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CORN

DISEASES

IN THE UNITED STATES

AND THEIR CONTROL

AGRICULTURAL RESEARCH

SERVICE • UNITED STATES

DEPARTMENT OF AGRICULTURE

IN COOPERATION WITH

PURDUE UNIVERSITY

AGRICULTURAL

EXPERIMENT STATION

I

-U.S. DEi-t. Of rf^RKUW

NÛV3. 41961

m.rter

AGRICUtTURE HANDBOOK NO. 199
CONTENTS

Page

Factors affecting the development of corn diseases i

Environment 2

Resistance of host 2

Causal organisms 2

Control of corn diseases 2

Seed rot and seedling blight 3

Stalk rots and root rots ,. 5

Diplodia stalk rot 6

Gibberella stalk rot 7

Charcoal rot 7

Pythium stalk rot 8

Other stalk rots .., 8

Pythium root rot 9

Ear rots 9

Diplodia ear rot 9

Fusarium kernel rot 10

Cob rot 10

Gibberella ear rot 11

Gray ear rot 11

Other ear rots 12

Storage rots and kernel disorders 12

Leaf diseases 14

Northern corn leaf blight , 15

Southern corn leaf blight 16

Helminthosporium leaf spot 17

Bacterial wilt 18

Minor leaf diseases 19

Bacterial leaf blight and stalk rot 20

Bacterial stripe 21

Zonate leaf spot 21

Purple sheath spot 22

Holcus spot 22

Cercospora leaf spot - 22

Anthracnose 22

Brown spot 22

Corn rusts 23

Common corn rust 23

Southern corn rust 24

Tropical corn rust 25

Downy mildews 25

Crazy top 25

Downy mildew 26

Virus diseases 27

Corn stunt 27

Sugarcane mosaic 27

Celery stripe 27

Leaf fleck 27

Corn smuts 28

Common smut 28

Head smut 29

Washington, P.C. Issued September 1961

For sale by the Superintendent of Documents, U.S. Government Printing OfBce

Washington 2.5, D.C. — Price 30 cents
CORN DISEASES

IN THE UNITED STATES AND THEIR CONTROL

By A. J. ULLSTRUP, plant pathologist,

Crops Research Division, Agricultural Research Service

The corn {Zea mays L.) crop

of the United States is subject to

a number of diseases that reduce

both yield and quality. Yearly

losses range from about 2 to 7 percent, but in some localized areas

one or more diseases may become

acute and destroy a considerably

higher proportion of the crop.

Ear and kernel rots decrease yield,

quality, and feeding value of the

grain. Stalk diseases may not only

lower yield and quality but also

make harvesting difficult. When

leaves are damaged by diseases,

the production of carbohydrates

to be stored in the grain is lessened, and immature, chaffy ears

result.

The diseases of com may be

classified as parasitic and nonparasitic. Most of the parasitic or

infectious diseases of com are

caused by fungi, a few by bacteria, and a few by viruses. Fortunately no known virus diseases

of corn have been found in the

Corn Belt of the United States.

Some parasitic diseases are caused

by nematodes. These very small,

slender, wormlike animals live in

the soil and may feed on the roots

of corn. They have not become

serious in the main corn-growing

areas of this country, but they are

prevalent in the Southern States.

Nonparasitic diseases result

from unfavorable climatic and soil

conditions. Deficiencies in the soil

of nitrogen, phosphorus, or potassium cause some of the most

frequently observed nonparasitic

diseases of corn. Occasionally

corn may suffer from the lack of

essential minor elements in the

soil.

In contrast to some of the diseases in certain other crops, the

diseases of corn seldom become

severe over very wide areas. The

production of corn in any given

locality of the United States has

not been limited by disease where

soil and weather conditions have

been favorable for the crop, nor

has it been necessary to stop

growing the crop over a wide

area because of disease.

In this handbook only the parasitic diseases caused by fungi, bacteria, and viruses will be treated

in detail.

FACTORS AFFECTING THE DEVELOPMENT OF

CORN DISEASES

Diseases of corn, like those of

other crops, vary in severity from

year to year and from one locality

or field to another depending on

the environment, the resistance of

the host, and the causal organism.

All three factors must be present

for the development of a disease.

For example, if the environment

is favorable for a disease and the

causal organism is present, but

the host is highly resistant, little

or no disease will develop. Similarly, if the causal organism is

present and the host is susceptible,

but the environment is unfavorable, the disease may not appear.
Environment

Many corn diseases develop best

when there is plenty of moisture

during the growing season. Either

rain or heavy dew is necessary

for spores of disease-producing

fungi to germinate and to penetrate the plant. Some diseases of

com such as seed rot and seedling

blight thrive when the soil temperature is low for an extended

period following planting. Bacterial wilt, or Stewart's disease, is

favored by mild winter temperatures. Under such conditions the

corn flea beetles (Chaetocnema

pulicaria Melsh.), which carry

the disease-producing bacteria

through the winter and spread the

disease from plant to plant, survive in large numbers. Crazy top

of corn becomes prevalent only

when the soil is waterlogged for

several days during the very

young seedling stage. The temperature and moisture of both soil

and air may thus determine the

development of corn diseases.

Soil fertility may affect the

severity of some infectious diseases of corn, particularly certain

stalk rots. Maintaining soils at

highly productive levels by judicious use of proper fertilizers

tends to produce vigorous plants

that do not die prematurely. However, some diseases seem not to be

affected to any great extent by

soil fertility, and a general statement cannot be made that a fertile

soil means healthy corn plants.

Resistance of Host

Great difl^erences exist among

inbred lines and hybrids as to

their relative resistance to various

diseases. Their inherent resistance or susceptibility may often

determine whether an epidemic of

a given disease will occur. Resistance to most corn diseases is

determined by several genes. In

only three diseases of corn is

resistance inherited as a monogenic dominant. It is the genetic

resistance of the host that can be

manipulated by the corn breeder

and through which he can modify

inbred lines and their hybrid combinations so as to produce high

levels of disease resistance.

Causal Organisms

No disease epidemic will occur

if the specific causal organism—a

fungus, bacterium, or virus — is

absent, even though the environment is favorable and the host

susceptible. The causal organisms

are as variable in their virulence

as the hosts they attack are in

their relative resistance. There

are, for example, several physiologic races of Puccinia sorghi

Schw., the fungus causing common corn rust. These vary only

in their virulence on different inbred lines of corn. However, in

the United States the problem of

physiologic races within the species of fungi and of bacteria causing diseases in corn has not been

a deterrent to breeding for disease resistance.

CONTROL OF CORN DISEASES

Two ways to control corn diseases are the use of disease-resistant hybrids and the application

of fungicides to the seed. Other

practices such as spraying plants

with fungicides, adjustment of

soil fertility by intelligent use of

fertilizers, and maintenance of

good drainage tend to reduce

losses from certain diseases, but

these have limited application.

The incorporation of genetic

resistance into agronomically

desirable hybrids by breeding

methods seems to be the most

efficient and permanent means of
Controlling corn diseases. None of

the hybrids in use are highly

resistant to all diseases and some

are extremely susceptible. Much

remains to be done in developing

disease-resistant hybrids by the

plant breeder and plant pathologist. It may be difficult to obtain

high resistance to all diseases, but

on the basis of past accomplishments it appears to be entirely

possible to develop adapted, highyielding corn hybrids that are

resistant to the major diseases in

a given area. The resistance of

a hybrid to a disease is generally

proportional to the number of

resistant inbred lines in its pedigree. Thus a hybrid comprised of

four resistant inbred lines is likely

to be more resistant than one

possessing only a single resistant

inbred line in its pedigree.

Where a disease is of sufficient

economic importance to warrant

control, local State agricultural

experiment stations should be

consulted for recommendations on

the use of resistant hybrids for

the particular area.

The treatment of seed corn

with a fungicide, either in a dust

or a slurry, may control seed rots

and seedling diseases but no other

diseases. Since 1935 considerable

advancement has been made in

improving seed corn treatments,

and good fungicides are on the

market that are specifically prepared for this purpose. These

should be used according to the

recommendations of the manufacturer.

Spraying corn plants with

fungicides to control leaf diseases

is successful in southern Florida.

This practice is economically feasible there because it is confined

to market-garden sweet corn,

which is a high value crop. In

many seasons leaf blights are so

severe in southern Florida that

unsprayed sweet corn fails to

yield marketable ears.

Crop rotation and destruction

of diseased plant parts have been

suggested as control measures for

certain plant diseases. Such practices are most effective where the

crop is grown in a limited area

or if the specific disease-producing

agent is strictly soilborne. In the

Corn Belt of the United States or

other areas where corn is extensively grown, it is unlikely that

destroying diseased plant parts

can be sufficiently thorough to be

effective in eliminating diseases.

With few minor exceptions rotation of crops has little effect on

reducing diseases of corn. In

river-bottom fields where, by

necessity, corn is often grown successively over several years, some

diseases appear to be no more

prevalent than where rotation is

practiced. Rotation is probably

more beneficial to corn in improving tilth and conserving fertility

than in reducing diseases.

Maintaining well-balanced fertility of the soil can help to lessen

the effects of some corn diseases.

Certain stalk rots are more severe

when corn is planted where potassium is deficient and nitrogen is

in excess. The effect of soil fertility on corn diseases depends

not only on the specific disease

but also on the particular mineral

deficiencies in the soil. Much is

to be learned about the relationship of soil nutrients to the diseases of corn. Since yield is a

primary factor in corn production,

every effort should be made to

build up and maintain soils at

maximum fertility levels.

SEED ROT AND SEEDLING BLIGHT

The period during which seed comes establised is very critical

germinates and the seedling be- in the life cycle of the corn plant.
Severe infection may kill the

embryo before germination.

