Transcript Control

Chapter 3
Corn/ Maize diseases
Introduction
Many corn fields develop disease problems every
year that affect yield and quality of the grain crop.
As history has shown repeatedly, corn diseases
can and do periodically cause significant yield
losses in patterns that are difficult to predict in
advance. Corn diseases typically cause minimal
damage over the entire state, however, some
acreage suffers significant disease damage each
year.
Introduction
Fortunately, corn has effective genetic resistance to
many of the important diseases, however,
numerous challenges remain in management of
corn diseases. This includes the seed and
seedling diseases, leaf diseases, stalk diseases,
and ear rots.
Introduction



The diseases of corn may be classified as parasitic
and nonparasitic.
Most parasitic (infectious) diseases of corn are
caused by fungi, a few by bacteria, and a few by
viruses.
Nonparasitic disorders result from unfavorable
climatic and soil conditions. Deficiencies of
nitrogen, phosphorus, or potassium cause some of
the most frequently observed nonparasitic
disorders of corn. Occasionally, corn may suffer
from lack of essential minor elements in the soil.
Introduction
The major corn diseases can be grouped into four
categories: leaf blights, stalk rots, ear rots, and
viral diseases.
Introduction



Ear and kernel rots decrease yield, quality, and
feeding value of the grain.
Stalk diseases not only lower yield and quality, but
also make harvesting difficult.
When leaves are damaged by disease, the
production of carbohydrates to be stored in the
grain is decreased; immature, chaffy ears are the
result.
Introduction
EAR ROTS
LEAF DISEASES
DIPLODIA EAR ROT
NORTHERN CORN LEAF BLIGHT
FUSARIUM KERNEL ROT
SOUTHERN CORN LEAF BLIGHT
GIBBERELLA EAR ROT
COMMON CORN RUST
GRAY EAR ROT
DOWNEY MILDEW OR CRAZY TOP STALK ROTS AND ROOT ROTS
COMMON SMUT
DIPLODIA STALK ROT
GRAY LEAF SPOT
GIBBERELLA STALK ROT
CURVULARIA LEAF SPOT
CHARCOAL ROT
VIRUS DISEASES
PYTHIUM STALK ROT
MAIZE DWARF MOSAIC
PYTHIUM ROOT ROT
MAIZE CHLOROTIC DWARF
BACTERIAL WILT
3-1 LEAF BLIGHTS
Northern Corn Leaf Blight
LEAF BLIGHTS


The most common are gray leaf spot, Stewart's
bacterial leaf blight, and northern corn leaf blight.
These diseases can be found in almost any field,
depending on the year and susceptibility of the
hybrid planted.
Some leaf-blight diseases are most often found
associated with continuous corn, especially in
reduced-tillage, continuous corn fields. These are
anthracnose, gray leaf spot, eyespot, and northern
leaf spot.
LEAF BLIGHTS


All leaf blight diseases cause loss of green leaf
tissue, resulting in fewer kernels and lightweight
grain.
Plants may be predisposed to stalk-rot diseases
when leaf damage is severe.
LEAF BLIGHTS

The amount of yield loss is usually related to the
time when the plant's upper leaves become
infected. The most severe yield loss occurs when
the upper leaves, the ear leaf, and those above the
ear, become infected at or soon after tasseling.
Yield losses will be minimal if disease does not
occur on these leaves until six to eight weeks after
tasseling.
LEAF BLIGHTS



Leaf blight diseases are most effectively controlled
by selecting hybrids with genetic resistance.
Contact your seed dealer for information on
hybrids with resistance to gray leaf spot, Stewart's
bacterial leaf blight and other leaf diseases
important in your area.
A one-to two-year rotation away from corn and
destruction of old corn residues by tillage may be
helpful if susceptible hybrids must be grown.
Fungicides are also available for control of leaf
diseases, but are economically viable only under
severe disease pressure.
Significance


Northern corn leaf blight (NCLB), caused by the
fungus Exserohilum turcicum previously called
Helmithosporium turcicum, can cause yield losses
in humid areas where corn is grown.
NCLB can occur throughout the state but usually
does not appear in fields before silking.
Significance
This
disease rarely causes significant yield losses
during dry weather, but during wet weather it may
result in losses of over 30% if established on the
upper leaves of the plant by the silking stage of
development. If leaf damage is only moderate or is
delayed until 6 weeks after silking, yield losses are
minimal.
Symptoms



Develop on lower leaves first and progress up the
plant under favorable weather conditions
( temperatures of 20－25℃ and high relative
humidity).
Several types of lesions may occur on leaves and
husks.
The type of lesion present is dependent on host
resistance genes.
Symptoms




The typical symptoms seen on a susceptible host
are long elliptical spots up to 15 cm in length.
Spots are grayish-green to tan in color.
Spore produced in the lesions are olive-green to
black and may be produced in concentric rings
giving the spot a target like appearance.
Spores from the primary lesions reinfect the host
producing secondary cycles of the disease.
Symptoms


Lesions produced on hybrids with polygenic
(quantitative) resistance are long and narrow
resembling those of Stewart's wilt. These lesions
may extend the entire length of the leaf. Fewer
lesions are produced on these hybrids and their
size, in term of surface area affected, is less than
on susceptible hybrids.
Lesions produced on hybrids with monogenic
resistance are characterized as small necrotic
spots that are surrounded by a chlorotic halo.
Spore is greatly reduced or absent in these
lesions.
Pathogen


