
Damicone)

COLOR PLATES
 70. Verticillium dahliae m icrosclerotia in root tissue. 71. Early web blotch sym ptom s on leaves. (Courtesy D. L.
(Courtesy H. Melouk) Cole)

A
72. Sym ptom s of advanced web blotch on a leaf. (Courtesy 73. Plants exhibiting severe sym ptom s of web blotch.
D. L. Cole) (Courtesy D. L. Cole)

74. Aspergillus flavus sporulating on a peanut seed. (Cour 75. Concealed damage in peanut seeds that have been
tesy B. Horn) split in half to reveal sporulating Aspergillus flavus. (Cour
tesy B. Horn)

76. A, Aspergillus flavus and B, A. parasiticus on Czapeks 77. Zonate leaf spot caused by Cristulariella pyram idalis.
agar m edium after 7 days at 30C. (Courtesy B. Horn) (Courtesy D. H. Smith)

COLOR PLATES
78. Bacterial leaf spot of peanut caused by Pseudom onas 79. Early sym ptom s (flagging) of bacterial wilt. (Courtesy
sp. in India. (Courtesy P. Subrahm anyam) D. M. Porter)

80. Dead branch of a plant infected with Pseudom onas 81. Advanced stage of bacterial wilt caused by P seu
solanacearum. (Courtesy D. M. Porter) dom onas solanacearum. (Courtesy D. M. Porter)

82. Vascular discoloration of a taproot infected with Pseu 83. Experimental plots with peanut cultivars resistant and
dom onas solanacearum. (Courtesy D. M. Porter) susceptible to bacterial wilt. (Courtesy A. C. Hayward)

If M
II
i
II
84. Roots and pods with galls caused by M eloidogyne are- 85. Left, pods from untreated soil with galls or w arts
naria. (Courtesy D. H. Smith) caused by M eloidogyne arenaria and right, pods from
nem aticide-treated soil. (Courtesy W. Horne)

COLOR PLATES
 87. Left, plants growing in soil treated with a nematicide
for control of M eloidogyne arenaria and right, plants in
untreated soil. (Courtesy R. Rodriguez-Kabana)

86. Root dam age caused by M eloido

gyne hapla. (Courtesy R. Rodriguez- 88. Eggs of M eloidogyne arenaria. (Courtesy N. Kokalis-
Kabana) Burelle)

89. M eloidogyne arenaria juvenile em erging from an egg 90. Giant cells induced by female M eloidogyne arenaria in
(Courtesy N. Kokalis-Burelle) root tissue. (Courtesy W. Horne)

91. M eloidogyne arenaria male. (Courtesy N. Kokalis- 92. Globose, pyriform fem ales of M eloidogyne arenaria
Burelle) extracted from root tissue. (Courtesy N. Kokalis-Burelle)

COLOR PLATES
93. Mature M eloidogyne arenaria fem ales in root tissue. 94. Sym ptom s caused by lesion nematodes on pods.
(Courtesy N. Kokalis-Burelle) (Courtesy J. L. Starr)

95. Stunting of plants in a peanut field infested with sting ne 96. Root system s dam aged by Belonolaim us longicau
matodes (Belonolaimus longicaudatus). (Courtesy A. Allison) datus. (Courtesy A. Allison)

97. Symptoms caused by Ditylenchus africanus on peanuts, 98. D itylenchus africanus, which feeds on peanut and on a
including discoloration of the pod, discoloration of the seed wide variety of fungi, including Penicillium spp. (Courtesy C.
testa, and premature seed germination. (Courtesy C. Venter) Venter)

99. C hlorotic rings caused by the tom ato spotted w ilt virus. 100. Plants with flaccid, drooping petioles caused by the
(Courtesy D. H. Smith) peanut bud necrosis virus. (Courtesy D. V. R. Reddy)

COLOR PLATES
 101. Chlorosis, leaf distortion, and line pattern caused by 102. Left, healthy seeds and right, seeds infected with the
the tom ato spotted w ilt virus. (Courtesy D. H. Smith) tom ato spotted w ilt virus. (Courtesy D. H. Smith)

103. Left, healthy plants and right, plants infected with the 104. Mosaic mottling and chlorotic rings on plants infected
Indian peanut clum p virus. (Courtesy D. V. R. Reddy) with the peanut clum p virus. (Courtesy D. V. R. Reddy)

105. Sym ptom s of chlorotic rosette. (Courtesy P. S ubralr 106. Chlorotic rosette symptom caused by the groundnut
manyam) rosette virus. (Courtesy D. V. R. Reddy)

107. Plants infected with the mosaic rosette virus. (Cour

tesy D. V. R. Reddy)

COLOR PLATES
 109. Inward curling of leaf edges and interveinal de
pression caused by the peanut m ottle virus. (Courtesy
D. V. R. Reddy)

108. Mosaic sym ptom s caused by the

peanut m ottle virus. (Courtesy D. V. R. 110. Stripes along the veins caused by the peanut stripe
Reddy) virus. (Courtesy J. W. Demski)

111. Green blotches caused by the peanut stripe virus. 112. Mild mottle sym ptom s caused by the peanut stripe
(Courtesy D. V. R. Reddy) virus. (Courtesy J. W. Demski)

113. Plant infected with the peanut stunt virus. (Courtesy 114. Stunted plants with leaflets showing rolled edges and
S. A. Tolin) necrosis induced by the cow pea mild m ottle virus.
(Courtesy D. V. R. Reddy)

COLOR PLATES
 115. Sym ptom s of chlorosis caused by the cucum ber 116. Distorted and puckered leaflets with necrosis caused
m osaic virus. (Courtesy Z. Xu) by the groundnut streak m osaic virus. (Courtesy P.
Subrahm anyam)

-A- *

117. Yellow spots caused by the peanut yellow spot virus. 118. Sym ptom s of witches-broom caused by a phyto
(Courtesy D. V. R. Reddy) plasma. (Courtesy D. V. R. Reddy)

119. Drought-stressed plants. (Courtesy D. H. Smith) 120. Sym ptom s of drought stress. (Courtesy D. M. Porter)

121. Frost injury. (Courtesy D. M. Porter) 122. Frost injury. (Courtesy D. M. Porter)

COLOR PLATES
123. Variegated leaves, a genetic abnormality. (Courtesy 124. Variegated leaflet, a genetic abnormality. (Courtesy
D. M. Porter) D. M. Porter)

125. Hail damage. (Courtesy R. Sturgeon) 126. Dicam ba injury. (Courtesy J. Beasley)

127. Paraquat injury. (Courtesy J. Everest) 128. C h lo roa ce ta m ide injury to seedlings.
(Courtesy C. Swann)

129. Acifluorfen injury. (Courtesy G. Sullivan) 130. Dinitroaniline injury to seedlings. (Courtesy G. Sullivan)

COLOR PLATES
 131. 2,4-DB injury. (Courtesy G. Sullivan) 132. Injury caused by s-triazine. (Courtesy C. Swann)

133. Metribuzin injury. (Courtesy C. Swann) 134. Vernolate injury. (Courtesy C. Swann)

135. Bentazon injury. (Courtesy C. Swann) 136. Norflurazon injury. (Courtesy G. Sullivan)

137. Lightning injury. (Courtesy S. Thom pson) 138. Nitrogen deficiency. (Courtesy R. Henning)

COLOR PLATES
139. Calcium deficiency. (Courtesy A. Narayanan)

V
f t '""'"'a ^ ..
Br jH

>i *J r '.'X

JKk
141. Iron chlorosis. (Courtesy D. H. Smith) 142. M anganese deficiency. (Courtesy R. Henning)

143. Chlorotic leaves caused by zinc toxicity. (Courtesy R.

Henning)

145. Stem splitting caused by zinc toxicity. (Courtesy D. M. 146. Field sym ptom s of copper deficiency. (Courtesy L.
Porter) Tripp)

COLOR PLATES
 x C' ^

... * .s#'
'Sate, '
<Njt , | I.., ; -s '"
.

y>

147, Leaves with m arginal chlorosis caused by copper 148. Boron toxicity. (Courtesy M. Walker)
deficiency. (Courtesy C. Gray)

149. Leaf injury caused by ozone. (Courtesy A. Heagle) 150. Larva of the fall arm yworm, Spodoptera frugiperda, on
a peanut leaf. (Courtesy R. E. Lynch)

151. Beet arm yworm, Spodoptera exigua, larva on a peanut 152. Adults of the beet arm yworm, Spodoptera exigua.
leaf. (Courtesy S. Poe) (Courtesy S. Poe)

153. Spodoptera litura larva feeding on a peanut leaf. 154. Egg m asses of the tobacco arm yworm, Spodoptera
(Courtesy ICRISAT) litura, on a peanut leaf. (Courtesy ICRISAT)

COLOR PLATES
155. Larva of the corn earworm , Helicoverpa zea, feeding 156. Larva of the gram pod borer, Heliothis armigera,
on peanut. (Courtesy R. E. Lynch) feeding on a peanut leaf. (Courtesy ICRISAT)

157. Larva of the velvetbean caterpillar, Anticarsia gem - 158. Larva of the groundnut leafminer, Aproaerem a modi-
matalis, on peanut. (Courtesy S. Poe) cella, feeding on a peanut leaf. (Courtesy ICRISAT)

159. Larva of the red-headed hairy caterpillar, Am sacta 160. Adult red-headed hairy caterpillar, Am sacta albistriga.
albistriga, on peanut. (Courtesy ICRISAT) (Courtesy ICRISAT)

161. Adult and cast nymphal skin of the potato leafhopper, 162. Adult of the groundnut jassid, Empoasca kerri, on
Empoasca fabae. (C ourtesy S. Poe) peanut. (Courtesy ICRISAT)

COLOR PLATES
 163. Hopper burn caused by potato leafhopper feeding. 164. Immature and adult tobacco thrips, Frankliniella
(Courtesy J. Stewart) fusca. (Courtesy R. Howell)

165. Cupping and crinkling of peanut leaves caused by 166. Aphids feeding on peanut terminals. (Courtesy D. M.
thrips injury. (Courtesy D. H. Smith) Porter)

167. Aphis craccivora feeding on peanut flowers. (Cour 168. Damage to peanut caused by tw ospotted spider
tesy ICRISAT) mites, Tetranychus urticae. (Courtesy J. C. Smith)

169. Adult of the sweetpotato whitefly, Bem isia tabaci, on 170. Larva of the lesser cornstalk borer, Elasm opalpus lig-
peanut. (Courtesy R. E. Lynch) nosellus. (Courtesy T. P. Mack)

COLOR PLATES
171. Female lesser cornstalk borer moth. (Courtesy T. P. 172. Male lesser cornstalk borer moth. (Courtesy T. P.
Mack) Mack)

173. Peanut pod externally scarified by the lesser cornstalk 174. Southern corn rootworm adult, the twelve-spotted
borer. (Courtesy R. E. Lynch) cucum ber beetle. (Courtesy J. C. Smith)

175. Larva of the southern corn rootworm, Diabrotica

undecim punctata howardi. (Courtesy R. E. Lynch)

176. Adult beetles, Lachnosterna se r

rata, an im portant white grub pest of
peanut. (Courtesy ICRISAT)

177. Larva or white grub of Lachnosterna serrata. (Courtesy

ICRISAT)

COLOR PLATES
 178. Termites, im portant pests of peanut in Africa and Asia. 179. Peanut pods externally scarified by term ites. (Cour
(Courtesy ICRISAT) tesy ICRISAT)

180. W ireworm larva and dam age to a peanut pod. (C our 181. Adult Indianmeal moth, Plodia interpunctella. (Cour
tesy R. Howell) tesy L. Zettler)

182. Adult rice moth, Corcyra cephalonica. (Courtesy 183. Larva and dam age caused by the rice moth, Corcyra
ICRISAT) cephalonica. (Courtesy ICRISAT)

184. Adults and larvae of the red flour beetle, Tribolium 185. Larva of the red flour beetle, Tribolium castaneum.
castaneum. (Courtesy L. Zettler) (Courtesy L. Zettler)

COLOR PLATES
186. Larva of the groundnut bruchid, Caryedon serratus, 187. The lygaeid bug Elasm olom us sordidus, a pest of
emerging from a peanut pod. (Courtesy ICRISAT) stored peanut. (Courtesy ICRISAT)

188. Alectra vogelii, a root parasite of peanut. (Courtesy P. 189. The connection between Alectra vogelii and the
Subrahm anyam ) peanut roots. (Courtesy D. H. Smith)

190. Striga herm ontheca, a root 191. Striga gesnarioides, a parasite of

parasite of peanut in W est peanut in M ozam bique. (Courtesy D.
Africa. (Courtesy K. V. Ramaiah) R. Butler)

CO LO R PLATES
 192. Dodder (Cuscuta campestris), a parasite of peanut in 193. Azygospore of Gigaspora sp. (Courtesy D. M. Porter)
the United States. (Courtesy D. H. Smith)

194. Extramatrical vesicles of Gigaspora sp. (Courtesy 195. Roots of two peanut cultivars nodulated by Rhizobium
D. M. Porter) sp. (Courtesy J. Wynne)

NC123 ININOCJNITROGEI

196. Plants inoculated with an effective Rhizobium strain 197. Agar im print of the abaxial surface of a field-collected
(NC 123), uninoculated plants, plants that received nitrogen peanut leaf colonized by a variety of bacteria (nutrient agar
fertilizer, and plants inoculated with an ineffective R hi contained chlorothalonil to inhibit fungal growth). (Courtesy
zobium strain (TAL420). (Courtesy J. Wynne) H. W. Spurr)

198. Leaf spot caused by Cercosporidium personatum col

onized by Dicyma sp. (Courtesy D. M. Porter)

COLOR PLATES
 Diseases Caused by Bacteria
regions, and the annual loss in pod yield caused by the disease
Bacterial Leaf Spot is estimated to be approximately 36,0001. The disease is wide
spread in the major peanut-growing areas of both northern and
Bacterial leaf spot of peanut, caused by an unidentified spe southern Vietnam and is most severe in dryland cropping sys
cies of Pseudomonas, has been observed in India, Vietnam, tems, especially on sandy upland or riverbank soils. Peanut is
and Zimbabwe. probably less susceptible to bacterial wilt than solanaceous
hosts such as tomato, potato, tobacco, and eggplant, except
Symptoms where peanut is intensely cropped under environmental condi
Lesions, which are small, circular to irregular, and light tions conducive to the disease and highly virulent strains of P.
brown, frequently occur on the lower leaves of young plants. solanacearum occur. Bacterial wilt is regarded as a potential
At early stages of disease development, the lesions are water threat to peanut production in several warm, humid areas of the
soaked and prominent on upper surfaces of leaflets. On the world as production expands into new areas or cultural prac
lower surfaces of the leaflets, lesions become visible only after tices change.
the spots on the upper surfaces are well developed. The lesions
enlarge, become irregular, and may develop chlorotic halos. Symptoms
When lesions are fully developed, their centers are light brown Infection of young plants can result in the sudden wilting of
with dark brown margins (Plate 78). Under favorable condi stems and foliage, although leaves on dead plants remain green
tions for disease development, the lesions coalesce, and the (Plate 79). Wilt symptoms can be observed 2-3 weeks after
leaflets become chlorotic and shed prematurely. sowing. The first sign of the disease is a slight drooping or
Bacterial colonies grown on D4 medium are pale white, curling of one or more leaves. In mature plants or in cultivars
circular, raised, and 1-2 mm in diameter. The bacterium (0.5- that are not highly susceptible, a gradual decline causes the
0.8 x 1.0-1.3 |im) is gram negative, nonfluorescent on Kings foliage to turn yellow. Wilt and death of single branches (Plate
medium, and rod shaped and has one or two polar flagella. 80) or of the entire plant (Plate 81) may follow. Alternatively,
the plant may show signs of recovery. The root systems of
Selected References infected plants display numerous discolored and dead roots.
Dying branches often curl to form a shepherds crook. Diag
Kado, C. I., and Heskett. 1970. Selective media for isolation of Agro nostic characteristics for this disease are a dark discoloration in
bacterium, Corynebacterium, Erwinia, Pseudomonas, and Xantho- the xylem and pith (Plate 82) and a milky white ooze com
monas. Phytopathology 60:969-976. posed of masses of bacteria that exudes from cut ends of stems
Raghava Reddy, J., McDonald, D., and Joshi, N. C. 1989. Bacterial placed in water.
diseases of ICRISAT legume crops and methods in plant bacteriol
ogy. Pages 37-55 in: Rep. Int. Legumes Pathol. Training Course, Causal Organism
8th. Int. Crops Res. Inst. Semi-Arid Trop. Legumes Pathol. Progr.
Rep. 10. P. solanacearum (Smith) Smith (syns. Burkholderia solana
Subrahmanyam, P., Wongkaew, S., Reddy, D. V. R., Demski, J. W., cearum (Yabuuchi et al.) and Ralstonia solanacearum (Yabu-
McDonald, D., Sharma, S. B., and Smith, D. H. 1992. Field diag uchi et al.)) is an aerobic, gram-negative, rod-shaped bacterium
nosis of groundnut diseases. Int. Crops Res. Inst. Semi-Arid Trop. that does not form spores and accumulates poly-p-hydroxy-
Bull. 36. butyrate as a carbon reserve. Although the bacterium does not
produce fluorescent pigments, it can produce a brown, diffus
(Prepared by P. Subrahmanyam) ible pigment on agar media containing tyrosine. The organism
does not grow at 41 C, and it cannot utilize arginine and
betaine as sole carbon sources. The bacterium is unable to
hydrolyze starch, and gelatin is liquefied weakly or not at all.
Bacterial Wilt There is variation in nitrate metabolism. Asian isolates from
peanut produce gas from nitrate, whereas those from the Amer
Bacterial wilt of peanut, caused by Pseudomonas solana- icas reduce nitrate to nitrite but without gas production. The
cearum, was first reported in Indonesia in 1905 and since then optimum temperature for growth is 30-35C.
has been reported in many regions throughout the world. The P. solanacearum is heterogeneous in phenotypic properties,
first report of the disease in the United States was in 1915 from such as ability to utilize specific carbon sources, and has been
Granville County, North Carolina, which had previously expe classified into five biovars on the basis of differences in oxida
rienced a high incidence of bacterial wilt of tobacco. Bacterial tion of particular hexose alcohols and disaccharides. Biovars 1,
wilt of peanut was responsible for heavy losses in Georgia in 3, and 4 have been reported as pathogens of peanut. In the
1913 but is now of minor importance in the United States. By United States, the disease is caused by biovar 1, whereas in
contrast, the disease is a major constraint to peanut production those Asian and African countries for which there is published
in several Asian and African countries, notably China, Indo information, it is caused by biovar 3 or 4. On the basis of hosts
nesia, Malaysia, Uganda, and Vietnam. of origin and host range, isolates of P. solanacearum have been
In Indonesia, bacterial wilt of peanut is most severe in tentatively divided into five races. The isolates from peanut are
western Java, southern Sulawesi, and southern Sumatra and is identified as race 1.
also important in central and eastern Java, Bali, and North The classification of strains of P. solanacearum has been
Sulawesi. In China, the disease is most severe in 16 southern greatly advanced by DNA analysis. Restriction fragment length
and central provinces, where it is estimated that more than polymorphism (RFLP) analysis has been used to differentiate
200,000 ha of peanut fields are infested with the wilt pathogen. P. solanacearum into RFLP groups 'by using nine probes to
The annual incidence of the disease is estimated to be 4-8% on regions of the chromosomal DNA associated with virulence
resistant cultivars and 10-30% on susceptible ones in some and the hypersensitive response. Similarity coefficients for all

43
 pairwise combinations of RFLP groups show two major divi peanut. In China, seven pathotypes have been identified on the
sions into which biovars and races can be placed (Table 4). The basis of their pathogenicity on six indicator cultivars having
same two divisions, one including biovars 1 and 2 and the different levels of wilt resistance. All six cultivars were sus
other biovars 3, 4, and 5, are also obtained by sequencing of ceptible to pathotype 7 and moderately resistant to pathotype 6.
the approximately 1,540 nucleotides in the 16S rRNA genes. Strains from southern China are generally more virulent to
The present nomenclature does not reflect this fundamental peanut than those from northern regions. Differences in viru
difference at the genetic level. It is conceivable that divisions I lence among isolates from peanut have been observed in Indo
and IE represent subspecies of P. solanacearum. It is of quaran nesia, but the degree of specialization to different cultivars does
tine significance that strains pathogenic to peanut are found in not warrant designation of pathotypes.
both divisions, biovar 1 of division H in the southeastern United
States and biovars 3 and 4 of division I in Asia and Africa Disease Cycle
(Table 5). Division II may have originated in the Americas and Bacterial wilt is a soilbome disease. Continuous cropping of
division I in Asia. a susceptible host or weed hosts will favor long-term survival
In culture, P. solanacearum undergoes spontaneous mutation of the pathogen. Some of the most common weed hosts in pea
involving multiple changes in phenotype; this phenomenon has nut fields in Asia are Ageratum conyzoid.es L., Crasso-
become known as phenotype conversion. Tliese pleiotropic cephalum crepidioides (Benth.) S. Moore, Crotalaria juncea
mutants show reduced extracellular polysaccharide production L., and Croton hirtus L. Infected crop residues also serve as
and endoglucanase activity and virulence and increased motil primary sources of inoculum.
ity. Highly motile, avirulent forms can rapidly dominate the Bacterial wilt is profoundly influenced by environmental
virulent form, especially in unaerated liquid media. Although conditions, particularly soil temperature and moisture content.
virulent forms are usually nonmotile, they may possess single High levels of soil moisture not only aid in the survival of the
polar flagella, which characteristically are straight rather than bacterium, but also increase bacterial dissemination and dis
wavy. Avirulent and virulent strains can be differentiated by ease development. Invasion of peanut occurs through wounds
growing the organism on a tetrazolium medium. Colonies of or natural openings in the roots followed by invasion of the
virulent strains are fluidal and irregular in shape and have water-conducting tissues, bacterial multiplication, blockage,
white to pink centers that darken with age. Avirulent colonies and interference with water transport. Root injury by soil
are round, butyrous, and uniformly red, even at early stages of insects and nematodes provides points of entry for the bac
growth. terium and may increase disease severity. Soil temperatures
Maintenance of virulence in culture requires continuous above 25C (at a soil depth of 5 cm) and high soil moisture
selection of the fluidal wild-type colony form from turbid sus favor the development of bacterial wilt. The disease is exacer
pensions kept at 15-20C or at room temperature (about 25C). bated by soil temperatures greater than 30C (air temperatures
Unselected cultures rapidly become dominated by the butyrous greater than 25C) for 10 days. Optimum*temperatures for wilt
colony form, giving rise to many reports in the literature of development are 28-33 C. In greenhouse-studies in Australia
loss of virulence by P. solanacearum in culture. with biovar 3, wilt severity was most pronounced under diurnal
In Indonesia and China, most of the peanut isolates belong to temperature regimes of 35/30C and 30/25C and was slight or
biovar 3, which is more virulent to peanut than biovar 1 occur absent under regimes of 25/20C and 20/15C.
ring in the United States. Peanut isolates are reported to be Reports on the incidence and severity of bacterial wilt in
more virulent on peanut than are isolates from other host crops. different soil types are contradictory. In Indonesia, the disease
Strains of P. solanacearum differ greatly in their virulence on has been most prevalent and severe in clay soils; in China, it is
predominant in sandy soils and relatively unknown in clay or
loam soils. The disease also occurs in red lateritic soils. In
TABLE 4. Classification of Pseudomonas solanacearuma Malaysia, the disease was shown to be more severe in clay soil
than in two types of sandy soils at the same moisture level.
~Disease severity increased significantly with an increase in
Biovars11 3,4, and 5 1 and 2 moisture for each of three different soil types. Continuous
Number of groups 16 12 planting of susceptible cultivars in wet soils leads to a rapid,
Similarity coefficient (%) buildup of inoculum.
Within division 78 9 62 19 Studies in China, Indonesia, Malaysia, and Vietnam have
Between divisions 13.5
shown that seed transmission occurs at a rate of 415%, the
aBased on restriction fragment length polymorphism involving nine highest rates occurring with freshly harvested seed. Infected
DNA probes to chromosomal DNA into 28 groups. seed is a potential source of primary inoculum, especially for
bRepresentatives of race 1 (Cook et al., 1989) are found in divisions I disease-free areas. However, there is rapid loss of viability of
and II, while races 2 and 3 are found in division II.
the bacterium as peanut seed dry to a moisture content below
9%. In areas where well-dried seed is used, seedbome infec
tion is unlikely to occur.
TABLE 5. Classification of strains of Pseudomonas solanacearum
from peanut Control
RFLPa Analysis Crop rotations are effective in reducing losses caused by
Country Biovar Division Groups
bacterial wilt but do not give complete control of the disease.
Rotations of peanut with crops that are immune or highly resis
Indonesia 3 I NDb tant to P. solanacearum and with nonhost crops such as rice,
Papua New Guinea 3 I ND com, soybean, and sugarcane are effective measures. Rotation
Philippines 3 I ND
Peoples Republic of China ND
of peanut with rice for 1-2 years or with other nonhost crops
3 I
4 I 11 and 17 such as sugarcane for 2-5 years is the most effective cultural
Sri Lanka 3 I ND control measure. Other cultural control measures include flood
Uganda 3 I ND ing peanut fields for 15-30 days before sowing and improving
4 I ND soil drainage. Sowing dates can be adjusted to avoid periods of
United States 1 II ND high temperature or ample soil moisture, conditions that favor
aRestriction fragment length polymorphism. bacterial infection and disease development. For example, in
bNo data available. the Hubei Province of China, early sowing in mid-April results
44
 in much lower incidence and severity of bacterial wilt than Selected References
sowing in June. Other measures include burning of crop resi
dues, removal of weeds, and cleaning of farm tools after opera Abdullah, H Maine, L. M. J., and Naib, H. 1983. The effects of soil
tions in infested fields. Chemical control measures have not types and moisture levels on bacterial wilt disease of groundnut
(Arachis hypogaea). Pertanika 6:26-31.
proved successful. In view of the potential for seedbome trans
Cook, D., Barlow, E., and Sequeira, L. 1989. Genetic diversity of
mission, seed movement should be strictly controlled to avoid Pseudomonas solanacearum-. Detection of restriction fragment length
spreading the pathogen to disease-free areas. polymorphisms with DNA probes that specify virulence and the
The use of resistant cultivars is the most effective and prac hypersensitive response. Mol. Plant-Microbe Interact. 2:113-121.
tical method to control bacterial wilt. Peanut is the first crop in Hayward, A. C. 1991. Biology and epidemiology of bacterial wilt
which resistance has been successfully used against P. caused by Pseudomonas solanacearum. Annu. Rev. Phytopathol
solanacearum (Plate 83). The high level of resistance in the 29:65-87.
cultivar Schwarz 21, first identified in Indonesia, has held up Hayward, A. C., and Hartman, G. L. 1994. Bacterial Wilt: The Dis
for more than 50 years, and strains capable of overcoming ease and Its Causative Agent, Pseudomonas solanacearum. C.A.B.
this resistance have, not evolved. A series of resistant culti International, Wallingford, England.
vars has been released and used in production in China since He, L. Y Sequeira, L., and Kelman, A. 1983. Characteristics of strains
the 1980s. of Pseudomonas solanacearum from China. Plant Dis. 67:1357-1361.
Kelman, A. 1953. The bacterial wilt caused by Pseudomonas solana
Field screening under uniformly high disease pressure in
cearum. N.C. Agric. Exp. Stn. Tech. Bull. 99.
wilt-infested plots at Cikeumeuh, western Java; Jambegede,
Mehari, V. K., Liao, B. S., Tan, Y. J., Robinson-Smith, A., McDonald,
eastern Java; Indonesia; and Hong An, Hubei Province, China, D., and Hayward, A. C. 1994. Bacterial wilt of groundnut. Int.
has proved to be a useful way to identify sources of resistance. Crops Res. Inst. Semi-Arid Trop. Bull. 35.
Wilt-resistant lines have approximately 80-95% plant survival Schaad, N. W. 1988. Laboratory Guide for Identification of Plant
compared with less than 10% survival in susceptible culti Pathogenic Bacteria. 2nd ed. American Phytopathological Society,
vars in infested fields. Lines showing wilt incidence of less St. Paul, MN.
than 10% are considered highly resistant and those with 10- Yabuuchi, E., Kosako, Y., Yano, I., Hotta, H., and Nishiuchi, Y. 1995.
20% incidence moderately resistant. Host-pathogen-environ- Transfer of two Burkholderia and an Alcaligenes species to Ral-
ment interactions may be responsible for the variability in stonia gen. nov.: Proposal of Ralstonia picketii (Ralston, Palleroni
disease reactions of some lines at different locations. For and Doudoroff 1973) comb, nov., Ralstonia solanacearum (Smith
example, the resistant Indonesian cultivars Gajah, Kidang, 1896) comb. nov. and Ralstonia eutropha (Davis 1969) comb. nov.
Microbiol. Immunol. 39:897-904.
Macan, and Banteng were only moderately resistant in some
areas of China. (Prepared by A. C. Hayward and L. Y. He)

Diseases Caused by Nematodes

Peanut plants infected with root-knot nematodes may show'
Root-Knot Nematodes various degrees of stunting and chlorosis. Severely infected
runner-type cultivars typically show limited growth, resulting
Root-knot nematodes (Meloidogyne spp.) are the nematodes in poor ground coverage at midseason (Plate 87). Root growth
causing the greatest yield losses in peanut. The conspicuous is restricted and the vascular elements of infected tissues are
root galls and warts caused by these nematodes resulted in
their early recognition as serious pathogens. Yield losses in
fields infested with the peanut root-knot nematode range from
20 to 90%. Root-knot nematodes can limit development of Rhi-
zobium nodules and aggravate damage caused by other soil
bome plant pathogens. In most fields of the southeastern United
States, continuous culture of the peanut results in increased
damage from root-knot nematodes and associated pathogens.

Symptoms
Peanut plants infected with the root-knot nematode com
monly develop enlarged roots and pegs, which appear as galls
of various sizes. The galls result from an internal swelling of
the roots and can be distinguished from Rhizobium nodules,
which are appended to the side of the root. Galls may attain a
diameter several times that of the adjacent root. Pegs and pods
also become infected and develop galls (Fig. 58). Galls on
roots, pegs, and pods (Plates 84 and 85) sometimes begin to
deteriorate by the time of crop maturity. Development of the
root system is often significantly reduced.
Symptoms of damage caused by the northern root-knot
nematode (M. hapla) are similar to those caused by the peanut
root-knot nematode (M. arenaria). Roots, pegs, and pods
become galled by both species, but individual galls caused by
M. hapla are smaller than those caused by M.. arenaria (Fig.
59). Roots infected with M. hapla often form branches near the
point of nematode invasion, producing a dense, bushy root Fig. 58. Pod galls caused by Meloidogyne arenaria. (Courtesy K.
system (Plate 86). Garren)

45
 disrupted, resulting in poor water and nutrient transport. In ous existence in warm climates: M. arenaria, M. incognita
fected plants show a tendency to wilt during periods of water (Kofoid & White), and M. javanica. The most common species
stress. of root-knot nematode north of 35 latitude in the northern
Damage from M. arenaria is aggravated by stem rot (caused hemisphere is M. hapla.
by Sclerotium rolfsii) and pod and peg rots. In some fields, Root-knot nematodes exist in the soil as egg masses, infec
there is a close association between densities of M. arenaria tive second-stage juveniles, and adult males. Individual eggs
juveniles in soil and incidence of stem rot (Fig. 60). are elongate and ovate (30-60 x 75-113 |om) (Plate 88). The
infective second-stage juveniles emerge from the eggs and
Causal Organisms move freely through the soil (Plate 89). Juveniles are slender
The principal species of root-knot nematodes attacking pea (430-470 |am long) with a stylet length of 10 |im. The infective
nuts are the peanut root-knot nematode (M. arenaria (Neal) juveniles penetrate roots, pegs, or pods and move intercellu-
Chitwood) and the northern root-knot nematode (M. hapla larly and intracellularly to a region near the vascular tissue.
Chitwood). Two races of M. arenaria are morphologically in There they lose their mobility and begin to feed on adjacent
distinct and are separated on the basis of ability to infect and plant cells. Giant cells are induced by feeding (Plate 90).
reproduce on Florunner peanut (race 1) or the failure to do so Under favorable conditions, the sedentary juveniles swell and
(race 2). In addition, the javanese root-knot nematode (M. develop into males (Plate 91) or enlarged (1-2 mm long),
javanica (Treub.) Chitwood) has been reported to attack peanut white, globose-pyriform, mature females (Plate 92), which pro
and produce symptoms similar to those of M. arenaria. duce large numbers of eggs (200-1,500 per female) in a gela
M. arenaria, M. hapla, and M. javanica are distributed tinous matrix. These egg masses may remain in the roots (Plate
worldwide. The area between 35S and 35N latitudes is wide 93) or be extruded into the soil (Fig. 61). After eggs hatch, the
ly infested by three species of Meloidogyne adapted to continu- new second-stage juveniles enter the soil surrounding the roots,
completing the life cycle. The cycle is influenced significantly
by soil temperature and moisture, but under normal conditions,
two or more cycles may occur during each season. Crop debris
containing galls may be spread by farming operations or
running water, producing widely distributed infestation sites.

DISEASE LOCI PER 100 M ROW

Fig. 60. Relationship between incidence of stem rot, caused by

Sclerotium rolfsii, and soil population densities of Meloidogyne
arenaria juveniles determined near harvest in Alabama.