Where infection takes place after

germination, seedlings may be

destroyed before or after emergence (pi. 1, A). Seedlings that

survive attack are usually retarded in vigor and develop into

less productive plants than plants

from healthy seedlings.

The prevalence of seedling

blight varies considerably depending, in part, on the weather conditions following planting. Seedling

diseases are more prevalent in

cold, wet soil than in warm soil.

Under the latter condition germination is rapid, and the seedling soon becomes established and

escapes infection by soil-inhabiting, pathogenic fungi. In cold,

wet soils germination is retarded

and the disease-producing fungi

can invade the embryo or young

seedling. A soil temperature of

about 50° F. is favorable for seedling blight, because at this temperature germination is very slow

and the soilborne pathogens can

grow and invade seed and seedlings.

In addition to the effect of cold,

wet soil, other factors such as

age of the seed, degree of finish

or maturity, mechanical damage,

and genetic resistance to invasion

by disease-producing fungi affect

the severity of seed rot and seedling blight. Seed stored for 2 or

more years often becomes increasingly susceptible to seed and

seedling diseases when planted

under unfavorable conditions. Dry

seed of 12-percent moisture or

less stored at about 35° F. at a

low humidity will generally germinate and grow in cold soil.

Immature or poorly finished seed

is almost invariably susceptible to

seedling blight. Mechanical damage to the seedcoat, such as breaks

or cracks that occur during harvesting or processing, affords avenues by which soilborne fungi can

invade the seed. Inbred lines and

their hybrid combinations differ

in their resistance to seed rot and

seedling blight. In general, sweet

corn is much more susceptible to

seedling diseases than is dent com,

and popcorn is most resistant.

This susceptibility may be due to

genetic factors, thinner seedcoat,

and ready availability of the

sugary endosperm as nutrition for

the pathogenic fungi.

With the introduction of hybrid

corn there has been less seed rot

and seedling disease than when

open-pollinated com was used because of better culling of seed

ears, rapid artificial drying, selection for resistance, and use of

effective seed-treating materials.

Symptoms.—The symptoms of

seed rot and seedling blight range

from complete killing of the embryo before seed germination in

severe infection to small discolored lesions on the roots and lower

part of the sprout in mild infection (pi. 1, B). Although several

fungi may parasitize the seed and

seedling, the symptoms are generally similar. Lesions on the

mesocotyl are often brown and

sunken. Invasion of roots by

pathogenic fungi is indicated by

discolored, water-soaked, flaccid

lesions. Aboveground symptoms

appear as wilting and dying of

the seedling leaves.

Causal Organisms.—A number

of fungi can cause seed rot and

seedling blight of corn. The niost

important of these are Pythium

irreguläre Buis., P. debaryanwm

Hesse, P. paroecandrum Drechs.,

P. ultimum Trow, P. splendens

Braun, P. vexans DBy., and ?

rostratum Butl. The members of

this genus are strictly soilborne.

Their distribution is determined

by the soil type and cropping history. Muck soils frequently have

a large population of one or more
species of Pythium that are pathogenic on com. In general, the

species attacking seed and seedhngs are able to thrive at temperatures somewhat lower than

those favoring rapid germination

of corn.

In addition to the several species

of Pythium, any one of the ear

rot fungi may also infect seed and

seedlings. These fungi are most

often seedborne and already established in the seed at harvest. One

of the most important economically is Diplodia viaydis (Berk.)

Sacc, which when in the seed

often destroys the embryo before

germination. Gibberella zeae

(Schw.) Fetch is found in the

cooler areas where corn is grown

and can cause severe seed rot and

seedling blight in cold soil. Pénicillium oxalicum Currie & Thorn

can cause seedling blight even in

warm soil. This fungus attacks

the mesocotyl near the seed and

secretes oxalic acid, which kills

cells in advance of the fungus.

Seedlings infected with P. oxalicum often show wilted and necrotic streaks on their leaves,

presumably due to toxic effects

of oxalic acid translocated from

the point of infection.

A few less virulent fungi sometimes associated with diseased

seedlings are Rhizoctonia zeae

Voorhees in the Gulf States, Rbataticola (Taub.) Butl., Nigrosporaoryzae (Berk. &Br.) Fetch,

and Aspergillu^ spp. Fu^arium

moniliforme Sheld. is often isolated from blighted seedlings, but

most of the work done with it

suggests that it is largely a secondary invader following a more

vigorous parasite. Several other

fungi have been found in diseased

corn seedlings, but their virulence

has never been proved.

Control.—The use of fungicides

for seed treatment is necessary to

control seedling diseases. Good

seed-treating materials are available and protect the seed from

invasion by soilborne pathogens

during the critical early stages

of germination. However, these

materials have little if any effect

on seedborne pathogens already

established within the seed prior

to planting. With the advent of

hybrid corn, the application of a

seed-treating material by the seed

producer has become almost universal.

Another way to reduce the predisposition of seed com to attack

by pathogens after planting is to

adjust harvesting and processing

machinery so that there is minimum physical injury to the seedcoat. The use of resistant hybrids

is still another means of avoiding

seedling diseases and insuring

good stands of com. Delay in

planting until the soil has become

warm and until the danger of

extended periods of cold weather

has passed minimizes the hazard

of poor stands due to seedling

blight.

STALK ROTS AND ROOT ROTS

Stalk rots and root rots of corn

are widespread in most areas

where the crop is grown. In seasons when these diseases are

severe, plants may die 2 to 3

weeks before becoming fully mature. As a result, the ears are

light weight and poorly finished.

However, more frequently the

greatest damage is caused by stalk

breakage and root lodging, which

make harvesting difficult, and

many ears are lost on the ground.

Three stalk rots—diplodia, gibberella, and charcoal rot—are

similar in that their respective

causal organisms show the same

general type of parasitism. The

fungi responsible for these dis-
eases do not ordinarily attack

young physiologically active

plants but those approaching maturity. However, pythium stalk

rot is a different type of disease,

because young plants may be

attacked well before the silking

stage.

Diplodia Stalk Rot

Probably the most common

stalk rot in the Corn Belt is

diplodia stalk rot. The factors

affecting the prevalence of the

disease are not fully known, but

dry weather in the early-gi'owing

season followed by ample rainfall

for 2 to 3 weeks after silking

appears to favor the development

of this disease. Severe infection

by any of the leaf diseases or

destruction of leaves by hail or

insects predisposes stalks to infection. Soil fertility may affect

the severity of diplodia stalk rot.

Observations and a few experiments have shown that more stalk

rot occurs where soils are excessively high in nitrogen and low

in potassium than where fertility

is ample and balanced.

Symptoms.—When infection

takes place before plants reach

maturity, the leaves suddenly become grayish green similar to the

effects of frost injury (pi. 2, A),

the lower parts of the stalk turn

from green to tan or brownish,

and the pith becomes soft (pi. 2,

B). When diseased stalks are

split open, the pith is disintegrated and discolored, and only

the water-conducting vascular

bundles are left intact (pi. 2, C).

Diseased stalks are weakened and

break readily in the wind and

rain. Occasionally minute black

pycnidia, the fruiting bodies of

the fungus, form in the fall just

beneath the surface of the lower

inteniodes of the stalk (pi. 2, E).

Cau,s « / 0rganism . — Diplodia

stalk rot is caused by Diplodia

maydis (D. zeae (Schw.) Lev.).

The fungus produces two types of

asexual spores. The most common

is long, elliptical, straight to

slightly curved, two celled, and

olive colored to brown. The second

spore type, less frequently seen,

is colorless, long, narrow, and

threadlike. Both are produced in

small, black, flask-shaped pycnidia,

which develop on infected parts

of the host in the field in either

the current year or the following

spring (pi. 2, E). When spores

are mature, they are exuded from

the pycnidia during warm, moist

weather and carried by the wind

to healthy plants where they infect the stalk or ear. No sexual

stage of the fungus is known.

Infection takes place most frequently at the crown of the plant

and spreads into the stalk and

the roots. Infection sometimes

occurs at the nodes between the

crown and the ear. Although the

fungus spreads some distance in

the stalk, it does not invade the

entire plant. Generally the fungus

does not grow from the crown

through the stalk and into the ear

to cause a rot there.

Control.—One way to reduce

stalk rot is to use resistant hybrids. Local State agricultural

experiment stations should be consulted for adapted resistant

hybrids. Full-season hybrids are

generally more resistant than ' those that mature early in a given |

area. Properly balanced soil fer- ,

tility will tend to reduce the abun- j

dance and severity of diplodia

stalk rot.

Where soil is infertile or potassium is deficient and nitrogen

proportionately excessive, this disease is often more severe. The

application of the proper kinds

and amounts of fertilizer based

on soil and tissue tests niay help

to minimize stalk rotting and

breakage.
Gibberella Stalk Rot

Gibberella stalk rot is widely

distributed in the United States

and more prevalent in the northern and eastern parts of the

country than diplodia stalk rot.

So far as is known the environmental factors affecting both diseases are similar. The diseases

are somewhat alike in that both

usually attack plants several

weeks after silking.

Symptoms.—The sudden onset

of grayish-green color of leaves

of early-infected plants resembles

the appearance of plants affected

with diplodia stalk rot at the same

stage of development. The softening and discoloration of the exterior of lower internodes are also

very similar in both diseases (pi.

3, A and B). When stalks affected

with gibberella stalk rot are split,

they will generally show a reddish

discoloration of the diseased area.

The shredded appearance of the

pith is otherwise much the same

as in diplodia stalk rot.