NCLB is caused by the fungus Exserohilum
turcicum, teleomorph Setosphaeria turcica. Both
the common name and causal organism have
several synonyms.
Conidiospores of E. turcicum have a slightly
protruding hilum which aids in identification of the
fungus.
Pathogen



Host of E. turcicum include corn, sorghum,
Sudangrass, Johnsongrass, gamagrass (鸭茅状摩
擦禾，产于美洲，饲料草) and teosinte(墨西哥类蜀
黍).
Exserohilum turcicum is divided into 5 races and
infection of hosts from different genera and species
is dependent on the race.
In addition, two biotypes have been identified from
maize.
玉米大斑病菌的生理分化
小种名
称
新命名
法小种
名称
玉米基因型
Ht1
Ht2
Ht3
HtN
毒力公式
（有效抗性基因
/无效寄主基因）
1
0
R
R
R
R
Ht1Ht2 Ht3
HtN/0
2
1
S
R
R
R
Ht2 Ht3 HtN/Ht1
3
23
R
S
S
R
Ht1 HtN/Ht2 Ht3
4
23N
R
S
S
S
Ht1 /Ht2 Ht3HtN
5
2N
R
S
R
S
Ht1 Ht3 /Ht2HtN
Disease cycle


The fungus causing NCLB overwinters as mycelia
and conidia on corn residues left on the soil
surface. The conidia are transformed into thickwalled resting spores called chlamydospores.
During warm, moist weather in early summer, new
conidia are produced on the old corn residue, and
the conidia are carried by the wind or rain to lower
leaves of young corn plants.
Disease cycle



Infection by germinating conidia occurs when free
water is present on the leaf surface for 6-18 hours
and the temperature is between 18-27℃. Lesions
develop within 7-12 days.
Secondary spread within fields occurs by conidia
produced on the leaf tissues.
The conidiospores germinate and penetrate leaf
tissue directly or through stomata. Infection occurs
when free moisture is present on the leaf surface.
Control


1. Resistant Hybrids
Planting resistant hybrids is the most effective
method for control of NCLB. Hybrids are available
with both monogenic and polygenic resistance
and should be used wheneverpossible.
Control


At least two types of resistance to NCLB are known:
small lesion size and few lesions (controlled by
multiple genes) and chlorotic lesions with little or no
sporulation and a yellowish halo (controlled by a
single gene). Thus, even where resistant hybrids
are planted, leaves may show some flecking or
small lesions, but no economic damage occurs.
Resistant hybrids should be planted in all
commercial dent corn production fields.
Control


2. Residue Management
Severe outbreaks of northern corn leaf blight
are sporadic but the potential for a major
outbreak is present where corn is being
continuously cropped in a conservation tillage
system. Since the fungus that causes the disease
survives between seasons on crop residue,
reduction of the residue should reduce the
amount of inoculum present in the spring.
Control


A one- to two-year rotation away from corn and
destruction of old corn residues by tillage may be
helpful in controlling the disease if susceptible
hybrids must be grown.
In this case a grower may find it useful to rotate
to an unrelated (non-host) crop such as soybeans.
Control



3. Fungicide Application
Several fungicides are labeled for control of
northern corn leaf blight. Mancozeb (代森锰锌)
and propiconazole（丙环唑） are labeled for field
corn, popcorn and sweet corn.
Fungicide sprays are recommended only for
fresh market sweet corn and hybrid seed
production fields. The spray schedule should start
when the first lesions appear on the leaf below the
ear.
小结





发生概况：分布？ 危害？产量损失轻病害识别：为
害？发病时期？症状特点？
病原：分类地位、形态特点、生理分化
病害发生发展规律：越冬、传播、入侵；
发病及其影响因素：品种抗性（抗病类型与抗病机
制）、气候、栽培管理
综合防治：抗病品种；改进栽培技术，减少菌源；
药剂防治（只适用于留种田）
3-2 STALK ROT
STALK ROT



Stalk rots are the most important and common
diseases of corn. Annual losses are estimated at 5
to 10 percent.
There are several stalk-rot diseases, but
Gibberella stalk rot and Anthracnose stalk rot
currently are the most prevalent.
Both are fungal diseases that result in premature
ripening, chaffy ears. The interior of the stalk
becomes rotted, tissues break down, and the stalk
is easily broken.
STALK ROT


Anthracnose stalk rot is usually associated with
continuous corn and is recognized by the
blackening of the outer surface of the stalk late in
the season.
Stalks with Gibberella stalk rot can be found in
nearly any field. Affected stalks often have pink to
reddish discolored internal tissues.
STALK ROT




Control of stalk rot diseases is based on reducing
plant stress from factors such as lack of moisture,
leaf diseases, insect injury, and nutritional stress.
Select hybrids with good stand ability and
resistance to leaf blight diseases.
Adjust soil fertility to recommendations based on a
soil test. Avoid excessive rates of nitrogen in
relation to potassium.
Follow a one- to three-year rotation away from
corn. Soybeans, forage legumes, and small grains
are acceptable in the rotation. The longer the
rotation away from corn the better.
STALK ROT



Plant at populations recommended for the hybrid
grown. Overplanting leads to increased moisture,
light and nutrient competition, and more plant
stress.
Harvest fields with the greatest level of rotted
stalks first to avoid lost ears on lodged plants.
Control insects, particularly root worms and stalk
borer. Insects cause injuries to plant roots and
stalks permitting stalk rot fungi to enter the plant.
小结