Fig. 59. Pod and root galls caused by Meloidogyne arenaria. Fig. 61. Meloidogyne arenaria female and egg mass in root
(Courtesy K. Garren) tissue. (Copyright J. Eisenback, used by permission)

46
 Root-knot nematodes can be distributed in a field through their Control
own movement but remain very localized. Ideally, control of parasitic nematodes should be based pri
Choosing the correct sampling time for nematode analysis is marily on the use of resistant cultivars, alone or in combination
critical for accurate diagnosis and selection of control mea with proper rotational crops and cultural techniques that reduce
sure's. Identification of Meloidogyne spp. is based on perineal soil infestation to a tolerable level. Presently, no commercially
patterns (Fig. 62), differential host responses, size of juveniles, available cultivars are resistant to root-knot nematodes; how
male morphology, and other characteristics. More recently, ever, a number of selections from crosses of Arachis hypogaea
molecular techniques such as polymerase chain reaction and with wild-type peanut species (e.g., A. glabrata) are resistant
DNA fingerprinting have been used successfully to identify to M. arenaria and have acceptable agronomic characteristics.
species of these nematodes. Population levels of root-knot There are significant differences in susceptibility to M. are
nematode juveniles in the soil vary widely throughout the year. naria and M. hapla among peanut cultivars. Also, for equally
In Alabama and other regions in the southeastern United susceptible peanut cultivars, those with late maturity dates sus
States, the number of juveniles of M. arenaria in soil increases tain greater populations of M. arenaria than those with earlier
through the growing season (April-September), reaching a maturity dates.
maximum (more than 200/100 cm3 of soil) in late July to Sep Continuous culture results in a gradual and steady decline in
tember and a minimum (fewer than 20/100 cm3 qf soil) be yield (Fig. 64). Yield losses of 100-150 kg/ha can be expected
tween January and early June. The up-rooting of peanut plants for each year of continuous culture. This trend in yield decline
causes a steep decline in the density of juveniles in the soil in response to continuous culture cannot usually be reversed
after harvest. Typically, numbers of juveniles during March with application of available nonfumigant nematicides. Rota
and April are less than 10% of those observed at harvest the tion of peanut with other crops can significantly decrease
previous year. Numbers of nematodes also change significantly levels of infestation of root-knot nematodes in soils. Rotations
in relation to soil depth (Fig. 63). In Alabama, significant of peanut with cotton, com, sorghum, and some soybean culti
numbers of juveniles are present throughout the year at a depth vars are effective in controlling or suppressing M. arenaria or
of 15-30 cm. In Florida, gelatinous egg masses of M. arenaria M. hapla. Although com and sorghum serve as hosts for M.
are present at soil depths of 0-75 cm from August through arenaria, the parasite does not develop as well on these crops
October; however, egg masses recovered from November (1
month after harvest) to July contained no viable eggs, sug
gesting that M. arenaria probably overwinters as second-stage
juveniles. These observations indicate that the probability of
detecting root-knot nematodes in any peanut field will be
greater if samples are taken during the last 2 months of the
growing season. This practice, while not helpful for the current
season, permits the establishment of expected levels of infes
tation for the following season. Samples collected during the
winter or early spring (off-season) invariably contain very low
numbers of plant-parasitic nematodes and require some form of
bioassay to establish the level of infestation with root-knot
nematodes.

( 25.SEPTEMBER.1986 B 28.MARCH.1987

Fig. 63. Relationship between soil depth and Meloidogyne are

naria juvenile population density in an Alabama field at harvest
(September 1986) and off-season after winter fallow (March
1987).

YEARS IN PEANUT
- O - N O NEMATICIDE NEMATICIDE

Fig. 62. Perineal pattern of adult Meloidogyne arenaria female. Fig. 64. Effects of number of years of continuous culture of pea
(Courtesy J. Eisenback) nut on yield in the southeastern United States.

47
 as on the peanut plant, so soil infestation can be reduced. The Rodnguez-Kabana, R., Kokalis-Burelle, N., Robertson, D. G., King,
reaction of individual cultivars to the nematode should be P. S., and Wells, L. W. 1994. Rotations with coastal bermudagrass,
determined before they are used as rotational crops. Cotton is cotton, and bahiagrass for management o f Meloidogyne arenaria
an excellent rotational crop for the management of M. arenaria and southern blight in peanut. J. Nematol. 26(suppl.):665-668.
in peanut since it is not a host to the nematode and its use Rodnguez-Kabana, R., Kokalis-Burelle, N., Robertson, D. G., and
Wells, L. W, 1994. Evaluation of sesame for control of Meloido
results in significant reductions in the incidence of root knot
gyne arenaria and Sclerotium rolfsii. Nematropica 24:55-61.
and stem rot (S. rolfsii). Rotations of peanut with Bahia grass
(.Paspalum notatum) or velvet bean (Mucuna deeringiana) are
(Prepared by N. Kokalis-Burelle
also very effective for the management of root knot and asso
and R. Rodrfguez-Kabana)
ciated diseases such as stem rot and pod rots. Other effective
rotational crops are castor bean (Ricinus communis), sesame
(Sesamum indicum), American joint-vetch {Aeschynomene
americana), partridge pea (Cassia fasciculata), and hairy in
digo {Indigophora hirsuta). Choice of a rotational crop is depen Root-Lesion Nematodes
dent on the economics and logistics of the production system.
Nematodes are attacked by a wide variety of microorgan Root-lesion nematodes were first observed on peanut plants
isms and invertebrates including viruses, bacteria, fungi, other in the United States in 1945. They have subsequently been
nematodes, protozoa, mites, and insects. Pasteuria penetrans, a found in all peanut-production areas of the United States and in
bacterial parasite of nematodes present in many peanut fields, most peanut-producing countries. Although these nematodes
has shown promise as a biological control agent against several are often found in fields with a history of peanut production,
plant-parasitic nematodes. they are not always associated with economic losses.
Two types of nematicides are widely used in peanut produc
tion: fumigants and nonfumigants with contact or systemic Symptoms
properties. The fumigants dibromochloropropane (DBCP) and Lesion nematodes are migratory endoparasites that attack
ethylene dibromide (EDB) were very effective for control of peanut roots, pegs, and pods, feeding primarily on parenchyma
root-knot nematodes and permitted continuous peanut culture cells (Fig. 65). Nematode feeding activity causes substantial
without significant decline in yield. However, health and envi tissue destruction and results in the development of necrotic
ronmental problems associated with these chemicals resulted lesions (Fig. 66). Under high disease pressure from large
in the removal of DBCP (in 1978) and EDB (in 1981) from nematode population densities, root lesions coalesce, causing a
agricultural use in the United States, but EDB is still used in general discoloration of the roots. Damaging population den
agriculture in some countries. Other fumigant nematicides sities of lesion nematodes are most frequently associated with
available for use in peanut are 1,3-dichloropropene (1,3-D) and coarsely textured, sandy soils.
metham sodium. These fumigants must be applied 1-2 weeks Pod lesions begin as tan to brown pin-point areas on the pod
before planting to avoid phytotoxicity. 1,3-D is most effective surface; as the nematodes feed and reproduce, the affected
when applied in the row at rates of 50-75 liters per hectare. areas enlarge and become darker (Plate 94). Older lesions are
Metham sodium decomposes in soil, generating nematicidal characterized by a blotchy appearance and indistinct margins,
methyl isothiocyanate; maximal peanut yield responses are which are caused by the darker necrotic parenchyma showing
obtained with in-the-row rates of 150-250 liters per hectare.
Efficacy of metham sodium is variable and depends on the
application methods and soil moisture and temperature.
Nonfumigant systemic nematicides available for use in
peanut production are-aldicarh._carbofuran. and phenamiphos.
These nematicides are most effective when applied at planting
at rates of 2-3 kg of active ingredient per hectare. For best
results, the application should be performed in a band 17-25
cm wide with light (2-4 cm deep) incorporation into the soil.
Other nonfumigant nematicides used with peanuts are ethoprop
and fensulfothion.

Selected References

Culbreath, A. K., Beute, M. K., Shew, B. B., and Barker, K. R. 1992.

Effects of Meloidogyne hapla and M. arenaria on black rot severity
in new Cylindrocladium-Ksistaxit peanut genotypes. Plant Dis.
76:352-357.
McSorley, R., Dickson, D. W., Candanedo-Lay, E. M., Hewlett, T. E.,
and Frederick, J. J. 1992. Damage functions for Meloidogyne
arenaria on peanut. J. Nematol. 24:193-198.
Minton, N. A., Csinos, A. S., and Morgan, L. W. 1990. Relationship
between tillage and nematicide, fungicide, and insecticide treat
ments on pests and yield of peanuts double-cropped with wheat.
Plant Dis. 74:1025-1029.
Noe, J. P., Holbrook, C. C., and Minton, N. A. 1992. Field evaluation
of susceptibility to Meloidogyne arenaria in Arachis hypogaea
plant introductions. J. Nematol. 24:712-716.
Rodrfguez-Kabana, R., and Canullo, G. H. 1992. Cropping systems
for the management of phytonematodes. Phytoparasitica 20:211-
224.
Rodnguez-Kabana, R., and King, P. S. 1985. Evaluation of selected
nematicides for control of Meloidogyne arenaria in peanut: A Fig. 65. Roots, pegs, arid pods with necrotic lesions caused by
multi-year study. Nematropica 15:155-164. Pratylenchus brachyurus.

48
through the outermost cells of the pod and making the necrotic Control
area look diffuse. Infection of pegs also results in the develop Identification of the nematode species within a particular
ment of necrotic lesions. Such lesions weaken the pegs, and field and determination of population density are basic to
pods are shed prematurely during the harvesting process. developing appropriate management programs. The most accu
Symptom development, damage to pods and pegs, and sup rate estimates of nematode population densities are obtained
pression of plant growth are related to initial nematode popula from samples collected during the autumn when densities are
tion densities and rate of population increase. Population den expected to be at maximum levels. It is critical that both soil
sities in excess of 5,000 nematodes per gram of fresh tissue and root populations be determined for this migratory endo-
have been observed in association with severe crop damage. parasite. Nematode extraction from pod, peg, and root tissues
Root-lesion nematodes may also affect the percentage of sound provides a more accurate estimate of population densities for
mature seed, seed weight, and value. lesion nematodes than soil analysis.
Other microorganisms may colonize nematode-damaged Soil treatment with fumigant or nonfumigant nematicides is
tissues. The combined effects of nematodes and associated effective in controlling lesion nematodes. It is often beneficial,
microorganisms can result in additional losses from decreased when initial nematode population densities are high, to split
pod yield and reductions in yield quality. nematicide applications and make the first application prior to
or at planting and the second at the time of peg initiation. With
Causal Organisms lower initial nematode population densities, the at-pegging
Two species of lesion nematodes, Pratylenchus brachyurus
(Godfrey) Filipjev & Schuurmans-Stekhoven and P. coffeae
(Zimmermann) Schuurmanns-Stekhoven, attack peanut plants
(Figs. 67 and 68). P. brachyurus, first reported in 1945, is the
most common and widely distributed species. Some evidence
suggests that populations of P. brachyurus may differ in viru
lence (aggressiveness). P. coffeae has been reported only from
India, where affected plants have a sickly appearance and
patchy, stunted growth. Other species of lesion nematodes have
been associated with peanut but have not been observed to
cause economic loss.

Disease Cycle
P. brachyurus survives extremes of temperature and mois
ture when the nematodes are within root and pod debris. Active
nematodes can be recovered from infected pods for several
months after harvest. It is likely that dissemination of the
nematode occurs through movement of infected pods and root
debris.
All developmental stages of the nematode are capable of
infecting roots, pegs, and pods. Initial infection may occur
immediately after germination of planted seed. The nematode
requires 4-5 weeks to complete its life cycle at optimal tem
peratures (2428C), and several generations can occur in a
single growing season. Because all developmental stages are Fig. 67. Pratylenchus brachyurus female. A, hind end; B and C,
infective, egg production by fecund females may begin within tail tips; D, head-end profile; E, head, face view; and F, entire
female. (Reprinted, by permission, from C.I.H. Descriptions of
a few days of infection. Root lesions also can be seen within a Plant-Parasitic Nematodes, Commonwealth Institute of Para
few days of the initial infection. Discrete generations have not sitology; 1986 C.A.B. Internationa!)
been observed in field populations because of the mix of life
stages that infect the developing root system.
application may provide economic control. Comparisons of knot or root-lesion nematodes, are for the most part ectopara
nematicide efficacy under conventional full tillage and that with sites; they are rarely found internally in roots or pods.
minimum tillage operations indicate that tillage does not affect
efficacy. Rotation is usually less effective and more difficult than Causal Organisms
chemical control because lesion nematodes have a wide host Sting nematodes parasitic on peanut plants are B. gracilis
range that includes numerous crop and weed species. Steiner or B. longicaudatus Rau. Before 1958, when B. longi
Moderate levels of host resistance have been identified but caudatus was described, all records on sting nematodes re
have not been incorporated into agronomically suitable peanut ferred to B. gracilis as the causal agent of disease on peanut.
genotypes. However, these records probably referred to B. longicaudatus,
which is the more common of the two species in the south
Selected References eastern United States.
Males and females of this nematode are morphologically
Boswell, T. E. 1968. Pathogenicity of Pratylenchus brachyurus to
similar. They range in length from 2 to 3 mm and have a
spanish peanuts. Ph.D. thesis. Texas A&M University, College
Station.
strongly striated cuticle. The stylet is very long (100-140
Chabra, H. K., and Mahajan, R. 1976. Pratylenchus coffeae, the root- pm).
lesion nematode in groundnuts and its control by granular nema-
ticides. Nematol. Mediterr. 4:241-242. Disease Cycle
Manual, J. S., Reynolds, D. A., Bendixen, L. E., and Riedel, R. M. Sting nematodes are migratory ectoparasites restricted to soil
1980. Weeds as hosts of Pratylenchus. Ohio Agric. Res. Dev. Cent. types with greater than 84% sand. The nematodes occur mainly
Res. Bull. 1123. in the upper 30 cm of soil, and their numbers fluctuate during
McClure, M., and Stowell, L. 1978. A simple method of processing the season. Sting nematodes are most active when soil temper
nematodes for electron microscopy. J. Nematol. 10:376-377. atures are 20-34C and reproduce fastest at 30C. Infested
Minton, N. A., Csinos, A. S., and Morgan, L. W. 1990. Relationship areas of a field vary in size and shape, but the boundary be
between tillage and nematicide, fungicide, and insecticide treat tween diseased and healthy plants is usually well defined,
ments on pests and yield of peanuts double-cropped with wheat.
indicating an aggregated distribution.
Plant Dis. 74:1025-1029.
Little is known about the life cycle of these nematodes.
(Prepared by T. E. Boswell and J. L. Starr) Sting nematodes in all stages of development are apparently
capable of feeding and causing damage.

Sting Nematodes Control

No commercially available peanut cultivars are resistant to
Sting nematodes (Belonolaimus spp.) have been known for this nematode. Sting nematodes have a very wide host range,
some time to be economically important pathogens of peanut in which includes com and other grasses, legumes (including soy
the United States. These nematodes are present in Virginia, bean), cotton, several vegetable crops, and sunflower. This wide
North and South Carolina, Georgia, Alabama, and Florida but are host range precludes the use of crop rotation as a practical con
of greatest importance in Virginia and the Carolinas. "field losses trol method. Fortunately, sting nematodes are easily controlled
can be slight or very severe (Plate 95). Sting nematodes have not with fumigant and nonfumigant nematicides; dosages required
been found in peanut-growing areas outside the United States. are generally lower than those needed to control root-knot
nematodes. Some nematicides, such as fensulfothion, that are
Symptoms effective against root-knot nematodes also afford good control
Sting nematodes cause peanut roots to become gnarled and of sting nematodes.
stubby; frequently the taproot is the only remaining root (Plate
96). Feeding by- these.nematodes causes tiny lesions along the Selected References
taproot, and plants become chlorotic with stubby, sparse root
systems. Roots and pods have small, dark, necrotic spots (Fig. Miller, L. I. 1972. The influence of soil texture on the survival of
69) caused by nematode feeding. Sting nematodes, unlike root- Belonolaimus longicaudatus. (Abstr.) Phytopathology 62:670-671.
Minton, N. A., and Baujard, P. 1990. Nematode parasites of peanut.
Pages 285-320 in: Plant Parasitic Nematodes in Tropical and
Subtropical Agriculture. M. Luc, R. A. Sikora, and J. Bridge, eds.
C.A.B. International, Wallingford, England.

(Prepared by N. Kokalis-Burelle
and R. Rodnguez-Kabana)

Ring Nematodes
An unidentified species of ring nematode was first reported
on peanut plants in a field in Georgia in 1953 and then in South
Carolina in 1955. This same nematode has been found since
then in a high percentage of the peanut fields in Georgia and is
widely distributed in the peanut-producing region of the United
States. Losses caused by the ring nematode have not been well
defined. Relatively large numbers of nematodes may be asso
ciated with peanut roots, although little discernible loss in yield
Fig. 69. Pods with lesions caused by the sting nematode, Belono or quality occurs. However, in North Carolina, negative cor
laimus longicaudatus (bottom), and unaffected pods (top). (Cour- relations were obtained between population levels and peanut
tesy K. Garren) yields. Also, in field experiments in North Carolina, positive
50
correlations were obtained between population levels of ring Causal Organism
nematodes and symptoms of Cylindrocladium black rot of pea C. ornata (Raski and Luc) (syns. Macroposthonia ornata
nut plants; in greenhouse tests, presence of the ring nematode (Raski) De Grisse & Loof and Criconemoid.es omatus Raski)
increased the incidence of the disease on the Florigiant cultivar are stout, fusiform nematodes about 0.36-0.44 mm long. They
but failed to affect disease severity on NC 3033, a resistant have a thick cuticle with deep fissures separating approxi
breeding line. mately 87-92 annules. The life cycle has not been reported.' C.
ornata, generally considered ectoparasitic, feeds by thrusting
Symptoms its stylet into an epidermal cell or into the cell of the cortex
Obvious damage to peanut plants is seldom caused by the directly beneath the epidermis (Fig. 70D). C. ornata feeds on
ring nematode, and large populations are usually necessary to peanut roots, pegs, and pods.
produce symptoms. Peanut plants growing in heavily infested
field soil have been described as chlorotic, and the condition Control
has been called peanut yellows. In microplots inoculated No known peanut cultivars have resistance to C. ornata.
with about 10,000 nematodes per plant, the roots and pods of Some of the crops grown in rotation with peanut (such as
peanut cultivars Argentine and Starr were severely discolored cotton, soybeans, com, and tobacco) reduce population levels
with brown necrotic lesions (Fig. 70A-C). Small, necrotic of this nematode. Fumigant and organophosphate nematicides
lesions were usually superficial, but necrosis in large lesions are usually effective in control.
extended deep into the roots and pods. Many root primordia
and young roots were killed, resulting in limited numbers of Selected References
lateral roots. Pod yields from nematode-infested plants were
half those of healthy plants. In microplot tests in North Caro Barker, K. R., Schmitt, D. P., and Campos, V. P. 1982. Response of
lina, as few as 178 freshly introduced Criconemella ornata per peanut, corn, and tobacco to Criconemella ornata. J. Nematol.
500 cm3 of soil stunted peanut plants. 14:576-581.

Fig. 70. A, Peanut pods inoculated with Criconemella ornata; B, uninoculated peanut pods; C, peanut roots and pods inoculated with C.
ornata (left) and uninoculated roots and pods (right); and D, C. ortata partially embedded in a peanut root. (Reprinted, by permission,
from Minton and Bell, 1969)

51
Diomande, M., and Beute, M. K. 1981. Effects of Meloidogyne hapla Control
and Macroposthonia ornata on Cylindrocladium black rot of pea Although the peanut pod nematode does not appear to cause
nut. Phytopathology 71:491-496. economic damage to other crops, it survives on a wide range of
Kinloch, R. A., and Lutrick, M. C. 1975. The relative abundance of rotation crops including com, sunflower, and tobacco. Since
nematodes in an established field crop rotation. Soil Crop Sci. Soc. the nematode also feeds on many weeds and fungi, including
Fla. Proc. 34:192-194. Penicillium spp. (Plate 98), commonly found in peanut fields,
Minton, N. A., and Bell, D. K. 1969. Criconemoides ornatus parasitic sanitation is one of the first steps in control. The use of nema
on peanuts. J. Nematol. 1:349-351.
tode-free seed is also important, and current research projects
(Prepared by N. A. Minton) are directed toward this goal. A recently released commercial
cultivar, Kwarts, has resistance to this nematode and will be
come more widely used when seed becomes available.
In South Africa, treatments with nematicides registered for
Peanut Pod Nematodes use against the peanut pod nematode include applications of
phenamiphos at planting, aldicarb at either planting or pegging,
Damage caused by Ditylenchus africanus was observed on and oxamyl at pegging. These nematicides reduce the numbers
peanut pods in South Africa as early as 1967; but because it of nematodes, but their cost effectiveness is often unreliable,
was confused with black hull, the first official report of the particularly in dryland production.
nematode did not appear until 1988. This nematode has been Recently, soils suppressive to the peanut pod nematode were
found in all major peanut-production areas of South Africa in identified in regions where peanuts have been grown in con
approximately 75% of all fields. D. africanus has not been tinuous culture for 10-30 years. A total of 13 species of
reported outside South Africa, although unpublished observa nematophagous fungi have been isolated from these soils. Two
tions report its occurrence in neighboring southern African Arthrobotrys species and two Monacrosporium species are the
countries. most commonly found and easily cultured. These fungi will be
tested for their potential for biocontrol of D. africanus.
Symptoms In fields infested with D. africanus, farmers are encouraged
The peanut pod nematode enters peanut pegs at the connec to practice early harvesting. Severity of pod symptoms corre
tion with the pod and penetrates various layers of the hull. The lates closely with seed quality. Pods with early symptoms re
first visible symptom is a gray, bruiselike discoloration of the ceive a second grade. Although yield increases with time, seed
pod at the peg connection. The seed coat becomes discolored, quality continues to decrease. Regular inspection for the first
and seed germinate prematurely (Plate 97). Those nematodes symptoms of nematode infection is required to determine a
that enter the hull exocarp migrate along the pod to the distal timely harvest.
end, causing a typical broad band of discoloration along the
sides of the pod. Many of the nematodes, however, penetrate to Selected References
the hull endocarp and migrate through the seed micropyle into
the seed coat and embryo. No visible damage is caused to the Rasson, S., De Waele, D., and Meyer, A. J. 1993. Survival of Ditylen
roots. chus destructor in soil, hulls and seed of groundnut. Fundam. Appl.
Breakdown of the pod may lead to early germination of up Nematol. 16:79-85.
De Waele, D., Jones, B. L., Bolton, C., and Van Den Berg, E. 1989.
to 25% of the seed. Seed weight may also be suppressed by
Ditylenchus destructor in hulls and seeds of peanut. J. Nematol.
20-50%. The greatest economic impact is to the market value
21:10-15.
of the crop. Discolored seed, according to South African regu De Waele, D., Wilken, R., and Lindeque, J. M. 1991. Response of
lations, are downgraded from first to second grade or even to potato cultivars to Ditylenchus destructor isolated from groundnut.
oil stock. The price decrease to second grade is approximately Rev. Nematol. 14:123-126.
15% and to oil stock approximately 65%. Jones, B. L.., and De Waele, D. 1988. First report of Ditylenchus
destructor in pods and seeds of peanut. Plant Dis. 72:453.
Causal Organism McDonald, A. H., and Van Den Berg, E. H. 1991. Evaluation of
D. africanus Wendt was first classified as D. destructor but nematicides for the control o f Ditylenchus destructor in groundnut
differs from the latter species in host plant specificity, charac fields. Phytophylactica 23:186.
teristics of morphology, and restriction fragment length poly Swart, A., and Jones, B. L. 1994. Interaction between Ditylenchus
morphisms (RFLPs) of ribosomal DNA. In South Africa, it is destructor and the nematophagous fungi Arthrobotrys dolioformis.
commonly referred to as the peanut pod nematode. (Abstr.) Proc. Symp. Plant Pathol. Soc. South Afr., 32nd.
Venter, C., De Waele, D., and Meyer, A. J. 1991. Reproductive and
Males and females of the peanut pod nematode are morpho
damage potential of Ditylenchus destructor on peanut. J. Nematol.
logically similar, slender, and approximately 0.9-1.0 mm long.
23:12-19.
The stylet is weak and approximately 8.7-8.9 |im long. Venter, C., De Waele, D., and Meyer, A. J. 1992. Minimizing damage
by Ditylenchus destructor to peanut seed with early harvest. J.
Disease Cycle Nematol. 24:528-532.
The peanut pod nematode is a migratory endoparasite that
completes its life cycle from egg to adult in 8 days at 30C. (Prepared by C. Venter)
The life cycle is slower and eggs are less viable at lower tem
peratures. The nematode enters the pods soon after pegging,
approximately 49 days after planting. It remains within the
hulls and seed and reproduces until harvest. At harvest, Other Nematodes
approximately 90% of the nematode population in or around a
plant is found within the pods. Only a small percentage is Several other species of nematodes parasitize peanut, but
found in the soil and roots. Around the time of harvest, large their occurrence is isolated and their importance uncertain. The
numbers of eggs are laid in both the hulls and seed. Nematodes testa nematode, Aphelenchoides arachidis Bos, has been de
in the hulls may enter anhydrobiosis. Many of the rotten pods scribed on peanut only in northern Nigeria. A. arachidis is a
and hulls remain in the soil, permitting survival from year to facultative endoparasite found mainly in the parenchymatous
year. Infested seed carry the nematode from field to field. tissue and around the tracheids of the seed, testae (seed coats),
Planting infested seed in clean soil or clean seed in infested shells, roots, and hypocotyls. Heavily infested seed coats be
soil will result in economic loss in yield. come discolored and translucent with dark vascular strands.

52
Seed coats may become unevenly thickened. All stages of the cavenessi has been found associated with most cultivated
nematode are found throughout the seed coat until the end of plants in Senegal and Mali. Leaving fields fallow between
the growing season, when mainly juvenile stages are found. A. crops provides excellent control but is not economically prac
arachidis predisposes seed to invasion by soilbome fungal tical.
pathogens such as Rhizoctonia solani, Sclerotium rolfsii, Macro Tylenchorhynchus brevilineatus Williams (syn. T. indicus
phomina phaseolina, and Fusarium spp., leading to reduced Siddiqi) has been reported only in the Kalahasti area and
seedling emergence. A. arachidis devalues the crop by reduc Nellore district of Andhra Paradesh, India. This nematode
ing seed quality. causes a brownish black discoloration of the pod surface and
A. arachidis can survive desiccation in stored pods for up to reduced pod size. Pegs and young pods may have brownish
12 months, while infected pods that are sun dried in the field yellow lesions with slightly raised margins. T. brevilineatus
before storage contain no active nematodes. Adult nematodes can be controlled and yields increased with application of
have been isolated from volunteer plants. Control of this nema aldicarb or carbofuran.
tode is mainly by preventive treatments that include immersing Dagger nematodes (Xiphinema spp.) are found consistently
seed in 60C water and sun drying pods after harvest. A. in peanut and often damage roots, producing galls and curly
arachidis can be disseminated in infected seed and therefore tips. Populations of dagger nematodes in peanut fields are
has the potential to become a widely distributed pest. typically very low and stable throughout the growing season,
Aphasmatylenchus structuratus Germani is a migratory endo- making the damage they cause relatively unimportant.
parasite and ectoparasite of peanut that has been reported only
in southwest Burkina Faso in western Africa. The nematode
Selected References
causes chlorosis, stunting, reduced development of the root
system and Rhizobium nodules, and yield reduction. A. struc
Germani, G. 1981. Pathogenicity of the nematode Scutellonema
turatus survives the dry season adjacent to roots of the karite cavenessi on peanut and soybean. Rev. Nematol. 4:203-208.
tree (Butyrospermum parkii L.) and does not enter into McDonald, D., Bos, W. S., and Gumel, M. H. 1979. Effects of infes
anhydrobiosis. This nematode spreads rapidly and parasitizes tation of peanut (groundnut) seed by the testa nematode, Aphelen-
other economically important leguminous plants in Burkina choides arachidis, on seed infection by fungi and on seedling
Faso. emergence. Plant Dis. Rep. 63:464-467.
Scutellonema cavenessi Sher has been found in northern Minton, N. A., and Baujard, P. 1990. Nematode parasites of peanut.
Nigeria, Senegal, and Mali. This nematode causes chlorosis, Pages 285-320 in: Plant Parasitic Nematodes in Tropical and
reduced root growth, and reduced Rhizobium nodulation. S. Subtropical Agriculture. M. Luc, R. A. Sikora, and J. Bridge, eds.
cavenessi is active during the rainy season and enters into anhy- C.A.B. International, Wallingford, England.
drobiosis when soil moisture drops to approximately 0.2%.
The extent of yield loss from this nematode is not known, but (Prepared by N. Kokalis-Burelle
the application of nematicides increases yield 20-220%. S. and R. Rodnguez-Kabana)

Diseases Caused by Viruses

relatively young plant is infected, the necrosis spreads toward
Tomato Spotted Wilt the base of the plant, resulting in its death. Secondary symp
toms include stunting and proliferation of axillary shoots. Leaf
and Peanut Bud Necrosis lets produced on the axillary shoots are reduced in size and
show puckering, mosaic mottling, and general chlorosis (Plate
The peanut bud necrosis virus (PBNV) and tomato spotted 101). Secondary symptoms are most common on early-infected
wilt virus (TSWV), both tospoviruses, cause economically plants, giving them a stunted and bushy appearance. Plants
important diseases in peanut. The distinction between PBNV infected later may also be stunted, but the symptoms may be
and TSWV has been recognized only recently. The disease restricted to a few branches or to the apical parts of the plants.
referred to. as bud necrosis, now shown to be caused by Seed from early-infected plants are small and shriveled, and
either TSWV or PBNV, was previously attributed only to the seed coats are red, brown, or purple with mottling (Plate
TSWV. TSWV and PBNV cannot be distinguished by symp 102). Although late-infected plants may produce seed of nor
toms alone on peanut or other hosts. TSWV is widely dis mal size, the seed coats are often mottled and cracked.
tributed in the Americas, Australia, Africa, and Europe, where
as PBNV appears to be restricted to southern and southeastern Causal Agents
Asia. Nevertheless, the thrips vectors of TSWV and PBNV TSWV and PBNV are found in all parts of affected plants.
occur in most peanut-growing countries. Therefore, in surveys Clusters of virus particles are often found in the cistemae of
for the occurrence of virus diseases in peanut, assays for both the endoplasmic reticulum. Individual particles are 80-120 nm
PBNV and TSWV should be conducted. in diameter and are covered with projections resembling spikes
(Fig. 71). TSWV and PBNV have an extremely low thermal
Symptoms inactivation point (45C for 10 min) and short longevity in
Symptoms caused by TSWV and PBNV in peanut are var vitro (less than 5 hr at room temperature). These properties can
iable. They may appear in young leaflets in the form of chlo be used, in conjunction with others, to identify TSWV and
rotic spots or a mild mottle (Plate 99) that develops into PBNV.
necrotic and chlorotic rings and streaks. Bud necrosis symp It is difficult to isolate TSWV or PBNV from infected plant
toms appear to be governed by ambient temperatures; when tissues. Additionally, neither TSWV nor PBNV is highly im
temperatures are above 30C during the day, petioles bearing munogenic. Polyclonal antibodies produced for an isolated
fully expanded leaflets with initial symptoms (as described vims may react with healthy plant extracts. Therefore, extreme
above) usually become flaccid and droop (Plate 100). This care should be taken in using polyclonal antisera and in inter
symptom is followed by necrosis of the terminal bud. When a preting the results of serological tests. Polyclonal or mono
53
clonal antibodies are widely used to study relationships among infected plants will create gaps in the field that may lead to an
tospoviruses and to diagnose disease. increase in the percentage of infected plants.
Good sources of resistance to both TSWV and PBNV have
Host Ranges been identified. The cultivar Southern Runner typically has
TSWV and PBNV have extremely wide host ranges that 50% lower disease incidence than the susceptible cultivar Flo-
include more than 370 species of plants in more than 50 runner. Peanut genotypes resistant to PBNV and T. palmi in
families. clude ICGV 86029, ICGV 86031, and ICGV 86388. Southern
Runner is also resistant to PBNV. Since the application of
Transmission insecticides increases disease incidence of both PBNV and
Both TSWV and PBNV are mechanically transmissible. TSWV, it is not advisable to apply insecticides for control.
Only chilled extracts containing antioxidants such as mercap-
toethanol or thioglycerol are suitable for transmitting the virus
by mechanical inoculations. Both TSWV and PBNV are trans
mitted by thrips. Probable vectors of TSWV in the United States Peanut Clump
are Frankliniella fusca (Hinds) and F. occidentalis (Pergande);
Thrips palmi (Kamy) transmits PBNV in India. The viruses are
and Indian Peanut Clump
acquired only by insect larvae but may be transmitted by larvae
or adults. TSWV multiplies in its thrips vector. Neither PBNV Peanut clump occurs in the Indian subcontinent and in west
nor TSWV is transmitted by seed in peanut. ern Africa (Senegambia, Burkina Faso, Niger, and the Ivory
Coast). The pathogen, a soilbome virus, causes severe crop
Control losses. Symptoms of peanut clump resemble those of green
Cultural practices such as early seeding, use of high-quality rosette (see Groundnut Rosette). As a result, it is likely that
seed treated with an approved seed protectant, and sowing at these two diseases have been confused.
the recommended rate and spacing to give optimum plant Studies on genome organization have revealed that isolates
population can reduce the incidence of TSWV and PBNV. The from India and western Africa are two distinct viruses. The
seedbed should be well prepared, and soil moisture should be virus from western Africa, referred to as peanut clump virus
sufficient to ensure good germination and seedling establish (PCV), and that from India, Indian peanut clump virus (IPCV),
ment. Given good growing conditions, the crop will rapidly are not serologically related. Differences in genome organiza
develop a close canopy and will not be as attractive to the tion between PCV and IPCV are apparent, and the complete
thrips vector as a patchy crop. The incidence of TSWV and nucleotide sequences of both genome RNAs are available.
PBNV under these conditions is much reduced. Because of the
extremely wide host ranges of TSWV and PBNV and their Symptoms
vectors, it is not practical to control the disease by destroying Diseased plants are severely stunted and dark green (Plate
weed reservoir hosts. Intercropping one row of a quick-grow 103). The disease occurs in patches in the field and recurs more
ing cereal crop such as sorghum or pearl millet with each three or less in the same position in the same field in successive peanut
rows of peanut can reduce disease incidence. Removal of crops. The symptoms first appear on young plants as mottling,
mosaic, and chlorotic rings on newly emerged quadrifoliates
(Plate 104). Subsequently, infected leaves turn dark green with or
without faint mottling. Early-infected plants are severely stunted
and may produce flowers, but any pods formed are not well
developed. Plants infected later are also stunted and h^ve short
ened intemodes and dark green leaflets. These plants may pro
duce pods, but seed weights may be reduced by up to 60%.

Causal Agents
PCV and IPCV have rod-shaped particles 24 nm in diameter;
there are two predominant lengths, approximately 185 and 250
nm (Fig. 72). The particles of PCV and IPCV each contain a
single polypeptide species with a molecular mass of 24 kDa.

Fig. 71. Particles of peanut bud necrosis virus covered with

spikes or projections. Fig. 72. Peanut clump virus particles.