Causal Organism. — Gibberella

stalk rot is a fungus disease

caused by Gibberella zeae. The

fungus has both asexual and sexual spores. The former are long,

curved, and spindle shaped, with

several cross walls. These spores

are produced on the mycelium of

the fungus, which grows from

diseased plant parts during warm,

moist weather. The asexual stage

is known as Fusarium graminearum Schwabe. The sexual

spores, or ascospores, are produced in black flask-shaped perithecia, which develop on the

surface of diseased cornstalks in

the fall or during the spring of

the following year (pi. 3, C).

Ascospores are exuded from the

perithecia during warm, moist

weather and carried by the wind

to infect ears or stalks. This fungus also attacks wheat and barley.

where it causes the disease known

as scab.

Control.—This disease may be

controlled by using full-season

resistant hybrids and by adjusting soil fertility to proper balance

where necessary.

Charcoal Rot

Charcoal rot is found mostly in

the drier areas where corn is

grown, principally in the eastern

Great Plains and in California.

Occasionally it becomes common

in the eastern Corn Belt.

Symptoms.—The disease first

attacks the roots of seedlings and

young plants. Lesions are brown

and water soaked and later become black. When the plant approaches maturity, the disease

spreads into the crown and lower

internodes of the stalk. Infected

stalks may often be recognized

by grayish streaks on the surface

of lower internodes. Internal

BN-n247X

FIGURE 1.—Typical shredding and

grayish-black lower internodes of a

cornstalk affected with charcoal rot.
parts of the stalk are shredded

and grayish black (fig. 1). Minute

black specks, or sclerotia, of the

fungus are scattered over the surface of the fibrovascular bundles.

Causal Organism.—Macrophomina phaseoli (Maubl.) Ashby

{Rhizoctonia bataticola) (Sclerotium bataticola Tauh.) is the causal

organism of charcoal rot. The

fungus appears to be composed of

several strains, v^rhich are differentiated on the basis of the size

of sclerotia and the presence or

absence of pycnidia. The spores

are colorless, oval, and single

celled and are borne in black flaskshaped pycnidia. Those strains of

the fungus attacking corn evidently do not form spores. The

sclerotia are black and globular to

irregular in shape. They are a

means by which the fungus is disseminated and by which it overwinters. The fungus has a wide

host range, attacking sorghum,

beans, and several other crops.

Control.—The disease may be

controlled by irrigation, where

practical, and by long rotations

with crops that are not natural

hosts of the fungus. Little is

known about the relationship of

soil fertility to the disease or the

relative resistance of inbred lines

and hybrids. Since the disease

invades the crown and stalk as

maturity is approached, balanced

soil fertility and the use of fullseason adapted hybrids would

probably tend to reduce the severity of charcoal rot.

Pythium Stalk Rot

Pythium stalk rot is a minor

disease that becomes acute only

in localized areas. It seems to be

confined to the Eastern and Southeastern United States, but it has

been reported in some parts of

Southern Europe and South

America. The disease is favored

by extended periods of hot, humid

weather. It is often encountered

in river-bottom fields when air

drainage is poor and humidity

high.

Symptoms.—The disease is generally first recognized when plants

fall over. The rotted part of the

stalk is usually confined to a single

internode just above the soil line.

The diseased area is brown, water

soaked, soft, and collapsed (pi. 3,

D). The stalks are not broken off

completely by the disease, and the

plants live for several weeks because the vascular bundles remain

intact.

Causal Organism.—Pythium

stalk rot is caused by Pythium

aphanidermatum (Edson) Fitz.

{P. butleri Subr.). The fungus

thrives at high temperatures, and

unlike other stalk-rotting fungi

it can attack young vigorously

growing plants before silking time

and the onset of maturity. The

fungus is strictly a soil inhabitant.

Control.—No specific control for

the disease is known, although

difl^erences in resistance are found

among inbred lines.

Other Stalk Rots

A bacterial disease attacking

both stalks and leaves of corn has

been observed in North Carolina

where overhead irrigation is used.

A similar disease has been found

in Wisconsin under comparable

conditions. Stalks become soft,

water soaked, and tan or brown.

They topple over at the point of

infection. Leaves are invaded at

their base near the sheaths and

ultimately become badly shredded.

The causal organism, which is

extremely virulent, appears to be

a species of the genus Erwinia

and distinct in certain characteristics from any other bacteria that

cause stalk rots of com.

Another bacterial stalk rot with

symptoms very similar to those

caused by Pythium aphaniderma8
turn has been reported on corn.

The causal organism is Erwinia

dissolvens (Rosen) Burkh. A third

stalk rot caused by the bacterium

Pseudomonas lapsa (Ark) Burkh.

has been reported from California.

Like the stalk rot caused by E.

dissolvens, it closely resembles

pythium stalk rot. Both of these

bacterial stalk rots seem to be

rare and limited in extent.

Pythium Root Rot

Pythium root rot is widely distributed, but evidently it is not

so destructive to corn as to sugarEAR

Corn is susceptible to a number

of ear rots, five of which are widespread throughout the main corngrowing areas of the United

States. They include diplodia ear

rot, fusarium kernel rot, cob rot,

gibberella ear rot, and gray ear

rot. The diseases can, at times,

reduce yield, quality, and feeding

value of the grain. However,

severe epidemics are usually

limited to localized areas and are

of less general economic importance than stalk rots.

Diplodia Ear Rot

Of the ear rots in the Corn

Belt, diplodia ear rot, or dry rot,

is the most common. In some

years and in restricted areas this

ear rot has caused appreciable

damage. Wet weather extending

from silking until 2 to 3 weeks

thereafter appears to be ideal for

infection of the ears, particularly

if the early summer has been

relatively dry so that spores of

the fungus have not been dispersed before the ears were

formed.

Symptoms.—Husks of ears infected early appear bleached (pi.

4, A) in contrast to the green

healthy ears. When infection takes

place within 2 weeks after silking,

cane and sorghum. Small feeding

roots are first attacked, and

lesions become light to dark brown

and flaccid. In later stages large

areas of the roots may become

infected and severe lodging results. Pythium debaryanum and

P. graminicola Subr., both of

which have a wide host range,

have been isolated from infected

roots. The disease usually becomes

severe where soil is poorly

drained, cold, and wet. Inbred

lines differ in resistance to the

disease.

ROTS

the entire ear becomes grayish

brown, shrunken, and very light

weight by harvest (see cover).

Such ears usually remain upright,

with husks stuck tightly together

owing to the growth of the fungus

between them. Black pycnidia of

the fungus are often found at the

base of the husks and on the sides

of the kernels of such badly infected ears. Ears infected later

in the growing season may show

no external signs of the disease

until the ear is broken or kernels

are removed. A white mold will

then be found growing between

the kernels, and their tips will

be discolored. Infection usually

begins at the base of the ear and

progresses toward the tip. Ears

appear to be most susceptible to

infection from silking until about

3 weeks later.

Causal Organism.—This ear rot

is caused by Diplodia maydis, the

same fungus associated with

diplodia stalk rot. It is described

under that disease.

Control.—Inbred lines vary in

their resistance to this ear rot and

tend to transmit their reaction to

this disease to their double-cross

combinations. No inbred line or

hybrid is completely resistant, but

the most susceptible inbreds are
usually discarded before they are

in hybrid combinations.

Fusarium Kernel Rot

Fusarium kernel rot is probably

the most widespread disease attacking corn ears. It is present

to some extent every year in the

Corn Belt, but it seems to be more

prevalent in the western part of

this area. In central California

the disease is sometimes particularly prevalent. Dry weather

seems to favor its spread and

development. The total loss caused

by the disease is probably less

than that caused by diplodia ear

rot because of the scattered infections rather than complete

involvement of the ears.

Symptoms.—The first symptom

of fusarium kernel rot is a pink

discoloration of caps of individual

kernels or groups of kernels scattered over the ear (pi. 4, B). The

color of infected kernels may vary

somewhat from faint pink to reddish brown depending somewhat

on the moisture content of the

grain. As the disease progresses,

infected kernels show a powdery

or cottony-pink mold grovrth. Infection often becomes established

around points where corn earworms (Heliothis zea (Boddie))

have entered the ear or channeled

between the rows of kernels.

Causal Organisms.—Fusarium

kernel rot is caused by Fusarium

moniliforme and a closely related

fungus, F. moyiiliforme var. suhglutinans Wr. & Reinking, both of

which produce an abundance of

small, colorless, one-celled spores

borne in chains or in false heads.

These are microconidia. A few

curved to spindle-shaped multicellular macroconidia are also

formed on the mycelium. Occasionally the sexual stages Gihherella fujikuroi (Saw.) Wr. and

G. fujikuroi var. subghitinans Edwards can be found on old cornstalks. They are represented by

small black perithecia, which bear

ascospores. The latter ooze from

the perithecia during warm, moist

weather. The sexual stage resembles that of G. zeae in some

respects.

Control.—No specific control for

the disease can be recommended

other than to avoid hybrids that

tend to be susceptible. Hybrids

with poor husk cover or with

weak seedcoats in which kernels

tend to "pop" or "silk cut" are

susceptible to infection.

Cob Rot

Cob rot is widely distributed

and present to some extent every

year. Corn that has been killed

or in which normal development

has been arrested because of stalk

rot, leaf blights, cold, or root injury is susceptible to cob rot.

Corn grown on poor soil appears

to be more susceptible than that

raised on fertile soil, possibly because of premature dying from

lack of proper nutrition.

Symptoms.—Afliected ears are

light weight, and the kernels are

slightly bleached, poorly finished,

and easily pressed into the cob.

Shanks and bases of badly infected ears are often shredded,

particularly when ears are picked

mechanically or later when they

are shelled. Close examination of

infected ears shows very small

black spore masses scattered in

the shredded pith of the cob and

on the tips of the kernels (pi. 4,

C). The chaff on infected ears is

often brown or chocolate colored

instead of the normal bright red.