发生概况：分布？ 危害？产量损失轻病害识别：为
害？发病时期？症状特点？
病原：有性态：
无性态：
病害发生发展规律：越冬、传播、入侵、发病及其
影响因素(寄主抗病性、气候、栽培管理、预测预
报)?
综合防治：抗病品种；种子处理；田间水肥管理；
化学防治；生物防治
3-3 Ear Rot
Ear Rot




Gibberella, Fusarium, and Diplodia ear rot
diseases occur in the world, but Gibberella ear rot
is the most important.
The Gibberella ear rot fungus is the same fungus
that causes Gibberella stalk-rot disease.
Gibberella enters from the silk end of the ear when
cool, wet weather persists for several weeks
through late silking of the crop.
Ear Rot

The occurrence of a whitish to pinkish mold on the
ear tip is diagnostic, but extensive mold growth
may not occur. On shelled grain, the symptoms
may be seen as a pinkish coloration in some of the
kernels.
Even though extensive rotting does not always occur,
the disease is serious because the fungus
frequently produces toxins that makes the corn
unfit for feeding. Hogs are particularly sensitive to
the toxins produced in moldy grain and may refuse
to eat it even when hungry. Some corn hybrids are
less susceptible than others to Gibberella ear rot.
Ear Rot


Diplodia ear rot appears to be more common in
continuous corn under reduced tillage. Ears
affected by Diplodia are covered with a thick mat of
white fungal growth.
Fusarium ear rot is common, but only individual
kernels are affected on ears.
小结




发生概况：分布？ 危害？产量损失轻病害识别：为
害？发病时期？症状特点？
病原：有性态：
无性态：
病害发生发展规律：越冬、传播、入侵、发病及其
影响因素(寄主抗病性、气候、栽培管理、预测预
报)?
综合防治：抗病品种；种子处理；田间水肥管理；
化学防治；生物防治
3-4 Virus Diseases
Virus Diseases




Maize dwarf mosaic and maize chlorotic dwarf, are
potentially destructive diseases where
johnsongrass is established.
The two viruses that cause these diseases are
able to survive in this perennial weed grass.
Aphids and leafhoppers feeding on johnsongrass
in the spring pick up the virus and inoculate nearby
corn.
Control is achieved by planting resistant or
tolerant hybrids. Efforts also should be made to
eradicate johnsongrass.
3-5 CORN SMUT
CORN SMUT

Corn smut occurs wherever corn is grown. It is
more prevalent, however, in warm and
moderately dry areas. Corn smut damages
plants and reduces yields by forming galls on the
aboveground parts of plants, including ears,
tassels, stalks, and leaves. The number, size,
and location of smut galls on the plant affect the
amount of yield loss.
CORN SMUT


Galls on the ear usually destroy it to a large
extent, whereas large galls above the ear cause
much greater reduction in yield than galls below
the ear.
Losses from corn smut range from a trace up to
10% or more in localized areas. Some individual
fields of sweet corn may show losses
approaching 100% from corn smut. Generally,
however, over large areas and with the use of
resistant varieties, losses in grain yields average
about 2%.
Symptoms



When young corn seedlings are infected, minute
galls form on the leaves and stems, and the
seedling may remain stunted or may be killed.
On older plants, infections occur on the young,
actively growing tissues of axillary buds, individual
flowers of the ear and tassel, leaves, and stalks.
Infected areas are permeated by the fungus
mycelium, which stimulates the host cells to divide
and enlarge, thus forming galls.
Symptoms
Galls are first covered with a greenish white
membrane. Later, as the galls mature, they reach a
size from 1 to 15 centimeters in diameter, and their
interior darkens and turns into a mass of powdery,
dark olive-brown spores. The silvery gray
membrane then ruptures and exposes the millions
of sooty teliospores, which are released into the air.
Galls on leaves frequently remain very small (about
1-2 cm in diameter), hard, dry, and do not rupture.
Pathogen


Ustilago zeae The fungus produces dikaryotic
mycelium, the cells of which are transformed into
black, spherical, or ellipsoidal teliospores.
Teliospores germinate by producing a four-celled
hasidiiim (promycelium) from each cell of which a
basidiospore (sporidium) develops.
Teliospores survives as a resistant spore in the
soil over winter, and possibly for 2 to 3 years. It can
be blown long distances with soil particles or
carried into a new area on unshelled seed corn and
in manure from animals that are fed infected corn
stalks.
Pathogen

The teliospores germinate in moist air and give rise
to tiny spores called sporidia. The sporidia bud like
yeast, forming new spores that germinate in rain
water that collects in the leaf sheaths. This leads to
infections that are visible in 10 days or more.
Wounds from various injuries provide points for the
fungus to enter the plant.
Pathogen

The smut fungus is sensitive to temperature and
moisture changes. In a warm season, the amount
of smut is related closely to the amount of soil
moisture, especially during June. When
temperatures are lower than normal, there may be
little smut even though soil moisture remains high.
Disease cycle