54
 Both IPCV and PCV are currently known to occur in several Mosaic rosette occurs only in eastern and central Africa.
serologically distinct variants. Among the IPCV variants, three Young leaflets show conspicuous mosaic symptoms (Plate
distinct serogroups have been identified. Variants can also be 107), which resemble those of chlorotic rosette except that
distinguished on the basis of their reaction on several hosts. stunting is less pronounced.
RNA1 of IPCV has been found to contain sequences conserved
among the variants and will be utilized to produce nucleic acid Causal Agents
probes capable of detecting several IPCV variants. Rosette disease of peanut is caused by a complex of two
viruses and a satellite RNA. Diseased plants contain a me
Host Ranges chanically transmissible virus, groundnut rosette virus (GRV),
PCV and IPCV have extremely wide host ranges, which which is classified as an umbravirus. GRV depends on the
include many monocotyledonous and dicotyledonous plants. groundnut rosette assistor virus (GRAV), a luteovirus, for
transmission by Aphis craccivora. GRAV causes no obvious
Transmission symptoms in peanut on its own. Variants of the satellite RNA
IPCV and PCV are readily sap transmissible. Both are trans are responsible for the different forms of rosette (chlorotic,
mitted by Polymyxa graminis. Both viruses are transmitted by green, and mosaic). These variants differ appreciably in nucle
seed in peanut (more than 6% frequency). Since IPCV is otide sequence, as do forms of the satellite from different parts
present in seed coats of all seed from infected plants, the seed of Africa.
coats should be removed before ascertaining seed transmission. GRAV, a typical luteovirus, can be detected by polyclonal
IPCV is seed transmitted in cereal crops such as finger millet, antisera produced against GRAV and by antisera to some other
foxtail millet, and pearl millet but not in sorghum. luteoviruses, such as potato leafroll virus (PLRV). It can also
The occurrence of IPCV is correlated with ambient air tem be detected by some monoclonal antibodies to PLRV. No virus
peratures. When ambient air temperatures are below 25C, particles have been reported for GRV, and so no antiserum is
only negligible IPCV incidence is observed. Therefore, in the available. Infected plants contain abundant infective single
tropics, crops grown after the rainy season in locations where stranded RNA.
temperatures are lower than 25C escape infection. High tem
peratures during the summer season followed by monsoon Host Range
rains appear to favor natural transmission. Peanut is the only natural host known for both GRAV and
GRV, though alternate hosts probably play an important part in
Control perpetuating the inoculum between crop seasons. Most species
IPCV incidence is higher when peanut crops are rotated with become infected with only one virus or the other. Host range
susceptible cereal crops. The incidence of virus can be reduced tests with GRV can be done also by mechanical inoculation.
by the application of soil biocides. Soil solarization (during hot GRV cultures' with or without the satellite RNA, induce
summer months for a period of 2 months) reduces IPCV inci necrotic lesions in host plants but not systemic infections.
dence. None of more than 9,000 Arachis hypogaea genotypes Necrotic rings are also produced on inoculated leaves. Most
showed resistance to IPCV when tested on infested soils. Since sensitive test plants produce mild veinal chlorosis or necrosis
the genomes of PCV and IPCV have been sequenced, there are on the first systemically infected leaves, which is followed by
excellent prospects for utilizing viral genes to induce resistance a faint mottle and moderate stunting.
by unconventional methods in A, hypogaea.
Transmission
The viruses associated with all three types of rosette disease
are transmitted by A. craccivora in a persistent or circulative
Groundnut Rosette manner. By analogy with other umbravirases, it is suspected
that GRV and its satellite RNA are encapsidated in GRAV coat
Groundnut rosette disease was first reported from Tanzania protein. Peanut is considered to be the main source of inocu
in 1907. Many epidemics of rosette were subsequently recorded lum from which the initial spread of the rosette disease occurs.
in Africa. One major epidemic in 1975 caused nearly $250 Neither GRAV nor GRV is seed transmitted in peanut. Because
million in crop losses in Nigeria alone. rosette-infected plants survive longer than healthy plants, they
Rosette has also been reported in Argentina, India, Indonesia, are not normally harvested and serve as an important source of
and the Philippines. In Africa, rosette disease is restricted to inoculum. Volunteer plants may also be a source of inoculum.
countries south of the Sahara. It is likely that A. craccivora colonizes these rosette-infected
plants and that moving rainy fronts are responsible for the
Symptoms dissemination of the aphids. Alate and apterous aphids are in
Three types of rosette disease, chlorotic, mosaic, and green, volved in the secondary spread. Diagnostic aids for the various
are recognized on the basis of symptoms. Chlorotic rosette components of rosette have recently become available and
occurs throughout Africa south of the Sahara. The disease first should permit epidemiological studies on rosette disease in
appears on young leaflets as faint mottling with a few green Africa.
islands. Leaflets produced subsequently are pale yellow with
green veins. Plants infected when young produce progressively Control
smaller, chlorotic, curled, and distorted leaflets. When older Rosette disease can be effectively controlled by cultural prac:
plants are infected, symptoms may be restricted to a few tices. These include destroying all volunteer and unharvested
branches or to the apical portion of the plants. Plants infected infected plants, planting early in the season and at a high seed
early are severely stunted (Plate 105) with thickened stems. Early ing rate, maintaining plant stands, and applying insecticides at
infection causes severe reduction in the number and size of pods. the correct time. Excellent sources of resistance to rosette
Green rosette disease occurs in western Africa and Uganda. disease are available in peanut germ plasm. Early-maturing,
Young leaflets show mild chlorotic mottling and isolated rosette-resistant genotypes recently have been identified and
flecks. Symptoms are masked in older leaflets, but leaflets are are being used in the development of rosette-resistant, early-
reduced in size, show outward rolling, and are not distorted. maturing cultivars. Since the coat protein gene of GRAV has
Plants infected early are severely stunted and are a darker been sequenced and constructs suitable for transformation have
green than healthy plants (Plate 106), somewhat resembling been prepared, prospects for producing rosette-resistant culti
plants infected with peanut clump virus. vars by insertion of the coat protein genes into peanut are good.

55
 virus-free seed is important. Genotypes in which PeMoV is not
Peanut Mottle seed transmitted have been identified and utilized in conven
tional breeding programs to produce acceptable, high-yield
Peanut mottle virus (PeMoV) was first reported in the breeding lines that do not transmit the disease via seed. Al
United States in 1961 and is currently present in all the major though resistance to PeMoV has been identified in wild species
peanut-growing countries. Its widespread distribution is prob of Arachis, it has not yet been transferred to A. hypogaea.
ably the result of dispersal of infected seed. An economic loss
of 5-6% from PeMoV was estimated in Georgia. In field tests
in India, susceptible cultivars suffered yield losses of up to
40%. Because of its worldwide distribution and potential for
Peanut Stripe
causing economic losses, PeMoV is considered to be of global
economic importance. The peanut stripe virus (PStV) was first reported in the
United States in 1983, having entered the country in peanut
Symptoms seed imported from China. PStV has been present in Southeast
Young leaflets show mild mottle symptoms or a mosaic of Asia since the early 1970s but has been often misidentified as
irregular, dark green islands (Plate 108). In older leaflets, peanut mottle virus (PeMoV). Peanut stripe poses a serious
mosaic symptoms are not obvious but can be seen by trans threat to peanut production in southern and southeastern Asia.
mitted light. In some genotypes, conspicuous interveinal de
pressions and an inward curling of the edges of leaflets are Symptoms
apparent (Plate 109). Infected plants are slightly stunted. Several symptom variants of PStV are known. The name
PeMoV reduces both numbers and size of pods on infected peanut stripe virus was first given to an isolate that induced
plants. discontinuous, dark green stripes along the lateral veins of
young leaflets (Plate 110). However, the most widely dis
Causal Agent tributed variant causes irregular green blotches on young leaf
PeMoV belongs to the potyvirus group. Particles are flexu- lets that persist as the leaflets age (Plate 111). A variant that
ous rods that measure about 750 x l2 nm (Fig. 73). The. coat induces chlorotic rings surrounding blotches on young leaflets
protein has an apparent molecular mass of 32-36 kDa. The was reported from Thailand and Indonesia. The most widely
thermal inactivation point is 55-64C, and the longevity in distributed isolate in China induces a mild mottle symptom
vitro is 1-2 days at room temperature. (Plate 112).
High-quality polyclonal antisera and monoclonal antisera
have been produced for PeMoV. They do not react with the Causal Agent
peanut stripe virus or the peanut green mosaic or groundnut PStV belongs to the potyvirus group. Although its particles
eyespot potyviruses that occur on peanut. resemble those of PeMoV. PStV is serologically distinct from
PeMoV. However, comparison of available full-length poty
Host Range virus nucleic acid sequences indicates that PStV is closely
PeMoV occurs in several important legume crops, including re lie d to the soybean mosaic virus.
peanut and soybean, and weeds.
Host Range
Transmission Natural hosts in the field are Centrosema pubescens, C.
PeMoV is readily transmitted by mechanical sap inoculation macrocarpum, Calopogonium caeruleum, Crotalaria striata,
and is seed transmitted at rates of 0-8.5%. PeMoV is also seed Desmodium siliquosum, and Pueraria phaseoloides. A number
transmitted in mung bean and cowpea but not in soybean. The of hosts can be systemically infected with PStV by sap inocu
virus can be detected in peanut seed by enzyme-linked immu lation. Since PStV does not produce local lesions on the
nosorbent assay. PeMoV is transmittedln a nonpersistent man Thaseolus vulgaris cultivar Topcrop, this host can be used to
ner by Aphis craccivora, A. gossypii, Myzus persicae, Hypero- distinguish it from PeMoV.
myzus lactucae, Rhopalosiphum padi, and R. maidis.
Transmission
Control PStV is transmitted by sap inoculation and by many aphid
Peanut seed appears to be the primary source of inoculum. species in a nonpersistent manner. Different symptom variants
Since many aphid species can transmit the virus, it is spread of PStV have different aphid transmission frequencies. Seed
rapidly to nearby plants. To avoid the disease, the planting of transmission of PStV can be as high as 37% when the seed are
derived from plants inoculated before flowering. Seed trans
mission frequency in naturally infected plants is normally less
than 5%. ITie virus is readily detected in seed by enzyme-
linked immunosorbent assay.

Control
Of approximately 10,000 peanut genotypes evaluated for
resistance to PStV in Indonesia, none was resistant. However,
some genotypes showed only mild symptoms, and some took a
longer time than the susceptible check to show overt symp
toms. The PStV genome has been sequenced, and the potential
exists for utilizing viral coat protein genes to incorporate resis
tance into Arachis hypogaea.
In areas where PStV is established, it occurs at high inci
dence, resulting in the harvest of virus-contaminated seed. The
common practice of using seed from the previous seasons crop
assures the continuous presence of PStV in the field. Therefore,
Fig. 73. Peanut mottle virus particles. Bar - 50Q .nm._(Courtesy production and distribution of virus-free seed should be given a
C. Kuhn) high priority in efforts to contain the spread of PStV.
 Causal Agent
Peanut Stunt CPMMV is a member of the carlavirus group of plant
viruses. The particles are slightly flexuous rods, 15 nm in
Peanut stunt was first observed in the United States in 1964. diameter and 610 nm long (Fig. 74). The thermal inactivation
It was economically important in the southeastern United point of CPMMV is 75-80C. High-quality polyclonal antisera
States in various forage legumes and beans, but it is now only to CPMMV also react with the groundnut crinkle virus re
a minor disease. The peanut stunt virus (PSV) occurs naturally ported from the Ivory Coast. CPMMV may be serologically
in peanuts from Sudan and China, where it can cause crop related to several aphid-transmitted carlaviruses.
losses of up to 75%.
Host Range
Symptoms The virus produces local lesions and systemic symptoms on
In the United States, PSV causes severe dwarfing of the many hosts.
entire plant or of one or more branches. In China, the virus
does not cause severe stunting. Shortening of the petioles, Transmission
reduction in the size of leaflets, chlorosis, and malformation CPMMV is readily sap transmissible. The whitefly, Bemisia
are observed in the United States, China, and Sudan (Plate tabaci, transmits the virus in a nonpersistent manner. CPMMV
113). Plants infected early in the growing season produce very is not seed transmitted in peanut.
few pods, and these are misshapen and frequently have a split
pericarp wall. The viability of seed from such pods is markedly Control
reduced. The virus causes epinasty with systemic mosaic and Peanut crops should not be planted adjacent to crops such as
malformation in cowpea (cultivar Blackeye). Systemic symp cowpea and soybean, which are frequently colonized by B.
toms produced by PSV in peanut, beans, and cowpea can be tabaci and are highly susceptible to infection by CPMMV in
used to distinguish it from the cucumber mosaic virus. areas where it occurs.

Causal Agent
PSV belongs to the cucumovirus group. The particles are
25-30 nm in diameter and encapsidate three single-stranded Cucumber Mosaic
RNAs. Two serologically distinct isolates from the United
States, PSV-E from the eastern region and PSV-W from the Natural occurrence of the cucumber mosaic virus (CMV) in
western region, and three serotypes from China, PSV-T, PSV- peanut has been reported only from China. The disease caused
2, and PSV-B2, have been reported. by CMV is referred to as peanut yellow mosaic and is currently
recognized as economically important in the northern regions
Host Range of China. CMV has caused crop losses of up to 40%.
PSV has a wide host range. It produces local lesions on
Chenopodium amaranticolor and C. quinoa. Symptoms
Initial symptoms are chlorotic spots and upward rolling of
Transmission young leaflets. Subsequently produced leaflets show a yellowing
PSV is transmitted by sap inoculation and in a nonpersistent of the lamina with green stripes along the lateral veins (Plate
manner by three aphid species, Aphis craccivora, A. spirae- 115). Occasionally, leaflets are deformed and plants are
cola, and Myzus persicae. It is seed transmitted at the lowest moderately stunted. The severe yellowing and mottling symp
frequency of all the other known seed-transmitted peanut toms observed on young plants are not apparent on older plants.
viruses. Up to 0.01% of large seed from plants infected late in
the season may contain the virus. Up to 0.2% of small seed
from less severely stunted plants may be infected;

Control
Since some forage legumes, such as white clover, are the
primary source of inoculum, peanuts should not be planted in
fields located near such legumes. Roguing of infected plants
from crops intended for seed production is recommended.
Ask. .
Currently, there are no peanut genotypes resistant to PSV.

Cowpea Mild Mottle

The cowpea mild mottle virus (CPMMV) is widely dis
tributed in Asia and Africa but has not been reported in the
United States. CPMMV incidence in peanut does not exceed
5%. Because of its wide distribution, potential to cause severe
crop losses, and occurrence at high incidence in peanut crops
intercropped or grown adjacent to crops such as soybean or
cowpea, incidence of CPMMV should be routinely monitored
in countries where it is endemic.

Symptoms
Initial symptoms on young leaflets are veinclearing followed
by downward rolling of the leaflet edges and veinbanding.
Subsequently, necrosis of leaflets and petioles occurs. Plants
are severely stunted and are conspicuous because of the rolled
edges and veinbanding of the leaflets (Plate 114). Fig. 74. Cowpea mild mottle virus particles.

57
Causal Agent Symptoms
Virus particles are 29 nm in diameter. Many strains of CMV Characteristic symptoms appear on young peanut leaflets as
occur in crop plants. Two strains of CMV naturally infect oval, chlorotic streaks along the veins. Leaflets are reduced in
peanut in China. A strain of minor importance, CMV-CS, is size, and early-infected plants are stunted. Symptoms are not
serologically related to the peanut stunt virus. The predominant distinct on older leaflets.
strain, CMV-CA, is serologically related to CMV-D but is
distinct from CMV-CS. Causal Agent
Purified virus particles of PC1SV are 52 nm in diameter.
Host Range Purified virus contains two polypeptides with molecular
CMV strains have wide host ranges. CMV-CA can infect 31 masses of 58 and 51 kDa. PC1SV DNA has recently been fully
plant species in six families by sap inoculation. sequenced, and the majority of the gene products indicate
significant relationships to other caulimoviruses. In enzyme-
Transmission linked immunosorbent assays, PC1SV does not react with
CMV-CA is easily transmitted by sap inoculation and by cauliflower mosaic, figwort mosaic, or soybean chlorotic
several aphids. Seed transmission is up to 4% in peanut. mottle viruses.

Control Host Range

Seed from infected crops should not be planted. Cultural The host range of PC1SV is unusually diverse compared with
measures such as mulching with transparent plastic sheets and other caulimoviruses. Chlorotic lesions with necrotic centers
roguing out diseased seedlings at early stages of crop growth produced on cowpea are very characteristic. Systemic infection
can reduce disease incidence. No resistance to CMV has been occurs on several Nicotiana species, Datura stramonium,
identified in the cultivated peanut. Glycine max, Petunia x hybrida, Spinacea oleracea, and Vigna
radiata.

Peanut Chlorotic Streak Transmission

PC1SV is readily mechanically transmissible. It is not trans
Peanut chlorotic streak was first observed in 1977 in Andhra mitted by Aphis craccivora, Myzus persicae, or Bemisia tabaci
Pradesh, India. In subsequent surveys, the causal agent, the and is not seed transmitted.
peanut chlorotic streak virus (PC1SV), was found to be widely
distributed in India. It was reported to be a new member of the Control
caulimovirus group. Recently, a symptom variant of PC1SV, The field incidence of PC1SV does not exceed 1%. However,
which is referred to as the veinbanding isolate and has minor the veinbanding variant of PC1SV was observed at an inci
differences in the physical map of the genome, has also been dence exceeding 20%. No control measures are currently avail
reported. able.

TABLE 6. Viruses That Naturally Infect Peanut8

Name Taxonomic Group Family Distribution
Cowpea chlorotic mottle virus Bromovirus Bromoviridae United States
Cowpea mild mottle virus Carlavirus NAb China, India, Indonesia, Ivory Coast, Nigeria, Thailand,
Philippines, Papua New Guinea, Sudan
Groundnut crinklevirus Carlavirus NA Ivory Coast
Peanut chlorotic streak virus Caulimovirus Pararetroviridae India
Peanut chlorotic streak virus
(veinbanding isolate) Caulimovirus Pararetroviridae India
Cucumber mosaic virus Cucumovirus Bromoviridae China
Peanut stunt virus Cucumovirus Bromoviridae Sudan, Japan, Spain, United States
Peanut clump virus Furovirus NA Niger, Burkina Faso, Ivory Coast, Senegal
Indian peanut clump virus Furovirus NA India, Pakistan
Groundnut yellow mosaic virus
(bean golden yellow mosaic virus) Geminivirus Geminiviridae India
Tobacco streak virus Ilarvirus NA Brazil
Groundnut rosette assistor virus Luteovirus NA All of Africa south of the Sahara
Sunflower yellow blotch virus Luteovirus NA Malawi, Kenya, Zambia, Tanzania
Groundnut veinal chlorosis virus Rhabdovirus Rhabdoviridae India, Indonesia
Groundnut chlorotic spotting virus Potexvirus NA Ivory Coast
Bean yellow mosaic virus Potyvirus Potyviridae United States
Groundnut eyespot virus Potyvirus Potyviridae Ivory Coast
Passion fruit woodiness virus Potyvirus Potyviridae Australia
Peanut green mosaic virus Potyvirus Potyviridae India
Peanut mottle virus Potyvirus Potyviridae Worldwide
Peanut stripe virus Potyvirus Potyviridae Brazil, China, India, Indonesia, Japan, Malaysia,
Philippines, Myanmar, Thailand, Taiwan, Vietnam,
United States
Peanut bud necrosis virus Tospovirus Bunyaviridae India, Nepal, Sri Lanka, China, Taiwan, Indonesia,
Thailand
Peanut yellow spot virus Tospovirus Bunyaviridae India, Thailand
Tomato spotted wilt virus Tospovirus Bunyaviridae North America, South America, South Africa, Nigeria
Groundnut yellow mottle virus Tymovirus NA Nigeria
Groundnut rosette virus Umbravirus NA All of Africa south of the Sahara
aListed alphabetically by taxonomic group.
bNot yet assigned.

58
 Herzog, E., Guilley, H., Manohar, S. K., Dollet, M., Richards, K
Other Viruses Fritsch, C., and Jonard, G. 1994. Complete nucleotide sequence of
peanut clump virus RNA1 and relationships with other fungus-
transmitted rod-shaped viruses. J. Gen. Virol. 75:3147-3155.
Many other viruses, including those that cause groundnut
Hobbs, H. A., Reddy, D. V. R., and Reddy, A. S. 1987. Detection of a
streak mosaic (Plate 116), groundnut crinkle, groundnut eye- mycoplasma-like organism in peanut plants with witches broom
spot, peanut green mosaic, peanut yellow spot (Plate 117), using indirect enzyme-linked immunosorbent assay (ELISA). Plant
peanut yellow mottle, groundnut streak, marginal chlorosis, Pathol. 36:164-167.
and rugose leaf curl, have been associated with peanuts Kormelink, R., de Haan, P., Peters, D., and Goldbach, R. 1992. Viral
throughout the world. Although these pathogens often cause RNA synthesis in tomato spotted wilt virus-infected Nicotiana
sporadic infections, yield losses can be significant. rustica plants. J. Gen. Virol. 73:687-693.
Known viruses that can infect peanut under natural con Manohar, S. K., Guillen, H., Dollet, M., Richards, K , and Jonard, G.
ditions, their geographical distributions, and the taxonomic 1993. Nucleotide sequence and genetic organization of peanut
groups to which they belong are listed in Table 6. clump virus RNA 2 and partial characterization of deleted forms.
Virology 195:33-41.
Murant, A. F. 1990. Dependence of groundnut rosette virus on its
satellite RNA as well as on groundnut rosette assistor luteovirus for
Witches -Broom transmission by Aphis craccivora. J. Gen. Virol. 71:2163-2166.
Murant, A. F., Robinson, D. J., Blok, V. C., Scott, K , Torrance, L.,
and Farmer, M. J. 1993. The groundnut rosette disease virus com
Witches-broom is caused by a phytoplasma (formerly called plex: Aetiology, transmission, diagnosis and novel approaches to
a mycoplasmalike organism). Unlike viruses, phytoplasmas are control. Annu. Rep. Scott. Crop Res. Inst. pp. 85-89.
cellular organisms related to bacteria. The disease is charac Reddy, D. V. R. 1991. Groundnut viruses and virus diseases: Dis
terized by stunting and excessive proliferation of shoots from tribution, identification and control. Rev. Plant Pathol. 70:665-677.
axils (Plate 118). Plants are bushy in appearance. Leaflets are Reddy, D. V. R., Richins, R. D., Rajeshwari, R., Iizuka, N., Manohar,
pale yellow and small. Pegs tend to grow upward, and pod S. K.,; and Shepherd, R. J. 1993. Peanut chlorotic streak virus, a
yields are severely reduced. new caulimovirus infecting peanuts (Arachis hypogaea) in India.
A high incidence of witches-broom on peanut has been Phytopathology 83:129-133.
observed in parts of Taiwan, Indonesia, and the Philippines. Reddy, D. V. R., Sudarshana, M. R., Ratna, A. S., Reddy, A. S Amin,
The pathogen is also known to occur in India, Thailand, China, P. W., Kumar, I. K., and Murthy, A. K. 1991. The occurrence of
and Papua New Guinea. A polyclonal antiserum has been yellow spot virus, a member of tomato spotted wilt virus group on
produced for the detection of phytoplasma by use of enzyme- peanut (Arachis hypogaea L.) in India. Pages 77-88 in: Proc.
Tomato Spotted Wilt Virus Workshop. U.S. Department of Agri
linked immunosorbent assay and can be used to distinguish
culture.
witches-broom from viral diseases characterized by severe Reddy, D. V. R., Wightman, J. A., Beshear, R. J., Highland, B., Black,
stunting and a bushy appearance. M., Sreenivasulu, P., Dwivedi, S. L., Demski, J. W., McDonald, D.,
Smith, J. W., Jr., and Smith, D. H. 1991. Bud necrosis: A disease
Selected References caused by tomato spotted wilt virus. Pages 1-20 in: Int. Crops Res.
Inst. Semi-Arid Trop. Bull. 31.
Bock, K. R. 1989. A review of research progress during 1985-89 with Satyanarayana, T., Sreenivasulu, P., Ratna, A. S., Reddy, D. V. R., and
special reference to groundnut streak necrosis disease. Pages 16-19 Nayudu, M. V. 1994. Identification of a strain of peanut chlorotic
in: Proc. Reg. Groundnut Workshop South. Afr., 3rd. International streak virus causing chlorotic vein banding disease of groundnut in
Crops Research Institute for the Semi-Arid Tropics, Patancheru, India. J. Phytopathol. 140:326-334.
India. Thouvenel, J. C., Fauquet, C., Fargett, D., and Fishpool, L. D. C.
Bock, K. R., Murant, A. F., and Rajeshwari, R. 1990. The nature of 1988. Peanut clump virus in West Africa. Pages 247-254 in:
resistance in groundnut to rosette disease. Ann. Appl. Biol. 117:379- Developments in Applied Biology 2: Viruses with Fungal Vectors.
384. J. I. Cooper and M. C. J. Asher, eds. Association of Applied Biolo
Demski, J. W., Reddy, D. V. R., Wongkaew, S., Xu, Z., Kuhn, C. W., gists, Wellesbourne, England.
Cassidy, B. G., Shukla, D. D., Saleh, N., Middleton, K. J., Xu, Z., and Barnett, O. W. 1984. Identification of a cucumber mosaic
Sreenivasulu, P., Prasada Rao, R. D. V. J., Senboku, T., Dollet, M., virus strain from naturally infected peanuts in China. Plant Dis.
and McDonald, D. 1993. Peanut stripe virus. Pages 1-16 in: Int. 68:386-389.
Crops Res. Inst. Semi-Arid Trop. Bull. 38. Xu, Z., Barnett, O. W., and Gibson, P. B. 1986. Characterization of
Dietzgen, R., Xu, Z., and Techeney, P.-Y. 1994. Digoxigenin-labeled peanut stunt virus strains by host reaction, serology, and RNA
cRNA probes for the detection of two potyviruses infecting peanut patterns. Phytopathology 76:390-395.
(Arachis hypogaea). Plant Dis. 78:708-711. Zhang, Z., Xu, Z., Chen, K., and Chen, J. 1993. Epidemiology of
German, T. L., Ullman, D. E., and Moyer, J. W. 1992. Tospoviruses: cucumber mosaic yirus (CMV) on peanut plants. Acta Phytopathol.
Diagnosis, molecular biology, phylogeny and vector relationships. Sin. 23:355-360.
Annu. Rev. Phytopathol. 30:315-348.
Gunasinghe, U. B., Flasinski, S., Nelson, R. S., and Cassidy, B. G.
1994. Nucleotide sequence and genome organization of peanut (Prepared by J. W. Demski and D. V. R. Reddy;
stripe potyvirus. J. Gen. Virol. 75:2519-2526. description of cucumber mosaic prepared by Z. Xu)

59
 Part II. Abiotic Diseases
The causal agent of necrotic etch has not been established.
Drought Stress Attempts to isolate fungi, bacteria, and viruses from necrotic
tissue have been unsuccessful. Disease expression is genet
At the onset of drought, peanut leaflets on affected plants ically controlled, and affected plants breed true for this condi
curl and become lighter in color than normal (Plates 119 and tion. Since necrotic etch is inherited as a qualitatively con
120). If the drought continues, leaflet curling becomes more trolled recessive trait, this disorder is considered to be of
pronounced and the abnormal coloration becomes even more genetic origin.
distinct. Eventually, leaflets turn brown and abscise. Wilted
plants usually recover, provided water becomes available. How Chlorophyll Deficiency
ever, if plants remain wilted for a prolonged period of time, Plants with chlorophyll deficiency ranging from complete
they will not recover. Pegs, either because of continued dry soil albinism to partial deficiency are noted occasionally in peanut
or pathogenic activity, weaken under severe drought stress. fields. Albino plants die shortly after germination. Variegated
Pods attached to weakened pegs often shed during harvest, leaflets, sometimes called chimeras, have areas of normal
especially if the soil is dry and hard. Shallow planting often green tissue as well as areas that lack chlorophyll (Plates 123
produces nonvigorous plants that lack deep roots and are ex and 124). These chlorophyll deficiencies are genetic in origin.
tremely sensitive to drought conditions.
Selected Reference
(Prepared by D. M. Porter)
Hammons. R. O. 1980. Inheritance of necrotic-etch -leaf disease in
peanuts. Peanut Sci. 7:13-14.

Frost Injury (Prepared by D. M. Porter)

Exposure of peanut plants to-below-freezing- temperatures

during the spring or fall can damage foliage. Tender, young
seedlings can be killed if subfreezing temperatures prevail for
Hail Injury
several hours. Exposure of mature plants to subfreezing tem
peratures during the fall results in various degrees of damage. Peanut plants at all stages of growth are occasionally dam-
Symptoms range fromTnarginal-and~tip~neerosis-to-death-ef- -aged-byhail,-Such-plants.. are characterized by shredded or
individual leaflets, branch terminals, and all aboveground plant tattered leaves, parts of which may remain attached to the
parts (Plates 121 and 122). Necrotic tissue is readily invaded by petiole while dislodged parts fall to the ground (Plate 125).
both saprophytic and parasitic fungi. With severe injury, defolia Unless damage is very severe, plants usually recover and pod
tion may be extensive. If plants are not carefully examined, frost yields are not noticeably reduced. Under severe conditions,
injury can be mistaken for symptoms of a biotic disease. stems may appear bruised. Bruised areas often become necrotic,
Seed in freshly dug pods are also subject to freeze injury. which can predispose plants to disease.
The cotyledons of frost-injured seed are off-white, water
soaked or translucent, and off-flavored. Seed have a rubbery (Prepared by D. M. Porter)
texture. Severely damaged seed can be used only for oil stock.

(Prepared by D. M. Porter)
Herbicide Injury
Herbicides are chemicals used to control, suppress, or kill
Genetic Disorders plants or severely interrupt their normal growth. Selective her
bicides are chemicals that are more toxic to certain plant;spe
Necrotic Etch cies (weeds) than to others (species that include the crop).
Necrotic etch, a foliar disease of unknown origin, was first Herbicides registered for use on peanut are selective because
observed in Georgia in 1962. Leaflet lesions, characterized at they usually cause only slight to moderate toxic effects on the
first by the death of three to five cells, are usually surrounded crop while controlling the weeds. Severe crop injury may re
by chlorotic zones of cells. The lesion center appears over a sult from use of excessive rates or from herbicide interaction
tertiary vein. The lesion expands rapidly; and within 2 days, with the environment or other pesticides. Herbicide injury may
the necrotic tissue doubles in size. The lesion moves rapidly also result from herbicide carryover from the previous crop,
through tertiary and secondary veins but not through the leaflet from drift, and from a wide array of application errors such as
midvein. Irregular, zonate lesions that occur on both sides of use of the wrong chemical, overlapping application, nonuni
the leaflet often approach 1 cm in diameter. form soil incorporation, or improper timing of application

60
(Table 7). Herbicide injury is shown in the following plates: related to sprayer swath or direction of sprayer operation,
dicamba (126), paraquat (127), chloroacetamide (128), aci- bands of injury related to treatments banded the previous
fluorfen (129), dinitroaniline (130), 2,4-DB (131), s-triazine year, and patterns related to areas treated with particular
(132), metribuzin (133), vemolate (134), bentazon (135), and tanks of spray mix can often provide evidence to identify the
norflurazon (136). source of the problem. Patterns related to improper mixing
The presence of distinct injury patterns is often helpful in techniques or inadequate agitation are also readily iden
diagnosing the source of herbicide injury. Overdose patterns tifiable.

TABLE 7. Symptoms and Control of Herbicide Injury to Peanuts

Herbicide
Classification and Names Symptoms Control Remarks
Benzoic Epinasty of stems, leaves, and petioles; Avoid drift. In application to Peanut yield loss may occur if dam
Dicamba (Banvel) splitting of stems and petioles; short adjacent crops, use ground age is sufficient to cause splitting
ening of intemodes; leaves often strap equipment and drift-control of stems and petioles.
like in appearance measures as noted on label.
Bipyridyliums Irregularly shaped white to light brown Use correct rate to minimize Peanut plants usually recover from
Paraquat (various trade names) spots or blotches with dark brown effects and apply at appro injury without yield loss.
margins priate growth stage.
Chloroacetamides Swelling of hypocotyl; curling of hypo- Use correct rate, and apply Injury is usually associated with
Alachlor (Lasso) cotyl; roots thickened and stubby in uniformly. heavy rainfall or irrigation soon
Metolachlor (Dual) appearance; delayed seedling emer after preemergence application,
gence and crop development; occa with low seed vigor, or both.
sionally, failure of seedlings to
emerge
Diphenyl ether Leaflets with bronze, speckled bum Use correct rate, and apply A contact herbicide injury is usually
Acifluorfen (Blazer) spots; leaflet crinkle; stem and petiole uniformly. most severe when temperature
bum. In severe cases, many injured exceeds 32C and humidity is
leaflets may drop. high.
Dinitroanilines Delayed seedling emergence and crop Use correct rate. Apply and Injury is usually associated with non-
Benefin (Balan) development; swollen hypocotyl; incorporate uniformly. uniform application or incorpora
Pendimethalin (Prowl) secondary roots thickened and stubby. Adhere to label directions tion or with use of excessive rates.
Trifluralin (Treflan) Meristem of primary root may die. concerning incorporation Factors other than dinitroanilines
Ethalfluralin (Sonalan) Leaves may be small. Plant may wilt depth. may cause swollen hypocotyl
readily under moisture stress. symptoms; however, roots will
usually be normal.
Phenoxys Epinasty of stems, leaves, and petioles; Avoid drift of 2,4-D to peanut Peanut injury with 2,4-DB is most
2.4-DB (Butoxone, Butyrac) occasional splitting of stems and plants. Use correct rate of likely to occur when high rates are
2.4-D (numerous trade names) petioles. 2,4-DB frequently causes 2,4-DB, and apply uniformly. applied under conditions of mois
base of peanut leaflet to become chlo Do not apply 2,4-DB to pea ture stress.
rotic and roll downward, resulting in nut plants under moisture
elongated appearance. Seed from stress.
plants treated with 2,4-DB are often
misshapen, with one cotyledon larger
than the other. In affected seed, the
larger cotyledon may fold around the
smaller, and the radicle is frequently
very prominent.
Substituted-ureas Interveinal chlorosis. In severe injury, Observe crop rotation restric Carryover of these herbicides is com
Fluometuron (Cotoran) entire leaflet becomes chlorotic., and tions noted on herbicide mon. It is most likely when pH is
Diuron (Karmex) necrosis proceeds inward from leaflet labels. Apply uniformly high and high rates are used.
tip and margins. and at correct rates.
s-Triazines Interveinal chlorosis. In severe injury, Observe crop rotation restric Carryover of these herbicides is com -
Atrazine (Atrazine, AAtrex) entire leaflet becomes chlorotic, tions noted on herbicide mon. It is most likely when pH is
Simazine (Simazine, Princep) and necrosis proceeds inward from labels. Apply uniformly high and high rates are used.
leaflet tip and margins. and at correct rates.
Other triazines Bleaching of leaflet at top and/or Avoid aerial application near Metribuzin does not present a carry
Metribuzin (Lexone, Sencor) margins peanut fields. over hazard to peanut plants.
Thiocaxbamate Delayed seedling emergence. On Use correct rate. Apply and Injured stands usually recover without
Vemolate (Vemam) newly emerged seedlings, leaflets of incorporate uniformly. yield reduction. Injury is most
youngest leaves are sealed at the likely under cool conditions on
margins. Affected seedlings are often coarse-textured soils with moisture
stunted. stress during seedling emergence.
Other herbicides Leaflet speckling; mottling or occa Use correct rate and apply uni Peanut plants usually recover from
Bentazon (Basagran) sionally marginal or complete chlo formly. Avoid application injury without yield loss.
rosis. Affected leaflets are retained with crop oil concentrates
within the crop canopy. except where necessary to
increase effectiveness of
weed control.
Norflurazon (Zorial) Veinal chlorosis (bleaching) of leaves Use correct rate. Apply to soil Peanut plants usually recover from
or in severe instances chlorosis of surface prior to crop injury without yield loss.
entire leaflets emergence.