In affected white hybrids the chaff

will be pale yellowish or gray.

Causal Organism.—Cob rot is

caused by Nigrospora oryzae

(Berk. & Br.) Fetch (Basisporium

gallarum Moll.), a fungus that

overv/inters on old plant refuse in

10
the field. Only an asexual stage

is known. Spores axe globular to

ovoid, black, and borne singly on

the mycelium.

Control.—Since the fungus attacks ears of weakened plants,

full-season adapted hybrids that

are resistant to stalk rot and leaf

blight are recommended.

Gibberella Ear Rot

Gibberella ear rot, sometimes

called red ear rot, is found more

frequently in the cooler, more

humid areas where corn is grown.

Com infected with this disease is

particularly toxic to hogs. When

such corn is offered on the ear,

the animals will refuse it, but

when it is ground into meal they

have no choice. Vomiting and

dizziness are symptoms after hogs

consume the infected corn. In

severe cases death may follow.

Symptoms.—A reddish mold

that starts at the tip of the ear

is the primary and distinguishing

symptom of gibberella ear rot (pi.

4, Z?). Ears infected early may

become completely rotted; the

husks adhere tightly and a pinkish mold grows between them.

Causal Organism.—This disease

is caused by Gibberella zeae, the

same fungus responsible for gibberella stalk rot. It is described

under that disease.

Control.—Since gibberella ear

rot has generally been of minor

economic importance, no efforts

have been made to control it

through breeding for resistance.

Gray Ear Rot

Gray ear rot seems to be widely

distributed over the Eastern

United States, but rarely has it

been severe and then only in very

restricted areas. Extended periods

of wet weather for several weeks

after silking seem to favor the

disease.

Symptoms.—In its early stages

this disease resembles diplodia ear

rot because of the grayish-white

mold that develops on and between the kernels near the base

of the ear. In ears that have been

infected early, the husks are

tightly adherent and bleached (pi.

5, A and B). At harvest such ears

are slate gray, and because of

their light weight they are held

upright. When an infected ear

is broken, the cob will often show

very small black specks, or sclerotia, scattered through it. Badly

infected kernels show black

streaks or specks beneath the

seedcoat (pi. 5, C). In advanced

stages the disease is easily distinguished from diplodia ear rot

by the slate-gray color of the ear

and black sclerotia in the pith of

the cob and under the seedcoat.

Causal Organism.—The disease

is caused by Physalospora zeae

Stout, which produces the perithecia of the sexual stage and

pycnidia of the asexual stage in

large lesions on corn leaves (pi.

5, D). Occasionally infection takes

place on the tassel neck or under

the sheath of the uppermost leaf

of the plant. The perithecia and

the pycnidia that may develop in

the same lesion are black and imbedded in the leaf tissue. Ascospores and pycnidiospores are

oval or ellipsoid, colorless to pale

green, and one celled. The fungus

overwinters on infected leaves,

and spores mature the following

growing season to infect leaves

and ears. Perithecia and pycnidia

are not found on the ears. Only

the sclerotia, which are small,

hard, black knots of the mycelium,

are found in the rotted ears and

kernels. These structures are resistant to extremes of the environment and serve as a means of

survival and propagation of the

fungus. The name of the asexual

stage of the fungus is Macrophoma zeae Tehon & Daniels.

11
Control. — No control for the

disease is known other than the

use of adapted hybrids. Since the

disease is so similar to diplodia

ear rot as to time and place of

infection on the corn plant, resistance to the two diseases might

be rather closely correlated.

Other Ear Rots

Several other ear rots and

kernel rots of corn have been described. However, they are confined to limited geographical

areas, occur very rarely, or are

otherwise of negligible consequence in the pathology of the

corn crop.

Physalospora ear rot is confined

largely to the Gulf States and is

similar in some respects to gray

ear rot. Severe infection is characterized by dark-brown to black

felty mold growth on all parts of

the ear. Mildly infected ears may

show a few blackened kernels confined near the base where most

infections begin. The causal

fungus Physalospora zeicola Ell.

& Ev. has both a sexual and an

asexual stage; the latter is called

Diplodia frumenti Ell. & Ev.

Pycnidiospores are oval, two

celled, and striate. They develop

on cornstalks infected by the

fungus. D. frumenti is distinguished from Macrophoma zeae on

the basis of size, shape, color, and

septation of the pycnidiospores.

Rhizoctonia ear rot, found also

in the Gulf States, is recognized

in its early stages by a salmonpink mold growth on the ear.

With age the infected ears become

dull gray, and numerous small

sclerotia ranging from white

through salmon color to brown

are formed on the outer husks.

The disease is caused by Rhizoctonia zeae, a fungus not known

to produce spores, but it is propagated and spread only by the

sclerotia. Warm, humid weather

seems favorable for infection.

Southern diplodia ear rot is

found in the Southeastern United

States. The symptoms of the disease are similar to those of

diplodia ear rot (see cover).

Southern diplodia ear rot is caused

by Diplodia macrospora Earle, a

fungus similar to D. maydis, but

dififering mainly in having larger

spores. The fungus also attacks

leaves of corn and produces small,

round to oval lesions.

Pénicillium ear rot is occasionally observed, particularly on inbred lines. The characteristic

appearance is a powdery green

mold on and between the kernels,

which are often bleached. Infections are frequently associated

with corn earworm channels. The

causal organism is most frequently Pénicillium oxalicum, but

occasionally other species of the

genus have been isolated from

diseased ears.

Aspergillus ear rot is another

disease that is comparatively rare.

Black powdery mold grows on and

between the kernels. Aspergillus

niger v. Tiegh. is the fungus most

frequently associated with this

ear rot, although other species,

some of which are greenish yellow, have been isolated from

diseased ears.

Cladosporium kernel rot occurs

occasionally in some years. Symptoms are characterized by dark

greenish-black kernels scattered

over the ear. Cladosporium herbarum S. F. Gray (Hormodendrum

cladosporioides (Fres.) Sacc.) is

the causal organism of the disease.

STORAGE ROTS AND KERNEL DISORDERS

Storage rots may develop on

either cribbed ear corn or shelled

corn in a bin if the moisture content of the kernels and the air

12
temperature are high enough to

permit fungi to grow. Storage

rots reduce both feeding value and

market grade of the corn.

Some of these typical storage

molds are able to grow on corn

with moisture contents as low as

14 to 18 percent.

%: %

Ifl« I t

S'-*.JK;

'.^ % '^

X ê

f

1 *

^

-I c

,"*

%

• *"--'< '^.

,. ''' v#^^

„^ ..

'') >,T^

-...>

c 1

BN-11246X, BN-11263X, BN-11249X

FIGURE 2.—Storage rots of corn : A and ß, Mold growth between and

at base of kernels; C, "blue-eye" of stored shelled corn. These rots

develop when corn is stored before moisture content is sufficiently

reduced.

Typical mold development on

and between kernels and at their

base are the first symptoms of

these rots (fig. 2, A and B). When

storage rots are allowed to develop, the kernels will cake together because of extensive mold

growth. One storage rot called

"blue-eye" is characterized by the

bluish-green germ due to growth

of the mold (fig. 2, C).

Storage rots can be due to any

one of the several fungi causing

ear and kernel rots in the field.

Several species of Aspergillus and

of Pénicillium are the most common storage-rot fungi and frequently are referred to as typical

storage molds. These are A.

glaucus Lk. ex Fr. (group), A.

flavus Lk. ex Fr., A. candidus Lk.,

A. niger, A. ochraceus Wilhelm,

P. rugulosum Thom, P. palitans

Westl., and P. chrysogenum Thom.

Storage molds can be controlled

by drying shelled com to 12-percent moisture or slightly less. Ear

corn stored in well-ventilated

cribs is ordinarily in no danger

from storage rots if the moisture

content is 18 percent or less. In

some seasons when weather conditions do not permit proper drying,

considerable mold may develop

on ears in the field. Such corn

should be artificially dried with

crib driers to a moisture content

low enough to stop mold growth.

Kernel disorders actually are

not diseases, but because they

provide opportunities for fungi

to invade kernels they are closely

related to corn pathology.

"Popped kernel" is a disorder

appearing as irregular breaks in

the seedcoat over the crown of

the kernel (fig. 3, A). The kernels

appear as partially expanded pop13
corn kernels. This disorder is

more common on a few inbred

lines than on hybrids.

"Silk-cut," another disorder, is

characterized by a horizontal cut

or split in the seedcoat over the

sides of the kernel (fig. 3, B). It

has nothing to do with the silk of

the ear, but it seems to be associated with certain inbred lines

and their combinations.

Both "popped kernel" and "silkcut" are caused by weak seedcoats, which appear to be unable

to expand as the kernels develop

and consequently break at the

weakest point. The rupturing of

the seedcoat exposes the starch of

the endosperm, which often becomes overrun with fungi, particularly Fusarium moniliforme.

»il.

'^^

BN-11265X, BN-11244X

FIGURE 3.—Kernel disorders: A, "Popped-kernel"; B, "silk-cut." These are due

to weakness of the seedcoat. Such breaks exposé the starch and predispose

kernels to infection by molds.

LEAF DISEASES

Certain leaf diseases of com more of these diseases were

have increased in economic impor- severe. The economic importance

^^^ce m the United States since of some of these diseases was al1940. Durmg this period there most coincident with the use of

were several seasons when one or hybrid com. However, this fact

14
does not mean that hybrid corn

is necessarily inferior to openpoUinated corn in resistance to

certain leaf blights.