The fungus overwinters as teliospores in crop
debris and in the soil, where it can remain viable for
several years.
In the spring and summer, teliospores germinate
and produce Basidiospores, which are carried by
air currents or are splashed by water to young,
developing tissues of corn plants.
Disease cycle
The smut fungus survives from year to year in old,
smutty corn stalks. Spores may be blown by wind
for considerable distances to new plants. The
fungus often enters plants through wounds made
by hail, cultivating equipment, or detasseling.
Infection may also occur through the silks.
Disease cycle
The fungus grows down the silks to the kernels and
causes galls on the ears. Silk infection must occur
in a 7-10 day period following silk emergence in
order for galls to form.
Disease cycle
Galls in older plants seem always to be the result of
local infections. Systemic infections occur
occasionally in very young seedlings. Frequently,
however, only a small number of the actual local
infections develop into typical, large galls, with the
others remaining too small to be visible.
Disease cycle
The mycelium in the gall remains intercellular during
most of gall formation, but before sporulation, the
enlarged corn cells are invaded by the mycelium,
collapse, and die. The mycelium utilizes the cell
contents for its further growth, and the gall then
consists primarily of dikaryotic mycelium and plant
cell remains.
Disease cycle
Most of the dikaryotic cells subsequently develop
into teliospores and, in the process, seem to
absorb and utilize the protoplasm of the other
mycelial cells, which remain empty. Only the
membrane covering the gall not affected by the
fungus, but finally the membrance breaks and the
teliospores are released.
Disease cycle
Some of released teliospores, if they land on young
corn tissues, may cause new infections and new
galls during the same season, but most of them
fall to the ground or remain in the corn debris,
where survive for several years.
Disease cycle
The factors that determine severity of common smut
are not fully understood. Hot, dry weather during
pollination, followed by rainy weather, seems to
favor disease spread and development. Corn
grown on heavily manured soils often develops
severe smut. Plants on such soil produce succulent
growth, which may be more susceptible to fungal
infection. Such soils may also provide a good
medium for the overwintering and germination of
the smut spores.
Control




1. Cultural Control
Corn smut is not a seed-borne disease;
therefore, seed treatment is of no value.
Collecting and destroying galls before the dark
fungal spores form will help reduce severity in small
plantings.
Crop rotation, in which corn is not grown more
often than one year in three, will help reduce fungal
inoculum in the soil.
Control



2. Resistance
The most effective control is to plant resistant
hybrids. No hybrid is completely immune to smut,
but most of the recommended hybrids of field corn
are reasonably resistant.
Dent corn is generally more resistant than
sweet or popcorn. In sweet corn, the larger, latergrowing varieties usually are more resistant than
the smaller, early varieties.
小结





发生概况：分布？ 危害？产量损失轻病害识别：为
害？发病时期？症状特点？
病原：形态特点、生理特性
病害发生发展规律：越冬、传播、入侵方式
发病及其影响因素：品种抗病性、菌源数量、环境
条件
综合防治：选用抗病品种；减少菌源；加强栽培管
理、种子处理；化学防治
3-6 Gibberella Stalk and Ear Rot
Introduction
Stalk rots of corn are often caused by different
combination of several species of fungi and
bacteria and affect plants when they are nearly
mature. The fungi most commonly responsible for
stalk rots in corn include several species of
Gibberella, Fusarium (F. verticillioides, F.
proliferaturn, and F. suhglutinans), Stenocarpella
(Diplodia), Colletcitrichum graminicola, and
Macrophomina. The stalk rot complex often
causes losses between 10 and 30%.
Introduction
In stalk rot, lower internodes become soft and
appear tan or brown on the outside while internally
they may appear pink or reddish. The pith
disintegrates; leaving only the vascular bundles
intact. The rot may also affect the roots. Stalk rot
leads to a dull gray appearance of the leaves,
premature death, and stalk breakage.
Introduction
The fungus that causes Gibberella stalk rot readily
survives in corn debris. Thus this disease may be
more prevalent in fields where continuous corn is
grown. Deep plowing, or a suitable rotation
strategy helps control the disease. An appropriate
choice of rotation crops is critical however. Use of
soybeans in rotation with corn is likely to provide
better disease control than use of small grains.
Introduction
Remember
that
Gibberella
zeae/Fusarium
graminearum attacks both corn and small grains,
and thus corn may serve as an inoculum source
for small grains and vice versa. Also, as is
generally true for stalk rots, proper soil fertility is
critical in controlling Gibberella stalk rot. A high soil
N/K ratio favors disease development. Finally, use
of resistant varieties can aid in disease control.
Introduction
Several fungi are able to infect corn ears and lead to
decay of corn kernels. Two common ear rots are
shown in this photo. The two ears on the left are
examples of Gibberella ear rot caused by
Gibberella zeae, the same fungus that causes
stalk rot of corn. The two ears on the right are
examples of Fusarium ear rot, caused by the
fungus Fusarium moniliforme. These two ear rots
are similar in that both causal fungi produce large
of amounts of whitish mycelium on the surface of
infected kernels.
Introduction
The two diseases can be distinguished by noting the
pattern of infection on the ear. In Gibberella ear rot,
infection starts at the tip of the ear and moves
toward the base. Typically the husk is also
infected and fuses to the ear. In Fusarium ear rot,
infection tends to be more uniform, with no real
concentration at the tip. Also, fusion of the husk to
the ear is relatively less common.
Introduction
In general, ear rots are of concern because they can
lead to yield reduction. In addition, many ear rot
fungi, including G. zeae and F. moniliforme,
produce toxic compounds (called mycotoxins) that
can adversely affect any animal that consumes
them. Toxic effects of mycotoxins in domesticated
animals vary depending upon the mycotoxin
consumed, but can include refusal to feed, loss of
weight, vomiting, increased occurrence of liver
tumors, loss of kidney function and abortion of
fetuses. Some mycotoxins are carcinogens.
小结





发生概况：分布？ 危害？产量损失轻病害识别：为
害？发病时期？症状特点？
病原：有性态：
无性态：
病害发生发展规律：越冬、传播、入侵
发病及其影响因素：寄主抗病性、气候、栽培管理
综合防治：抗病品种；种子处理；田间水肥管理；
化学防治；生物防治
3-7 Potato Diseases
POTATO LATE BLIGHT
Introduction