61
 Injury caused by herbicide drift may result from movement and then, as they become thickened and leathery, a dull, dark
of spray particles or vapors from treatment sites adjacent to green. In time, the older leaves turn orange yellow (their veins
peanut fields. Drift damage is usually most severe in areas may be reddish brown). The entire leaf becomes brown and
nearest the application site and declines in intensity with dis finally drops. Stems may become purplish because of an accu
tance from that site. Drift damage usually can be detected in mulation of anthocyanins.
sensitive vegetation in and around both the field of origin and
the contaminated site. Potassium
Herbicide injury resulting from either herbicide carryover or Potassium deficiency is expressed in chlorosis of the leaves,
improper soil treatments is often associated with soil con beginning at leaflet margins. Some chlorosis may be inter-
ditions. Where excessive dosages of herbicides are used, injury veinal, but most yellowing occurs at the leaf edges. These re
is usually most severe in coarse-textured (sandy) soils low in gions change to reddish brown and then become necrotic or
organic matter. Herbicide carryover is usually associated with scorched. Severely affected older leaves are shed. Leaf margins
high clay content or high organic matter content or both. may curl upward somewhat, and the tips of branches may
Herbicide injury problems can be minimized by using the redden and die.
correct product at the proper rate and time and using recom
mended application techniques. Calcium
Peanut is especially sensitive to calcium deficiency. In solu
Selected Reference tion culture, a lack of this nutrient is expressed not only quick
ly, but with marked effects. Roots are severely affected, be
Skroch, W. A., and Sheets, T.. J. 1977. Herbicide injury symptoms and
coming short, stubby, and discolored. Young leaves soon wilt,
diagnosis. N.C. Agric. Ext. Serv. Bull. AG-85.
apical buds die, and regions of the petiole break down. Stem
elongation ceases, so plants are stunted. In less severe cases,
(Prepared by C. W. Swann)
leaves are small and plants take on a bushy appearance. Leaves
may develop numerous brown spots or pitted areas, resulting in a
bronze color (Plate 139). Flowering and fruiting are inhibited.
Lightning Injury In the field, calcium deficiency is expressed more commonly
by abnormal fruiting. Extreme deficiency of calcium in the
Plant injury by lightning occurs infrequently. When it does, fruiting zone results in no pods being formed. Cultivars vary,
it is spectacular and may be confused, without close observa however, in their sensitivity to a lack of this nutrient in the
tion, with an initial locus of a potentially pandemic disease fruiting zone. With a less extreme deficiency, the seed often
such as rust (Puccinia arachidis). Injury is characterized by the abort and only the shells develop, resulting in empty pods that
death of peanut plants in isolated, round spots within the field have been called pops. Seed that do develop often have a
(Plate 137). Plants not killed may have black streaks of necro darkened plumule (Fig. 75). The viability of seed, including
sis running along their branches. The demarcation between those that do not have darkened plumules, is directly related to
uninjured and injured plants in the field is usually distinct. At their calcium concentration.
the fringe of the strike, plants with varying degrees of injury
are scattered among unaffected plants. Magnesium
Leaves deficient in magnesium exhibit interveinal chlorosis.
(Prepared by D. M. Porter) The yellowing begins at the margins and extends toward the
midrib. The edges may become orange and crinkle or curl.
Older leaves develop necrotic areas and then drop from the
Nutrient Imbalances plant.

A nutritional imbalance in peanut plants is usually expressed Sulfur

in patterns of abnormal growth. The symptoms, whether from Terminal growth of the peanut plant is affected by lack of
deficiency or toxicity, depend on the severity of the conditions. sulfur. Under deficient conditions, root development is re
To produce clear symptoms of known cause, researchers have stricted and new leaves become pale green or yellow (Plate
occasionally used solution culture studies. Some of the descrip 140). Leaf chlorosis resembles that caused by lack of nitrogen,
tions in this section are from such observations. Symptoms in except that because of the greater immobility of sulfur within
plants grown in the field may be much less distinct and more
difficult to diagnose.

Nitrogen
Nitrogen deficiency is characterized by varying degrees of
general chlorosis (Plate 138). Young plants not yet adequately
colonized by rhizobia may become lighter green than normal.
In more severe cases, the entire leaf becomes a uniform, pale
yellow, and stems may be thin and elongated. As the plant de
velops, the lower, older leaves are most affected and drop from
the plant. Growth is stunted, and stems may become reddish.
In the field, foliar chlorosis can result from lack of nodulation,
from ineffective nitrogen fixation induced by molybdenum
deficiency (usually associated with extreme soil acidity), from
translocation of the limited supply of nitrogen to developing
pods late in the season, or from waterlogged conditions.

Phosphorus Fig. 75. Healthy cotyledon and plumule (right) and darkened plu
Plants deficient in phosphorus are stunted; leaf size is espe mules exhibiting calcium deficiency symptoms (left and center).
cially reduced. Affected leaves may first become bluish green (Courtesy D. Hallock)

62
the plant tissues, it occurs predominately at growing points. may occur in affected regions. Necrosis develops in the tips
Plants deficient in sulfur may be stunted but appear quite and margins, progressing inward until the petiole drops. The
upright because of reduced branching. bud areas are affected, resulting in stunted plants with short
branches. Yields are reduced.
Iron
Iron deficiency occurs in calcareous soils with alkaline pH. Molybdenum
It may develop so rapidly that intermediate or mild conditions Deficiency of molybdenum may occur if the soil is extreme
are difficult to observe. Young leaves exhibit interveinal chlo ly acid. The symptom produced, however, is that of nitrogen
rosis and may have somewhat crinkled margins. Very soon, deficiency. Apparently, the critical level of molybdenum
however, these young leaves become very pale yellow, almost needed for nitrogen fixation is greater than the level needed for
white (Plate 141). Even the petiole is very light in color. other physiological processes.
Affected leaves then develop brown spots or necrosis on the
laminae. In the field, plant growth may be restricted and leaf Boron
size reduced. Severe deficiency of boron causes leaves to turn deep green.
Water-soaked areas may develop, and lesions may occur on
Manganese leaves, petioles, and stems. Growth is restricted: terminal leaves
Manganese deficiency is expressed by interveinal chlorosis become small and deformed, intemode length is reduced, and
in the leaves (Plate 142). Symptoms range from mild, in which secondary branching occurs, making the plant appear stumpy
leaves are light green and the regions immediately adjacent to and short. The lower branches may split. Flowering and pod
the veins and the veins themselves remain green, to severe, in production are reduced. The pods of certain varieties may
which the entire interveinal area is chlorotic. After a period of exhibit fine cracks. Lateral root growth is restricted, and root
interveinal chlorosis, some bronzing may occur; then older tips become swollen.
leaves develop necrotic spots and drop from the plant. Stems The most common boron deficiency symptom in field-grown
are slender and weak. Fruiting, and thus yields, are reduced. peanut plants occurs in the pod. Seed do not develop properly.
Manganese deficiency occurs in soils inherently low in this The inner face of the cotyledon is depressed in the center, and
nutrient, especially-if they have been limed more than neces that region often turns brown, especially when roasted. The
sary. symptom has been termed hollow heart (Fig. 76).
Excess manganese, associated with high-manganese soils Boron toxicity symptoms are likely to occur if more than 0.5
and very low pH, results in manganese toxicity symptoms. kg of boron per hectare is applied. Leaflet margins become
Leaves have slight interveinal chlorosis near the leaf margin, chlorotic and then necrotic (Plate 148). In severe cases the
and small brown spots develop in the affected regions. Flow leaves shed from the plant.
ering and rate of maturation are delayed, so pod development
is impaired. Selected References

Zinc Cox, F. R., Adams, F., and Tucker, B. B. 1982. Liming, fertilization
Lack of zinc results in interveinal chlorosis of recently ma and mineral nutrition. Pages 139-163 in: Peanut Science and
tured leaves. In severe cases, they will later turn red brown and Technology. H. E. Pattee and C. T. Young, eds. American Peanut
Research and Education Society, Yoakum, TX.
then drop from the plant. However, retarded growth is the
Reid, P. H., and York, E. T., Jr. 1958. Effect of nutrient deficiencies
dominant deficiency symptom. Intemodal length is reduced; on growth and fruiting characteristics of peanuts in sand cultures.
plants are stunted; terminal growth is retarded; and new leaves Agron. J. 50:63-67.
develop very slowly. Terminal leaflets are small, thickened,
leathery, and exceptionally dark green. Yields are reduced. (Prepared by N. L. Powell and F. R. Cox)
Yields are also restricted by zinc toxicity. Severely affected
plants exhibit chlorosis (Plate 143) and stunting (Plate 144).
Stems and petioles become purplish. Lesions resulting in a
split stem (Plate 145) occur at the plants base, and progressive
necrosis may cause the plant to die prematurely.
Ozone Damage
Copper Ozone, sulfur dioxide, and fluorides are the major air pollu
Under copper deficiency conditions, young leaves become tants likely to affect peanuts. Ozone is by far the most impor
deformed and are greenish yellow or chlorotic (Plate 146). tant air pollutant because it occurs throughout peanut produc
Terminal leaflets are small, and their margins may curl inward, tion areas at concentrations that cause foliar injury and
giving a cupped appearance (Plate 147). Yellowish white spots decrease yield. Classical foliar symptoms caused by sulfur
dioxide or fluorides have been described for crops grown near
industrial point sources. However, injury from sulfur dioxide
or fluorides has not been documented for peanuts.

Sources
Ozone is formed in the troposphere by complex photochem
ical reactions between oxides of nitrogen and hydrocarbons
that originate chiefly from gasoline engines and the burning of
other fossil fuels. These primary pollutants are transported long
distances by regional weather patterns. Concentrations of ozone
are likely to be high enough to injure peanuts during calm,
sunny days when primary pollutants from urban areas are
present. Seasonal concentrations of ozone in the southeastern
peanut-production areas are higher than in most other areas of
Fig. 76. Cotyledons with hollow heart symptoms (left two) caused the United States because of the frequent transport of nitrogen
by boron deficiency compared with cotyledons from healthy oxides and hydrocarbons from urban areas and the frequent
plants. (Courtesy D. Hallock) periods of bright sunshine.
63
Symptoms A healthy peanut leaf from a plant grown in a field chamber
Ozone enters leaves through stomata during normal gas receiving charcoal-filtered air (i.e., reduced ozone concentra
exchange. As strong oxidants, ozone or secondary products tions) and a leaf from a plant grown in the open that has injury
resulting from oxidation by ozone (e.g., free radicals) cause a caused by ozone are shown in Plate 149.
variety of symptoms that appear within 2 days after exposure.
Most symptoms are subtle and difficult to separate from those
caused by normal senescence (e.g., chlorosis). Sometimes, how Selected References
ever, a distinct, light tan, powdery appearance (fleck) and/or tiny,
darkly pigmented areas (stipple) can occur on upper leaf surfaces Heagle, A. S. 1989. Ozone and crop yield. Annu. Rev. Phytopathol.
between the veins. Both of these symptoms appear mostly on 27:397-423.
middle-aged leaves and are caused by the death of individual Heagle, A. S., Letchworth, M. B., and Mitchell, C. A. 1983. Injury
cells. With time and continuing daily exposure to ozone, these and yield responses of peanuts to chronic doses of ozone in open-
symptoms are gradually blurred by chlorosis and other symptoms top field chambers. Phytopathology 73:551-555.
of general senescence. Flecking, stippling, and symptoms of Heck, W. W. 1968. Factors influencing expression of oxidant damage
early senescence on peanut leaves occur in the field and have to plants. Annu. Rev. Phytopathol. 6:165-188.
been duplicated by controlled exposures to ozone. Field chamber
experiments have shown that ambient concentrations of ozone
can decrease peanut yield in the southeastern United States. (Prepared by A. S. Heagle)

64
 Part III. Insects and Arthropods
Insects and related arthropod pests occupy every conceivable a developing terminal; and the com earworm, Helicoverpa zea,
niche on the peanut plant. Insects feed in terminal buds and which consumes terminals, young foliage, flowers, and imma
flowers; on leaves, roots, and pods; behind leaf axils and pet ture pegs. The major mechanism of yield reduction in legumes
ioles; on plant fluids by inserting their mouthparts into cells or such as peanut, caused by feeding of foliar insects, is the re
directly into the nutrient transport system; in tunnels that they moval of photosynthetically active tissue, which thereby re
form in the leaves, main stem, lateral branches or roots; and on duces the production of photosynthate. Many lepidopterous
or in peanut pods and seed. They damage the plant directly by defoliators of peanut prefer to feed on young leaves and ter
removing photosynthate that would otherwise be used for minals found in the upper plant canopy. The upper canopy is
vegetative or reproductive plant growth; damaging cells in more active in light interception and production of photo
photosynthetically active tissue; removing foliage that pro synthate than shaded leaves of the mid- and lower canopy.
duces photosynthate; feeding on developing pegs, pods, and
seed; damaging the root-hypocotyl region by the removal of Armyworms
periderm, cortex, and phloem tissue; and increasing the rate of Several species of armyworms are major defoliators of pea
water loss from an injured, stressed plant. To add to this bio nut, including the fall armyworm, Spodoptera frugiperda (J. E.
logical complexity, arthropod pests generally do not occur in Smith) (Plate 150), and the beet armyworm, S. exigua (Hiibner)
single-species groups but in groups of several species. (Plates 151 and 152), in the United States; the tobacco army
Equally important as the direct damage to plants by insects worm, S. litura (Fabricius) (Plate 153), in Asia; and the Afri
is the indirect damage that may result from the injury they can armyworm, S. littoralis (Boisduval), in Africa and western
cause. Insects are vectors of plant pathogens such as the ground Asia. Armyworm moths lay masses of 20-1,000 eggs on the
nut rosette, bud necrosis, and tomato spotted wilt viruses. In leaves and stems of peanut (Plate 154). The egg masses often
addition, injured plant tissue is vulnerable to secondary infec are covered with body scales and silk webbing, giving them a
tion by pathogens such as Aspergillus flavus and Sclerotium green to golden bronze color. Newly emerged larvae feed cryp
rolfsii. Economic losses attributable to plant pathogens trans tically on the undersides of leaflets, in terminals, or between
mitted by insects-often exceed losses caused by the insects the leaf petioles and stems while older larvae feed openly on
themselves. For example, the peanut rosette virus, transmitted the plant on terminals and younger leaves. Older S. litura lar
by Aphis craccivora Koch, was credited with decimating pea vae feed primarily at night and hide under debris or soil clods
nut production in West Africa in 1975. Likewise, the plant at the base of the plant during the day. The fall armyworm
viruses that cause bud necrosis and tomato spotted wilt are prefers to feed' on young leaf tissue and consumes about 100
transmitted by thrips and cause significant crop losses in Asia cm2 of foliage during larval development, 80% of which is
and the Uiiited States, respectively. consumed during the last two instars. Fall armyworm larvae
The feeding by multiple species of insect pests can best be require almost twice as much foliage to complete development
understood by grouping the insects into feeding guilds based when feeding on older foliage than on younger foliage. In
on the plants physiological response to the injury they cause. India, defoliation of peanut by Spodoptera larvae has a greater
There are six categories of plant injury or crop damage caused effect on yield during the dry season (December-April) than
by insect feeding: stand reduction, leaf-mass removal, assimi during the rainy season (June-October). This difference in
late removal, water balance disruption, pod destruction, and susceptibility to injury probably occurs because of the plants
architectural modification. inability to compensate for the effects of defoliation during the
For the purpose of this discussion, insects and other arthro short, cooler, dry season.
pods that cause damage to peanut are divided into the follow Armyworm larvae feed on a wide variety of cultivated and
ing guilds: foliage feeders, intracellular feeders, root and pod wild host plants. Mature larvae may reach a length of 3-4 cm,
feeders, and stored-product feeders. A general description of have a characteristic inverted Y pattern on their head capsules,
the injury caused by arthropod pests and its physiological and vary from light green to brown or black with longitudinal
effect on the plant is presented with a brief description of stripes along their sides. These insects are called armyworms
selected species in each guild. because young larvae feed together on a host and crawl en
masse to adjacent fields after all the foliage in one area has
been consumed.
Foliage Feeders Helicoverpa (Heliothis) spp.
Helicoverpa larvae are plant pests in all temperate, tropical,
The foliar feeding guild of insects that injure peanut is com and subtropical regions of the world. In the New World, the
posed primarily of immature lepidopterans. Plant injury by com earworm, bollworm, or tomato fruitworm (all approved
these larvae is diverse. Examples include the groundnut leaf- common names), Helicoverpa zea (Boddie) (Plate 155), and
miner, Aproaerema modicella, which initially feeds between the tobacco budworm, Heliothis virescens (Fabricius), are the
the epidermal layers of the leaf and forms mines while feeding most important pest species. In Africa and Asia, the most
on the mesophyll tissue; the rednecked peanutworm, Stegasta important pest species is the old world bollworm or gram pod
bosqueella (Chambers), which feeds almost exclusively within borer, Heliothis armigera (Htibner) (Plate 156). On peanut, the
65
eggs are laid singly, primarily on the undersides of leaves in the because of the numerous, long hairs on the bodies of older
outer plant canopy. Larvae of all these species feed on flowers larvae. Hairy caterpillars have one generation per year. Moths
and pods of numerous hosts including cotton, okra, pigeonpea, are brownish white with a wing span of 40-50 mm (Plate 160).
peanut, soybean, and cowpea. Early instars feed in leaf ter They emerge shortly after the first rains of the rainy season and
minals while older larvae feed openly on terminals and young lay clusters of 50-100 eggs in or around any available plant.
foliage. Helicoverpa larvae reach a length of almost 4 cm and As a peanut seedling emerges, young larvae move and feed en
may be rose pink, yellow green, brown, or almost black on masse on the undersides of leaves. Older larvae disperse
their dorsa, with alternating light and dark longitudinal stripes through the field and feed on terminals, leaves, and flowers.
on their sides and a lighter color on their undersides. Spiny Larvae reach a length of 5 cm and may completely defoliate all
projections are also quite noticeable on the surfaces of Hel peanut plants in a field before migrating and feeding in an
icoverpa larvae. A single com earworm larva consumes 175- adjacent field.
200 cm2 of peanut foliage during development, of which 75-
97% is consumed by the last two instars. In India, H. armigera
feeds primarily on flowers, and its greatest effect on peanut is
to extend the fruiting period of the plants.
Intracellular Feeders
Velvetbean Caterpillar Peanut hosts a number of intracellular feeders including
The velvetbean caterpillar, Anticarsia gemmatalis Hiibner, is aphids, leafhoppers, thrips, mites, and whiteflies. These insects
a tropical to subtropical New World pest. It does not overwin generally have rasping or piercing-sucking mouthparts and
ter in peanut-producing regions of the United States and sur directly damage plants by consuming photosynthate. Several of
vives the winter only in the most southern latitudes. The moths the intracellular feeders, especially thrips and aphids, are vec
migrate northward each year. Damage by the velvetbean cater tors of plant pathogens. Feeding by the potato leafhopper, Em-
pillar (Plate 157) in the United States is most severe in north poasca fabae, on leaves reduces photosynthesis and increases
ern Florida and southern Georgia, where high larval densities respiration. A reduction in photosynthesis occurs immediately
often occur on peanut late in the growing season. Eggs are after E. fabae feeds. The duration of photosynthesis reduction
usually laid singly on the undersurfaces of leaves. Larvae feed is related to the length of the feeding period, the stage of plant
openly on the plant, initially consuming terminals and young development, and the stage of leafhopper development. Injured
foliage. With increased larval age, this preference declines, and plants partially recover photosynthetic activity, but the reduc
larvae consume leaves of all ages. They are voracious feeders tion is permanent, affects all stages of plant development, and
on peanut, soybean, kudzu, and velvetbean and may rapidly- is most pronounced in bloom and postbloom growth stages. In
and completely defoliate plants. A larva consumes approxi plants damaged by the twospotted spider mite, Tetranychus
mately 100 cm2 of leaf tissue during its development. urticae, both photosynthesis and transpiration are reduced in
Larvae of the velvetbean caterpillar reach a maximum length severely damaged cells while moderate' damage may increase
of 4.5-5 cm and are characterized by a yellow head capsule transpiration and cause development of smaller, deformed
and a body color ranging from light green to black with yellow leaves with a lower chlorophyll content. Increased leaf tran
to white longitudinal stripes along the entire length of the body. spiration also increases water loss, resulting in plant stress and
The last pair of prolegs projects backward, and the legs are closure of leaf stomates.
prominent when larvae are at rest. When larvae are disturbed,
they often drop to the ground and thrash from side to side in Leafhoppers
rapid, twitching contortions characteristic of the insect. Several species of leafhoppers, especially members of the
genus Empoasca, are pests of peanut. These include the potato
Groundnut Leafminer leafhopper, E. fabae (Harris) (Plate 161), in North America;
The groundnut leafminer^ Aproaerema modicella Deventer, the groundnut jassid, E. kerri Pruthi (Plate 162), in India; and
is a primary pest of peanut in India and Southeast Asia. The E. facialis Jacobi and E. dolichi Paoli in West Africa. Both
hosts of this leafminer are primarily legumes, and peanut and adult and nymphal leafhoppers feed primarily on the under
soybean are among its most important crop hosts. Moths sides of peanut leaflets or leaves by inserting their mouthparts
deposit eggs singly on the undersides of leaves or on petioles into the midribs and extracting plant fluids. Adult leafhoppers
and stems. First-instar larvae tunnel into the leaflet and feed on are 3-5 mm long, wedge shaped, and light green to yellow.
the mesophyll between the upper and lower epidermis, forming Leafhopper feeding causes leaves and leaflets to turn yellow
blotch mines. Severe infestations may result in complete loss from the point of injury to the tip in a typical V shape (Plate
of photosynthetic tissue and defoliation as leaflets turn brown, 163), probably as a result of the injection of salivary toxin or'
shrivel, and desiccate. Third-stage larvae leave their mines, toxins before feeding. The symptom, called hopper bum,
web two or more leaflets together, and continue to consume may become so severe that the injured area dies. In the United
foliage as they complete their development (Plate 158). At States, the potato ,leafhopper does not survive the winter in
maturity, larvae reach a length of 6-8 mm and pupate within northern latitudes and overwinters only in mild climates along
webbed leaflets. Populations of leafminers increase during the the gulf coast. Adults disperse northward during the growing
rainy season and may become severe pests during the pod- season on wind currents associated with weather fronts, reach
filling stage. Problems caused by this pest may intensify when ing as far north as Canada by early June. In the United States,
irrigation allows peanut production to extend beyond the rainy injury to peanut by leafhoppers is generally most severe during
season into the dry season. Moths then move from fields with June and July; in India, injury is most severe during August
mature plants to fields with immature plants, which are par and September of the rainy season and February and March of
ticularly susceptible to damage by this species. the dry season.

Hairy Caterpillars Thrips

Arctiid larvae of the genus Amsacta are among the most In the United States, the tobacco thrips, Frarikliniella fusca
important defoliators of peanut in India, although they produce (Hinds) (Plate 164), is the most abundant species of thrips on
only sporadic losses on peanut. The red-headed hairy cater peanut, while in Southeast Asia, Scirtothrips dorsalis Hood
pillar, A. albistriga Walk. (Plate 159), is most important in and Thrips palmi (Bagnall) are the most abundant species on
southern India, and A. moorez. (Butler). is., most important in this crop. Thrips are extremely small (1.5-2 mm), delicate in
northern India. These insects are named hairy caterpillars sects that feed in peanut leaf buds and flowers. Eggs are depos
66
ited in plant tissue and hatch in 5-7 days. Immature stages The silverleaf whitefly lays its eggs on the undersides of
resemble the adults but lack the fringed wings. Immatures are peanut leaves, and immatures can be found on both the upper
pale yellow to white, while adults range from light yellow to and lower leaf surfaces, which does not occur on most other
gold to black. Thrips have rasping mouthparts and feed by hosts. The nymphs are distributed equally among the tetrafo-
scraping the upper surfaces of developing terminals and imbibing liates of a peanut leaf and pass through four nymphal instars.
the exuded fluid. Thrips injury to terminals results in deformed They are most abundant on leaves three, four, and five, and
leaves that are crinkled and slightly cupped upon emergence then abundance declines as leaf age increases. Adult whiteflies
(Plate 165). Thrips damage to peanut foliage is most severe are white and approximately 2 mm long and are found on the
during the first 30 days after plant emergence. Once plants begin lower leaf surfaces (Plate 169). Plant damage is by direct
to bloom, most thrips are found in the peanut flowers. removal of photosynthate from the phloem and by the produc
Results from several studies indicate that thrips injury to tion of honeydew, which drips onto leaves below the nymphs
peanut does not significantly decrease pod yield..However, two and is colonized by a sooty mold, Capnodium spp., that re
recent findings have altered opinion on the importance of duces light interception and photosynthesis.
thrips. Thrips injury and herbicide injury to seedlings inter
acted to significantly reduce main stem height, canopy width,
yield, and value of peanut. Secondly, and probably most impor
tantly, thrips transmit the bud necrosis and tomato spotted wilt Root and Pod Feeders
viruses, both of which cause important diseases in peanut.
However, control of thrips does not reduce virus incidence. Several soil-inhabiting insects and other arthropods are key
pests of peanut worldwide and represent a diverse group of
Aphids species, including white grubs, wireworms, earwigs, ants, lepi-
Several aphid species have been reported on peanut, but the dopterous larvae, termites, and millipedes. These pests feed on
cowpea or groundnut aphid, Aphis craccivora Koch, is the roots, stems, and pods, causing stunting; decreased leaf area;
most important. This aphid occurs in the United States, Asia, diminished root, pod, and seed dry weight; reduced xylem
and Africa, but it is a major vector of the groundnut rosette pressure; reduced photosynthate flow in the phloem; decreased
virus only in Africa. The adult aphid is black, rounded, and nitrogen fixation; and wilting of plants caused by insufficient
slightly oblong with brown legs, a prominent cauda, and thin, transport of water. In addition, injury to plants by insects pre
black cornicles. They reproduce asexually, and nymphs are disposes them to invasion by secondary pathogens such as
dark brown. As populations increase on peanut, winged aphids Aspergillus flavus.
are produced and disperse to form new colonies. Nymphs and
adults feed primarily on new tissue including leaf buds and Lesser Cornstalk Borer
unfurling leaves (Plate 166), pegs, and flowers (Plate 167) by The lesser cornstalk borer, Elasmopalpus lignosellus (Zeller)
inserting their piercing-sucking mouthparts into the phloem (Plate 170), is among the most important insect pests of peanut
and extracting sap. in the United States. This insect is a pest of numerous crops,
including peanut, when soil moisture is deficient; it seldom
Twospotted Spider Mite causes damage when soil moisture is high. This insect also is
The twospotted spider mite, Tetranychus urticae Koch, is a more important as a pest on peanut grown in sandy soil than in
major pest of peanut in the United States, especially in Virginia heavier soil that has a higher organic content and greater water-
and North Carolina. The adult mite is approximately 0.5 mm holding capacity. Soil moisture affects every stage of E. ligno
long and light green to yellow with two black dots on the sellus. Under wet conditions, moths lay eggs singly on the
dorsum. The mites injure plants by inserting their piercing- plant and larvae feed between leaf axils and stems or in flower
sucking mouthparts into plant cells and sucking out the con buds. Under dry conditions, moths lay eggs just below the soil
tents. They overwinter as diapausing females or, in areas with surface around the base of the plant and larvae feed under
a mild winter, as actively reproducing adults. In the spring, leaves touching the ground or on the main stem at or just
mites initially feed on early hosts and then become established below the soil surface. Larvae form feeding tubes in the soil
on com. Populations increase rapidly on tasseling com and from which they feed on roots and developing pods. They also
then disperse as it begins to senesce. Dispersal from senescing may tunnel through the main stem or lateral branches of plants.
com occurs during flowering and pod development on peanut, Moths are approximately 12.5 mm long; females are charcoal
stages that are favorable for mite establishment and population gray to black, often with brown markings toward the anterior
increase (Plate 168). Mite outbreaks in peanut are thought to be (Plate 171), and males are buff to light yellow with charcoal
induced by application of fungicides and insecticides; the gray bands on their wings (Plate 172). Young larvae are bright
interaction between the two pesticides reduces the number of red, and older larvae have dark mahogany and blue green
natural enemies that regulate mite populations on peanut. alternating bands around their bodies and may reach 2 cm in
length. Larvae prefer to feed on immature peanut pods and
Whiteflies damage developing seed when they penetrate. Older larvae
The sweetpotato whitefly, Bemisia tabaci (Gennadius), is a feed externally on more mature pods by scarifying the exocarp
relatively new pest of peanut in the United States, but it has without actually penetrating the pod (Plate 173). This external
been a pest of peanut in India for many years. The first white- damage to pods is sufficient to enhance infection by A. flavus
fly infestations on peanut in the United States coincided with and the formation of aflatoxin.
the identification of a new strain, B, that devastated vegetable A model for predicting an infestation by the lesser cornstalk
crops in Florida, California, Arizona, and Texas during 1987 borer (LCB) has been developed. The model is used to cal
and 1988. Strain B was also found on peanut in Georgia. Re culate LCB days, i.e., the number of hot, dry days (on which
cent research on strain B of the sweetpotato whitefly has the temperature is at or above 35C and rainfall is less than
shown that it may be a new species, and the names silverleaf 2.54 mm) minus the number of cool, wet days (on which the
whitefly and B. argentifolii Bellows & Perrin have been pro temperature is less than 35C and rainfall is at or above 2.54
posed. This whitefly is a serious threat to peanut because of its mm). Scouting for LCB damage is recommended when the
ability to increase its population rapidly, its occurrence on the running total of LCB days approaches zero. Values below zero
undersides of leaves where it is difficult to control with indicate that the LCB is unlikely to be a problem in peanut,
insecticides, its resistance to a number of insecticides, and its while values of 10 or greater represent conditions under which
role as a vector of plant viruses. outbreaks of this insect are likely to occur.
67
Southern Corn Rootworm insects with three pairs of inconspicuous legs on the front half
The southern com rootworm, Diabrotica undecimpunetata of the body. They range in color from yellow to light brown
howardi Barber, is a major pest of peanut in Virginia and North and at maturity average 15-25 mm in length. Larvae feed on
Carolina and of peanut grown on poorly drained soils in the all underground parts of the peanut plant, but they are espe
southeastern United States. The adults, often called spotted cially damaging to the pods (Plate 180). Wireworms make
cucumber beetles, are about 6-6.5 mm long and are easily jagged entry holes in the pods and feed on the developing seed,
recognized by the twelve spots on their greenish yellow elytra often completely consuming the seed and leaving empty pods.
(Plate 174). Adults prefer to oviposit at the bases of plants in
moist, dark soil with moderate levels of organic material and Millipedes
clay. The presence of weeds among peanut plants increases Millipedes are a serious pest of peanut in several developing
opposition. The larvae are slender, fragile, and white with dark nations, particularly in western Africa. Of the 13 species of
brown to black head capsules and anal plates and may reach a millipedes that damage peanut in Senegal, Peridontopyge spp.
length of 12.5-18.0 mm at maturity (Plate 175). Adult rootworm are the most prevalent. Millipedes spend the dry season deep in
beetles feed above the ground on peanut leaves, and larvae feed the soil below stumps and in or under termite mounds. During
below ground on roots or developing pegs and pods. Larvae the rainy season, more than 50% of the millipedes are found in
make almost cylindrical entry holes and feed on the immature the upper 10 cm of soil, whereas during the dry season, more
pods and developing seed. Damage by rootworm larvae also than 90% are found below 10 cm. They emerge from the soil
predisposes pods to invasion by fungi that induce pod rot. Three shortly after the first substantial rains of the wet season and feed
to four generations may occur each year in the southern latitudes, on seedling plants, including peanut, often reducing plant density
while only one generation occurs in the northern latitudes. by up to 20%. They also feed on developing pods and may
reduce yield by 30-40%. Millipedes primarily attack immature,
White Grubs developing peanut pods, while termites attack more mature pods.
White grubs are the larvae of scarab beetles and are con
sidered among the most important pests of peanut worldwide,
especially in the developing nations of Africa and Southeast
Asia. Several species of the genera Lachnosterna, Adoretus,
Stored-Product Feeders
Anomala, Eulepida, Leucopholis, and Schizonycha feed on
peanut roots and pods. Adult beetles, called cockchafers, are Peanuts in storage are attacked by a variety of stored-product
fairly large, 18-20 x 6 mm. They emerge from the soil at dusk pests that can rapidly reduce seed quality. More than 100 spe
during the first few weeks of the rainy season. They often con cies of insects and related arthropods infest stored peanuts.
gregate on trees to mate and feed (Plate 176) before returning Most stored-peanut pests penetrate the pod and feed on the
to the soil to lay their eggs. Eggs are laid singly or in small seed. However, several species have difficulty penetrating un
clusters 5-15 cm below the soil surface. Larvae are C shaped damaged peanut pods, and thus seed damage tends to be more
and white with brown to black head capsules and anal plates severe in damaged or cracked pods. Other pest species easily
(Plate 177). Larvae of some species are up to 50 mm long and bore through the pod to feed on the protein- and oil-rich seed.
20 mm in diameter. Older (third-instar) larvae may feed on the Heavy infestations with stored-product insects may leave dam
taproots, resulting in patches of stunted, wilted, or dead plants. aged seed or seed contaminated with frass, webbing, insects, or
Most injurious species of white grubs on peanut-have one gener insect parts, all of which can make the product unsuitable for
ation per year. human consumption.

