chapter 3 corn/ maize diseases
DESCRIPTION
Chapter 3 Corn/ Maize diseases. Introduction. - PowerPoint PPT PresentationTRANSCRIPT
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.
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
Introduction
STALK ROTS AND ROOT ROTS
DIPLODIA STALK ROT
GIBBERELLA STALK ROT
CHARCOAL ROT
PYTHIUM STALK ROT
PYTHIUM ROOT ROT
BACTERIAL WILT
EAR ROTS
DIPLODIA EAR ROT
FUSARIUM KERNEL ROT
GIBBERELLA EAR ROT
GRAY EAR ROT
LEAF DISEASES
NORTHERN CORN LEAF BLIGHT
SOUTHERN CORN LEAF BLIGHT
COMMON CORN RUST
DOWNEY MILDEW OR CRAZY TOP
COMMON SMUT
GRAY LEAF SPOT
CURVULARIA LEAF SPOT
VIRUS DISEASES
MAIZE DWARF MOSAIC
MAIZE CHLOROTIC DWARF
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.
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.
LEAF BLIGHTS
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.
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.
Significance
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.
Symptoms
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.
Pathogen
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 毒力公式（有效抗性基
因 / 无效寄主基因）Ht1 Ht2 Ht3 HtN
1 0 R R R RHt1Ht2 Ht3
HtN/0
2 1 S R R RHt2 Ht3 HtN/Ht1
3 23 R S S RHt1 HtN/Ht2
Ht3
4 23N R S S SHt1 /Ht2 Ht3HtN
5 2N R S R SHt1 Ht3 /Ht2HtN
The fungus causing NCLB overwinters as mycelia and conidia on corn residues left on the soil surface. The conidia are transformed into thick-walled 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.
Disease cycle
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.
Control
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 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.
STALK ROT
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
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.
Ear Rot
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
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.
Virus Diseases
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.
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%.
CORN SMUT
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.
Symptoms
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.
Pathogen
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.
Disease cycle
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, later-growing varieties usually are more resistant than the smaller, early varieties.
Control
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
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.
Introduction
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
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.
Introduction
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.
POTATO LATE BLIGHT
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.
Symptoms
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.
Pathogen
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.
Disease cycle
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
Control
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
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.
Significance
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.
Major Potato Viruses
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.
Control
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 diseases3-9 sweet potato diseases
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.
Introduction
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.
Sweet potato black rotSweet potato black rot
•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.
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
Pathogen
•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
Host range
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.
Biology
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.
Control
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