Today, potato is the fourth most important food
crop in the world, with annual production
approaching 300 million tons.
A single medium-sized potato contains about half
the daily adult requirement of vitamin C. Other
staples such as rice and wheat have none.
Potato is very low in fat, with just 5 percent of the
fat content of wheat, and one-fourth the calories
of bread. Boiled, it has more protein than maize,
and nearly twice the calcium.
POTATO LATE BLIGHT
Late blight is still the greatest potential disease
threat to the potato crop, accounting for significant
annual losses world-wide. It can destroy foliage
extremely quickly (it is capable of escalating from
low
levels
of
infection
to
complete
haulm
destruction in little more than 2 weeks), causing
reduced tuber yields and altered size grades.
POTATO LATE BLIGHT
The extent of yield loss is dependent on when haulm
loss occurs in relation to tuber bulking, but
responses to fungicide treatment as high as 30
tonnes/ha have been recorded. More sinister is the
potential for infection of the daughter tubers, which
reduces quality or marketable yield and, in severe
cases, can lead to rotting in the ground before
harvest or later in store.
POTATO LATE BLIGHT

Late blight is difficult to diagnose in the early
stages yet, once it is clearly evident, it is virtually
impossible to eradicate except by destroying the
host crop. Spores released from infected plants
are known to be capable of wind-borne migration
over several kilometres. No other disease
demands such collective responsibility to
safeguard potato production.
POTATO LATE BLIGHT

This disease is most destructive in areas with
frequent cool, moist weather. Zones of high late
blight severity include the northern United States
and the east coast of Canada, Western Europe,
central and southern China, southeastern Brazil,
and the tropical highlands. Late blight is also very
destructive to tomatoes and some other members
of the family Solanaceae.
POTATO LATE BLIGHT

Late blight may kill the foliage and stems of potato
and tomato plants at any time during the growing
season. It also attacks potato tubers and tomato
fruits in the field, which rot either in the field or
while in storage. Late blight may cause total
destruction of all plants in a field within a week or
two when weather is cool and wet. Even when
losses in the field are small, potatoes may become
infected during harvest and may rot in storage.
Symptoms
Symptoms appear at first as water-soaked spots,
usually at the edges of the lower leaves. In moist
weather the spots enlarge rapidly and form brown,
blighted areas with indefinite borders. A zone of
white, downy mildew growth 3 to 5 millimeters wide
appears at the border of the lesions on the
undersides of the leaves. Soon entire leaves are
infected, die, and become limp under continuously
wet conditions, all tender, aboveground parts of the
plants blight and rot away, giving off a
characteristic odor.
Symptoms
Entire potato plants and plants in entire fields may
become blighted and die in a few days or a few
weeks. In dry weather the activities of the
pathogen are slowed or stopped. Existing lesions
stop enlarging, turn black, curl, and wither, and no
oomycete appears on the underside of the leaves.
When the weather becomes moist again the
oomycete resumes its activities and the disease
once again develops rapidly.
Symptoms

Affected tubers at first show purplish or brownish
blotches consisting of water-soaked, dark,
somewhat reddish brown tissue that extends 5 to
15 millimeters into the flesh of the tuber. Later the
affected areas become firm and dry and somewhat
sunken. Such lesions may be small or may involve
almost the entire surface of the tuber without
spreading deeper into the tuber interior.
Symptoms

The rot, however, continues to develop after the
tubers are harvested. Infected tubers may be
subsequently covered with sporangiophores and
spores of the pathogen or become invaded by
secondary fungi and bacteria, causing soft rots and
giving the rotting potatoes a putrid, offensive odor.
Pathogen



Phytophthora Infestans
The mycelium produces branched
sporangiophores that produce lemon-shaped
sporangia at their tips. At the places where
sporangia are produced, sporangiophores form
swellings that are characteristic for this oomycete.
Sporangia germinate almost entirely by
releasing three to eight zoospores at
temperatures up to 12 or 15°C, whereas above
15°C sporangia may germinate directly by
producing germ tube.
Pathogen
Branched hyphae or sporangiophores emerge from
the stomata of infected leaves in humid
conditions. They release sporangia that are
spread by rain-splash to neighbouring plants and
there, in the right conditions, infect the new host.
Sporangia are the main means by which blight is
spread but they require a film of moisture on the
leaf surface for at least 12 hours for germination
to occur.
Pathogen
Reproduction in late blight, Phytophthora infestans,
is primarily asexual. The oomycete requires two
mating types for sexual reproduction. However, in
the early 1950’s, two mating types of late blight,
occurring with roughly equal frequency and called
A1 and A2, were discovered in the Toluca Valley of
Mexico.
Pathogen
The population that occurred elsewhere in the world
appeared to comprise the A1 mating type only.
The absence of the A2 type outside Mexico
explained why sexual reproduction had not been
observed since serious studies of the disease
started in the late 1840’s.
Pathogen
Then in the early 1980’s, after a reported discovery
of an A2 isolate in Switzerland, European
researchers started to check their collections of
isolates and discovered the widespread presence
of the A2 mating type, alongside A1. They could
show that the A2 type had been in Europe at
least since 1980. What is more, modern genetic
studies using molecular markers have enabled
workers to identify a new population of the A1
mating type that arose in Europe at the same
time as the A2 mating type.
Pathogen