Termites Indianmeal Moth

Termites (Plate 178) of many genera, especially Odonto- The Indianmeal moth, Plodia interpunctella (Htibner), is an
termes and Microtermes, are major pests o f peanut in Africa important-pest of-stored peanut worldwide. Moths are readily
and Asia. Termites tend to be a major problem on peanut distinguishable by the unusual color of the forewings; the front
during periods of insufficient rainfall, whereas white grubs are half of the forewing is white to gray while the outer one-half is
more of a problem in those areas where soil moisture is ade reddish brown to purple with a copper luster (Plate 181). The
quate for proper plant growth. Harvester termites feed at the wings are folded close to the body when the moth is resting,
bases of stems and, like beavers, can fell the whole plant. and each is marked with a prominent, reddish brown band. Adult
Other species cover a plant with soil and feed on the leaves, moths have a wing spread of nearly 19 mm and a length of 8-13
but the greatest damage is caused by species that feed on pods mm when the wings are folded. Females lay eggs singly or in
or tunnel into the taproot, main stem, or lateral branches. Ter small groups. Larvae feed on shelled seed or on seed in damaged
mites damage pods in two ways: by externally scarifying the or cracked pods. Larvae form a silken, matted web on the seed;
pod without pod penetration (Plate 179) and by penetrating the and under severe infestation, the entire surface of seed may be
pod and feeding on the seed. Damage to pods is most severe covered with webbing. At maturity, larvae average about 15 mm
late in the growing season when they are left in the soil past in length and are light yellow to creamy white, often with a
optimum maturity or during periods of insufficient rainfall. pinkish hue. Damage is in the form of partially consumed seed,
Damage by termites reduces yield and, equally important, en cast skins, and webbing on the pods and seed.
hances A. flavus invasion and aflatoxin contamination of seed.
Rice Moth
Wireworms The rice moth, Corcyra cephalonica (Stainton), like many
Wireworms, immature stages of click beetles, are increas other stored-product pests, is considered a secondary pest of
ingly important pests of peanut in the southeastern United stored peanut because it is unable to penetrate and damage
States. Several species of the genus Conoderus have been col seed in sound pods. Moths of this species are gray brown to
lected from peanut; C. scissus (Schaffer) and C. amplicollis tawny with a wing span of 14-24 mm and a length of 12-15
(Gyllenhal) are encountered most frequently. Wireworms have mm with the wings folded along the sides of the abdomen
life cycles lasting 1-6 years, depending on the species. They (Plate 182). Veins in the wings are slightly darkened. Eggs are
tend to be more of a problem in moist soils and during years of laid singly, and larvae feed on loose, shelled seed or on seed in
higher than normal rainfall. Adult click beetles emerge from cracked pods (Plate 183). Larvae form silken tubes that are
the soil during spring to early summer and lay eggs in the soil attached to the seed on which they feed. They also spin a
close to a plant host. Wireworm larvae are slender, hard-bodied dense, tough, silken cocoon for pupation. A mature larva is
68
about 15 mm long and white to dirty gray with numerous long Research, New Delhi.
hairs and a dark brown head and pronotum. Bellows, T. S., Jr., Perring, T. M Gill, R. J., and Headrick, D. H.
1994. Description of a species of Bemisia (Homoptera: Aleyro-
Flour Beetles didae). Ann. Entomol. Soc. Am. 87:195-206.
The red flour beetle, Tribolium castaneum (Herbst), and the Brandenburg, R. L and Kennedy, G. G. 1987. Ecological and agri
confused flour beetle, T. confusum Jacquelin du Val, average cultural considerations in the management of twospotted spider
mite (Tetranychus urticae Koch). Agric. Zool. Rev. 2:185-233.
3-4 x 1.5-2.0 mm and are oblong and slightly flattened, red
Brust, G. E., and House, G. J. 1990. Influence of soil texture, soil
dish brown beetles that attack stored peanut worldwide (Plate moisture, organic cover, and weeds on oviposition preference of
184). The two species are very similar in appearance, habits, southern corn rootworm (Coleoptera: Chrysomelidae). Environ.
and life history. An adult may lay up to 450 eggs among peanut Entomol. 19:966-971.
pods and seed. Larvae are yellowish white with a brown head Chamberlin, J. R., Culbreath, A. K., Todd, J. W., and Demski, J. W.
capsule and forked anal plate (Plate 185). Both , adults and 1993. Detection of tomato spotted wilt virus in tobacco thrips
larvae feed on the surface of peanut seed and burrow into the (Thysanoptera: Thripidae) overwintering in harvested peanut
seed. As a result of this feeding, seed become powdery and fields. J. Econ. Entomol. 86:40-45.
dusty and are unfit for human consumption. This damage also Deitz, S. S., Chapin, J. W., and Adler, P. H. 1992. Feeding-site prefer
increases the percentage of split seed when pods are shelled. ence of fall armyworm, corn earworm, and granulate cutworm
(Lepidoptera: Noctuidae) on Florunner peanut. Peanut Sci. 19:63-
Groundnut Bruchid 68,
Demange, J. M. 1975. Les Myriapodes Diplopodes nuisibles a
The groundnut bruchid, Caryedon serratus Oliver, is an im
larachide au Senegal. Oleagineux 30:19-24.
portant pest because it can attack unshelled, undamaged peanut Hutchins, S. H., Higley, L. G., and Pedigo, L. P. 1988. Injury equiva-
pods. It is a major pest of peanut in Asia and Africa. The adult lating as a basis for developing multiple-species economic injury
is 47 x 5 mm, dark gray to brown, and slightly mottled and levels. J. Econ. Entomol. 81:1-8.
has large hind legs. Eggs are laid on the pods, and larvae chew Jones, J. W., Barfield, C. S., Boote, K. J., Smerage, G. H., and
directly through the eggshell and pod to feed on the seed. Thus, Mangold, J. 1982. Photosynthetic recovery of peanuts to defo
damage is not visible externally on the pods without careful liation at various growth stages. Crop Sci. 22:741-746.
observation. Often the first evidence of infestation is a hole cut Lynch, R. E., and Mack, T. P. 1995. Biological and biotechnical
in the pod by a larva before it pupates; the hole allows an adult advances for insect management in peanut. Pages 95-159 in:
to emerge from the pod. Larvae sometimes emerge and pupate Advances in Peanut Science. H. E. Pattee and H. T. Stalker, eds.
outside an infested pod (Plate 186). Infestation may occur American Peanut Research and Education Society, Rocky Mount,
shortly after plants are inverted and while the pods are drying NC.
in the windrow or while the pods are stored in the open during Lynch, R. E., and Simmons, A. M. 1993. Distribution of immatures
and monitoring of adult sweetpotato whitefly, Bemisia tabaci (Gen-
the dry season.
nadius) (Homoptera: Aleyrodidae), in peanut, Arachis hypogaea.
Environ. Entomol. 22:375-380.
Pod-Sucking Bug Mack, T. P., Davis, D. P., and Lynch, R. E. 1993. Development of a
The Wang, Elasmolomus sordidus (Fabricius), which may system to time scouting for the lesser cornstalk borer (Lepidoptera:
attack peanut pods while they are drying in the field or during Pyralidae) attacking peanuts in the southeastern U.S. J. Econ.
storage, is a widespread pest of peanut in India. The adult is a Entomol. 86:164-173.
dark brown, 10- x.2-mm, typical lygaeid-shaped bug with long Pencoe, N. L., and Lynch, R. E. 1982. Distribution of Heliothis zea
legs and antennae (Plate 187). The adult pierces a pod with its eggs and first-instar larvae on peanuts. Environ. Entomol. 11:243-
long, slender mouthparts and feeds on the oil in the enclosed 245.
seed. This injury causes the seed to become wrinkled with dark Wightman, J. A., Dick, K. M., Ranga Rao, G. V., Shanower, T. G.,
spots and increases the probability of rancidity. In the field, the and Gold, C. G. 1990. Pests of groundnut in the semi-arid tropics.
eggs are laid either in the soil or on vines, and in storage they Pages 243-427 in: Insect Pests of Tropical Food Legumes. S. N.
are laid among the pods. First-instar nymphs have bright red Singh, ed. John Wiley & Sons, New York.
Wightman, J. A., and Ranga Rao, G. V. 1993. A groundnut insect
abdomens, while later instars become progressively darker.
identification handbook for India. Int. Crops Res. Inst. Semi-Arid
Trop. Bull. 39.
Selected References

Amin, P. W. 1988. Insect and mite pests and their control. Pages 393- (Prepared by R. E. Lynch, J. A. Wightman,
452 in: Groundnut. P. S. Reddy, ed. Indian Council for Agricultural and G. V. Ranga Rao)

69
 Part IV. Other Organisms
Parasitic Flowering Plants
Alectra vogelii Striga spp.
Alectra vogelii Benth. (Scrophulariaceae) is a root parasite More than 60 species of Striga (Scrophulariaceae) have been
of peanut and several other leguminous crop plants. It has been reported as parasites of several cereal and leguminous crop
reported in various countries in Africa (Angola, Burkina Faso, plants. S. hermontheca Benth. has been reported on peanut in
Malawi, Mozambique, Nigeria, Swaziland, Zambia, and Zim West Africa and S. gesnarioides (Willd.) Vatke (witchweeds)
babwe). A high disease incidence (about 90%) has been re on peanut in Mozambique and on Arachis repens in Nigeria.
ported in Burkina Faso and Malawi. A. picta Hemsl. para S. hermontheca is a cross-pollinated species with wide varia
sitizes peanut in glasshouse experiments. tion in plant type and floral morphology. It is an annual, erect
A mature plant of A. vogelii reaches a height of about 0.5 m herb reaching a height of about 0.5 m (Plate 190). Leaves are
with stems branching out at the base (Plate 188). Flowers are a. green and 20-60 mm long. Flowers are sessile, irregular, and
prominent lemon yellow with horseshoe-shaped stigmata. Roots bright pink. The calyx is distinctly five ribbed, and the corolla
are orange and poorly developed. The connection between the tube, 11-17 mm long, bends characteristically at an angle
parasite and the peanut roots can be seen by carefiilly removing immediately over the tip of the calyx. Bracteoles are 2-3 mm
the soil in the root zone (Plate 189). wide. The fruits (capsules) contain vast numbers of minute
Parasitized peanut plants become stunted, and yields are seed.
reduced. The potential pod yield loss has been estimated at S. gesnarioides is an annual, erect herb reaching a height of
about 40% in Nigeria. about 0.15 m (Plate 191). Leaves are scalelike, rarely exceed

Dodder seed Infected p la n ts in c e n t e r o f i n f e c t i o n

overw inte ri ng re m ain stunted and may die. Do d d e r
c o n t in u e s to s p re a d to a d ja c e n t
in soil

Fig. 77. Life cycle of dodder. (Modified and reprinted, by permission, from G. N. Agrios, 1978, Plant Pathology, 2nd ed., Academic Press,
New York. Prepared by Nancy Browning)

70
ing 5 mm in length. Compact branches arise from ground level. bell-shaped flowers are produced in small clusters. The life
The plant forms a large haustorium (feeding structure) with the cycle of C. campestris is outlined in Figure 77.
host root, unlike S. hermontheca. Flowers are irregular and
vary greatly in size and color but are usually creamy white, Selected References
bluish, or pink.
Ramaiah, K. V., Parker, C., Vasudeva Rao, M. J., and Musselman,
L. J. 1983. Striga identification and control handbook. Int. Crops
Res. Inst. Semi-Arid Trop. Bull. 15.
Cuscuta campestris Riches, C. R., Hamilton, K. A., and Parker, C. 1992. Parasitism of
grain legumes by Alectra species (Scrophulariaceae). Ann. Appl.
Biol. 121:361-370.
Cuscuta campestris Yunck. (Convolvulaceae) (dodder) is a
Subrahmanyam, P., Wongkaew, S., Reddy, D. V. R., Demski, J. W.,
stem parasite that attacks a wide range of flowering plants. It is McDonald, D., Sharma, S. B., and Smith, D. H. 1992. Field diag
a parasite but not an important pest of peanut in the United nosis of groundnut diseases. Int. Crops Res. Inst. Semi-Arid Trop.
States. C. campestris lacks true roots and leaves and produces Bull. 36.
a tangle of wiry branches (Plate 192) that coil around the
branches of host plants and produce haustoria. The branches
are orange to golden yellow and devoid of chlorophyll. Minute, (Prepared by P. Subrahmanyam)

Beneficial Organisms
Most research has focused on the effects of these fungi on
Mycorrhizae growth of inoculated plants in the greenhouse and in sterilized
soils. In general, mycorrhizal fungi have a positive effect on
The peanut root, like roots of most other herbaceous plants, peanut growth. Individual species differ significantly in their
is commonly colonized by vesicular-arbuscular endomycor- effectiveness in promoting growth. Growth response may be
rhizal fungi (Figs. 78 and 79). Species of the genera Glomus, enhanced by inoculation with mixtures of glomalean fiingi
Gigaspora, Scutellospora, Sclerocystis, and Entrophospora and/or Bradyrhizobium. Vegetative growth has been enhanced
have been reported to be naturally associated with peanuts. The by more than 300% in peanuts inoculated with various species.
association is characterized by the formation of arbuscules Some reports indicate increases in seed yield. Other reports
(haustoriumlike structures) in the roots and of chlamydospores indicate no positive response. Experiments have been con
and azygospores (Fig. 80; Plates 193 and 194) in the roots and ducted on the effects of metals, phosphorus, water, pesticides,
soil. Sporocarps may also be formed in the soil. and other soil microorganisms on the activity of mycorrhizal
fungi associated with peanuts.
Progress in research pertaining to endomycorrhizal fungi and
their effects on peanuts (and all other plants) has been ham
pered by the fact that the taxonomy of these glomalean fungi is
little understood. Identification of species is difficult. It in
volves interpretation of spore color, spore size, structure and
chemical reactions of cell wall layers, presence or absence of
sporocarps, and morphological characteristics of the sporo
carps. None of the species can be grown and maintained in
pure culture in the laboratory. Cultures must therefore be
grown in association with living host roots in the greenhouse
and separated from the soil or other growth medium for use as

Fig. 78. Vesicular-arbuscular mycorrhizal fungi in peanut roots. Fig. 79. Hyphae of a mycorrhizal fungus in a peanut root (note
(Courtesy M. Yeh) penetration site). (Courtesy D. M. Porter)

71
inoculum. In the future, it will be necessary to reevaluate the
ecology and importance of individual species on the basis of
Rhizobia
new species concepts.
Bacteria of the genus Rhizobium infect peanut and other
Selected References legume roots, establishing a relationship that is generally bene
ficial to both the bacteria and the plant. The bacteria, which are
Garber, R. 1992. Interactions of Glomus species and Meloidogyne
abundant in soils where peanuts have been previously grown,
arenaria on growth and development of Arachis hypogaea. Ph.D.
diss. Texas A&M University, College Station.
can assimilate or fix atmospheric nitrogen in a symbiotic rela
Hag, L. L., and Taber, R. A. 1985. Characterization of vesicular- tionship with the peanut plant.
arbuscular endomycorrhizal fungi from peanuts in the Philippines. Although both symbiotic and nonsymbiotic bacterial nitro
Page 441 in: Proc. North Am. Conf. Mycorrhizae, 6th. gen fixation (BNF) occur among a diverse array of prokaryotes,
Krishna, K. R., and Bagyaraj, D. J. 1985. Phosphatases in the rhizo- the former is much more important. It has been estimated that
spheres of mycorrhizal and non-mycorrhizal groundnut. J. Soil symbiotic nitrogen fixation can yield 30-300 kg of nitrogen per
Biol. Ecol. 5:81-85. hectare per year, while nonsymbiotic fixation yields only 1-3 kg
Morton, J. B. 1993. Problems and solutions for the integration of of nitrogen per hectare per year. This difference is caused by the
glomalean taxonomy, systematic biology, and the study of endo- high requirements for energy, varying from a minimum of 12
mycorrhizal phenomenon. Mycorrhiza 2:97-109. moles to 29 moles of AIT consumed in reducing 1 mole of N2.
Nopamornbodi, O., Vasuvat, Y., and Taber, R. A. 1985. Character Since the major source of this required energy is photosynthate,
ization of vesicular-arbuscular endomycorrhizal fungi from peanuts the symbiotic systems are much more efficient. It has been
in Thailand. Page 442 in: Proc. North Am. Conf. Mycorrhizae, 6th.
estimated that about 1-2 metric tons of plant carbohydrate (from
Parvathi, K., Venkaqteswarlu, K., and Rao, A. S. 1985. Influence of
photosynthesis) may be consumed annually in BNF.
root-infecting fungi on development of Glomus mosseae in ground
nut. Curr. Sci. 54:1006-1007. It is estimated that 60 million metric tons per hectare of
Taber, R. A., Smith, O. D., Smith, D. H., Segner, S. L., Taber, W. R., nitrogenous fertilizer are used globally, while annual BNF is
Pettit, R. E., Neck, J. S., Rajapakse, S., and Harman, W. F. 1994. estimated to be about 175 metric tons per year. Symbiotic
Growth response of peanut to field inoculation with vesicular- nitrogen fixation by agricultural legume crops is about 50
arbuscular endomycorrhizal fungi and Bradyrhizobium. Peanut Sci. metric tons per year. Peanuts possess a comparatively high
21:104-112. symbiotic nitrogen-fixing capacity. Field studies with Ni5
Vazquez, L., Taber, R. A., and Elkan, G. H. 1986. A comparison of isotope methodology showed 68-152 kg of nitrogen fixed per
the indigenous population of vesicular-arbuscular mycorrhizal hectare per season. Of the total plant nitrogen, 54-90% was
fungi at two locations in North Carolina. (Abstr.) Page 245 in: derived from BNF. The totals varied depending upon the
Annu. Meet. Am. Soc. Microbiol., 86th. Bradyrhizobium, strain used, the peanut cultivar, and cultivar-
(Prepared by R. A. Taber) strain interaction. The bacterial strain used, however, accounts
for the larger part of the variability observed for nodulation ancL
nitrogen fixation.
Early researchers considered all rhizobia to be a single spe
cies capable of nodulating all legumes. Extensive cross-testing
on various legume hosts led to taxonomic characterization of
rhizobia based on bacteria-plant cross-inoculation groups,
which were defined as groups of plants within which the root
nodule organisms are mutually interchangeable. The concept
of cross-inoculation groupings as taxonomic designators has
gradually fallen into disrepute, although some of this philoso
phy is retained in the current taxonomic scheme.
Bacteria of the family Rhizobiaceae lack endospores and are
normally rod shaped, aerobic, and gram negative. They are
motile and have one polar or subpolar flagellum or two to six
peritrichous flagella. The bacteria utilize many carbohydrates,
and considerable extracellular slime may be produced during
growth on carbohydrate-containing media. Best growth is usu
ally achieved at 25-30C on relatively simple heterotrophic
media. A number of monosaccharides serve as suitable energy
sources, and several organic or inorganic nitrogen sources can
be used. Dinitrogen is the primary nitrogen source in symbiosis
with a leguminous host. Some strains of rhizobia show a close
relationship in DNA base composition with bacteria of the
genus Agrobacterium.
Traditionally, rhizobia have been divided into two groups
according to growth rate: fast growers and slow growers.
Fast growers are the rhizobia commonly associated with al
falfa, clover, bean, and pea, which in culture grow much faster
(less than one-half the doubling time of slow growers or less
than 6 hr); slow growers are exemplified by soybean and cow
pea rhizobia (generation time greater than 6 hr). Most bacteria
that infect peanut roots are slow growers, often with a mean
generation time exceeding 12 hr. Although there is phenotypic
and genotypic diversity within these major groupings and some
overlap, numerous studies have demonstrated the validity of
this classification.
Fig. 80. Azygospore of Gigaspora sp. (top) and chlamydospore of The relative fastidiousness of the slow growers has been
Glomus sp. (bottom). substantiated by recent studies. While the major biochemical

72
pathways seem to be similar, evidence suggests that the pre cient in Rhizobium strains. When few bacteria are present,
ferred nitrogen-fixation pathway may be different. Analyses plants show typical nitrogen-deficiency symptomsyellowing
(16S RNA) o f the fast- and slow-growing rhizobia confirm that and low protein content of foliage (Plate 196) and low yields of
these groupings indeed represent different genetic phyla. Re pods and seed. When effective nodules are formed on young
cent studies in which numerical taxonomy, carbohydrate seedling roots, the plants grow rapidly and have adequate
metabolism, antibiotic susceptibilities, serology, DNA hybrid nitrogen to maintain green leaves. More than 200 kg of nitro
ization, RNA analysis, and DNA base ratio were used all gen per hectare can be fixed by well-nodulated peanut roots.
demonstrated the validity of the fast- and slow-growing group Environmental conditions that favor peanut plant growth
ings. also favor nodule development and nitrogen fixation. Nitrogen
The taxonomy of the rhizobia is in a state of transition. As fixation is decreased by drought, low temperatures, and low
more molecular information accumulates, such genetic data light intensities.
will, no doubt, further displace cross-inoculation approaches to When peanut is planted in fields that lack effective Rhizo
classification. On the basis of the difference between the fast- bium strains, a significant yield increase usually results from
and slow-growing rhizobia, the traditional rhizobia have been inoculation with an effective strain (Plate 196). Commercial
divided into two genera. The slow-growing strains were placed Rhizobium inoculants are available and are best applied in the
in the genus Bradyrhizobium, containing two species, B. furrow at planting time. Once desirable strains are established
japonicum and B. elkanii, which nodulate soybeans. Other in a field, it is not necessary to add new inoculum each year,
bradyrhizobia occur (e.g., the peanut bradyrhizobia) but have since the rhizobia can survive on organic matter for several
not been classified to species or biovar levels. Until further years.
taxa within the genus are proposed, these should be described When desirable strains of Rhizobium provide the peanut
with the appropriate host plant given in parentheses, e.g., the plant with adequate nitrogen, inorganic nitrogen fertilizer is of
peanut rhizobiaBradyrhizobium sp. (Arachis). little use. Added nitrogen actually inhibits nodulation and
The fast-growing rhizobia have been placed in the genus reduces nitrogen fixation.
Rhizobium, containing six species, R. leguminosarum, R. meli- The infected tissue of the nodule ordinarily shows no change
loti, R. loti, R. galeage, R. fredii, and R. tropici. Three former for some weeks or months and then eventually breaks down
species, R. phaseoli, R. trifolii, and R. leguminosarum, have and disappears. Degeneration begins with tissue breakdown at
been combined into the species R. leguminosarum. R. fredii is the base of the nodule and progresses toward the apex until all
a new species consisting of fast-growing rhizobia that effec of the nodule is destroyed. The nodule may enter the degenera
tively nodulate Chinese soybean cultivars ordinarily nodulated tive phase at an early stage if growth conditions are unsuitable
by B. japonicum. for the host or if the bacteria and the host are inherently incom
Peanuts are able to form effective symbioses with a number patible.
of genetically diverse, slow-growing bradyrhizobia. Since
many of the tropical and semitropical legumes are nodulated Selected References
by bradyrhizobia, there exists a large diversity of potential
symbionts, which probably accounts for the large strain varia Elkan, G. H. 1992. Biological nitrogen fixation. Pages 285-295 in:
tion in BNF. Encyclopedia of Microbiology, vol. 1. J. Lederberg, ed. Academic
Bacterial nodules arise in the junctions of lateral roots along Press, New York.
both primary and secondary roots of the peanut. Possibly such Giller, K. E., and Wilson, K. J. 1991. Nitrogen Fixation in Tropical
Cropping Systems. C.A.B. International, Wallingford, England.
areas provide favorable intercellular sites for rhizobial multi
Ratner, E. I., Lobel, R., Feldhay, H., and Hartzook, A. 1979. Some
plication and penetration in the cortex, since no infected root characteristics of symbiotic nitrogen fixation, yield, protein and
hairs have been observed in peanut roots. Small indentations of soil accumulation in irrigated peanuts (Arachis hypogaea L.). Plant
the host cell wall, which may be the initial entry sites, occa Soil 51:373-386.
sionally are found. The nodule is recognizable before intracel van Rossum, D. 1994. The Groundnut-Bradyrkizobium Symbiosis.
lular rhizobia can be found. Rhizobia are distributed in the Vrije Universiteit, Enschede, Netherlands.
nodules by cell division, and only invaded cells in the bacterial Wynne, J. C., Bliss, F. A., and Rosas, J. C. 1987. Principles and prac
zone seem to divide. One possible consequence of such a mode tice of field designs to evaluate symbiotic nitrogen fixation. Pages
of infection is that the plant has the ability to form nodules 371-390 in: Symbiotic Nitrogen Fixation Technology. G. H. Elkan,
with a wide range of Rhizobium strains. Roots of most peanut ed. Marcel Dekker, New York.
genotypes nodulate readily with cowpea rhizobia (Plate 195).
Symbiotic nitrogen fixation is a more specific property, how (Prepared by G. H. Elkan)
ever; and often the nodules are ineffective or inefficient.
Nodules on peanut roots are round or oval. The nodules may
have a broad attachment to the root, with bacteroid tissue
embedded in the root cortex so that the nodules appear hemi
Bacillus subtilis
spherical; the husk tissue may even grow around the subtending
lateral root. Nodule number and development are determined Bacillus subtilis is well known for its ability to produce anti
by the interaction of the host and bacteria and are, furthermore, biotics. Since the 1950s, researchers have evaluated this bac
affected by competition for photosynthate among nodules on a terium for its potential as a biological control agent. During the
plant, the distribution of plant hormones, and environmental early 1980s, researchers began to study P. Broadbents A-1'3
factors such as moisture and temperature. isolate of B. subtilis as a possible biological seed treatment for
Rhizobia vary in their ability to fix nitrogen in peanut. The peanuts. This isolate was compatible with most common seed-
same strain can form effective nodules on one host plant and treatment fungicides, and when it was mixed with fungicides
ineffective nodules on another of a different genotype. Rhizobium as a preplant seed treatment, improved vigor was demonstrated
strains that lack the ability to form functional nodules can have through earlier emergence and larger, more robust plants.
an adverse effect on plant growth and may inhibit other strains Germination studies revealed that seed treated with B. sub
with good nodulating ability. The interior of a fresh, effective tilis germinated earlier and produced longer taproots with more
nodule is dark red from the leghemoglobin that it contains, while lateral roots than untreated seed. This response was more
ineffective nodules are pink, light green, or colorless. apparent at 20C than at 27C and was also more apparent on
Where legumes have never been grown or where several seed produced by environmentally stressed plants than on seed
years have elapsed since they were grown, soils may be defi from unstressed plants. Since this response occurred in the
73
 absence of seedbome pathogens (on seed treated with a fungi
cide) and in the absence of soil, the initial interpretation was
Leaf-Surface Epiphytes
that the bacterium must be stimulating plant growth through
hormone production. Although peanut foliage is host to numerous microorgan
Field studies demonstrated that hormonal stimulation was isms, only a small fraction negatively interact with the peanut
one mechanism of growth enhancement of B. subtilis-treated plant to the extent that we consider them to be pathogens. The
plants. Yields were improved by 17% when B. subtilis treat other microbes on the leaf surface are poorly understood but do
ments were combined with fungicides compared with fungi not appear to interact with the plant in a negative way. Plant
cide alone. These data indicate that control of root-infecting pathologists have long recognized the existence of epiphytic
fungi, such as Rhizoctonia solani AG-4, is a second possible microflora, but only recently has research been initiated to
mechanism for improved peanut growth. A third possible better describe and quantify this population. Interest in foliar
mechanism is improved nutritional status of plants resulting microflora comes with a recognition of its potential application
from enhanced nodulation by Bradyrhizobium. Significant in for foliar disease control. Although the influence of these epi
creases in leaf and stem nitrogen and in boron and potassium phytes on the epidemiology of peanut diseases is largely unex
were noted after treatment with B. subtilis. Vesicular mycor plored, available evidence indicates a strong potential for using
rhizae were unaffected. the epiphytic population for reducing disease. According to
A regional test conducted in 24 field locations in the south classic theory, biological control can be achieved through
eastern United States with commercial seed-treatment applica several mechanisms of antagonism, including competition, anti
tion and planting procedures assessed yield improvements, the biosis, and parasitism or predation. Available evidence indi
relationship of disease severity to yield, and the efficiency of cates that epiphytic populations can exhibit some of these
root bacterization. All locations were effectively inoculated mechanisms of biological control.
with B. subtilis at harvest, and yield improvements were re First, epiphytic microbes may reduce disease through com
lated to rotational history and time of planting. The average petition by consuming nutrients or occupying infection sites.
yield increase was 7.6%. Locations that were planted to The degree of competition pathogens experience is unknown,
legumes in either of the previous 2 years averaged a 12% yield but research is underway to characterize the microbial popula
increase. Locations at which seed were planted early in cool tions of peanut foliage. Microbial populations can reach one
soils averaged an 11.4% increase, while seed planted late in million or more per square centimeter (Plate 197). The epi
warm soils averaged a 6.8% yield increase when inoculated phytic microflora of peanut leaves is quite complex and in
with B. subtilis. Areas with conditions that supported patho cludes bacteria, yeasts, and filamentous fungi. For example, a
gens such as Rhizoctonia (poor rotations and cool, early- large survey of epiphytic bacteria showed that Methylobac-
planted soils) showed the greatest yield improvements when B. terium, Curtobacterium, Rathayibacter, Bacillus, Clavibacter,
subtilis-treated seed were planted. and Aureobacterium are the predominant bacterial genera on
Evaluation of mature plants grown from seed treated with B. peanut foliage in North Carolina. The degree to which compe
subtilis strain A -13 revealed that only the upper 10 cm of the tition might reduce disease depends on the biology of the patho
taproot was effectively colonized. Furthermore, branch roots gen. For example, pathogens that use exogenous nutrients
more than 2 cm from the taproot were typically not effectively might be more inhibited by competition from epiphytic flora.
colonized. These data indicate that the yield benefits come More research is needed to fully understand the impact of
about after colonization of only a small percentage of the total microbial competition on foliar diseases.
root mass. Second, antibiosis by beneficial microorganisms may have a
B. subtilis forms highly stable spores, making it extremely role in reducing disease. Field tests have been conducted with
resistant to environmental stress. Commercial preparations antagonistic bacteria for controlling Cercospora arachidicola
maintain their ability to inoculate for years. The A -13 strain of on peanut. Foliar applications of Bacillus thuringiensis or
B. subtilis was adapted to cotton by multiple host passages and Pseudomonas cepacia were applied at 14-day intervals during
then renamed GB03. This strain is marketed under the trade the season. Both organisms are strongly antagonistic to C.
name Kodiak for use on seven crops, including peanut and arachidicola in vitro. P. cepacia strains produce several anti
cotton. During 1994, less than 5% of the peanut crop was biotics including pyrrolnitrin. The antagonistic mechanism of
treated with this biological fungicide (and plant growth pro B. thuringiensis strain HD-1 is unknown, but B. thuringiensis
moter), but more than 4 million acres of cotton were treated. is closely related to B. cereus, which does produce antifungal
For the 1995 season, it was projected that almost 90% of all antibiotics. Disease control, although statistically better than
cotton grown in the United States would be treated with this that in unsprayed controls, was generally poor and was con
biological control agent. sidered unacceptable compared with standard fungicide treat
ment. The poor survival of the biological control agents on
Selected References foliage probably afforded little opportunity for antibiotic pro
duction on the leaf surface. Enzymatic mechanisms of anti
Backman, P. A., Brannen, P. M., and Mahaffee, W. F. 1994. Plant biosis may hold more promise. When chitin amendments were
response and disease control following seed inoculation with applied to peanut foliage, chitinolytic bacteria increased from
Bacillus subtilis. Pages 3-8 in: Improving Plant Productivity with 1% of the total population to 40%. When a chitinolytic strain
Rhizosphere Bacteria. M. H. Ryder, P. M. Stevens, and G. D. of B. cereus was applied to peanut foliage along with chitin, a
Bowen, eds. CSIRO, Glen Osmond, Australia. 60% reduction in infection by C. arachidicola was observed.
Broadbent, P., Baker, K. F., and Waterworth, Y. 1971. Bacteria and
While it is clear that epiphytic microorganisms can reduce
actinomycetes antagonistic to root pathogens in Australian soils.
Aust. J. Biol. Sci. 24:925-944. disease through antibiosis, more work is needed to develop the
Kenny, D. S., Howell, C. R., and Minton, E. B. 1992. Studies on the full potential of this type of control.
mode of action of Bacillus subtilis as a biocontrol agent in cotton. Third, mycoparasitism by foliar epiphytes may also play a
Page 198 in: Proc. Beltwide Cotton Prod. Res. Conf. National role in reducing disease. In laboratory tests, Verticillium lecanii
Cotton Council, Memphis, TN. reduced infection of detached peanut leaves by Cercospor
Turner, J. T., and Backman, P. A. 1991. Factors relating to peanut idium personatum and Puccinia arachidis, particularly when
yield increases after seed treatment with Bacillus subtilis. Plant leaves were preinoculated with V. lecanii. In another study, V.
Dis. 75:347-353. lecanii and Penicillium islandicum were the most effective of
several mycoparasites evaluated in the laboratory and field for
(Prepared by P. A. Backman) biological control of P. arachidis. Direct parasitism of C. per-
74
sonatum by mycoparasites has been evaluated under field con cosporidium personatum. It has not been reported on early leaf
ditions. spot. It has been found in several countries, including the
In summary, while the epiphytic population has a clear po United States, where it was first found in Texas and later in
tential for reducing disease, more research and development Virginia and Florida. The fungus may almost completely cover
are needed before these epiphytes can be used as biological the abaxial sporulating surface of C. personatum, where it
controls. For the present, these epiphytic organisms are per penetrates and destroys the conidiophores, conidia, and sub
haps best viewed as a factor that reduces the severity of foliar tending cells. The entire leaf spot appears gray on the abaxial
disease and allows greater flexibility in the use of other control surface (Plate 198). D. pulvinata was capable of colonizing up
measures. to 87% of the lesions under field conditions. Although not
effective in preventing infection, D. pulvinata might have a
Selected References role in reducing sporulation. Colonies on potato-dextrose agar
are gray to olivaceous gray. Conidia are spherical to sub-
Ghewande, M. P. 1990. Biological control of groundnut (Arachis spherical, hyaline to light colored, and 4-7 jim in diameter and
hypogaea L.) rust (Puccinia arachidis Speg.) in India. Trop. Pest may be minutely echinulate. Considerable experimental work,
Manage. 36:17-20. both in the laboratory and in the field, has indicated potential
Knudsen, G. R., and Spurr, H. W., Jr. 1987. Field persistence and for biological control of late leaf spot.
efficacy of five bacterial preparations for control of peanut leaf
spot. Plant Dis. 71:442-445.
Kokalis-Burelle, N., Backman, P. A., Rodrfguez-Kabana, R., and Selected References
Ploper, L. D. 1992. Potential for biological control of early leafspot
of peanut using Bacillus cereus and chitin as foliar amendments. Mitchell, J. K., Jeger, M. J., and Taber, R. A. 1987. The effect of
Biol. Control 2:321-328. temperature on colonization of Cercosporidium personatum leaf
Subrahmanyam, P., Reddy, P. M., and McDonald, D. 1990. Parasitism spot of peanuts by the hyperparasite Dicyma pulvinata. Agric.
of rust, early and late leafspot pathogens of peanut by Verticillium Ecosyst. Environ. 18:325-331.
lecanii. Peanut Sci. 17:1. Mitchell, J. K., Smith, D. H., and Taber, R. A. 1987. Potential for
biological control of Cercosporidium personatum leafspot of pea
(Prepared by V. J. Elliott and H. W. Spurr, Jr.) nuts by Dicyma pulvinata. Can. J. Bot. 65:2263-2269.
Porter, D. M., and Taber, R. A. 1992. First report in Virginia of
Dicyma pulvinata colonizing Cercosporidium personatum, the
causal agent of late leaf spot of peanut. Plant Dis. 76:1185.
Dicyma pulvinata Shokes, F. M., and Taber R. A. 1983. Occurrence of a hyperparasite
of Cercosporidium personatum on peanut in Florida. (Abstr.) Phy
topathology 73:505-506.
The fungus Dicyma pulvinata (Berk. & M. A. Curtis) Arx
(syn. Hansfordia pulvinata (Berk. & M. A. Curtis) S. J.
Hughes) is a mycoparasite on the late leaf spot fungus, Cer- (Prepared by R. A. Taber)