Several reasons may account

for this apparent association of

the prevalence of some leaf blights

and the use of hybrid corn. (1)

During the late 1930's and early

1940's there were several years

when weather conditions favored

the development of both northern

corn leaf blight and southern corn

leaf blight in the eastern Corn

Belt. This was at a time when

hybrid corn was just being introduced into this area and there was

much interest in the crop. (2)

Hybrid corn is genetically much

more uniform than open-pollinated corn. Consequently, when a

disease attacks, the plants all tend

to react similarly. Whereas openpollinated corn, although not

highly resistant, is much more

heterogeneous, and the degree of

resistance to diseases may vary

from one plant to another.

Leaf blights vary in prevalence

and severity from year to year

and from one locality to another,

depending largely on environmental conditions. Humid weather

along with heavy dew favors the

spread and development of leaf

blights caused by fungi. Leaf

blights can be found on corn in

both poor and rich soil. Soil fertility does not seem to affect these

diseases as much as weather conditions and genetic constitution

of the plants.

Northern Corn Leaf Blight

Northern corn leaf blight is

found in most humid areas where

corn is grown. In the United

States it frequently occurs in the

eastern Corn Belt and extends to

the Atlantic coast and southward.

Under favorable conditions it may

occasionally become locally severe

in the northern and central Corn

Belt. The time when the disease

first appears is determined largely

by weather conditions. In some

years it may be found before silking, whereas under less favorable

conditions, such as hot, dry

weather, there may be no trace

of it. In southernmost Florida

where temperature and humidity

favor growth and reproduction of

the fungus during most of the

year, infection may become established on seedlings.

Reductions in grain yield maj;

exceed 30 percent or more if the

disease becomes well established

2 to 3 weeks after silking. The

later the disease appears, the less

yield is reduced. In addition to

losses in yield during a severe

epidemic, the feed value of fodder

is lowered and plants become predisposed to stalk rot.

Symptoms.—Northern corn leaf

blight is recognized by long, elliptical, grayish-green or tan spots

on the leaves. When fully expanded the spots may be IVa by 6

inches (pi. 6, A). These lesions

appear first on the lower leaves,

and as the season progresses the

number increases until, under

severe conditions, nearly all the

leaves are covered with them and

little green tissue remains. Under

such circumstances the plants appear dead and gray, as though

injured by frost. Many spores of

the fungus are produced on the

lower surface of the lesions under

humid conditions. Often the

spores are arranged in concentric

zones, and a faint targetlike pattern in the lesions is evident.

Lesions may form on the husks.

Since the kernels are not attacked,

the possibility of distributing the

disease by seed is remote.

Causal Organism.—Helminthosporium turcicum Pass, is the

fungus causing northern corn leaf

blight. The fungus and the disease

were first described in Italy in

15
1876. The fungus overwinters on

infected corn leaves, and during

the following summer spores are

formed on the mycelium located

in and on old lesions. The newly

formed spores are carried by the

wind to growing corn leaves

where, if moisture is present, they

germinate and penetrate and thus

establish the disease. The fact

that spores are carried for some

distance during the summer may

account for isolated epidemics in

the northern Corn Belt. Germination and penetration take place

within 6 to 18 hours when water

is on the leaves and the temperature is within 65° to 80° F.

Lesions are recognizable 7 to 12

days after infection, and new

spores are formed on them to continue the disease cycle. Asexual

spores are long and spindle shaped

and have one to nine cross walls.

A sexual stage, Triciiovietas'phaeria turcica Luttrell, has been

described, in which small black

perithecia bearing ascospores

were produced. This stage was

obtained in pure culture in the

laboratory by mating appropriate

isolates of the fungus.

Besides corn the fungus also attacks sorghum (Sorghum vulgäre

Pers.), sudangrass (S. sudanense

(Piper) Stapf.), Johnsongrass (S.

halepense (L.) Pers.), and teosinte

( Euchlaena m e x i cana Schrad.).

Cross inoculations with isolates

from these hosts suggest the presence of physiologic races within

the fungus. No differential pathogenicity has been found among

isolates from corn. This fact

makes the work of the corn

breeder less complicated, because

he does not need to breed for resistance to different races of the

fungus.

Control.—^The most effective

and efficient means of controlling

northern corn leaf blight is to use

resistant hybrids. Resistant hybrids adapted to southern Indiana,

Illinois, and Ohio are available!

Other resistant hybrids of different adaptation are being developed.

Resistance to this disease is

determined by a large number of

genetic factors, or genes, but it is

possible through breeding to

transfer such resistance to susceptible but otherwise desirable

inbred lines for use in hybrid

combinations. The amount of resistance in a double-cross hybrid

is generally proportional to the

number of blight-resistant inbred

lines in the pedigree.

To control the disease on sweet

corn in southern Florida, the

plants are sprayed with a fungicide. This practice is economically feasible because of the

premium paid for the crop. Seed

treatment or crop rotation has no

effect on the disease.

Southern Corn Leaf Blight

Southern corn leaf blight, like

northern corn leaf blight, is found

wherever corn is grown under

humid conditions. It is confined

chiefly to the Southeastern United

States, but it does occur in Missouri, Illinois, Indiana, Ohio, and

eastward to the Atlantic coast.

The disease thrives at slightly

higher temperatures than northern corn leaf blight, and consequently it is notfound so far north

as the latter.

Symptoms.—Typical lesions of

this leaf blight are parallel sided

and grayish tan, ranging from

minute spots up to % by l'/^

inches (pi. 6, B). The tips of

ears and the silks of sweet corn

may be attacked during an extremely heavy infestation. Similar

infections have not been observed

in dent corn.

Causal Organism.—The disease

is caused by the fungus Helmvnthosporium waydis Nisik. & Miy16
ake. Spores are long, narrow, and

slightly curved; they have from

3 to 13 cross walls. A sexual

stage, Cochliobolus heterostrophus

Drechs., bears long threadlike

ascospores in black flask-shaped

perithecia. Since the sexual stage

is found rarely in nature, it is

doubtful whether it functions in

propagating the fungus. No

specialized pathogenic races of the

fungus are known, although the

disease has been reported to attack teosinte.

Control. —• Like northern corn

leaf blight, the control of this

disease is best accomplished by

using resistant hybrids. The few

released hybrids previously referred to as resistant to northern

corn leaf blight also are highly

resistant to southern com leaf

blight. The disease is controlled

in southern Florida by spraying

with a fungicide. Resistance is

determined by several genes,

which appear to be independent

of those governing resistance to

northern corn leaf blight. The

resistance of a double-cross hybrid

is proportional to the number

of resistant inbred lines in the

pedigree.

Helminthosporium Leaf Spot

Helminthosporium leaf spot is

of minor economic importance. It

is encountered on a few susceptible inbred lines. Farmers are

not troubled with the disease, because it does not occur on commercial single- or double-cross

hybrids. There are two physiologic races of the fungus: Race

I is highly virulent and specialized

in its parasitism to a few inbred

BN-11252X, BN-11257X

FIGURE 4—A Leaf lesions typical of those caused by race I of Helminthosporium

carbonum; B, corn ear infection typical of that caused by race I or race 11

of this fungus.

17
lines of corn ; race II is much less

virulent and shows no distinct

host specialization. Humid weather favors rapid spread of the

disease.

Symptoms.—The disease caused

by race I of the pathogen is recognized by tan, oval to circular

lesions, ranging from very small

spots up to % by 1 inch (fig. 4,

A). A pattern of concentric zones

is often evident in the lesions.

Under ideal conditions lesions become abundant and the fungus

produces spores profusely on leaf

sheaths. The ears are also readily

attacked and have a black felty

mold over the kernels and the ear

appears charred. Symptoms produced by race II on field-grown

plants are oblong chocolate-colored

spots ranging from very small up

to % by 1 inch. The ear rot

caused by race II is indistinguishable from that caused by race I

(fig. 4, B). The leaf disease

caused by race II is very rarely

found.

Causal Organism.—Helminthosporium. carhonum Ullstrup is the

fungus responsible for the disease.

Asexual spores are olive brown,

long-elliptical to spindle shaped,

with rounded ends bearing from

2 to 12 cross walls. The two races

of the fungus are alike in cultural

behavior, size, shape, and color of

spores, but they are distinguished

only on the basis of symptoms

produced on corn leaves and the

specialization in parasitism of

race I to a few inbred lines. A

sexual stage of the fungus, Cochliobolm carbonus Nelson, has been

produced in pure culture by growing in association appropriate

mating types of the fungus. The

perithecia and ascospores resemble those of C. heterostrophus in

size, shape, and color.

Control.—This disease can be

easily controlled by using resistant inbred lines. Since a single

gene determines resistance, it is

rather simple to incorporate resistance into a susceptible line by

breeding methods.

Bacterial Wilt

Bacterial wilt, sometimes referred to as Stewart's disease, is

widespread over the Eastern

United States. It is much more

severe on sweet corn than on

dent corn.

This disease, unlike the three

previous fungus diseases, does not

require damp weather and heavy

dew for spread and development.

Bacterial vdlt is carried through

the winter within the bodies of

com flea beetles. When these insects come out of hibernation late

in the spring, they feed on young

corn plants and thus start infections on the leaves. During the

growing season the beetles continue to spread the disease from

infected to healthy plants. The

prevalence of bacterial wilt varies

from year to year depending oii

the number of corn flea beetles

that survive the winter. When

winters are mild, usually large

numbers of beetles survive and

thus start infections and spread

the disease during the growing

season. Cold winters reduce the

number of beetles, and consequently there is little primary infection and spread of the disease

is retarded.

Symptoms.—In sweet corn, susceptible hybrids wilt rapidly and

resemble plants with an inadequate water supply (pi. 6, C).

Infected plants that do not die are

stunted and may produce no ears.

Diseased plants frequently show

long, irregular, pale-green to yellowish streaks on the leaves.