The A2 and the new population of A1 have
displaced the original population of A1 mating
type that had been present in Europe for perhaps
a period of 140 years. The speed at which this
displacement occurred indicates that the new
population of Phytophthora infestans is fitter than
the old population.
Pathogen

Techniques using molecular markers have shown
that the diversity of virulence and the complexity
of races have increased greatly since 1980.
Whilst both strains reproduce asexually, when
they occur together they are able to combine
sexually and produce thick-walled oospores, a
natural survival (resting) phase for the disease.
These oospores can survive for several years in
the soil and can subsequently germinate to infect
potato plants.
Pathogen
It is not clear to what extent oospores are now
responsible for “transmitting” disease to new
crops, if at all. It is clear, however, that blight
strains have become more genetically diverse
and aggressive, and have the potential to
develop resistance to fungicides more readily. We
should not be unduly alarmed but need to be
mindful that the disease has changed and
continue to treat it with respect and vigilance.
Disease cycle
The pathogen strains that prevailed until the 1980s
belonged to mating type Al and reproduced in the
absence of its compatible mating type A2, i.e.,
asexually. Therefore, they did not produce
oospores and overwintered only as mycelium in
infected potato tubers.
Disease cycle
Spread of the compatible mating type A2 from
Mexico to the rest of the world has made possible
the sexual reproduction of the pathogen, which
results in the production of oospores in infected
aboveground and belowground potato and tomato
tissues. Oospores may survive in the soil for 3-4
years. Such oospores not only can overwinter in
the soil, they also make possible the production of
new more virulent strains through genetic
recombination of pathogenic characteristics of the
mating strains.
Disease cycle
During infection, a number of potato defense-related
genes are induced (activated) by the pathogen,
including genes coding for β-l,3-glucanase, known
to be induced in many host-pathogen systems,
genes
coding
for
enzymes
involved
in
detoxification, and several other types of genes
involved in plant defense against pathogens.
Disease cycle
The mycelium from infected tubers or from
germinating oospores and zoospores spreads into
shoots produced from infected or healthy tubers,
causing discoloration and collapse of the cells.
When the mycelium reaches the aerial parts of
plants, it produces sporangiophores, which
emerge through the stomata of the stems and
leaves and produce sporangia.
Disease cycle
The sporangia, when ripe, become detached and
are carried off by the wind or are dispersed by rain;
if they land on wet potato leaves or stems, they
germinate and cause new infections.
The germ tube penetrates directly or enters through
a stoma, and the mycelium grows profusely
between the cells, sending long, curled haustoria
into the cells. Older infected cells die while the
mycelium continues to spread into fresh tissue.
Disease cycle
A few days after infection, new sporangiophores
emerge from the stomata of the leaves and
produce numerous sporangia, which are spread
by the wind and infect new plants. In cool, moist
weather, new sporangia may form within four
days from infection; thus, a large number of
asexual generations and new infections may be
produced in one growing season.
Disease cycle
Wherever the two mating types Al and A2 are
present together in the same plant tissue,
fertilization may take place and oospores may be
produced. The frequency of oospore formation
and their role in the development of the disease
within a growing season are not yet known. In any
case, as the disease develops, established
lesions enlarge and new ones develop, often
killing the foliage and reducing potato tuber yields.
Disease cycle
The second phase of the disease, the infection of
tubers, varies between potato varieties and
pathogen isolates. It begins in the field when,
during wet weather, sporangia are washed down
from the leaves and are carried into the soil.
Emerging zoospores germinate and penetrate
the tubers through lenticels or through wounds.
Disease cycle
In the tuber the mycelium grows mostly between the
cells and sends haustoria into the cells. Tubers
contaminated at harvest with living sporangia
present on the soil or on diseased foliage may
also become infected. Most of the blighted tubers
rot in the ground or during storage.
Disease cycle
The development of late blight epidemics depends
greatly on the prevailing humidity and temperature
during the different stages of the life cycle of the
oomycete. The oomycete grows and sporulates
most abundantly at a relative humidity near 100%
and at temperatures between 15 and 25°C.
Disease cycle
Temperatures above 30°C slow or stop the growth of
the oomycete in the field but do not kill it, and the
oomycete can start to sporulate again when the
temperature becomes favorable, provided, of
course, that the relative humidity is sufficiently
high.
Control





1. Eliminate sources of infection
– Prevent growth on dumps
– Control volunteer potatoes
– Use high quality seed
– Don’t risk home-saved seed in high blight
years
Control



2. Use more resistant cultivars or ensure varietal
sensitivity influences the control strategy
3. Make well-formed, firm ridges that adequately
cover the daughter tubers
4. Start the spray programme early – no later than
when the plants meet along the row and earlier if
high risk conditions prevail
Control



5. Select fungicides to suit the growth stage of
the crop
6. Watch out for blight forecasts but monitor local
conditions closely
7. Apply fungicides at intervals appropriate to the
risk
Control



8. Be flexible with fungicide programmes - alter
the routine in response to heightened risk
9. Take care that irrigation does not increase the
risk of disease spread, particularly tuber infection
10. Be timely with desiccation: delay lifting until
the foliage has been completely dead for at least
14 days
小结