75
 Part V. Management of Peanut Diseases
Pathogenic biota, mycotoxins, insects, mites, and rodents Exclusion on a small scale may involve site selection within
threaten the peanut crop in the field and during storage and a farm to avoid problem fields or sanitation of equipment and
processing. To realize maximum profit, growers must manage vehicles after activity in infested fields. Site selection can also
peanut diseases so that losses are minimized and inputs are as be used to minimize exposure to endemic pathogens or insect
low as possible. vectors.
Temperature, precipitation, soil type, elevation, endemic Contacts between a pathogen and peanut plants may be re
pathogens, and cropping systems influence the disease com duced by using cultural practices that physically remove inocu-
bination in a growing area. Thresholds for unacceptable levels la from positions of greatest damage potential and that reduce
of peanut disease also vary. For example, yield loss caused by the duration of environmental conditions favoring fungal growth
late leaf spot may not occur if the level of Cercosporidium per and pathogenesis. These include burial of host crop debris with
sonatum infection is low. However, stem rot caused by Sclero a moldboard plow, cultivation that does not throw soil onto the
tium rolfsii reduces yield even at low levels of infection. plants (nondirting), crop rotation, weed control, optimal seed
Management of a particular disease may integrate regulatory ing rate and date, and foliar disease management.
measures, cultural practices, cultivar resistance, and pesticide Ideal plant populations are important for management of
usage. Growers need to know the effectiveness of management stem rot, Sclerotinia blight, and the tomato spotted wilt virus.
practices, how and when to use them, and the expected results. Dense plant populations may increase the first two, and sparse
Safety of producers and consumers and the long-term program populations may increase the third.
sustainability should also be considered. Production practices For pathogens that develop either early Or late in the grow
vary from labor intensive in some developing countries to ing season, disease severity canbeminimized by planting early
nearly completely mechanized in the United States. Similarly, or late, thus allowing plants to mature before environmental
disease management ranges from minimal to intensive and conditions conducive to disease prevail. Examples of diseases
may include practices that minimize host-pathogen contact and for which this strategy is effective are rust and Sclerotinia
pathogen populations and reduce pathogen increase. blight. An early planting date could be a part of peanut rust
disease management in southern Texas, since early planting and
early maturity allow for crop development before the arrival of
Strategies infective rust spores on wind currents from the south. Late-
planted fields infested with Sclerotinia minor are under in
Minimizing Host-Pathogen Contacts creased risk of Sclerotinia blight during cool, wet, fall weather
and Pathogen Populations in some areas. Planting very early or very late in some areas
Exotic pathogens should be prevented from entering a pro may increase the incidence of the tomato spotted wilt virus.
duction area. Movement of pathogens among countries or Crop rotation with species in the grass (Poaceae) family are
regions via seed, other plant material (living or dead), soil, or particularly useful in managing several endemic peanut path
other means can have serious repercussions. Once introduced, ogens (Fig. 81). High peanut yields are often obtained after
pathogens may be very difficult or impossible to eradicate.
Extensive knowledge of a pathogen and the risk it poses for
production is necessary for exclusion to be effective. Exclusion
is especially critical if an exotic pathogen has a wide host
range or survives for long periods in the absence of peanut, if
the disease caused is difficult to manage, and if resistant culti
vars are not available. For example, Cylindrocladium para
siticum was probably introduced into the United States from
Asia on a host plant other than peanut. The fungus later be
came established in peanut fields, and Cylindrocladium black
rot now causes major losses in the United States.
Exclusion on a large scale can be accomplished by regulatory
legislation. Regulations may include embargo, quarantine, and
inspection. Laboratory testing of seed and imports and inspection
of seed-production fields in some countries or growing areas may
be necessary to prevent the introduction of exotic pathogens.
The basis of seedling disease management is high-quality,
pathogen-free seed planted under conditions that favor rapid
germination and emergence. These conditions include optimal
timing for proper soil moisture and temperature. Most seed
bome peanut pathogens can infect a wide range of plants. Seed Fig. 81. Leaf spot ratings (Florida 1 -1 0 scale) for continuous
treatments prevent long-distance spread of certain seedbome growth of peanut (P) and peanut grown after 3 years of Bahia
pathogenic fungi. grass (B). (Courtesy T. B. Brennemann)

76
rotation with Bahia grass (Paspalum notatum). Such increases Peanut disease predictive systems help producers make fun-
are attributed to inoculum reduction, disease suppression, weed gicide-application decisions for leaf spot management. Weath
control, improved soil tilth, or other factors. Rotation with non er information such as leaf wetness, relative humidity, and
grass crops, certain nonlegumes, and even resistant peanut cul temperature can be used by growers or computer models that
tivars can also be effective in reducing inoculum levels and schedule fungicide treatments. A predictive system may call
increasing peanut yields, even where diseases do not appear to for fewer, the same, or even a greater number of fungicide
be limiting. applications than a calendar-based schedule.
Tillage and other practices that destroy crop residue can re Disease control strategies should consider fungicide effects
duce overwintering inoculum of most peanut foliage- and stem- on nontarget organisms. For example, use of chlorothalonil for
infecting fungi. Destruction of peanut crop residue is most leaf spot control increases incidence of Sclerotinia blight, so
effective as a disease-control technique during rotations with alternative leaf spot fungicides should be considered. Some
nonhosts. The majority of these pathogens survive between fungicides may increase spider mite populations.
peanut crops on or in infested residue. Enhanced residue decay Risk of pathogen insensitivity to fungicides increases with
after tillage favors nonpathogenic soil microorganisms over prolonged, exclusive use of single-mode-of-action products.
pathogens, and pathogen survival decreases. Risk-management strategies may involve tank mixes, pre
packaged mixtures, or alternating two or more effective prod
Reducing Pathogen Increase ucts with different modes of action. Partner fungicides may be
Peanut producers often have options during a growing sea systemic or protectant. The risk of developing insensitivity is
son for reducing the rate of disease increase. Rate-limiting further reduced by using all other available disease control
practices include the use of protective and curative (systemic) strategies, including resistant cultivars, crop rotation, and cul
agrochemicals, cultural practices, biological control practices, tural practices.
and resistant cultivars. Use of disease-resistant cultivars that sustain competitive
Fungicide seed-treatment combinations generally increase yield and quality is the most economical and efficient disease
germination and emergence and reduce losses from damping- control method. Even with yields lower than those of suscep
off induced by soilbome and seedbome pathogens. Seed treat tible cultivars, resistant cultivars may be useful in rotations on
ments applied immediately after shelling reduce further colo a prescriptive basis. Genetic resistance has been identified for
nization by seed fungi and pathogen spread during storage. most major peanut diseases, but acceptable cultivars with these
Mechanical damage to seed, which can be particularly severe desirable traits are in many cases not available (Table 10).
when seed have a moisture content of less than 7%, should be There are many breeding efforts underway around the world
minimized during handling and planting. A partial list of some with goals of developing cultivars with resistance to one or
seed-treatment fungicides is given in Table 8. more peanut diseases.
Fungicides and nematicides applied to peanut plants and soil Biological control agents may be applied to either the seed,
by ground equipment, airplane, and chemigation may increase plant, or soil or stimulated by cultural practices or the addition
yields through the control of pathogens o f foliage and below- of amendments. The rationale is to favor the crop, disfavor
ground plant parts. Without good foliar disease management, pathogens, or stimulate plant resistance mechanisms. The bac
pod detachment before and during harvest may be severe. Mini terium Bacillus subtilis (Ehrenberg) Cohn is an example of an
mal fungicide drift and thorough canopy penetration are critical effective biological seed treatment.
to the success of /oliar fungicide programs. Vehicle damage Cultural practices that maximize plant health include main
from ground spray equipment can increase the incidence of taining soil pH and optimal availability of plant nutrients and
several diseases. A partial list of fungicides labeled for foliar water. Crop residues should be shredded in the fall and deep
application is given in Table 9. turned with a moldboard plow equipped with litter-covering
devices near the time of planting. Tillage is a cultural prac
tice that integrates disease control, residue and water man
TABLE 8. Some Fungicides Used Alone or in Combination agement, physical weed control, soil compaction and salinity
as Seed Protectants on Peanut alleviation, and herbicide and fertilizer incorporation. Exces
Common Name Chemical Name sive herbicide or improper placement may cause root damage
and predispose seedlings and plants to infection by soilbome
Captan d is-Af-((Trichloromethyl)thio)-4-cyclohexene- pathogens.
1,2-dicarboximide
5,6-Dihydro-2-methyl-Af-phenyl-1,4-oxythiin-
Soil calcium and salinity management are necessary to
Carboxin
3-carboxamide reduce the pod rot complex in some growing areas. Whether
PCNB Pentachloronitrobenzene the source is calcium sulfate (gypsum or landplaster) or cal
Thiram Tetramethylthiuram disulfide cium carbonate (lime or ground limestone), adequate calcium
in the pegging zone during pod fill minimizes nutrition-related
This table should not be construed as a list of recommended fungicides.
Disease-management recommendations are published annually by the pod rots and is one aspect of producing high-quality seed. Cal
extension service of each peanut-producing state. cium sulfate supplements in conjunction with deep tillage to

TABLE 9. Some Fungicides Labeled for Control of Foliar Diseases of Peanuta

Common Name Chemical Name Foliar Diseases
Basic copper sulfate Cupric sulfate Leaf spot
Benomyl Methyl l-(butylcarbamoyl)-2-benzimidazolecarbamate Leaf spot, web blotch
Chlorothalonil Tetrachloroisophthalonitrile Leaf spot, rust, web blotch
Copper hydroxide Cupric hydroxide Leaf spot
Mancozeb Zinc ion and manganese ethylene bisdithiocarbamate b Leaf spot, web blotch
Propiconazole 1- [2-(2,4-dichlorophenyl)-4-propyl-l ,3-dioxolan-2-ylmethyl] -1H-1,2,4-triazole Leaf spot
Tebuconazole oc-[2-(4-chlorophenyl)-ethyl]-a-(l,l-dimethylethyl)-lff-l,2,4-triazole-l-ethanol Leaf spot, rust
aThis table is not to be construed as a list of recommended fungicides. Disease-management recommendations are published annually by the extension
service in each of the peanut-producing states.
bCoordination product of manganese, 16%; zinc, 2%; and ethylene bisdithiocarbamate, 62%.

77
break up a plow layer help to displace sodium (Na) from soil Selected References
particles and facilitate its leaching out of the pod and root
zone. Application of high levels of calcium sulfate suppresses Henning, R. J., Allison, A. H., and Tripp, L. D. 1982. Cultural prac
Pythium pod rot in some soils. tices. Pages 123-138 in: Peanut Science and Technology. H. E.
Harvesting at optimal maturity can decrease pod rot losses. Pattee and C. T. Young, eds. American Peanut Research and Edu
cation Society, Yoakum, TX.
Maintaining proper storage temperature and relative humidity
Lucas, G. B., Campbell, C. L., and Lucas, L. T. 1985. Introduction to
equilibrium will slow or preclude the growth of storage fungi,
Plant Diseases: Identification and Management. AVI, Westport, CT.
including those that produce mycotoxins. Melouk, H. A., and Shokes, E M., eds. 1995. Peanut Health Manage
Good disease management will pay dividends in high yields ment. American Phytopathological Society, St. Paul, MN.
of good-quality peanuts. Disease management practices vary Porter, D. M., Smith, D. H., and Rodrfguez-Kabana, R. 1982. Peanut
among growing areas, cultivars used, and the disease complex plant diseases. Pages 326-410 in: Peanut Science and Technology.
unique to each growing area. Good management is seldom H. E. Pattee and C. T. Young, eds. American Peanut Research and
simple and requires a plan that integrates wise cultivar and site Education Society, Yoakum, TX. .
selections, proper use of cultural practices, judicious chemical Shokes, F. M., and Smith, D. H. 1990. Integrated systems for manage
applications, and biological controls into a practical program ment of peanut diseases. Pages 229-238 in: Pest Management in
(Table 10). It also involves timely planting, harvesting, and Agriculture, vol. 3. 2nd ed. D. Pimentel, ed. CRC Press, Boca
storage of the peanut crop. Disease control requires a plan Raton, FL.
based on research knowledge and extension of that knowledge
to the producer. (Prepared by F. M. Shokes and M. C. Black)

TABLE 10. Principles of Peanut Disease Control and Relative Effectiveness of Management Practices
Harvest,
Control Cultural Crop Resistant Pathogen- Handling,
Disease Principle8 Practices'1 Rotation0 Cultivarcli Free Seed0 Pesticides ce and Storage0
Fungal diseases of foliage
and upper stems
Early and late leaf spots I, R P, W, WC 2 2 F-l
Rust R D ,P,W 2 F-l
Web blotch R W 3 2 F-l
Pepper spot and leaf scorch R 3 F-2
Scab E, R 2 2 1 F-2
Fungal diseases of lower stems,
pegs, pods, roots, and seeds
Stem rot (southern blight, white mold) I, R D, P, S, T, W, WC 2 2 F-2
Sclerotinia blight E, I, R D, P, S,W 3 3 1 F-3, ST-2, N-3
Cylindrocladium black rot E.I.R . D, S, SF 2 2 1 N-2, ST-1
Pythium diseases R S, SF, W 3 3 F-3, ST-3
Rhizoctonia diseases I,R D. T, W 2 3 ST-3, F-I
Charcoal rot R D,W ST-3 ...
Diplodia collar rot I, R W 3 RI F-3
Black hull I, R T 3 3 F-3
Verticillium wilt E, I, R W, WC 2 RI N-2
Botrytis blight R D ,P,W 3 F-2
Aspergillus crown rot RT V7T7W RI 3 ST-3 3
Phymatotrichum root rot I, R pH, S, SF, T 3
Aflatoxin I, R D, W 3 RI SI-3 1
Pod rot complex I, R SF, T, W 3 3 F-2
Penicillium and Rhizopus seed rots I, R ST-1 1
Viral diseases
Peanut mottle E, I S RI 1
Peanut stunt E, I S, WC RI 1
Peanut stripe E RI 1
Peanut clump/Indian peanut clump E D, S 3 1 N-3
Groundnut rosette I, R P,WC 1 SI-1
Spotted wilt R D, P, S, WC 2
Bud necrosis R D, P, WC 2
Yellow spot R
Nematode-induced diseases
Peanut root knot E; I, R S 2 RI N-2
Northern root knot E, I, R S 2 RI N-2
Javanese root knot E, I, R S 2 RI N-2
Root-lesion nematodes I S 3 RI N-2
Sting nematodes I s 3 N-l
Ring nematodes I s 3 N-2
Potato nematodes E, I s 1 1
Bacterial wilt E, I, R 2 1 3
aE = exclude or avoid introduction of initial pathogen inoculum; I = reduce inoculum of an endemic pathogen; and R = reduce the rate of pathogen
increase and spread.
bT = tillage, including crop residue management; SF = optimal soil fertility; P = plant population or density; D = seeding date; W = water management;
WC = weed control; pH = adjustment of soil pH; and S = site selection.
0Relative effectiveness of practices: 1 = highly effective; 2 = moderately effective; and 3 = slightly effective.
dRI = resistance identified in plant introductions or breeding lines but not available in commercially acceptable cultivars.
eF = fungicide; SI = soil-applied insecticide; N = nematicide or soil sterilant; and ST = seed treatment, either fungicide or biological control bacterium.

78
 been made to achieve resistance against the two leaf spots and
Genetic Modification rust. Particularly successful have been the efforts of the re
searchers at the International Crops Research Institute for the
Peanut is an important grain legume in both the semiarid Semi-Arid Tropics (ICRISAT), who have screened the entire A.
tropics and warm temperate regions of the world. The species hypogaea germ plasm collection and conducted extensive
originated in the region of southern Bolivia and northern crossing programs. Other individuals, especially in China, have
Argentina, and at least seven centers of diversity are present in attempted to create variation within the cultivated species
South America and Africa. Several large germ plasm collec through induced mutations. These studies have led to the re
tions exist in North America, South America, Asia, and Africa, lease of 33 cultivars.
which together have more than 12,000 entries. Within the cul Unlike the cultivated species, a large amount of morpho
tivated species are two morphologically distinct subspecies logical and genetic variation at the molecular level has been
(hypogaea and fastigiata), containing two and four botanical documented among the wild species of Arachis. An RFLP
varieties, respectively. Additionally, both genetic and cyto linkage map was recently constructed from an A. stenosperma
plasmic differences have been observed among intersubspe- x A. cardenasii diploid hybrid, and if the wild species and
cific hybrids. Although the germ plasm collection is large, cultivated genomes are homosequential, then these studies
genetic characterization of Arachis hypogaea is limited com should have applications for analyzing A. hypogaea. Included
pared with that of other important crop species. among wild peanut species are accessions that exhibit extreme
Inheritance of only a few morphological or agronomic traits ly high levels of disease resistance (Table 11). Several species
has been determined, and fewer than 10 linkage groups have have multiple resistance to the most widespread peanut dis
been reported. No aneuploid series is available to help asso eases. The genus has been divided into nine botanical sections
ciate genes with chromosomes. To date, no genetic map for the with four tetraploid (2n = 4x = 40) and 65 diploid (2n = 2x =
cultivated peanut has been made, nor has any gene been asso 20) species. Of these, approximately 25 will hybridize with A.
ciated with a specific chromosome. Genetic characterization of hypogaea-, but ploidy level and genomic differences result in a
peanut has been especially difficult because it is an allopoly high degree of sterility, even when it is possible to produce F;
ploid (2n = 4x = 40) that arose from two distinct species with progeny. Very little is known about reciprocal differences
similar genomes. Hybrids originating from crosses of mutant among crosses, however; and most hybrids can be obtained
genotypes thus result in polyploid genetic ratios that are com only when the cultivated species is used as the female parent.
plicated by gene duplications and interactions among genomes. Moving genes that confer disease resistance from wild to
At the molecular level, studies with isozymes, restriction frag cultivated peanut species has been a primary objective of
ment length polymorphisms (RFLPs), and randomly amplified several breeding programs since the mid-1960s. Efforts have
polymorphic DNAs (RAPDs) have indicated that polymor concentrated on obtaining additional germ plasm from South
phisms can be detected in a relatively small percentage of the America, studying crossing and biosystematic relationships,
genomes of the cultivated species. Thus, it has not yet been .investigating mechanisms of incompatibility and fertility resto
possible to construct a linkage map for the cultivated peanut. ration, and selecting advanced-generation tetraploid progenies
Plant breeding efforts since the 1970s have led to steady with high levels of resistance. Making the initial interspecific
increases in yields, the result of selection of plants in which crosses is difficult but has proven to be much easier than in
photosynthate is preferentially partitioned into reproductive ducing genetic recombination between chromosomes of the
structures and metabolism. However, less progress has been wild and cultivated species. Thus, relatively few lines with
made in the improvement of other traits such as resistance to high levels of disease resistance have been selected in 40-
diseases. In large part, this has been because of the multigenic chromosome hybrid derivatives. Germ plasm releases have
inheritance of disease resistance and/or multiple components of recently been made from interspecific peanut hybrids that
resistance in the host plant. A limited number of cultivars with confer resistance to peanut pathogens including Cercospora
enhanced disease resistance have been released. These include arachidicola and Meloidogyne arenaria. Because these lines
NC 8C and its replacement, NG 10C, which have moderate have relatively low yields and poor agronomic quality, secon
resistance to Cylindrocladium black rot, caused by Cylindro dary breeding programs will be necessary to incorporate this
cladium parasiticum-, the Virginia market type VA 8 IB and resistance into genotypes with potential for cultivar release.
spanish type Tamspan-80, which are resistant to Sclerotinia Barriers to interspecific hybridization have led to many
blight; and the small-seeded runner market type Southern studies of reproductive development and crossing barriers in
Runner, which is resistant to late leaf spot, stem rot, and the peanut. Reproductive development in peanut is complicated by
tomato spotted wilt virus. Additional breeding progress has the interactions of the embryo with the geotropic growth of the

TABLE 11. Number of Accessions with High Levels of Disease Resistance in Botanical Sections of Arachis
Number with High Resistance2
Number
Disease Evaluated Ara.h Cau. Ere. Ext. Het. Rhi. Tri. Unk.
Early leaf spot 97 1 2 3 24
Late leaf spot 96 15 4 12 3 50 1
Cylindrocladium black rot 21 16
Web blotch 50 24 4 1 1 1
Rust 61 18 4 1 34 1
Peanut clump 38 1
Peanut mottle 91 4 1 4 1 39
Peanut ringspot 1 1 1 5
Peanut rosette 13 1 1 1 1
Peanut stripe 8 1 3
Peanut stunt 90 3 1 4 39
Tomato spotted wilt 42 3 1
aAra. = Arachis; Cau. = Caulorrhizae; Ere. = Erectoides, including species in both sections Erectoides and Procumbentes (formally section Erectoides
ser. Procumbentes)', Ext. = Extranervosae; Het. = Heteranthae; Rhi. = Rhizomatosae; Tri. = Triseminatae; and Unk. = section unknown.
bSection Arachis species are cross-compatible with A. hypogaea.

79
 peg from the stem into the soil. After fertilization, the embryo high-velocity particles can penetrate intact cell walls to carry
grows, becomes quiescent for a week or longer, and then reini transforming DNA into the cell. DNA carried by the particles
tiates growth as the pod forms. Foremost among techniques can then be integrated with the chromosomal DNA of the plant
used to overcome interspecific hybridization barriers are the cell. Integrated genes are usually inherited stably, and the
use of growth regulators to enhance fertilization and promote transformed plants typically express the protein encoded by the
peg elongation and embryo growth and the in vitro culture of introduced gene.
ovules and embryos. To overcome the failure of peg growth, An important goal of peanut transformation is to produce
gibberellic acid can be applied at the base of the flower hypan- transgenic germ plasm sources with improved resistance to
thium at the time of pollination. Although this hormone effec pathogens, particularly certain fungi and viruses. Enhanced
tively stimulates peg elongation, it also inhibits embryo growth. resistance to fungi has been observed in plants of other species
Applications of kinetin and indoleacetic acid to the peg appear that express high levels of plant chitinase and other alien gene
to be necessary to maintain reproductive growth. Even with the products.
addition of growth regulators, however, the embryonic tissues Alien gene products also can act synergistically when they
will not fully develop, and in vitro culture is necessary to are expressed simultaneously in plant tissues, e.g., by the co
obtain plants. expression of chitinase and glucanase. In this case, each of the
Ovule culture in peanut was first successful during the early two gene products could be expected to catalyze hydrolysis of
1970s. However, results have been highly variable, and plants a specific component of the fungal cell wall, causing exposure
have rarely been recovered. Failure of this system is attributed of the cell membrane and thus making the fungus highly sus
to the undifferentiated state (globular stage) of embryos con ceptible to disruption by osmotic shock.
tained within ovules. When the peg is placed into culture with Enhancement of virus resistance in plants may be obtained
the meristem left intact, it will elongate, grow geotropically, by the expression of capsid protein or other virus-encoded pro
and expand into pods and may produce well-developed seed teins. This effect has been demonstrated in a wide array of
after 90 days. This technique appears to increase success rates plant species for several major classes of viral pathogens. It is
for obtaining plants from very young embryos. If reproductive anticipated that such a strategy would also be effective in pea
tissues abort after embryos have differentiated into a heart nut.
shape, then in vitro culture of excised embryos has been highly At the present time, the technology for enhancing disease
successful. Although several unique hybrids have been ob resistance through gene transfer to peanut is not yet fully
tained through embryo culture, many of those reported in the developed. However, key elements are now available. The
literature also have been obtained through conventional cross technology for enhancing resistance to viral pathogens is well
ing procedures. developed and has been demonstrated in numerous crop spe
Protoplast fusion is potentially useful as a means of broaden cies for major classes of pathogenic viruses. Strategies for
ing the genetic base in many cultivated species. The use of enhancing resistance to fungi are less well defined; but several
protoplast technologies may be forthcoming in peanut, espe rational strategies for combating fungi -have-been advanced,
cially if wild species can be used as source tissues to hybridize and genes needed for testing them have been cloned.
with A. hypogaea. In general, genetic modification and improvement of the
Studies with in vitro tissue culture have indicated that most peanut has been a steady but slow process since the 1950s.
peanut explants can be induced to form callus tissues. At the Polyploidy, little knowledge of genetic systems, few genes
present time, there is no evidence of plant regeneration from characterized, multiple genes conditioning traits of agronomic
undifferentiated A. hypogaea tissues (callus or single-cell sus interest, and relatively few investigators working in peanut
pensions). Thus, the state of the art for plant cell culture in breeding and genetics have hindered progress. During the
peanut restricts the use of many techniques applicable for im 1980s and into the 1990s, however, increased effortsespe
provement of other crop species. cially in the areas of molecular genetics, tissue culture, and
The use of haploid breeding procedures for A. hypogaea has gene transformationhave significantly broadened the knowl
been generally unsuccessful. Although studies on floral bud edge base o f peanut genetics. Applications of recent basic
size and anther color have allowed selection of tissues at the scientific advances should be forthcoming as previously com
correct developmental stage for in vitro culture of anthers or plex and obscure procedures become routine and can then be
pollen, development beyond a few cell divisions has not been used to solve practical problems in genetics and pathology.
observed.
Several important advances have been recently made in pea Selected References
nut tissue culture and plant regeneration. In the most promising
of these procedures, plants are regenerated from explants such Broglie, K., Chet, I., Holliday, M., Cressman, R., Biddle, P.,
as immature cotyledons or leaves or from meristematic tissues Knowlton, S., Mauvals, C. J., and Broblie, R. 1991. Transgenic
in shoot tips. Treatments such as the addition of antiviral plants with enhanced resistance to the fungal pathogen Rhizoctonia
agents or altered temperatures can be combined with these solani. Science 254:1194-1197.
procedures to provide a source of virus-free plants and tissues. Knauft, D. A., and Ozias-Akins, P. 1995. Recent methodologies for
Plant gene transfer (transformation) is a relatively new tech germplasm enhancement and breeding. Pages 54-94 in: Advances
nology by which genetic elements conferring disease resistance in Peanut Science. H. E. Pattee and H. T. Stalker, eds. American
can be transferred to crop plants. Transformation theoretically Peanut Research and Education Society, Rocky Mount, NC.
permits genes derived from virtually any source to be intro Lodge, J., Kaniewski, T., and Turner, N. 1993. Broad-spectrum virus
duced into the crop species. The genetic base of the crop is resistance in transgenic plants expressing pokeweed antiviral pro
thus greatly expanded with the possibility that novel, disease- tein. Proc. Natl. Acad. Sci. USA 90:7089-7093.
McKently, A. H., Moore, G. A., Wang, A., and Doostdar, H. 1993.
resistant genotypes might be produced. Significant advances
Agrobacterium-mediattd transformation of peanut zygotic embryos
have been made toward development of a practical gene- and regeneration of transgenic plants. In Vitro 29A:65.
transfer, technology for peanut. Ozias-Akins, P., Schnall, J. A., Anderson, W. E, Singsit, C.,
Of the several strategies that have been attempted for peanut Clemente, T. E., Adang, M. J., and Weissinger, A. K. 1993. Re
transformation, microprojectile bombardment of either intact generation of transgenic peanut plants from stably transformed
tissues or embryogenic cultures appears to be the most suc embryogenic callus. Plant Sci. 93:185-194.
cessful. In microprojectile bombardment, microscopic gold or Schnall, J. A., and Weissinger, A. K. 1993. Culturing peanut (Arachis
tungsten particles are coated with the transforming DNA and hypogaea L.) zygotic embryos from transformation via micropro-
then accelerated to high velocity in a gunlike apparatus. The jectile bombardment. Plant Cell Rep. 12:316-319.

80
 Stalker, H. T., and Simpson, C. E. 1995. Germplasm resources in rust. Resistance has been identified and used successfully in
Arachis. Pages 14-53 in: Advances in Peanut Science. H. E. Pattee some breeding programs.
and H. T. Stalker, eds. American Peanut Research and Education Peanut roots, pegs, pods, and stems are attacked by a wide
Society, Rocky Mount, NC.
range of soilbome fungi, nematodes, and insects. Useful resis
tance to soilbome fungal pathogens has been identified but is
(Prepared by H. T. Stalker and A. K. Weissinger) generally incomplete and polygenic.

Cylindrocladium Black Rot

0Cylindrocladium parasiticum)
Disease- and Insect-Resistant Peanut breeders in Georgia, Florida, and Virginia have
screened the germ plasm collection for resistance to Cylindro
Cultivars cladium black rot (CBR) and released 10 germ plasm lines with
varying degrees of resistance. One of these lines (NC 3033)
Successful breeding and screening programs for disease, in has been used in the development of two resistant virginia-type
sect, and nematode resistance require close cooperation be cultivars (NC 8C and NC 10C). Three spanish-type cultivars
tween a breeder/geneticist and pathologist, entomologist, and/or (Tamnut 74, Toalson, and Spancross) were identified as resis
nematologist. Immunity to pathogens, insects, or nematodes tant after release. However, the resistant germ plasm and span
has not been reported in cultivated peanut (A. hypogaea L.). ish cultivars all have relatively low yield potential.
However, many genotypes have been found with usable levels Studies have shown that resistance in NC 3033 is probably
of resistance for most of the major pathogens and insects the result of a lack of infection at inoculum densities less than
(Tables 12 and 13). Nematode resistance has been less avail 50 microsclerotia per gram of soil and tolerance to infection at
able. In many cases, pest resistance is great enough to allow greater densities. The resistance in spanish types is similar.
reduced levels of pesticides or to enhance the level of control Inoculum level, environment, and other factors can also affect
currently available with pesticides. As sources of resistance are disease expression.
identified, they must be incorporated into an ongoing breeding Resistance to CBR has been attributed to additive genetic
program. Generally, emphasis is placed on developing resis effects and is appreciably heritable. However, root and pod
tance to those pathogens and other pests for which other con resistance may be inherited separately, thus complicating
trol measures (cultural or chemical) are not available or are too breeding for resistance. The potential exists for race develop
expensive. Incorporating the many quality and agronomic char ment in C. parasiticum.
acteristics needed to make a new cultivar acceptable to peanut
growers and the industry requires an intensive breeding effort. Sclerotinia Blight (Sclerotinia minor)
Of the fungal diseases, early leaf spot, caused by Cercospora Screening for resistance to Sclerotinia blight in the United
arachidicola (CA); late leaf spot, caused by Cercosporidium States has been concentrated in the Virginia-Carolina and
personatum (CP); and rust, caused by Puccinia arachidis, are southwestern peanut areas where Sclerotinia blight is a major
nearly worldwide in occurrence and frequently have great eco problem. These efforts have resulted in the release of two
nomic impact on the crop. Considerable effort has been given virginia-type peanut cultivars (VA 81B and VA 93B) and one
to identifying sources of resistance to CA, CP, and rust. All spanish-type cultivar (Tamspan-90) with varying degrees of
breeding programs in the United States, at ICRISAT (India and partial resistance. Twelve germ plasm lines have also been
Africa), and in most other countries with peanut-breeding pro released with resistance to Sclerotinia blight. Resistance varies
grams have addressed one or more of these disease problems. in these lines from moderate (VGP 1 to VGP 9) to very high
Most sources of resistance to the leaf spots are only partial or (Chico and TXAG 1, 2, 4, and 5).
rate reducing. Mechanisms or components of resistance com The resistance in highly resistant lines and cultivars is
monly reported include extended latent periods, decreased thought to be largely the result of a morphological escape
sporulation, smaller lesions, reduced necrotic area, reduced mechanism rather than one based on physiological characters.
infection frequency, and reduced defoliation. The growth habit in all of these genotypes is upright with an
Resistance to CA, CP, and rust appear to be independently open canopy structure, which creates a microclimate less
inherited. Major genes for resistance have been identified for favorable for colonization and infection.
rust but not for the leaf spots. Additive genetic factors pre Preliminary studies have shown that the physiologic resis
dominate in resistance to the leaf spots, but nonadditive factors tance in some plants may be at least partially controlled by a
are also important. Resistance to CP seems to be more com cytoplasmic factor. Other studies have shown low-narrow and
monly available than that to CA in cultivated peanut. broad-sense heritability for resistance, indicating the involve
Many wild Arachis species and their interspecific deriva ment of several genes and/or large environmental variance.
tives from cultivated peanut have been reported to have resis Resistance to Sclerotinia blight is also often associated with
tance approaching immunity for some foliar diseases, especial early maturity. Reliable laboratory screening procedures are
ly CP and rust. A. diogoi, A. cardenasii, and A. stenosperma needed in order to definitively determine the inheritance of
are among Arachis spp. with near immunity to CP. resistance to Sclerotinia blight.
Late maturity and low pod yields have been associated with
foliar disease resistance, especially to leaf spots. Southern Stem Rot (Sclerotium rolfsii)
Runner is a runner cultivar with moderate resistance to CP and Breeding programs in all major peanut-producing areas of
rust that has yields and grades comparable to currently avail the United States have included screening for resistance to
able cultivars. However, Southern Runner matures 10-20 days stem rot. One germ plasm line (NC 3033) and two cultivars
later than the widely grown susceptible cultivar Florunner, (NC 2 and NC 8C) with resistance to stem rot have been
which may limit its adaptability to certain growing areas. released. In addition, six other cultivars (Toalson, Southern
Other cultivars or germ plasm lines released from breeding Runner, Pronto, Georgia Browne, and Sunbelt Runner) have
programs in the United States with partial resistance to CA or been identified since release as resistant. Recent studies have
CP include Altika (CA/CP), GP-NC 343 (CA), NC 3033 (CA), shown that resistance is not related to growth habit. While no
PI 109839 (CA), Tifrust 1 (CA/CP, rust), Tifrust 2 and 3 (CP, specific genetic models for control of stem rot resistance have
rust), Tifton 8 (CA/CP), and VGP 2 to VGP 7 (CA/CP). been reported, it has been suggested that the defense
Web blotch (Phoma arachidicola), a foliar disease that can mechanism is different from that for resistance to pod rot
be very damaging, is generally less common than CA, CP, or caused by Pythium myriotylum.