These streaks become dry and

brown. The vascular bundles in

the plants become filled with bac18
teria. When the stalks are cut,

yellowish masses of bacteria ooze

out on the cut surface. If small

pieces of infected leaf tissue are

placed in a drop of water and

observed under a microscope,

masses of bacteria will be seen

flowing out from the cut ends of

the vascular bundles. In severely

infected plants cavities may form

in the pith of the stalk. In such

plants the bacteria spread

throughout the vascular system,

passing through the cob into the

kernels. Infected kernels may

thus be a means of spreading the

disease to new localities.

Dent corn is generally much

more resistant than sweet corn

and seldom does the disease

spread through the entire plant,

except in a few very susceptible

inbred lines, and then the symptoms are as described for sweet

corn. In dent corn the characteristic symptoms on the leaves are

the long, irregular, pale-greenish

streaks that turn yellow, then die,

and become straw colored (pi. 6,

D). This is known as leaf blight

or late-infection phase, since it

generally becomes prevalent after

tasseling. These dead, dry lesions

sometimes become covered with

saprophytic fungi, which mistakenly may be assumed to cause

the disease. The long streaks always originate at the feeding

wounds of corn flea beetles. Where

infection is severe, much of the

leaf area may be destroyed, the

yield is reduced, and the plants

become more susceptible to stalk

rot. The infection of dent corn

kernels is exceedingly rare and

occurs only where the disease is

most severe on susceptible inbred

lines.

Causal Organism. — Bacterial

wilt is caused by a species of

bacterium, Xanthomonas stewartii (E. F. Sm.) Dows. The cells

are short, nonmotile rods. Colonies on nutrient agar are small,

slow growing, and pale yellow.

Control.— The most practical

way to control this disease is to

use resistant hybrids. The hybrid

Golden Cross Bantam was the

first sweet corn developed for resistance to this disease. It is

vddely adapted over most of the

eastern Corn Belt. Several other

sweet corn hybrids have been

developed that combine resistance

to bacterial wilt with high yield

and quality. In both sweet and

dent corn the earlier and shorter

inbred lines appear to be more

susceptible than the later and

taller inbred lines. In sweet corn,

Country Gentleman and Evergreen are generally more resistant

than the Bantam types.

Early spraying or dusting

plants with an insecticide to kill

corn flea beetles is partly effective

in reducing spread of the disease.

There is some indication that adequate levels of potassium in the

soil tend to minimize the disease,

whereas high levels of nitrogen

predispose plants to susceptibility. Seed treatments or spraying plants with fungicides has no

efl'ect on controlling the disease.

In dent corn there appears to

be a positive correlation between

resistance to the late-infection

phase of this disease and resistance to northern corn leaf blight.

Studies conducted several years

ago on bacterial wilt indicate that

two major genes and one minor

.(rene operate in determining resistance to the disease.

MINOR LEAF DISEASES

Several fungi and bacteria attack corn leaves but are of little

economic importance, either because they rarely occur or because

they do little damage. They will

be treated briefly.

19
Bacterial Leaf Blight and

Stalk Rot

Bacterial leaf blight was first

described about 1930 as occurring

in some of the southern and central areas of the United States.

The disease seems to be favored

by rather high temperature. It

ding, especially after wind and

rain.

Stalk rot usually occurs just

above the point where the ear is

attached and causes a dark-brown

rot of the pith (fig. 5, B). As the

rot progresses, the tops of the

plants die. Afl'ected plants are

dwarfed and often develop mulBN-11251X, BN-11246X, BN-n24SX

FIGURE 5.—Bacterial leaf blight and stalk rot: A, Leaf lesions; B, stalk rot,

showing discoloration of internode; C, multiple ear formation on a plant

affected with bacterial leaf blight and stalk rot.

has been of minor economic importance.

Symptoms. — The disease may

appear in localized areas in the

field. Leaf lesions range from

small elliptical spots to long narrow stripes, extending nearly the

full length of the leaf (fig. 5, A).

These lesions often coalesce and

affect most of the leaf width. At

first the lesions are olive green

and water soaked and later become tan and dry. Badly diseased

leaves show characteristic shredtiple ears, which are usually

sterile (fig. 5, C).

Causal Organism. — The bacterium causing the disease isPsev.-

domonas aIbo])recipitans Rosen.

The cells are short, rod shaped,

and motile. The organism was

first described on foxtail grass

(Setaria spp.), where it causes a

leaf disease.

Coniro/.—Because of its minor

economic importance, no control

measures have been developed for

this disease.

20
Bacterial Stripe

Bacterial stripe seems to thrive

during and after extended periods

of warm, wet weather. Lesions

and is the same organism responsible for bacterial stripe of Sorghum species. This disease is not

of economic importance and has

BN-11256X, UN-H250X

FIGURE 6.—Bacterial stripe: A, Typical narrow linear lesions on lower leaves;

B, striped bleached leaves, which are not infected, develop after severe

infection on lower leaves.

are long/narrow, generally parallel sided, olive to amber colored,

and water soaked (fig. 6, A).

They first appear on the lowest

leaves. On very susceptible inbred

lines most of the leaves below the

ear may be killed by the disease.

Under such conditions where infection is severe, the upper leaves

at first have pale-yellow or greenish-white stripes. The stripes

enlarge, coalesce, and continue to

become lighter until the upper

leaves are almost completely white

(fig. 6, B). These bleached leaves

are not infected but show a secondary efli'ect of infection on the

lower leaves. Pseudomonas andropogonis (E. F. Sm.) Stapp is the

bacterium causing this disease

been acute only on a few very

susceptible inbred lines of corn.

Zonate Leaf Spot

Zonate leaf spot is found in the

Gulf States. Lesions are reddish

brown and water soaked. As they

enlarge up to 1 to 2 inches in

diameter, a very definite targetlike or zonate pattern appears.

The disease occurs on sorghum,

sudangrass, johnsongrass, and

sugarcane (Saccharum officinanim L.), as well as on corn. The

causal organism is the fungus

Gloeocercospora sorghi D. Bain &

Edg., which produces numerous

long, narrow, needlelike spores in

a slimy matrix on the surface

of the lesions.

21
Purple Sheath Spot

Purple sheath spot is rather

widespread, but as far as can be

determined it causes no measurable damage to plants. Purplishbrown irregular spots of varying

sizes become conspicuous on the

leaf sheaths, usually after silking

BN-11280X

FIGURE 7.—Purple sheath spot.

(fig. 7). Beneath these spots the

inner surface of the leaf sheath

shows a discoloration and breakdown of the tissue. Inbred lines

differ considerably in their reaction to this disease. Investigations have shown that several

fungi and bacteria live saprophytically on debris that collects behind the leaf sheaths and become

mildly parasitic as the host ages.

Holcus Spot

Holcus spot attacks the leaves

of several grasses, including foxtail millet {Setaria itálica (L.)

Beauv.), sudangrass, johnsongrass, and some varieties of sorghum, in addition to corn. The

lesions are first dark green and

water soaked; later they become

dry and brown with a reddish

margin. They are round to elliptical and range from small spots

up to about one-half inch in diameter. The causal organism is the

bacterium Pseudomonas syringae

V. Hall, which invades its hosts

through stomata.

Cercospora Leaf Spot

Occasionally cercospora leaf

spot is found on corn leaves as

they approach maturity. The spots

are gray to tan and narrow, ranging from small spots up to Vi by

2 inches. The causal organisms

Cercospora zeae-maydis Tehon &

Daniels and C. sorghi Ell. & Ev.

differ slightly in the size of spores

and in the symptoms they produce.

Anthracnose

Anthracnose is rarely found in

the United States. Localized outbreaks have occurred under extremely humid conditions. Small,

oval, tan spots on the leaves are

the characteristic symptoms

caused by Colletotricum graminicolum (Ces.) G. W. Wils.

BROWN SPOT

Brown spot, or physoderma dis- far west as Kansas and north to

ease, of corn is often prevalent in

the Southeastern United States,

although it has been reported as

South Dakota. Warm, humid

weather favors its development

and spread. ^

22
Symptoms. — Initial symptoms

occur mainly below the ear on

leaf blades, leaf sheaths, and

stalks. Lesions first appear near

the base of the leaf blade as yellowish spots that later turn brown

(pi. 7, A). Spots coalesce to form

large blotches. Infections on the

leaf sheath resemble purple sheath

spot (pi. 7, B). Stalks become

infected at the nodes beneath the

sheaths. Cells of infected tissues

disintegrate and expose pustules

containing the reddish-brown sporangia of the fungus. In severe

infection stalks break at the nodes

and leaf sheaths below the ear

(pi. 7, C) and most of the leaves

die prematurely (pi. 7, D).

Causal Organism,.—The fungus

causing brown spot, Physoderma

maydis Miyabe (P. zeae-m.aydis

Shaw), is relatively simple in

structure. Sporangia, which are

produced abundantly in the pustules, are golden brown, smooth.

thick walled, and generally globe

shaped except for a flat area on

one side. When sporangia germinate, a cap or lid opens to release

a vesicle, which ruptures and

liberates several uniciliate zoospores. These motile cells require

water on the leaf surface to move

about. They come to rest, round

up, and penetrate the host. Germination of sporangia requires

water and a temperature range

from 73° to 85° F. The fungus

overwinters in the sporangial

stage on infected tissue.

Coniro^.—Marked differences

exist between inbred lines in resistance to this disease. Where

brovm spot is troublesome. State

agricultural experiment stations

should be consulted for recommended resistant hybrids. Crop

rotation and sanitation are ineffective in practical control of the

disease.