发生概况：分布？ 危害？产量损失轻病害识别：为
害？发病时期？症状特点？
病原：形态特征；侵染过程；有性态的有无及其作
用
病害发生发展规律：越冬、传播、入侵、中心病株
发病及其影响因素：气象因素，寄主抗病性、栽培
管理、预测预报
综合防治：抗病品种；建立无病留种田；加强栽培
管理；化学防治
3-8 Virus and Viroid Diseases
of Potato
Significance
Potatoes are a vegetatively propagated crop, and
many disease organisms including several viruses
and a viroid are disseminated in tubers. The
important role that tubers play in virus spread is
recognized by the strict requirements for foundation
or certified seed production.
Significance
For example, all four classes of New York foundation
seed shall not show a total in excess of 1/2 percent
of mosaic, leafroll, or spindle tuber viroid based
upon a winter test performed in Florida. Seven
viruses and spindle tuber viroid are recognized as
important in the state from either a production or a
seed certification standpoint. The viruses include
potato leafroll virus, potato viruses Y, X, A, S, M,
and alfalfa mosaic virus, with the first three being
the most important.
Major Potato Viruses

Potato leafroll virus (PLRV) causes an important
disease of potatoes affectine the auantitv and
quality of production and may cause a crop to be
ineligible for certification. Foliar symptoms of
PLRV can be divided into primary and secondary
infections.
Major Potato Viruses

Primary infection results when an initially healthy
plant is inoculated via aphids during the current
season. Symptoms first appear where inoculation
occurs. The upper leaves become pale, upright,
and rolled and show some reddening of the tissue
a round the leaf edges. The lower leaves may or
may not have symptoms.
Major Potato Viruses
Secondary infection occurs when an infected tuber
is planted, giving rise to an infected plant. The
lower leaves are severely rolled and leathery to
the touch. The plant frequently has an overall
stunted, upright, chlorotic appearance. The oldest
leaves may show reddening on the margins or
chlorosis. The upper leaves may not have obvious
symptoms.
Major Potato Viruses
Some varieties such as Russet Burbank are very
susceptible to PLRV and to tuber symptoms of
internal net necrosis. Many varieties grown in the
Northeast are not subject to net necrosis. PLRV
can be difficult to detect because foliar symptoms
are not always obvious. Thus infected tubers or
tubers with net necrosis may result from plants
without visual symptoms.
Major Potato Viruses
PLRV is transmitted in a persistent manner by
several aphid species, the most important
being the green peach aphid (Myzas
persicae). In addition to infecting potato, the
virus infects other solanaceous crops and
weeds (tomato, tobacco, jimsonweed, etc.).
Control consists of suppressing aphid
populations with systemic and (or) foliar
insecticides and planting certified seed.
Major Potato Viruses


Potato virus Y
Potato virus Y (PVY) is one of the most
important viruses infecting potatoes. It is
readily spread by aphids in a nonpersistent
manner as well as mechanically by human
activity and may result in severely depressed
yields. PVY is tuberborne and can interact
with other viruses such as PVX and PVA to
result in heavier losses.
Major Potato Viruses
Symptoms caused by PVY infection can vary
depending upon the strain and potato variety
grown. A rugose mosaic symptom is characteristic
for some strains, but is most commonly ascribed to
a mixture of PVY and PVX. Other strains produce
a general mosaic or a hypersensitive (severe
necrotic) reaction.
Major Potato Viruses
Necrosis may progress to total leaf collapse,
with the dead leaflet clinging to the stem.
Some
varieties
with
a
strong
hypersensitivity reaction display field
resistance, and the progeny from such
plants may be healthy. Besides infecting
potato, PVY affects other solanaceous
crops (tomato, pepper) and weeds
(nightshade, groundcherry).
Major Potato Viruses
Potato Virus X (PVX) is one of the most widely
distributed viruses of potatoes because no
symptoms develop in some varieties (latent
mosaic), the full extent of damage with PVX is not
recognized. Mixed infections of PVX with other
viruses like PVY and PVA cause more damage
than PVX alone. PVX is tuberborne and is readily
mechanicaly transmitted by human activities.
Tobacco, pepper, and tomato are additional hosts
for this virus.
Control
Potato viruses represent a large portion of the
disease problems that routinely face the potato
industry. Control of these virus diseases is
expensive, but has been accomplished using seed
certification programs. In recent years, however,
potato breeding programs have introduced a
number of cultivars that have good agronomic
characteristics, but often lack adequate virus
disease expression.
Control
Efforts to control diseases in these potatoes (virus
susceptible, but with an almost latent disease
expression) have been of major concern to
certification
programs.
Through
good
communication between the breeding and
certification programs, the newest cultivars being
released appear to have both agronomic
characteristics and some level of virus resistance.
Additionally, screening programs are weeding out
those cultivars with latent expression to major
viruses.
Control
Other recent efforts by commercial companies and
universities have incorporated virus resistance
into existing cultivars through biotechnology.
Further development of this science has been
slowed by lack of consumer acceptance. Finally,
import of new cultivars from outside of the typical
U.S. system are also straining the system
regarding
cultivar/virus
interactions
and
symptomology.
Control
Potato viruses influence not only the processing and
fresh pack industries, but commercial growers,
seed growers and the general public. Control of
virus diseases requires the use of chemical
pesticides, thus there is intense scrutiny by the
public and EPA about environmental contamination
and food safety.
Control
Efforts made by researchers, regulators, and
producers to limit virus spread helps reduce
pesticide use and limits pest resistance problems.
These practices ultimately produce lower costs
and result in a healthier potato industry.
小结






发生概况：分布？ 危害？产量损失
病害识别：不同毒源的症状特点
病原：毒源种类
病害发生发展规律：越冬、传播方式
发病及其影响因素：介体与气候条件，品种因素，
栽培与耕作因素
综合防治：抗病品种；防治传毒蚜虫，加强栽培管
理，化学防治
3-9 sweet potato diseases
Introduction