81
Pod Rot (.Pythium, Rhizoctonia, and Fusarium spp.) more lignified cell walls in the epicarp; and sclerenchymatous
Three breeding lines (NC 3033, TXAG 4, and TXAG 5) and mesocarp of cell walls in the pods.
two cultivars (Toalson and Tamspan-90) with resistance to pod
rot have been released. Although resistance has been reported Rhizoctonia Limb Rot (.Rhizoctonia solani)
in some cultivars, the level is not high enough to prevent seri One virginia-type cultivar (VA 8 IB) and one spanish-type
ous yield losses. Resistance to pod rot has been associated with cultivar (Toalson) were reported as resistant to Rhizoctonia
more compact palisade mesophyll cells in leaf tissue; thicker, limb rot after their release for resistance to other soilbome

TABLE 12. Peanut Germ Plasm Lines and Cultivars, Released and/or Registered in the United States,
That Have Resistance to Diseases, Nematodes, or Insects
Description
Type (Crop Science
Identity Resistance" Sourceb Year vol.:page)
Germ plasm
GP-NC 343 SCRW, CA NC 1970 11:605
Chico SBC USDA-ARS, GA, VA, OK 1973 15:105
PI337394F AF USDA, AL, GA 1974 15:106
PI 337409 AF USDA, AL, GA 1974 15:106
NC 10247 LH NC 1975 15:738-739
NC 10272 LH NC 1975 15:738-739
NC 15729 LH NC 1975 15:738-739
NC 15745 LH NC 1975 15:738-739
PI 109839 CA USDA, GA 1979 20:292
NC 3033 CBR, SR, PR, LS, CA NC 1976 16:887
VGP 1 CBR, SB USDA-ARS, VA 1979 20:419
CBR-R1 to R6 CBR USDA-ARS, GA 1981 21:992-993
Tifrust 1 to 14 R, CA, CP USDA, GA 1981 22:452-698
F 334 AB-14 CR USDA-ARS, GA, FL 1983 23:1019-1020
GFA 1 and 2 AF USDA, GA 1983 23:1020-1021
AR 1 to 4 AF USDA, GA 1983 23:1021
Tifton 8 CBR, LS, SCRW, CR, CA, CP USA-ARS, VA, GA 1984 25:203
TXAG 1 and 2 SBC TX 1985 26:391
VGP 2 to 7 SB, LS, SCRW, CA, CP USDA-ARS, VA 1986 27:1319
TXAG 4 and 5 PR, SB TX, OK, USDA-ARS 1989 30:429
ICGV 87157 CP, TSWV, SR, LM, LH ICRISAT 1990 32:837
ICGV 86031 T, LH, LM, BW ICRISAT 1991 33:220
GP-NCW 1 to 4 CA, CP NC 1992 33:1117
TXAG 6 and 7 R, CA, CP, RK TX 1992 33:1148
VGP 9 SB, CBR USDA-ARS, VA 1993 34:1132-1133
Cultivar
Spancross CBRC USDA-ARS, GA, OK 1970 10:459
NC 2 SR NC 1952 10:459-460
Tamnut 74 CBRC TX, OK, GA 1974 15:603-604
NC 6 SCRW NC 1976 17:346
Toalson PR, CBR,c SR,CRLC TX 1979 19:742
VA81B SB, RLC USDA-ARS, VA 1982 22:1085-1086
Sunbelt Runner AF, SRC USDA-ARS, GA 1981 22:1086
NC8C CBR, SR NC 1982 23:183-184
Pronto SRC USDA-ARS, OK, GA 1980 23:184
Southern Runner LS, R, WB, SR,CTSWVC FL 1986 27:817
NC 10C CBR NC 1988 31:484
Tamspan-90 SB, PR TX, USDA-ARS 1990 31:1711
Florunner WBC FL 1969 9:850
GA 119-120 BW USDA, GA 1954 11:313
Altika CA, CP FL 1972 14:339
ICGV 87-87128 TSWV ICRISAT (India) 1988 30:959
ICGS 11 TSWV ICRISAT (India) 1986 30:960
NC V I1 SRC NC, USDA-VA 1989 31:484-485
ICGV 87141 TSWV ICRISAT 1989 31:1096
ICG SI TSWV ICRISAT 1990 31:1382-1383
ICGV 87187 TSWV ICRISAT 1990 32:278-279
ICGV 87160 R, CP, TSWV, SR, LM ICRISAT 1990 32:1075
Sinkarzei RCA ICRISAT 1989 33:212
ICGV 86590 R, CP, SR, LH, CR ICRISAT 1991 33:357-358
Georgia Browne SR, RL, TSWV GA 1992 34:1125-1126
VA93B SB USDA-ARS, VA 1993 34:1126
aSCRW = Southern com rootworm; SB = Sclerotinia blight; CBR = Cylindrocladium black rot; SR = stem rot (white mold); PR = pod rot; LS = leaf spot;
CR = Diplodia collar rot; RL = Rhizoctonia limb rot; WB = web blotch; CA = early leaf spot (Cercospora arachidicola)', CP = late leaf spot (Cerco
sporidium personatum)', R = rust (Puccinia arachidicola)', TSWV = tomato spotted wilt virus; LM = leafminer {Aproaerena modicella); BW = bacterial
wilt {Pseudomonas sp.); LH = leafhopper (Spodoptera sp.); T = thrips {Thrips palmi)', RK = root-knot nematode {Meloidogyne spp.); and AF =
Aspergillus flavus.
bNC = North Carolina Agricultural Research Service; USDA-ARS = U.S. Department of Agriculture-Agricultural Research Service; AL, GA, FL, OK,
and VA = agricultural experiment stations in Alabama, Georgia, Florida, Oklahoma, and Virginia, respectively; and ICRISAT = International Crops Re
search Institute for the Semi-Arid Tropics.
c Resistance identified after release.

82
diseases. It has been suggested that an open canopy structure, are derived from complex interspecific crosses with A. car-
such as that needed for Sclerotinia blight resistance, may be denasii Krap. et Greg. nom. nud., A. chacoensis Krap. et Greg.
associated with resistance to Rhizoctonia limb rot. However, nom. nud., A. batizocoi Krap. et Greg., and A. hypogaea (Flo-
greenhouse studies have indicated that morphological barriers runner). Some reports of resistance in other Arachis species
or active plant response may also be associated with resistance. and low to moderate levels of resistance in A. hypogaea have
Early maturity could be a good escape mechanism, since pea been made.
nuts could be dug before environmental conditions (low tem
peratures) are suitable for disease development. Peanut Pod Nematode (Ditylenchus africanus)
Peanut germ plasm was screened in South Africa for resis
Diplodia Collar Rot (Diplodia gossypina) tance to D. africanus, and two breeding lines, US 40-1 and PI
One spanish-type germ plasm line (F 334 AB-14) with high 298233, with excellent partial field resistance were found. One
levels of resistance to Diplodia collar rot has been released. A cultivar with partial resistance to the peanut pod nematode has
virginia-type germ plasm line (Tifton 8), unrelated to F 334 been released.
AB-14, has been released with resistance to Diplodia collar rot
at low inoculum densities. While F 334 AB-14 is in the back Viruses
ground of some cultivars being grown today, the resistance has Sources of resistance have been reported in cultivated peanut
not been transferred to these cultivars. to the viruses that cause groundnut rosette, peanut stunt, and
tomato spotted wilt (TSWV). ICRISAT has been a primary
Black Hull (Chalara elegans) source of germ plasm resistant to groundnut rosette (Africa)
The introduction of resistant cultivars successfully restored and TSWV (India), whereas breeding programs in Florida,
peanut production in irrigated areas of South Africa where this Georgia, and Texas have had some success in developing
disease once dominated. Different sources of genetic resistance material resistant to TSWV. The recently released variety
to C. elegans were identified, and new spanish cultivars with Georgia Browne has significant resistance to TSWV.
resistance were officially released.
Southern Corn Rootworm
Aflatoxin (Aspergillus flavus and A. parasiticus) Programs screening for resistance to southern com rootworm
Screening for resistance to aflatoxin-producing fungi has have resulted in the identification of several sources with
been carried out in several countries by using laboratory tech various levels of resistance. Three germ plasm lines (GP-NC
niques, rehydrated seed, and field-stress studies. Studies have 343, Tifton 8, and VGP 7) have been released. CP-NC 343 has
evaluated resistance to both infection by the fungus and pro been used to develop the partially resistant cultivar NC 6.
duction of aflatoxin. Pis 337394F and 337409, GFA 1 and GFA Resistance is thought to be based on antibiosis or biochemical
2, AR 1 to AR 4, and Sunbelt Runner were selected as having processes in most resistant lines identified and appears to be
resistance to infection by the fungus on rehydrated seed. Selec heritable and multigenic in nature.
tions from Senegal, 55-437 and 73-30, show field resistance
under severe drought stress. Various other reports of resistance Thrips and Leafhoppers
can be found in the literature listed. No cultivar with a high Only limited work has been done or is currently being done
level of resistance to aflatoxin-producing fungi has been made to search for resistance to foliage-feeding insects in peanuts.
commercially available in the United States. This is largely because of the ready availability of acceptable
insecticides for their control and the higher priority assigned to
Root Knot (Meloidogyne arenaria and M. hapla) diseases and other pests for which satisfactory controls are
There has been only limited success in identifying resistance unavailable or limited.
to the peanut root-knot nematode, and there are no reports of Four germ plasm lines (NC 10247, NC 10272, NC 15729,
high levels of resistance in A. hypogaea. TXAG 6 and TXAG and NC 15745), with resistance to the potato leafhopper, were
7, A. hypogaea germ plasm lines from the Texas Agricultural developed from the irradiation breeding program in North
Experiment Station with high levels of resistance to root knot, Carolina and have been released. NC 10247 is considered a
Virginia type, while the other three are runner market types.
ICRISAT has released two germ plasm lines (ICGV 87157 and
TABLE 13. Disease- and Nematode-Resistant ICOY. 86031) and one cultivar (ICGV 86590), all spanish
Peanut Cultivars from Africa types, with resistance to leafhoppers. ICGV 86031 also has re
sistance to thrips. Inheritance studies indicate leafhopper resis
Cultivar Resistance* Origin
tance is probably controlled by a few major genes.
RMP12 CP, RV Burkina Faso
RMP91 CP, RV Burkina Faso
Falcon WB Zimbabwe
Selected References
RMP40 RV Burkina Faso
RGI RV Malawi Anderson, W. F., Wynne, J. C., Green, C. C , and Beute, M. K. 1986.
KH 149A RV Burkina Faso Combining ability and heritability of resistance to early and late
RH 241D RV Burkina Faso leafspot of peanut. Peanut Sci. 13:10-14.
OH 243C RV Burkina Faso Barnes, J. S., Csinos, A. S., and Branch, W. D. 1990. Sensitivity of
69-101 RV Senegal Rhizoctonia solani isolates to fungicides and evaluation of peanut
59-426 RV Senegal cultivars to Rhizoctonia limb rot. Peanut Sci. 18:62-65.
Harts BH South Africa Branch, W. D., and Brenneman, T. B. 1993. White mold and Rhizoc
Jasper BH South Africa tonia limb rot resistance among advanced Georgia peanut breeding
Kwarts BH, PN South Africa lines. Peanut Sci. 20:124-126.
Robbie SB South Africa Branch, W. D., and Csinos, A. S. 1987. Evaluation of peanut cultivars
55-437 AF Senegal for resistance to field infection by Sclerotium rolfsii. Plant Dis.
73-30 AF Senegal 71:268-270.
aCP = Cercosporidium personatum; RV = rosette virus; WB = web blotch Campbell, W. V., and Wynne, J. C. 1985. Influence of the insect-
CPhoma arachidicola); BH = black hull (Chalara elegans)', BB = resistant peanut cultivar NC 6 in the field. J. Econ. Entomol.
Botrytis blight (Botrytis cinerea); SB = Sclerotinia blight (Sclerotinia 63:1825-1827.
minor); PN = peanut pod nematode (Ditylenchus africanus); and AF = Chiteka, Z. A., Gorbet, D. W., Knauft, D. A., Shokes, E M., and
Aspergillus flavus. Kucharek, T. A. 1988. Components of resistance to late leafspot in

83
 peanut. II. Correlations among components and their significance Influence of maturity and fruit yield on susceptibility of peanut to
in breeding for resistance. Peanut Sci. 15:76-81. C. personatum. Peanut Sci. 17:52-58.
Chiteka, Z. A., Gorbet, D. W., Shokes, F. M., Kucharek, T. A., and Norden, A. J., Smith, O. D., and Gorbet, D. W. 1982. Breeding of the
Knauft, D. A. 1988. Components of resistance to late leafspot in cultivated peanut. Pages 95-122 in: Peanut Science and Technol
peanut. I. Levels and vaxiability-Implications for selection. Peanut ogy. H. E. Pattee and C. T. Young, eds. American Peanut Research
Sci. 15:25-30. and Education Society, Yoakum, TX.
Coffelt, T. A., and Herbert, D. A. 1994. Evaluation of virginia-type Pixley, K. V., Boote, K. J., Shokes, F. M., and Gorbet, D. W. 1990.
peanut cultivars for resistance to southern corn rootworm. Peanut Growth and partitioning characteristics of four peanut genotypes
Sci. 21:81-91. differing in resistance to late leafspot. Crop Sci. 30:796-804.
Coffelt, T. A., and Porter, D. M. 1982. Screening peanuts for resis Porter, D. M., Coffelt, T. A., Wright, F. S., and Mozingo, R. W. 1992.
tance to Sclerotinia blight. Plant Dis. 66:385-387. Resistance to Sclerotinia blight and early leafspot in Chinese pea
Culbreath, A. K., Todd, J. W., Demski, J. W., Branch, W. D., Hol nut germplasm. Peanut Sci. 19:41-43.
brook, C. C., and Gorbet, D. W. 1991. Field evaluation of peanut Porter, D. M., and Hammons, R. O. 1975. Differences in plant and
genotypes to resistance to tomato spotted wilt virus, 1990. Biol. pod reaction of peanut lines to infection by Diplodia gossypina.
Cult. Tests Controlling Plant Dis. 6:52. Peanut Sci. 2:23-25.
Gorbet, D. W., Knauft, D. A., and Shokes, F. M. 1990. Response of van der Merwe, P. J. A., and van der Merwe, L. P. 1988. Hosts: A
peanut genotypes with different levels of leafspot resistance to groundnut cultivar with resistance to black pod rot (Chalara
fungicide treatment. Crop Sci. 30:529-533. elegans). Appl. Plant Sci. 22:81-82.
Grichar, W. J., and Smith, O. D. 1992. Variation in yield and resis Venter, C., Dewaele, D., and Meyer, A. J. 1991. Reproductive and
tance to southern stem rot among peanut (Arachis hypogaea L.) damage potential of Ditylenchus destructor on peanut. J. Nematol.
lines selected for Pythium pod rot resistance. Peanut Sci. 19:55-58. 23:12-19.
Hadley, B. A., Beute, M. K., and Wynne, J. C. 1979. Heritability of Wildman, L. G., Smith, O. D., Simpson, C. E., and Taber, R. A. 1992.
Cylindrocladium black rot resistance in peanut. Peanut Sci. 6:51- Inheritance of resistance to Sclerotinia minor in selected Spanish
54. peanut crosses. Peanut Sci. 19:31-34.
Holbrook, C. C., and Noe, J. P. 1992. Resistance to the peanut root- Wynne, J. C., Beute, M. K., and Nigam, S. N. 1991. Breeding for
knot nematode (M. arenaria) in Arachis hypogaea. Peanut Sci. resistance in peanut (Arachis hypogaea L.). Annu. Rev. Phyto
19:35-37. pathol. 29:279-303.
Knauft, D. A., Gorbet, D. W., and Norden, A. J. 1988. Yield and mar
ket quality of seven peanut genotypes as affected by leafspot
disease and harvest dates. Peanut Sci. 15:9-13. (Prepared by D. W. Gorbet, T. A. Coffelt,
Miller, I. L., Norden, A. J., Knauft, D. A., and Gorbet, D. W. 1990. and P. J. A. van der Merwe)

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 Glossary
A acre apterouswingless
C centigrade or Celsius arbuscule (adj. arbuscular)branched, haustoriumlike, intracellular
cm centimeter (0.39 in.; 1 cm = 10 mm) development of mycorrhizal fungi
FFahrenheit ascigerousbearing asci
ftfoot ascocarp sexual fruiting body of an ascomycetous fungus
ggram (453.59 g = 1 pound) ascomaa sporocarp having asci
hahectare ascomycete (adj. ascomycetous)fungus that produces sexual spores
hrhour (ascospores) within a saclike structure, the ascus
mmeter ascospore sexual spore borne in an ascus
mtmetric ton ascus (pi. asci) saclike structure containing ascospores (typically
mlmilliliter eight) and borne in an ascocarp
mmmillimeter (0.04 in.; 10 mm = 1 cm) aseptatehaving no cross walls
pgmicrogram (1 gg = 10-6 g) asexualvegetative; without sex organs, as a type of spore
Hmmicrometer (1 pm = 10m) attenuate (v. or adj.)to narrow; to weaken or decrease in virulence
runnanometer (1 nm = 10~9 m) or pathogenicity
ppbparts per billion avirulentunable to cause disease; nonpathogenic
ppmparts per million axenicpertaining to a culture free of living bacteria or other organ
isms; pure culture
abaxial directed away from the stem o f a plant; pertaining to the axil the angle formed by the leaf petiole and the stem
lower surface of a leaf axillarypertaining to or placed within an axil
abioticpertaining to the absence of life, as diseases not caused by azygosporespore morphologically similar to a zygospore
living organisms
abscise (n. abscission) to cut off, separate basidiomycete (adj. basidiomycetous) fungus that forms sexual
acervulus (pi. acervuli)erumpent, saucerlike fungal fruiting struc spores (basidiospores) on a basidium
ture bearing conidiophores, conidia, and sometimes setae basidiosporesexual spore produced on a basidium
acicularneedle-shaped basidium (pi. basidia, adj. basidial) short, club-shaped, haploid pro
acutepertaining to symptoms that develop suddenly (as opposed to mycelium produced by basidiomycetous fungi
chronic) basipetaltoward the bottom
adaxialpertaining to the upper leaf surface biguttulatehaying two globules or vacuoles
adventitious arising or occurring sporadically from unexpected tis biocide a pesticide lethal to all living material
sue origin bioticrelating to life, as disease caused by living organisihs
aedum (pi. aecia) cuplike fruiting body of rust fungi bitunicate double-walled
aerial occurring in the air blightgeneral term for sudden, severe, and extensive spotting, dis
aerobicliving only in the presence of oxygen coloration, wilting, or destruction of leaves, flowers, stems, or
aflatoxinchemical by-product from Aspergillus flavus and A. para entire plants
siticus harmful to humans and other animals botryose shaped like a bunch o f grapes
agargelatin from seaweed used in making laboratory culture media butyrousbutterlike
alatehaving wings
albino (n. albinism) white or light-colored; having a marked de calcareousresembling or containing calciurr
ficiency in pigmentation calyxoutermost flower whorl; sepals, collectively
alternate hostanother plant host for a given organism carlavirus one of a group of related viruses, including the cowpea
amphigenousgrowing on both sides of a leaf mild mottle virus
anaerobicliving in the absence o f oxygen carpel structural unit or units of the pistils of certain flowers
anamorphicpertaining to the imperfect (asexual) state of a fungus carpogenicgiving rise to fertile cells
anastomosisfusion between branches of the same or different carpophorestalk of a fruiting body in fungi
structures (e.g., hyphae) to make a network carpospore a diploid spore
annulegrooved band in the cuticle of some nematodes catenatein chains
antagonistan organism that limits the action o f another caudatail
anteriortoward the front or head (as opposed to posterior) chelicera sharply pointed appendage at the front of a sucking insect
antherpollen-bearing portion of a flower chimeraa plant or part composed of two or more genetically differ
antheridium (pi. antheridia)male sexual organ found in some fungi ent tissues
anthesis the period of the opening of a flower chlamydosporethick-walled or double-walled asexual resting spore
antiserumportion of blood containing antibodies formed from hyphal cells (terminal or intercalary) or by transfor
apex (adj. apical) tip mation of conidial cells
aphicide agent, usually a chemical, that kills or inhibits aphids chlorophyll (adj. chlorophyllous) one of a group of green pigments
apothecium (pi. apothecia) saucer-shaped, ascus-bearing fruiting found in chloroplasts and important in photosynthesis
body chlorosis (adj. chlorotic)failure of chlorophyll development, caused
appressorium (pi. appressoria) swollen or flattened portion of a by disease or a nutritional disturbance (e.g., lack of iron, zinc, or
germ tube or hypha that attaches to the host during an early stage of magnesium); fading of green plant color to light green, yellow, or
infection white

85
cilium (pi. cilia) appendage like a flagellum, which propels cells epidermis (adj. epidermal) surface layer of cells of leaves and other
(especially zoospores) through water plant parts
cirrus (pi. cirri) column or tendril of mucus laden with spores epinasty abnormal, clawlike, downward curling of leaves
clavate, claviform club-shaped epiphyllouson the upper surface of a leaf
coalesce to run together equatorial poreunthickened spot at the equator of a spore through
coenocyticpertaining to a multinucleate mass of protoplasm with which a germ tube may emerge
out cross walls eradicateto destroy or remove (a pest or pathogen)
collarthe portion of the seedling near the surface of the ground erumpentbursting or erupting through the substrate surface
colonization establishment of a pathogen within a host plant extra-large kernels seed of Virginia market-type cultivars that do
confluentcoming together not pass through a 21.5/64-in. screen
conicalcone-shaped exudateliquid (ooze) excreted or discharged from diseased tissues,
conidiogenesismethod of spore formation from roots and leaves, or by fungi
conidiogenousproducing and bearing conidia exudeto ooze or be discharged through pores
conidiophore simple or branched, fertile hypha on which conidia
are produced facultative parasite organism that is normally self-dependent but is
conidium (pi. conidia, adj. conidial) asexual spore borne at the tip capable of being parasitic
or side of a specialized hypha (conidiophore) falcate curved like the blade of a scythe or sickle
corniclehornlike projection fallowto leave soil unseeded after plowing
cortex (adj. cortical)region of parenchyma tissue between the epi fascicle (adj. fasciculate) small group, bundle, or cluster of flowers,
dermis and phloem in stems and roots; a more or less thick outer leaves, stems, or roots; also used with fungi
covering field capacity(of water) amount of water retained by a soil after all
cotyledon seed leaf gravitational water is drained away
crownregion of a seed plant at which stem and root merge filamentthin, flexible, threadlike object; anther-bearing stalk of a
cruciform arranged in the shape of a cross stamen
cucumovirus one of a group of related viruses, including the peanut filamentous or filiform threadlike
stunt virus flagellum (pi. flagella)hairlike, whiplike, or tinsellike appendage
cultivar cultivated variety of a motile cell (bacterium or zoospore) that provides locomotion
culture artificial growth and propagation of organisms on nutrient fleckminute, discolored spot in green tissue
media or living plants flexuoushaving turns; not rigid
cuticlewaxy, noncellular layer formed on the outer walls of plant focus small area of diseased plants
epidermal cells; outer sheath or membrane of a nematode or plant foliarpertaining to leaves
cylindric of the same diameter throughout the length forma specialis (f. sp.)taxonomic category reflecting incomplete
cytoplasmliving protoplasm in a cell, except the nucleus knowledge of structure
fructificationgeneral term for spore-bearing organs in both macro
damaged kernels damaged seed that reduces the market value of fungi and microfungi
peanuts fumigantvapor-active (volatile) disinfectant used against micro
damping-offrapid, lethal decline of a germinating seed or seedling organisms and other pests
before or after emergence fungicide substance lethal to fungi
declinous about to fall over; drooping funiculus stalk of the ovule
defoliateto deprive of leaves prematurely fusiform spindlelike; narrowing toward the ends
deliquescent dissolving, liquefying, or melting away fusoid;somewhat fusiform
dematiaceous darkly pigmented
digitatehaving lobes radiating from a common center gall abnormal swelling or localized outgrowth, often roughly spheri
dilution end point stage of a serial dilution of cells or preparations cal, produced by a plant as a result of attack by a fungus, bacteri
at which growth or infection from a standard sample of the suspen um, nematode, insect, or other organism
sion no longer occurs gametangium (pi. gametangia) cell containing gametes or nuclei
dimorphic (n. dimorphism)=havmg1worfonns that act as-gametes
dissemination spread of infectious material (inoculum) from dis gamete sex cell
eased to healthy plants geniculatebent, like a knee
distichous in two lines genome set or group of chromosomes
dolioformbarrel-shaped genotype genetic constitution of an individual or group; class or
dormancy (adj. dormant) state of reduced physiologic activity group of individuals sharing a specific genetic makeup
geocarp fruit (e.g., peanut pod) that ripens beneath the ground
echinulate having small, pointed spines projecting from cell walls geocarposphere soil near a pod
ectoparasiteparasite living on the exterior of its host geotropism (adj. geotropic) growth curvature induced by gravity
effuse (adj.) stretched out, especially a filmlike growth germ pore differentiated thin area within a spore wall (especially in
egg mass group of eggs held together by a gelatinous matrix rust fungi) through which a germ tube can emerge
ellipsoid elliptic in optical section germ tubehypha resulting from an outgrowth o f the spore wall
elliptichaving the shape of a foreshortened circle and/or cytoplasm
elongateto lengthen germinate (n. germination)to begin growth (as of a seed, spore,
elytrum (pi. elytra) one of the anterior wings on some insects that sclerotium, or other reproductive body)
serve to protect the posterior functional wings germlinggerminating spore
enation abnormal outgrowth from the surface of a stem or leaf girdleto circle and cut through; to destroy vascular tissue in a
endocarp inner layer of a pericarp (fruit wall) canker that encircles the stem or stolon
endoconidium (pi. endoconidia) conidium formed inside a hypha globosealmost spherical
endoparasiteparasite living inside its host globuletiny globe or ball
endoplasmic reticulum system of interconnected cytoplasmic gnotobioticpertaining to growth of an organism in the absence
membranes that transports materials within the cell of other organisms or in the presence of only known organ
endosperm nutritive tissue developed around an embryo in the ovule isms
endospore an asexual spore developed within the cell graft transmissiontransmission of a pathogen by vegetative propa
epicotylportion of a plant embryo or seedling above the node at gation
which the cotyledons are attached gram-negative, gram-positivepertaining to bacteria that release or
epidemic general and serious outbreak of disease retain, respectively, the violet (red) dye in Grams solution
epidemiology (adj. epidemiologic) study of factors influencing the granulous covered with a granulelike substance
initiation, development, and spread of infectious disease guttulatehaving one or more oillike drops inside

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gynophore stalk bearing the female reproductive structures; in pea leaflet one of the separate blades or divisions of a compound leaf
nut, commonly called a peg legume simple, dry, dehiscent fruit that develops from a simple
pistil and splits at maturity along two seams
hamatehooked lenticular shaped like a double convex lens
haulmstem or stalks, collectively lesionwound or delimited diseased area
haustorium (pi. haustoria)specialized hyphal branch of a parasite, lignincomplex organic substance or group of substances that im
especially one within a living host cell, for absorbing food (often pregnate the cell walls of xylem vessels and certain other plant
associated with rust fungi, downy and powdery mildew fungi, cells
parasitic flowering plants, and other obligate parasites) local lesionlocalized spot produced on a leaf upon mechanical
herbaceous having little or no woody tissue and usually persisting inoculation with a virus
for a single growing season longevity in vitro amount of time a virus remains infective when
hilum scar on a seed where it was attached to the funiculus stored at room temperature
hollow heart a boron deficiency symptom expressed as a ridged Iygaeidsmall, sucking insect
hollow between the cotyledons
holomorphthe whole organism macerateto soften by soaking; to cause disintegration of tissues by
homothallism (adj. homothallic) condition in which sexual repro separation of cells
duction can occur without the interaction of two different thalli, macroconidiumlarge conidium produced usually at a different
both sexes being present in the same mycelium period or on a different structure than microconidia
honeydewsugary ooze or exudate, typically from aphids masked symptom symptom that is absent under certain environ
hostliving plant attacked by or harboring a parasite and from which mental conditions but that appears when the host is exposed to cer
the invader obtains part or all of its nourishment tain temperature and light conditions
host rangekinds of plants attacked by a given pathogen maturationprocess of becoming mature
hullouter coat of a seed mechanical damagedamage inflicted by equipment
hyalinetransparent or nearly so; translucent (often used in the sense mechanical transmission (or inoculation) spread or introduction of
of colorless) inoculum to an infection court (especially a wound) accompanied
hymenium spore-bearing layer of a fungal fruiting body by physical disruption of host tissues
hypanthiumenlargement of the floral receptacle medium (pi. media)chemical environment providing nutrition for
hypha (pi. hyphae, adj. hyphal) tubular filament of a fungal thallus growth
or mycelium; the basic structural unit of a fungus meiosisthe process during which gametes are formed
hypocotylportion of a seedling below the cotyledons melanized darkened
membranousmembranelike
icosahedralhaving 20 faces, as a virus particle meristem (adj. meristematic)formative plant tissue
immunogenicproducing immunity mesocarpmiddle coat of a pericarp
imperfect state asexual part of the life cycle of a fungus, during mesophyllleaf tissue between the epidermal layers; cells contain
which asexual spores (such as conidia) or no spores are produced ing chlorophyll
in vitro in glass, on artificial media, or in an artificial environment; metabasidiumthe part or stage of the basidium in which meiosis
outside the host occurs
in vivo within a living organism metula (pi. metulae) a sporophore branch having phialides
inclusionsbodies suspended in the cytoplasm microconidium (pi. microconidia) the smaller conidium of a fun
indehiscentpertaining to fruit that does not split open at maturity gus that also has macroconidia
infection (v. infect)process of a pathogen entering and parasitizing microsclerotium (pi. microsclerotia)microscopic, dense aggregate
a host plant of darkly pigmented, thick-walled hyphal cells
infection court site in or on a host plant where infection can occur mildewthin coating of mycelial growth and spores on the surfaces
infection pegvery fine hypha that is thrust through the cuticle or of infected plant parts
epidermis of a host cell mitochondrion (pi. mitochondria) various cellular organelles out
infestation (v. infest) attack by animals, especially insects or nema side the nucleus
todes; aggregation of inoculum or other organisms on a plant sur mitosporeuninucleate, diploid zoospores
face monadelphouspertaining to stamen filaments united into a tube or
inflorescenceflower or flower cluster column
initial inoculum the total population of a pathogen at the onset of morphology (adj. morphologic) form and structure of organisms
an epidemic mosaicvirus disease characterized by dark and light green mottling
injuryresult of transitory operation of an adverse factor such as of the foliage
insect feeding, action of a chemical, or unfavorable environmental motile capable of self-propulsion by means of flagella, cilia, or
condition amoebic movement
inoculate (n. inoculation)to place inoculum in an infection court multinucleatehaving more than one nucleus per cell
inoculum (pi. inocula)pathogen or its parts capable of establishing muriformhaving transverse and longitudinal septa
a live colony when transferred to a favorable location mycelium (pi. mycelia, adj. mycelial)mass of hyphae constituting
inoculum density a measure of the number of propagules of a patho the body (thallus) of a fungus
genic organism mycelogenicpertaining to germination of sclerotium by production
intercalarybetween the apex and the base of mycelium
intercellular between or among cells mycoflorafungi characteristic of an environment
intercrop to grow one crop between the rows a f another crop mycoparasitefungus that attacks another fungus
intemode (adj. internodal) area of stem between two nodes mycophagousfeeding on fungi
interveinalbetween (leaf) veins mycoplasmaprokaryotic organism, smaller than conventional bac
intracellularthrough or within cells teria, lacking rigid cell walls and variable in shape
isolate (n.)pure microbial culture separated from its natural origin mycoplasmalike organismorganism with the apparent features of
isometric equally long a mycoplasma but not proven to be a mycoplasma
mycorrhiza (pi. mycorrhizae, adj. mycorrhizal) association between
keelthe two anterior, united petals of a butterflylike legume flower a symbiotic, nonpathogenic, or weakly pathogenic fungus and the
kernelsee seed roots of plants

laminaexpanded part of a leaf necrosis (adj. necrotic) death (of tissue), usually accompanied by
larva (pi. larvae)juvenile; growth stage between embryo and adult discoloration
latentpresent but not manifested or visible, as a symptomless infec nematicide agent, usually a chemical, that kills or inhibits nema
tion by a pathogen todes