CORN RUSTS

In the United States two rusts

are found on corn—common corn

rust, which is almost universal

where corn is grown, and southern corn rust, which is confined

generally to the southeastern

areas. Tropical corn rust is found

in some of the tropical areas of

the Western Hemisphere. Common corn rust generally does not

cause much damage to the plant,

although exceptions have been

noted, especially in sweet com,

where severe infection reduced

yield. Southern corn rust has

never been reported as severe in

the United States, but in parts

of Africa the disease has caused

heavy yield losses.

Common Corn Rust

In the Corn Belt common corn

rust often appears soon after silking, although in some years it

may appear much earlier. Cool,

humid weather favors development of this disease.

Symptoms.—This rust is recognized by oval to elongate cinnamon-brown pustules scattered

over both surfaces of the leaves

(pi. 8, A). As corn matures, the

pustules become brownish black

owing to the replacement of the

reddish summer spores, or urediniospores, by black winter

spores, or teliospores. The pustules

may appear on any of the aboveground parts of the plant, but

they are most abundant on the

leaves. The pustules of this rust,

or uredinia and telia, break

through the epidermis early in

their development. This one characteristic differentiates this rust

from southern com rust.

Causal Organism. — Puccinia

sorghi is the fungus causing

common corn rust. The urediniospores are globose, finely echinu23
late, and cinnamon brown. They

are carried by the wind and under

favorable temperature and moisture conditions germinate and

penetrate corn. Teliospores are

two celled, brownish black, smooth,

thick walled, and ellipsoid. Each

spore is attached to a pedicel

twice the length of the spore.

Teliospores germinate after a

ripening period—usually over

winter — to form small basidiospores, which are delicate, thin

walled, and single celled. These

spores cannot infect corn, but

they parasitize species of Oxalis,

where the pycnial and aecial, or

cluster-cup, stages arise after infection by the basidiospores. On

the upper side of Oxalis leaves

pycnia are formed. They contain

minute spores, or spermatia.

Fusion of these with receptive

structures of the opposite mating

type initiates the development of

aeciospores in "cluster cups" on

the lower surface of Oxalis leaves.

The aeciospores are globoid to

ellipsoid, finely verrucose, and

pale yellow. They are carried by

the wind to corn leaves, where

they start infections that again

give rise to the urediniospores. In

the Central and Southern United

States the urediniospores may

overwinter and servie to initiate

infection in the spring, thus bypassing the necessity of the alternate host Oxalis.

Control.—In the United States

there has been no urgent need to

control common corn rust. Most

inbred lines are susceptible, but

a few have shown resistance to

one or more physiologic races of

this rust. One collection of the

Cuzco variety from Peru appears

to be highly resistant to all cultures of P. sorghi. Since resistance is determined by a single

dominant gene, transfer of such

resistance to agronomically desirable inbred lines should be

relatively simple.

Southern Corn Rust

Southern corn rust was first

reported in the United States

from Massachusetts in 1879. Since

then it has been found in several

Southern States and as far north

as Wisconsin. It is frequently

encountered in the warm, humid

areas of Central and South America. It has become economically

important in parts of Africa and

has been found in several countries in the Eastern Hemisphere.

Southern com rust apparently requires somewhat higher temperatures than common corn rust.

Symptoms. — The uredinia of

this rust, which occur on both

surfaces of the leaves, are definitely lighter in color, somewhat

smaller, and more circular than

those of common corn rust. The

epidermis remains intact over

the pustules for a longer time

than in common corn rust. Teha

are chocolate brown to black and

often in circles around the initial

uredinia (pi. 8, B). They are

easily distinguished from those of

common corn rust, because they

are smaller and the leaf epidermis

over their surface is retained for

a longer time.

Causal Organism. — Puccinia

polysora Underw. is the causal

organism of southern corn rust.

Urediniospores are moderately

echinulate, yellowish to golden,

globose to ovoid, and slightly

larger than those of P. sorghi

Teliospores are chestnut brown to

black, angular, ellipsoid, and

slightly shorter and thicker than

those of P. sorghi. The spores are

two celled, the apical wall is only

slightly thickened, and they are

borne on a short pedicel onefourth or less the length of the

spore. No alternate host for Ppolysora has been reported; con24
sequently, only the uredinial and

telial stages are known.

Control.—This disease has not

become sufficiently important economically in the United States to

develope resistant hybrids. However, in Africa, where it has become a real problem, resistant

hybrids have been produced. Two

physiologic races of the rust have

been reported there. A single

dominant gene determines resistance to one of these races.

Tropical Corn Rust

Tropical com rust is found only

in the warm, humid parts of the

Western Hemisphere and has not

been reported in the United

States. The uredinia that occur

mainly on the upper leaf surface

are oblong, pale yellow, and covered by the epidermis, except for

a small pore or sUt. The telia are

chocolate brown, encircle the uredinia, and remain covered by the

leaf epidermis for a long time.

The causal organism is Physopella

zeae (Mains) Cummins & Ramachar (Angiopsora zeae Mains).

Urediniospores are ovoid, colorless

to yellow, and moderately echinulate. Teliospores are golden

brown, one celled, oblong, angular,

and borne in sessile chains of two

spores. No alternate host has been

found. Nothing is known about

this rust as to inheritance of

resistance.

DOWNY MILDEWS

Seven downy mildew diseases

are known to attack com. Only

crazy top and downy mildew occur

in the United States. The others

are found in the Eastern Hemisphere, particularly in the Philippines, Indonesia, Southeast Asia,

India, and Africa. All these diseases are caused by closely related

species of Sclerospora and Sclerophthora. The symptoms are

somewhat similar. They are characterized by chlorotic streaking,

mottling, stunting, malformation

of tassels and ears, and excessive

tillering. Warm, very humid

weather favors those downy mildew diseases found outside the

United States.

Crazy Top

Crazy top is widespread over

the United States. It has been

reported from New York to California and from Wisconsin to

Texas. However, it is seldom so

prevalent as to cause any appreciable damage. The primary environmental factor determining the

presence of the disease is flooding

or waterlogging of the soil during

the period from germination of

the kernels until seedlings are

4 to 6 inches high.

Symptoms.—The most conspicuous symptom characterizing this

disease, and from which its name

is derived, is the partial to complete proliferation of the tassel

(pi. 8, C). Instead of the normal

floral structures, these parts continue to grow and take on the

shape of small leaves so that the

tassel looks like a large plumy

mass (fig. 8, A). Excessive ear

shoots and an increased number

of intemodes above the ear and

in the shank are characteristics of

this disease. Pronounced stunting,

narrow straplike leathery leaves,

excessive tillering, and complete

suppression of tassel and ear formation are typical symptoms of

severely infected plants (fig. 8,

B).

Causal Organism. — Sclerophthora macrospora (Sacc.) Thirum.

(Sclerospora macrospora Sacc.)

is the fungus causing crazy top

25
BN-11296X, BN-11254X

FIGURE 8.—A, Typical crazy top symptoms; B, severe infection by Sclerophthora

macrospora, showing complete suppression of tassels and ears and the narrow

straplike leaves.

of corn. Sexual spores, or

oöspores, are relatively large,

thick walled, and yellowish. These

presumably germinate to form

sporangia, the asexual phase of

the fungus. Sporangia, which are

exceedingly rare on corn in the

United States, are lemon shaped

and germinate by releasing

kidney-shaped biciliate zoospores.

Little is known regarding the

mode of infection, but it is likely

that penetration takes place by

zoospores, which are released

when oöspores germinate in saturated soil. The parasitic mycelium is completely systemic.

Oöspores are formed in great

abundance in leaf sheaths and in

the straplike narrow leaves of

badly infected plants.

Sclerophthora macrospora, like

all fungi causing downy mildews,

is an obligate parasite. A large

number of wild grasses are attacked by this fungus. These

hosts may be a means by which

the parasite maintains itself in

the absence of com.

Control. — The most direct

means of control is to provide

proper soil drainage. Nothing is

known concerning the relative resistance of hybrids. Seed treatment has no effect in controlling

this disease.

Downy Mildew

Downy mildew is exceedingly

rare. It has been reported on corn

only twice in the United States_

Grayish blotching and mottling of

the leaves, together with chlorotic

streaking and stunting, are symptoms on corn. The fungus Sclerospora graminicola (Sacc.) Schroet.

attacks foxtail grass (Setana

spp.) occasionally. The size and

shape of spore forms, although

26
somewhat similar to those of the two species. The disease is

Sclerophthora macrospora, are of no economic importance in the

sufficiently distinct to separate United States.

VIRUS DISEASES

The virus diseases of corn that

occur in the United States are

corn stunt, sugarcane mosaic,

celery stripe, and leaf fleck. They

have been of little economic importance, and none occur in the

Corn Belt. In certain tropical

areas of the world some virus

diseases of corn have become economically important.

Corn Stunt

Corn stunt was first found in

California and later in the Rio

Grande Valley of Texas. A distinctive symptom of this virus

disease is the abnormal growth

from the nodal buds below the

ear. This growth gives a bushy

appearance to the plants (pi. 8,

D). These lateral branches may

become 2 to 3 feet long. Where

infection takes place early, all the

internodes of the stalk are shortened so that the plant appears

stunted. In later infections only

the internodes above the ear are

shortened. Leaves are light green

and streaked with pale blotches.

Often the tips and margins are

reddish bronze. Several ears are

frequently produced, but these are

small and often only partially

filled. The disease is transmitted

by at least two leafhoppers —

Dalhidus niaidis (DeL. & W.) and

D. eliynatus (Ball). It does not

seem to be transmitted through

the seed. There are marked differences among inbred lines in

resistance to the disease.

Sugarcane Mosaic

Sugarcane mosaic is sometimes

found in the Gulf States on corn

when grown near sugarcane.

Streaking and mottling of the

leaves, together with partial or

complete sterility of the ears, are

the characteristic symptoms. The

virus has a wide host range within

the grass family. It is transmitted

by the corn leaf aphid (Rhopalosiphum maidis (Fitch)) and two

additional species of plant lice.