The most common sweet potato diseases are
stem rot (wilt), nematodes, black rot, and soft rots.
These diseases and others can cause heavy
losses in the field and in storage.
They can be prevented or controlled by following
recommended practices in selecting resistant
varieties, selecting seed stock, producing
transplants, selecting fields, and growing
practices.
Introduction


black rot, and stem rot usually come from disease
infested seed stock and can be controlled by a
fungicide dip before bedding seed roots.
Nematodes can come from infested plant growing
beds or infested soil. Fields known to be infested
with nematodes or other sweet potato diseases
should be avoided. A three to five year rotation
should be practiced.
Introduction

Soft rots and other storage disease problems can
be reduced by sanitation and disinfection of the
storage house, proper curing, and careful
handling of the sweet potatoes during harvesting,
curing, and storage.
Sweet potato black rot
Black rot is caused by the fungus Ceratocystis
fimbriata. The disease can cause significant
losses during storage, in the transplant bed, and
in the field. The pathogen not only reduces yield
and quality but also gives the sweet potatoes a
bitter taste.
•Early symptoms: small, circular, slightly sunken,
dark brown or grey spots on the sweet potato
surface.
Right: Sweet potatoes
in storage with early
symptoms of black rot,
including some white,
fluffy, mycelial growth
of Ceratocystis
fimbriataon the black
rot lesions.
•Advanced symptoms: large, circular, sunken, dark
brown to black spots on the sweet potato surface.
The brownish colored rot usually remains
shallow, but can extend into the inner part of
the potato, leading to rot by secondary
organisms which can destroy the entire root.
Sunken cankers and lesions appear on sweet
potato underground stems; roots can rot.
Pathogen




Ceratocystis fimbriata(fungus)
Originally described on Ipomoea batatas(sweet
potato) in 1890 (Halstead, 1890).
There are several apparently host-specialized
strains that are sometimes called ‘types’,
‘races’or ‘forms’, and many of these may prove to
be distinct species.
Cross-inoculation studies between Ceratocystis
from different host plants has proven the host
specificity of some of these types
Host range








•Theobromacacao(cacao)可可
•Mangiferaindica(mango)芒果
•Ipomoea batatas(sweet potato)
•Coffea sp. (coffee)咖啡
•Eucalyptus spp. 桉树
•Citrus spp. 柑橘
•Crotolaria juncea(sunn hemp)印度麻
•Hevea brasiliense(rubber)橡胶
Host range








•Colocasia esculenta*(taro)芋头
•Xanthosoma sp.(dasheen)黄体芋属
•Syngonium sp.*合果芋
•Ficus carica(fig)无花果
•Spathodea campanulata(African Tulip tree)火焰树
•Acacia mearnsii 果荆树
•Erythrina sp.荆桐
•Manihot esculenta(cassava)花叶木薯
Biology



Dispersal or spread of the black rot fungus: The
fungus is spread by wind, water, soil, on harvesting
baskets, on farm machinery, by some insects, by
humans (clothing), by contaminated tools
Survival of the fungus: The fungus survives in soil, in
water, and on decaying organic matter such as
sweet potato debris left in the field. It can survive for
several years in the soil.
Infection of sweet potato: Wounds on the sweet
potato skin are important entry points for infection by
the fungus. Sweet potato roots and stems are also
susceptible to infection.
Control






Crop rotation: perhaps the most important practice
for controlling black rot.
Sweet potatoes should not be planted in the same
field more than once every third or fourth year.
Rotation crops should not be hosts for C. fimbriata.
Bedding site selection
Sweet potatoes should not be bedded in sites that
have been used to grow sweet potatoes within the
last three years.
New land should be used for bedding.
Control





Selection of seed roots
Only sweet potato cuttings free of disease
should be selected for bedding for plant production.
Do not plant infected sweet potato roots.
Cutting of transplants
It is critically important for transplants to be cut at
least 2 cm above the soil line, to exclude infected
underground portions of the stem.
Control






Careful handling
The crop should be handled carefully during
growth and harvesting operations to minimize
wounding to the potatoes.
Field sanitation
The sweet potato crop debris should be removed
from the field after harvest.
Cull diseased potatoes before washing
Do not wash and package sweet potatoes from
crops that show any signs of infection, as the
incidence of disease may increase drastically
following this operation, and equipment may
become contaminated.
Control






Washing
Clean, fresh water should be used to wash the
potatoes. The water should not re-circulate.
Storage
The potatoes should not be stored or covered
when they are wet. Allow them to dry after
washing. Store in well-ventilated location.
Shippers: Do not allow boxes to get wet get wet
during shipping or at any time.
Ventilated boxes are much better for controlling
black rot disease.
Control




Decontamination of tools and equipment
Any equipment or materials that come into
contact with an infected crop (washing machines,
storage crates, storage structures) should be
decontaminated.
Spray empty washing machines and crates
with a fungicide.
Storage facilities should be thoroughly
cleaned before harvest.
小结






发生概况：分布？ 危害？产量损失
病害识别：为害？发病时期？症状特点？
病原：分类地位，形态特征
病害发生发展规律：育苗期，大田期，贮藏期
发病及其影响因素：寄主抗病性、伤口、温湿度
综合防治：严禁病薯、病苗调运；建立无病留种田，
培育无病壮苗；加强苗床管理；搞好耕作栽培管理；
做好旧窖消毒及贮藏期管理；选用抗病品种