87
nematode small, wormlike animal, parasitic in plants or animals or phyllotaxyarrangement of leaves on a stem in relation to one
free living in soil or water another
nodebranch point on a stem at which leaves and buds arise phytoplasmamycoplasmalike organism
nodule (n. nodulation) small knot or irregular, rounded lump; on phytotoxic (n. phytotoxicity) harmful to plants
leguminous plants, structures on roots that contain nitrogen-fixing pigmentany coloring matter in the cells of plants or fungi
bacteria pinnatefeatherlike; having parts arranged along two sides of an
nonpedicellate not borne on a slender stalk axis
nonpersistentpertaining to viruses that are infectious within insect pistilthe ovary, stigma, and style o f a flower
vectors for short periods and are transmissible without a latent pithparenchymatous tissue occupying the center of the stem
period and without prior multiplication and translocation within the plasmodium (pi. plasmodia)naked, multinucleate mass of proto
vector plasm moving and feeding in amoeboid fashion
pleomorphicable to assume various shapes
obclavateinversely clavate; widest near the base plumulebud of an ascending axis of a plant while still in the
obligate parasite organism that in nature can survive only on or in embryo
living tissues podfruit of a peanut plant that contains from one to six seed
oblongtwice as long as wide and having somewhat truncate ends pollenmale sex cells produced by anthers of flowering plants
obovate, obovoidreversely egg-shaped, with the broader end upper pollinationtransfer of pollen from anther to stigma or from a
most staminate cone to an ovulate cone
obtuserounded or blunt; greater than a right angle potyvirusone of a group of related viruses
oidium spermatium formed on a hyphal branch; flat-ended, asexual predisposeto make prone to infection and disease
spore formed by the breaking up of a hypha into cells; a mildew primary inoculuminoculum that initiates disease
olivaceous olive or olive green in color primary rootroot that develops directly from the radicle of an
oogonium (pi. oogonia) one-celled female sex organ of some fungi embryo rather than from a crown or node
oospore thick-walled resting spore produced by the union of an primordial (n. primordia)first in order of appearance; pertaining to
oogonium and an antheridium the earliest stages o f development
ostiole (adj. ostiolate)pore; opening in the papilla or neck of a peri- prokaryotic (n. prokaryote)without internal membrane-bound or
thecium or pycnidium through which spores are released ganelles
ovaryenlarged basal portion of a pistil containing the ovules and promycelium (pi. promycelia)in rusts and smuts, a germ tube issu
developing into the fruit ing from the teliospore and bearing the basidiospores
ovate, ovoid oval; egg-shaped propaguleany part o f an organism capable of independent growth
overwinter to survive over the winter period pseudoparenchymafungal cells that resemble the parenchyma of
ovule enclosed structure that, after fertilization, becomes a seed higher plants
pseudothecium (pi. pseudothecia)peritheciumlike fruiting body
palisade tissue found beneath the upper epidermis of leaves com containing asci and ascospores
posed of elongate, tubular cells arranged upright in the manner, of pulvinatecushion-shaped
posts in a palisade fortification pustule small, blisterlike elevation of epidermis formed as spores
papilla (pi. papillae, adj. papillate) small, blunt projections emerge
paraphysis (pi. paraphyses) sterile, upward-growing, basally at pycnidiosporespore produced within a pycnidium
tached hypha present in some kinds of fungal fruiting structures pycnidium (pi. pycnidia)asexual, globose or flask-shaped fruiting
parasite organism that lives in or on another organism and obtains body produced by fungi
food from it pyramidalpyramid-shaped
parenchyma (adj. parenchymatous)thln;walTed'pTanrcells........... pyriformpear-shaped
pathogen (adj. pathogenic) agent that causes disease
pathogenicity ability to cause disease
quadrifoliatecompound leaf composed o f four leaflets
pedicel small stalk; stalk of an individual flower
quarantinelegislative control of the transport of plants or plant
pegyoung fruit during the stalklike phase of development that
parts to prevent spread of disease
comes after the unionof~gametes-and-before-the~enlargement-of-the
fruit
penetrationinitial invasion of a host by a pathogen race subgroup or biotype within a species or variety distinguished
perfect statethe sexual stage in the life cycle of a fungus from other races by behavior (virulence, symptom expression, or
pericarpripened and modified walls o f a plant ovary (fruit) host range) but not by morphology
perinealthe area between the anus and the posterior part of the radiate (adj.)spreading from or arranged around the center
external genitalia radiclepart of the embryo that develops into the primary root
perithedum (pi. perithecia)flask-shaped or subglobose. thin- raspingusing a roughened surface
walled fungal fruiting body (ascocarp) containing asci and asco reniformkidney-shaped
spores (spores are expelled or otherwise released through a pore, resistance (adj. resistant)property of a host that prevents or im
the ostiole, at the apex) pedes disease development
persistentpertaining to viruses that are infectious within insect reticulatehaving the form of a net
vectors for long periods rhizobium nodules galls on roots caused by Rhizobium spp.
pest any organism that injures plants or plant products rhizomorphvisible strand or cord of compacted mycelium, often
pesticide a chemical used to control pests dark colored
petiole stalk portion o f a leaf rhizospheremicroenvironment in soil immediately around plant
pHmeasure of acidity and alkalinity (pH 7 is neutral; below pH 7 is roots
acidic; above pH 7 is alkaline) rickettsialike organismpleomorphic or rod-shaped, nonfilterable
phaeosporoushaving dark, one-celled spores bacterium that causes disease (many are arthropod-borne; most
phanerogama seed plant or flowering plant have not been cultured in artificial media)
phialide (adj. phialidic) end cell of a conidiophore or a conidio RNAribonucleic acid
phore of fixed length with one or more open ends through which a rogueto remove and destroy by hand individual plants that are
basipetal succession of conidia develops diseased, infested by insects, or otherwise undesirable
phialospore conidium produced on a phialide rosette disease symptom characterized by short, bunchy growth
photosynthesismanufacture of carbohydrates from carbon dioxide habit resulting from shortened intemodes but no comparable reduc
and water in the presence of chlorophyll(s) during which light tion in leaf size
energy is used and oxygen is released rugosewrinkled
phototropismgrowth movement o f plants induced by light runner plantnew plant produced asexually on a runner or stolon
phragmospore spore having two or more transverse septa russetbrownish, roughened tissue resulting from cork formation

88
saprophyte (adj. saprophytic) organism that feeds on dead organic produces new plants; runner; in fungi, hypha that grows horizon
matter tally along the surface
scabroughened, crustlike diseased area on the surface of a plant stoma (pi. stomata) small pore bordered by guard cells found in the
organ epidermis of leaves, stems, and other plant parts and through which
sclerenchyma (adj. sclerenchymatous)thick tissue made up of exchange of gases occurs
thick-walled plant cells striated (n. striations)marked with delicate lines, grooves, or ridges
sclerotium (pi. sclerotia) hard, frequently rounded, usually darkly stroma (pi. stromata) compact mass of mycelium (with or without
pigmented resting body of a fungus composed of a mass of spe host tissue) that supports fruiting bodies or in which fruiting bodies
cialized hyphal cells (the structure may remain dormant for long are embedded
periods and then germinate to produce a stroma, fruiting body, stuntreduction in height of a vertical axis resulting from a pro
mycelium, or conidiophores when favorable conditions return) gressive reduction in the length of successive internodes or a
scorch any symptom, such as a lesion or system of lesions, that decrease in their number
suggests the action of flame or fire on the affected part, especially style slender part of many pistils located between the stigma and
on extending organs such as green leaves or petals the ovary and through which the pollen tube grows
secondary infectioninfection resulting from the spread of infec stylet stiff, slender, hollow feeding organ of plant-parasitic nema
tious material produced after a primary infection or from other todes
secondary infections without an intervening inactive period stylospore spore on a pedicel or hypha, especially a urediospore; an
secondary rootbranch from a primary root elongated pycnidiospore
sedimentation coefficientmeasure (expressed in Svedberg units subacute somewhat acute
[S] and proportional to molecular weight) of the velocity with subcarbonaceousalmost like charcoal or cinders
which a compound or structure is spun down during ultracentrifu subepidermal occurring beneath the epidermis
gation subflexuous almost flexuous
seedripened ovule consisting of an embryo and stored food en subglobosealmost globose
closed by a seed coat subhyaline somewhat or imperfectly clear
seedbome carried on or in a seed sublethal almost fatal or lethal
self-pollinationtransfer of pollen from the anthers to the stigma of submicroscopic smaller than can be seen with a compound micro
the same flower scope
senesce (adj. senescent, n. senescence)to decline, as with matura subspherical almost spherical
tion, age, or disease stress substrate substance on which organisms grow
sepal one of the modified leaves comprising a calyx symptomindication of disease by reaction of the host
septum (pi. septa, adj. septate) cross wall symptomless carrier a plant that, although infected with a patho
serology (adj. serologic) study, detection, and identification of anti gen (usually a virus), produces no obvious symptoms
gens, antibodies, and their reactions syn. synonym(s)
sessilelacking a petiole, as in some leaves, or a pedicel, as in some syndromepattern or sequence of disease development; a complex
flowers and fruits of symptoms
seta (pi. setae)bristle or bristle-shaped body, usually deep yellow synergism (adj. synergistic) concurrent parasitism of a host by two
or brown pathogens in which the symptoms or other effects are of greater
setuladelicate, hairlike appendage arising from the end of a magnitude than the sum of the effects of each pathogen acting alone
conidium synnemata a group of conidiophores cemented together and form
sexual spore spore produced as a result of meiosis ing an elongated, spore-bearing structure
shell tissue in which seed are enclosed systemicpertaining to chemicals or pathogens that spread through
sinuoushaving many curves, bends, or turns out a plant rather than remaining localized
soilborne carried on or beneath the soil surface
sorus (pi. sori) compact fruiting structure, especially spore masses taprootprimary root that grows vertically downward and ives off
in rust and smut fungi; occasionally a group of fruiting bodies smaller lateral roots
sound mature kernelsundamaged seed large enough to ride the taxonomy (adj. taxonomic) the science dealing with naming and
officially designated screen size for a specific market type of classifying organisms
peanut teleomorphperfect (sexual) state of a fungus
sowto plant seed teliosporethick-walled resting spore that germinates to form a
sp. (pi. spp.) species (a genus name followed by sp. means that the basidium
particular species is undetermined; spp. after a genus name means telium (pi. telia) sorus that produces teliospores
that several species are being-referred -to-without being-named testa (pi. testae) seed coat
individually) thermal inactivation pointlowest temperature at which heating for
spermagonium (pi. spermagonia)walled structure in which sper- a limited period (usually 10 min) is sufficient to cause a virus to
matia are produced lose its infectivity or an enzyme its activity
spermatium (pi. spermatia) a sex cell tissue group of cells, usually of similar structure, that perform the
sporadic appearing at irregular intervals same or related functions
sporangium (pi. sporangia) structure in lower fungi containing torulose cylindric but having swellings at intervals
asexually formed spores toxicity capacity of a substance to produce injury
spore one- to many-celled reproductive body in fungi and lower toxinpoison produced by a living organism
plants translocationtransfer or movement of foods and other products of
sporodochium (pi. sporodochia) superficial, cushion-shaped, metabolism
asexual fruiting body translucent so clear that light may pass through
sporulate to produce spores transpirationthe giving off of water vapor from living plants
stamen (adj. staminal)pollen-producing organ of a flower, usually truncate ending abruptly as though the end had been cut
consisting of a filament and an anther turgidplump or swollen as a result of internal water pressure
stellatepertaining to starlike extensions on spores
sterigma (pi. sterigmata) small, usually pointed protuberance or unicellular one-celled
projection that supports a spore uniloculatecontaining a single cavity
stigmaportion of a flower that receives pollen and on which the urediniosporebinucleate, repeating spore of rust fungi
pollen germinates urediniumfruiting body o f rust fungi that produces urediniospores
stipe stalk
stipule small, leaflike appendage at the base of a leaf petiole, variety (adj. varietal)group of closely related plants of common
usually occurring in pairs origin within a species that differ from other varieties in certain
stolon a long, slender, modified stem arising from the crown that minor details such as form, color, flower, and fruit

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vascularpertaining to fluid-conducting (xylem and phloem) tissues water-soakeddescribing a disease symptom of plants or lesions
vector agent that transmits inoculum that appear wet, dark, and usually sunken and translucent
vegetative asexual; somatic whorlcircular arrangement of like parts
veinbanding symptom of viral disease in which regions along veins wiltlack of freshness; drooping of leaves from lack of water (inade
are darker green than tissue between veins quate water supply or excessive transpiration); a vascular disease
veinclearing disappearance of green color in or around leaf veins that interrupts the normal uptake and distribution of water
vesicle (adj. vesicular)thin, bladderlike sac or structure in which
zoospores are differentiated or released; the bulbous head ter xerophyteplant adapted to a limited water supply
minating a conidiophore of Aspergillus', sporelike structure formed xylemwater-conducting tissue in plants
by mycorrhizal fungi
viable able to live; able to survive, as spores
yellows a plant disease characterized by yellowing and stunting of
viroplasm cellular inclusions that are sites of synthesis of viral
the host plant
components and the assembly of virus particles
virulence degree or measure of pathogenicity; relative capacity to
cause disease zonatemarked with zones; targetlike; appearing in concentric
virulentstrongly pathogenic rings
volatile evaporating rapidly zoosporemotile spore
volunteer self-set plant; plant seeded by chance zygosporeresting spore formed from the union of like gametangia

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 Index
Adoretus spp., 68 Aspergillus crown rot, 7-8,78; Pis. 2-4 Caulorhizae, 3
Aeschynomene americana, 48 Aspergillus Centrosema
Aflatoxin, 40-42, 67; Pis. 74-76 flavus, 40-42, 67; Pis. 74-76 macrocarpum, 56
cultivars with resistance to, 82, 83 cultivars with resistance to, 82, 83 pubescens, 56
management practices for, 78 fumigatus, 37 Ceratobasidium sp., 31
Ageratum conyzoides, 44 niger, 7-8; Pis. 2-4 Cercospora arachidicola, 17-20, 25, 26, 31;
Agrobacterium sp., 72 nomius, 41 Pis. 24-26
Alectra parasiticus, 40-42, 83; PL 76 biological control of, 74
picta, 70 pulverulentus, 8 genetic resistance to, 79, 81
vogetii, 70; Pis. 188, 189 Athelia rolfsii, 36 Cercospora leaf spot, 17
Alternaria Aureobacterium sp., 74 Cercosporidium personatum, i7-20, 25, 26,
altemata, 7 31; Pis. 24-26
arachidis, 7 Bacillus, 74 biological control of, 74, 75; Pl. 198
Alternaria leaf spot, 7; Pi. 1 cereus, 74 genetic resistance to, 81, 83
Amsacta subtilis, 73-74 Chaetomium sp., 37
albistriga, 66; Pis. 159, 160 thuringiensis, 74 Chalara elegans, 8-10, 83; Pl. 5
moorei, 66 Bacteria, 4, 5 Charcoal rot, 11-12, 78; Pis. 12-14
Anomala spp., 68 Bacterial leaf spot, 43; PI. 78 Chenopodium
Anthracnose, 7 Bacterial wilt, 43-45; Pis. 79-83 amaranticolor, 57
Anticarsia gemmatalis, 66; PI. 157 cultivars with resistance to, 82 quinoa, 57
Aphasmatylenchus structuratus, 53 management practices for, 78 Chlorophyll deficiency, 60; Pis. 123, 124
Aphelenchoides arachidis, 52-53 Bean golden yellow mosaic virus, 58 Chlorotic rosette, 55; Pis. 105, 106
Aphids Bean yellow mosaic virus, 58 Choanephora sp., 12
feeding damage caused by, 67; Pis. 166, Belonolaimus Choanephora leaf spot, 12
167 gracilis, 50 Clavibacter sp., 74
and transmission of viruses, 55, 56, 57 longicaudatus, 5, 50; Pis. 95, 96 CMV. See Cucumber mosaic virus
Aphis Bemisia Colletotrichum, 26
craccivora, 55, 56, 57, 58, 67 argentifolii, 67 arachidis, 1
gossypii, 56 tabaci, 57, 58, 67; Pi. 169 dematium, 7
spiraecola, 57 Black hull, 8-10; PI. 5 mangenoti, 1
Aproaerema modicella,65, 66; PI. 158 cultivars with resistance to, 83 Conoderus, Pl. 180
Arachis, 2-3, 79-80 management practices for, 78 amplicollis, 68
cardenasii, 79, 81 Black pod, 23 scissus, 68
chacoense, 3 bollworm, 65; PI. 155 Copper deficiency, 63; Pis. 146, 147
chacoensis, 3 Boron deficiency and toxicity, 63; Corcyra cephalonica, 68-69; Pis. 182, 183
diogoi, 3, 81 PI. 148 Cotton root rot, 27
duranensis, 3 Botryodiplodia theobromae, 16 Cowpea chlorotic mottle virus, 58
glabrata, 2, 47 Botryotiniafuckeliana, 10 Cowpea mild mottle virus (CPMMV), 57, 58;
hypogaea, 1, 2,79, 80 Botrytis blight, 10-11; Pis. 6-11 Pl. 114
subsp. fastigiata, 79, 80 cultivars with resistance to, 83 CPMMV. See Cowpea mild mottle virus
var. aequatoriana, 3 management practices for, 78 Crassocephalum crepidioides, 44
var. fastigiata, 2, 3, 8 Botrytis cinerea, 1011, 83; Pis. 6-11 Criconemella ornata, 15, 50-52
var. peruviana, 3 Bradyrhizobium, 71, 72, 74 Criconemoides omatus, 51
var. vulgaris, 3 elkanii, 73 Cristulariella
subsp. hypogaea, 79, 80 japonicum, 73 moricola, 42
var. hirsuta, 2, 3 Brown leaf spot, 17 pyramidalis, 42; PL 77
var. hypogaea, 2, 3, 79, 80 Bud necrosis, 53 Crotalaria
pintoi, 2 Burkholderia solanacearum, 43 juncea, 44
pusilla, 3 Butyrospermum parkii, 53 striata, 56
repens, 2 Croton hirtus, 44
spegazzinii, 3 Calcium Cucumber mosaic virus (CMV), 57-58; Pl. 115
stenosperma, 2, 79, 81 deficiency, 62; PI. 139 Cultivars, with disease and insect resistance,
villosulicarpa, 2 and the peanut pod rot complex, 24 81-84
Armyworms, feeding damage caused by, 65; Caloglyphus spp., 24 Curtobacterium sp., 74
Pis. 150-154 Calonectria Cuscuta campestris, 70, 71; Pl. 192
Arthrobotrys spp., 52 crotalariae, 13 Cylindrocladium
Ascochyta ilicicola, 13,14; PL 17 crotalariae, 13
adzamethica, 39 Calopogonium caeruleum, 56 parasiticum, 12-15; Pis. 15-17
arachidis, 39 Caryedon serratus, 69; PL 186 cultivars with resistance to, 79, 81, 82
Ascochyta leaf spot, 39 Cassia fasciculata, 48 management practices for, 78

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Cylindrocladium black rot, 12-15; and seedling damping-off, 20 Leucopholis spp., 68
Pis. 15-17 f. sp. phaseoli, 21 Lightning injury, 62; PL 137
cultivars with resistance to, 79, 81, 82 tricinctum, 21
management practices for, 78 Macrophoma phaseolina, 11
and ring nematodes, 51 Genetic disorders, 60; Pis. 123, 124 Macrophomina phaseolina, 11-12, 53;
Genetic modification, for disease Pis. 12-14
Dagger nematodes, 53 management, 79-81 Macroposthonia ornata, 51
Damping-off Gigaspora spp., 71-72; Pis. 193, 194 Magnesium deficiency, 62
caused by Aspergillus niger, 8 Gliocladium, 35 Malbranchea pulchella var. sulfurea, 37
caused by Fusarium spp., 20, 21 roseum, PI. 8 Manganese deficiency and toxicity, 63;
caused by Pythium spp., 27, 29 Glomus spp., 71-72 Pl. 142
caused by Rhizoctonia solani, 30 Glycine max, 58 Melanosis, 22
Datura stramonium, 58 Gram pod borer, 65; PI. 156 Meloidogyne, 82
Delimited shell spot, 15-16; Pis. 18, 19 GRAV, 55, 58 arenaria, 45-48; Pis. 84, 85, 87-93
Desmodium siliquosum, 56 Green rosette, 55 cultivars with resistance to, 83
Diabrotica undecimpunctata howardi, 68; Groundnut bruchid, 69; Pi. 186 genetic resistance to, 79
Pis. 174, 175 Groundnut chlorotic spotting virus, 58 and the peanut pod rot complex, 24, 29
and the peanut pod rot complex, 24 Groundnut crinkle virus, 57, 58, 59 hapla, 15, 45-48, 83; Pl. 86
Dicyma pulvinata, 75; PI. 198 Groundnut eyespot virus, 58, 59 incognita, 46
Didymella arachidicola, 39 Groundnut leafminer, 65, 66, 82; PI. 158 javanica, 46
Didymosphaeria arachidicola, 39 Groundnut rosette assistor virus (GRAV), 55, Methylobacterium sp., 74
Diplodia collar rot, 16-17; Pis. 20-23 58 Microtermes spp., 68
cultivars with resistance to, 82, 83 Groundnut rosette virus (GRV), 55, 58; Millipedes, 68
management practices for, 78 Pis. 105-107 Mites, 20
Diplodia gossypina, 16-17, 83; Pis. 20-23 genetic resistance to, 79, 83 and delimited shell spot, 16
Disease management management practices for, 78 and the peanut pod rot complex, 24, 29
disease- and insect-resistant cultivars for, Groundnut streak virus, 59 Molybdenum deficiency, 63
81-84 Groundnut streak mosaic virus, 59; PI. 116 Monacrosporium spp., 52
and genetic modification, 79-81 Groundnut veinal chlorosis virus, 58 Mosaic rosette, 55; Pl. 107
strategies of, 76-78 Groundnut yellow mosaic virus, 58 Mucorpusillus, 37
Ditylenchus Groundnut yellow mottle virus, 58 Mucuna deeringiana, 48
africanus, 52,83; Pis. 97,98 GRV. See Groundnut rosette virus Muddy spot, 39
destructor, 52 Gypsum, and the peanut pod rot complex, Mycoplasmalike organism. See
Drought stress, 60; Pis. 119, 120 24, 29 Phytoplasmas
and aflatoxin contamination, 40, 41 Mycorrhizae, 71-72; Pis. 193, 194
and Aspergillus crown rot, 8 Hail injury, 60; PI. 125 Mycosphaerella
and the lesser cornstalk borer, 67 Hairy caterpillars, 66; Pis. 159, 160 arachidicola, 39
Hansfordia pulvinata, 75 arachidis, 17
Early leafspot, 17-20, 31, 79; Pis. 24-26 Helicoverpa zea, 65-66; PL 155 argentinensis, 39
cultivars with resistance to, 81, 82 Heliothis berkeleyi, 18
management practices for, 78 armigera, 65; PI. 156 Mycosphaerella leaf spot, 17
Earworm, 65; PI. 155 virescens, 65 Myrothecium
Elasmolomus sordidus, 69; PI. 187 Herbicide injury, 60-62; Pis. 126-136 gramineum, 23
Elasmopalpus lignosellus, 36, 67-68; compared with leaf spot symptoms, 17 roridum, 23; PL 29
Pis. 170-173 Heteranthae, 3 Myrothecium leaf blight, 23; PL 29
and aflatoxin contamination, 41 Hollow heart, 63 Myzus persicae, 56, 57, 58
Empoasca Hopper-bumr 66t-Pl l63
dolichi, bb Humicola lanuginosa, 37 Necrotic etch, 60
fabae, 66; PI. 161 Hydnum omnivorum, 27 Nematodes, 5, 6, 45-53; Pis. 84-98
facialis, 66 Hyperomyzus lactucae, 56 and the peanut pod rot complex, 24
kerri, 66; PI. 162 Nemophila spp., 9
Entrophospora spp., 71 Indian peanut clump virus (IPCV), 54-55, Neocosmospora, 13
Epiphytes, use of for biological control of 58, 78; Pl. 103 vasinfecta, 23
disease, 74-75; PI. 197 Indianmeal moth, 68; Pl. 181 Neocosmospora foot rot, 23
Erectoides, 3 Indigophora hirsuta, 48 Net blotch, 39
Eulepida spp., 68 Insects, feeding damage caused by, 65-69; Nicotiana spp., 58
Extranervosae, 3 Pis. 150-187 Nitrogen deficiency, 62; Pl. 138
IPCV. See Indian peanut clump virus Nitrogen fixation, 72-73; Pis. 195, 196
Flour beetles, 69; Pis. 184, 185 Iron deficiency, 63; Pl. 141 Nutrient imbalances, 24, 62-63;
Frankliniella Pis. 138-148
fusca, 54, 66; PI. 164 Lachnosterna serrata, 68; Pis. 176, 177
occidentalis, 54 Lasiodiplodia theobromae, 16 Odontotermes spp., 68
Frost injury, 60; Pis. 121, 122 Late leafspot, 17-20, 31; Pis. 24-26 Oidium arachidis, 27
Fungi, 4, 5 cultivars with resistance to, 79, 81, 82 Old world bollworm, 65; Pl. 156
Fungicides, 77 management practices for, 78 Olpidium brassicae, 23
Fusarium, 5, 53; PI. 27 Leaf scorch, 2425, 78; Pl. 32 Olpidium root discoloration, 23
avenaceum, 21 Leafhoppers Ozone damage, 63-64; Pl. 149
equiseti, 21 cultivars with resistance to, 82, 83 Ozonium root rot, 27
moniliforme, 21 feeding damage caused by, 66;
oxysporum, 20, 21 Pis. 161-163 Paspalum notatum, 48
scirpi, 21 Leptosphaerulina crassiasca, 5, 24-25; Passion fruit woodiness virus, 58
solani, PI. 28 Pis. 31, 32 Pasteuria penetrans, 48
and the peanut pod rot complex, Lesser cornstalk borer, 36, 67-68; PBNV. See Peanut bud necrosis virus
23-24, 27, 29; PL 30 Pis. 170-173 PC1SV. See Peanut chlorotic streak virus
and root rot, 20-21 and aflatoxin contamination, 41 PCV. See Peanut clump virus

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Peanut bud necrosis virus (PBNV), 53-54, Pseudomonas, 43; Pl. 78 Sclerotium
58, 78; Pl. 100 cepacia, 74 bataticola, 11
Peanut cercosporosis, 17 solanacearum, 5, 43-45; Pis. 79-83 cinnamomi, 42
Peanut chlorotic streak virus (PC1SV), 58 PStV. See Peanut stripe virus rolfsii, 20, 36-37, 53; Pis. 60-65
Peanut clump virus (PCV), 54-55, 58; PSV. See Peanut stunt virus cultivars with resistance to, 81, 82
Pl. 104 Puccinia arachidis, 20, 31-33, 62, and root-knot nematode damage, 46, 48
genetic resistance to, 79 Pis. 48, 49 Sclerotium rot, 36
management practices for, 78 biological control of, 74 Scutellonema cavenessi, 53
Peanut green mosaic virus, 58, 59 cultivars with resistance to, 81, 82 Scutellospora spp., 71
Peanut mottle virus (PeMoV), 56, 58; Pueraria phaseoloides, 56 Sesamum indicum, A8
Pis. 108, 109 Pythium, 5, 21, 78 Sistotrema brinkmannii, 27
genetic resistance to, 79 aphanidermatum, 28 Sore shin, 30; Pl. 39
management practices for, 78 debaryanum, 28 Southern blight, 36, 78
Peanut pod nematode, 52, 83; Pis. 97, 98 irregulare, 28 Southern com rootworm, 68; Pis. 174, 175
Peanut pod rot complex, 21, 23-24; Pl. 30 myriotylum, 27-30; Pis. 37, 38 cultivars with resistance to, 82, 83
cultivars with resistance to, 82 and the peanut pod rot complex, 23-24, and the peanut pod rot complex, 24, 29
management practices for, 78 30; Pl. 30 Southern stem rot, 36
Peanut ringspot, 79 ultimum, 28 Sphaceloma arachidis, 33-34; Pis. 50, 51
Peanut stripe virus (PStV), 56, 58; Spinacea oleracea, 58
Pis. 110-112 Ralstonia solanacearum, 43 Spodoptera, 82
genetic resistance to, 79 Rathayibacter sp., 74 exigua, 65; Pis. 151,152
management practices for, 78 Rednecked peanutworm, 65 frugiperda, 65; Pl. 150
Peanut stunt virus (PSV), 57, 58; Rhizobium, 72-73; Pis. 195, 196 littoralis, 65
Pl. 113 fredii, 73 litura, 65; Pl. 153, 154
genetic resistance to, 79 gale age, 73 Sporotrichum sp., 37
management practices for, 78 leguminosarum, 73 Springtails, 29
Peanut yellow mosaic, 57 loti, 73 Stegasta bosqueella, 65
Peanut yellow mottle, 59 meliloti, 73 Stem rot, 36-37; Pis. 60-65
Peanut yellow spot virus, 58, 59, 78; Pl. 117 phaseoli, 73 cultivars with resistance to, 81, 82
Peanut yellows, 51 trifolii, 73 management practices for, 78
PeMoV. See Peanut mottle virus tropici, 73 and root-knot nematode damage, 46, 48
Penicillium, 35, 52; Pl. 98 Rhizobium nodules Stemphylium botryosum, 22
islandicum, 74 affected by nematodes, 53 Stemphylium leaf spot, 22
Penicillium seed rot, 78 compared with nematode galls, 45 Sting nematodes, 50, 78; Pis. 95, 96
Pepper spot, 2425, 78; Pl. 31 Rhizoctonia, 78 Striga
Peridontopyge spp., 68 bataticola, 11 gesnarioides, 70-71; Pl. 191
Pestalotiopsis solani, 5, 53, 30-31, Pis. 39-47 hermontheca, 70-71; Pl. 190
arachidis, 26 biological control of, 74 Sulfur deficiency, 62; Pl. 140
neglecta, 26 and the peanut pod rot complex, 23-24, Sunflower yellow blotch virus, 58
Pestalotiopsis leaf spot, 26 82; Pl. 30
Petunia x hybrida, 58 Rhizoctonia limb rot, 30, 31, 82; Talaromyces (Penicillium) dupontii, 37
Phaeoisariopsis personata, 18 Pis. 42, 44 Termites, 68; Pis. 178, 179
Phanerochaete Rhizoglyphus sp., 16 and aflatoxin contamination, 41
chrysorhiza, 26 Rhizomatosae, 3 Testa nematode, 52-53
omnivora, 26 Rhizopus seed rot, 78 Tetranychus urticae, feeding damage caused
Phaseolus vulgaris, 56 Rhopalo'siphum by, 66, 67; Pl. 168
Phoma arachidicola, 39-40, 83; Pis. 71-73 maidis, 56 Thanatephorus cucumeris, 30
Phoma leaf spot, 39 padi, 56 Thermoascus aurantiacus, 37
Phomopsis blight, 26 Rice moth, 68-69; Pis. 182, 183 Thermomyces lanuginosus, 37
Phomopsis sojae, 26 Ricinus communis, 48 Thermophilic fungi, 37
Phosphorus deficiency, 62 Ring nematode, 50-52, 78 Thielavia
Phyllosticta' Root-knot nematodes, 45-48; albomyces, 31
arachidis-hypogaea, 26; Pl. 34 Pis. 84-93 basicola, 9
sojaecola, 26 cultivars with resistance to, 82, 83 Thielaviopsis basicola, 9
Phyllosticta leaf spot, 26; Pis. 33, 34 management practices for, 78 Thrips
Phymatotrichopsis omnivora, 27 and the peanut pod rot complex, 24, 29 cultivars with resistance to, 82, 83
Phymatotrichum omnivorum, 27; Pis. 35, 36 and Verticillium wilt, 38 feeding damage caused by, 66-67;
Phymatotrichum root rot, 27, 78; Pis. 35, 36 Root-lesion nematodes, 48-50, 78; Pis. 164, 165
Phytoplasmas, 5, 6, 59; Pl. 118 Pl. 94 and transmission of TSWV and PBNV, 54
Pigweed, infected with Rhizoctonia solani, Rugose leaf curl, 59 Thrips palmi, 54, 66, 82
Pl. 47 Rust, 31-33, 62; Pis. 48,49 Tikka leaf spot, 17
Pisum spp., 9 cultivars with resistance to, 81, 82 Tobacco budworm, 65
Plodia interpunctella, 68; Pl. 181 fungicides effective on, 77 Tobacco streak vims, 58
PLRV, 55 genetic resistance to, 79 Tomato fruitworm, 65; Pl. 155
Pod breakdown, 23, 27 management practices for, 78 Tomato spotted wilt vims (TSWV), 53-54,
Pod-sucking bug, 69; Pl. 187 58; Pis. 99, 101, 102
Polymyxa graminis, 55 Scab, 33-34, 78; Pis. 50,51 cultivars with resistance to, 82, 83
Potassium deficiency, 62 Schizonycha spp., 68 genetic resistance to, 79
Potato leafroll virus (PLRV), 55 Scirtothrips dorsalis, 66 management practices for, 78
Potato nematodes, 78 Sclerocystsi spp., 71 Torula basicola, 9
Powdery mildew, 27 Sclerotinia blight, 3436; Pis. 52-59 Tribolium
Pratylenchus cultivars with resistance to, 81, 82, 83 castaneum, 69; Pis. 184, 185
brachyurus, 48-50 management practices for, 78 confusum, 69
coffeae, 48-50 Sclerotinia minor, 3436, 81, 83; Trichoderma, 35, 36; Pl. 59
Procumbensae, 3 Pis. 52-59 harzianum, 37

93
 dahliae, 37-39; Pis. 67, 68, 70 Whiteflies
Trierectoides, 3
lecanii, 74 feeding damage caused by, 67; Pl. 169
Triseminalae, 3
Verticillium wilt, 37-39, 78; Pis. 66-70 and transmission of CPMMV, 57
TSWV. See Tomato spotted wilt virus
Vigna radiata, 58 Wireworms, 68, Pl. 180
Twospotted spider mite, 20
Viruses, 6, 53-58, 83; Pis. 99-117 Witches-broom, 59; Pl. 118
feeding damage caused by, 66, 67; Pl. 168
Tylenchorhynchus
Web blotch, 39-40, 79; Pis. 71-73 Xiphinema spp., 53
brevilineatus, 53
indicus, 53 cultivars with resistance to, 82, 83
fungicides effective on, 77 Yellow mold, 40-42; Pis. 74-76
Velvetbean caterpillar, 66; Pl. 157 management practices for, 78
White grubs, 68; Pis. 176, 177 Zinc deficiency and toxicity, 63; Pis. 143-145
Verticillium
White mold, 36, 78 Zonate leaf spot, 42; Pl. 77
albo-atrum, 37-39

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