The disease is not seedborne. With

the introduction of resistant

varieties of sugarcane, the incidence of the disease on corn has

been reduced to a level where it

is no longer of economic importance.

Celery Stripe

Celery stripe is a virus disease

on corn in Florida. Longitudinal

light-green streaks on the leaves

and marked stunting constitute

the main symptoms of the disease.

Darkening of the vascular bundles

in the stalk has been observed in

old infected plants. The virus has

a rather wide host range, among

which are a number of wild plant

species. The cotton or melon aphid

{Aphis gossypii Glov.) is a natural

vector of the virus. There is no

evidence that the disease is of

appreciable economic consequence.

Leaf Fleck

Leaf fleck is a virus disease of

corn, which has been reported

from California. Small pale spots

that later become yellowish and

ultimately affect the entire plant

are the main symptoms. A single

species of a wild grass, hardinggrass (Phalaris tuberosa var.

stenoptera (Hack.) Hitchc), is

27
the only other host. The disease nomic importance. Three species

is not seedborne and of no eco- of aphids can spread the disease.

CORN SMUTS

Corn is attacked by two smuts.

Common smut, or boil smut, is

widely distributed over the world

and is present in nearly every

area where corn is grown. Head

smut of corn is of minor economic

importance in the United States.

It is found mainly in some of the

Western States and rarely east

of the Great Plains. Head smut

is more prevalent in the Eastern

Hemisphere than in the Americas.

Common Smut

Losses from common smut in

the United States are variable,

ranging from a trace up to about

6 percent in localized areas. It is

doubtful whether losses in grain

yield exceed 2 percent over very

wide areas. However, in sweet

corn the losses may be considerably higher. The number, size,

and location of galls on the plant

affect the amount of yield reduction. Large galls on and above

the ear are more destructive than

galls below the ear.

The relationship between weather conditions and the prevalence

and severity of common smut is

not clear. Dry weather generally

favors smut. In the western Corn

Belt common smut appears to be

more prevalent. It is not known

if the dry weather generally prevailing in that area predisposes

the plants to infection or simply

provides better means for the

spread of the fungus. The incidence of smut seems to be higher

among plants grown in soil especially high in nitrogen and particularly where heavy applications

of barnyard manure have been

made. Injuries due to hail or

incurred during cultivation increase the amount of smut by

exposing tissue to invasion by the

pathogen. Injuries resulting from

detasseling in seed fields increase

smut infection at that point of

the stalk where the tassel is

pulled out.

Symptoms.—^The symptoms of

common corn smut are usually

conspicuous and easily recognized.

All aboveground parts of the corn

plant are susceptible (pi. 9,A-D).

Galls are at first covered with a

glistening white membrane. The

interior of these galls soon becomes black and powdery, with

the membrane rupturing to expose the sooty mass of spores.

Galls on leaves seldom develop

beyond the size of a pea. They

become hard and dry and contain

few spores (pi. 9, D). Embryonic

tissue is particularly susceptible

to attack. It is in areas where

such tissue is abundant that galls

are most frequently observed (pi.

9, A and B). Early infection may

cause death of young plants, but

this is very uncommon.

Causal Organism. — Ustilago

maydis (DC.) Cda. is the fungus

causing common com smut. The

chlamydospores, which constitute

much of the black sooty galls, are

brownish black, thick walled,

heavily echinulate, and spherical

to oval. They germinate to form

a promyceHum, on which onecelled, colorless, and very small

elliptical basidiospores are borne.

These basidiospores, or sporidia:

are usually haploid, whereas the

chlamydospores are diploid. Germination of the black chlamydospores takes place in water at

about 50° to 95° F. Infection may

take place by means of infection

28
hyphae either arising directly

from the germinating chlamydospore or developing after the

fusion of sporidia of the opposite

mating types. Infection hyphae

are binucleate; haploid hyphae

are ordinarily incapable of penetrating the host. Penetration

takes place through stomata,

wounds, or directly through cell

walls. The parasitic mycelium

stimulates host cells to increase in

size and number. Eventually

chlamydospores develop in the

mycelium within the galls and

soon they are entirely converted

to a black, powdery, spore mass.

Control.—The most effective

means of control is to avoid very

susceptible hybrids. Control

through crop rotation and destruction of galls has been recommended, but it is unlikely that

such methods would be effective

or even practical where corn is

extensively grown. In small garden plots the removal of galls may

help to reduce the abundance of

spores.

j Head Smut

! Head smut is unimportant economically in the United States

and only rarely have local outbreaks in the Great Plains and

some of the Western States been

of consequence. The disease in

sorghum caused by a different

physiologic race of the same

fungus appears to be more prevalent. Infection may take place

over a wide range of soil temperatures. Dry soil is more favorable

for infection than wet soil.

Symptoms. — The first symptoms of head smut are seen when

tassels and ears appear. These

, parts may be partly or completely

', converted to a mass of brownishblack spores. The galls are first

, covered with a membrane that

soon breaks open to expose the

powdery spore mass and vascular

bundles of the host. These vascular bundles in the galls are one

of the several features distinguishing this disease from common smut. If only parts of tassels

and ears are converted to galls,

it is not uncommon to find leafy

proliferations on these parts. This

stimulation of the formation of

leaves in place of floral parts does

not occur in common smut.

Causal Organism. — Sphacelotheca reiliana (Kühn) Clint, is

the fungus causing head smut of

corn. The chlamydospores are

brown to black, thick walled, and

generally spherical. They germinate to form a promycelium, on

which sporidia are borne. The

sporidia are small, colorless, thin

walled, and single celled. Penetration of the host follows fusion

of sporidia of the opposite mating

types. The binucleate infection

hyphae arising from such fusions

penetrate the young seedling. The

parasitic mycelium develops

systemically in the host, and galls

form after ears and tassels appear. The morphology and life

cycle of the fungus are somewhat

similar to those of Ustilago maydis. Seedling infection and the

systemic nature of the parasitic

mycelium differentiate head smut

from common smut.

Control.—Because of the minor

economic importance of the disease and its occurrence outside

the main corn-growing areas of

the United; States, little is known

regarding the relative resistance

of inbred lines and hybrids. Seed

treatment is somewhat effective in

destroying externally borne spores

on the seed, but it will not protect

against infection in smut-contaminated soil. Crop rotation and seed

treatment are recommended as

partial control practices.

29
AKi-iculture Handbook 199. U.S. Dept. of Agriculture PLATE 1

IP

.*

""fBH

?TMKJ^ ^^^^IJ^^2^ '-'''M^HHHHH

HHHJJ

4, Poor stand of corn resulting from inadéquat« seed treatment and cold,*«

weather after planting. B, Typical symptoms of seed rot and seedling DUgM.

plant on left is healthy.
Agriculture Handbook 199, U.S. Dept. of Agriculture

BN-11269X

A, Premature death due to diplodia stalk rot; compare with healthy green stalks

in background. B, Lower internodes of infected plants. C, Same stalk as

in B but split open to show disintegration of pith. D, Lower internodes of

healthy plant. È, Pycnidia of Diplodia mnydis on infected stalk.
Agriculture Handbook 199, U.S. Dept. of Agriculture PLATE 3

BN-i:276X D

A, Crown of plant affected with gibberella stalk rot; B, breakdown and pin^

discoloration of pith of stalk affected with gibberella stalk rot; C, peritnecid

of Gibberella zeae on diseased stalk; D, pythium stalk rot, showing discoloiation and collapse of lower internodes.
Agriculture Handbook 199, U.S. Dept. of Agriculture

A B

PLATE 4

BN-11274X BN-11275X

A, Diplodia ear rot, showing bleached husks; B, fusarium kernel rot; C, cob rot

with typical shredding and black spore masses at tips of kernels; D, gibberella ear rot.
ARriculture Handbook 199. U.S. Dept. of Agriculture PLATE 5

BN-11287X

A, Discolored husks of ears affected with a;ray ear rot; B, husked ears, showing

typical .Symptoms of gray ear rot; C^ sc'lerotia, or minute black specks, oí

causal fungus beneath seedcoat; D, perithecia and pycnidia of Physalosp

zeae in a leaf lesion.

loro
Agriculture Handbook 199, U.S. Dept. of AM:ricultuTe PLATE 6

BN-U263X D

BN-11265X

A. Typical l.si». .( north. corn let big«; B EXTaf^Ä'', ;'S, .

ar.rifvL°'.yr!irinSr¿:'&,5e^S „ha« o, b.c.er,., -1.

on dent corn.
Agriculture Handbook 199, IT.S. Dept. of Agriculture PLATE 7

BN-11262X

A, Brown spot disease, showing symptoms at base of leaf blades; B, ^y P

of brown spot on leaf sheaths ; C, stalk breaking resulting from severe oro«

spot infection; D, dead lower leaves and stalk infection typical ot DIO

spot disease.
Agriculture Handbook 199, U.S. Dept. of Agriculture

BN-11289X BN-11282X

Common corn rust, showing pustules rupturing epidermis of leaf. B, Telia

of southern corn rust, showing their circular pattern around uredinia ;

epidermis of leaf remains intact over telia for a long period. C, Leaf proliferation of tassel affected with crazy top. D, Corn stunt, showing stunting,

bushiness, and yellowish-green streaking of leaves that typify the disease.
Agriculture Handbook 199. U.S. Dept. of Agriculture PLATE 9

BN-U286X Q

BN-11284X

A, Common corn smut on tassel; B, common corn smut affecting ear; C, infection

of nodal buds; D, small dried smut galls on corn leaf.

:ir U.S. GOVERNMENT PRINTING OFFICE, 1961 0^