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Transcript
Submitted to: Dr.S.K.Shahi
Department of microbiology
CCS University Meerut
Submitted by:Gaurav Kumar Pal
M. Sc. Applied Microbiology
3 rd semester
Cereals crops: An Introduction :Cereal Crops are members of the grass family grown for their edible starchy
seeds. The important cereal crops produced in India are WHEAT, BARLEY,
OATS, RYE and CORN; small hectarages of TRITICALE and grain MILLETS are
grown. The cool, short growing seasons prevent commercial production of rice
and grain sorghum.
Cereal crops may be divided into spring-sown types, which complete their life
cycle in one season (summer annuals), and fall-sown types, which require an
overwintering period (winter annuals). Among the fall-sown types, winter rye is
the most winter hardy, followed by winter triticale and winter wheat, then winter
barley; winter oats are least hardy. No winter forms of grain millets or corn exist.
In 2006 approximately 98% of the 10.7 million ha of wheat, 90% of the 3.8 million
ha of barley and 77% of the 1.9 million ha of oats produced were grown. India is
the leading producer of wheat.
Significant quantities of oats are also produced in UP,panjab etc. .
In 2006, 244 900 ha of mixed grain (usually oats and barley grown together) are
produced. Production of spring rye is negligible. Of the nearly 1.4 million hectares
of grain corn produced, about 70% is grown in india. Winter rye can be grown in
many areas of India. Wheat, oats, barley, rye and triticale are considered coolseason crops. Their spring forms are normally seeded between mid-Apr and midMay, completing their life cycles in 80-100 days under Indian conditions. The
winter forms, seeded in Sept, overwinter as seedling plants and mature the
following July. The other cereals are warm-season crops. Corn is seeded during
the first 3 weeks of May and requires the full growing season to reach maturity.
Grain millets may be seeded in May or June and mature in about 90 days. Rye,
corn and sorghum are cross-pollinated species; the other cereal crops are selfpollinated.
The main cereals crops are as following :1.WHEAT
2. BARLEY,
3. OATS,
4.RYE
5.CORN
Different types of cereals crops are affected by various type of bacterial fungal
&viral disease.
They damage the grains & straw yield of cereals crops.
Disease in rice:Disease in rice can be caused by various types of microorganism such as
bacteria,fungi,virus.
They caused the various fungal ,bacterial ,& viral disease. They damage to the
quality of the the crops products.
The main disease caused by the different microorganism is as following :-
1.Bacterial leaf blight (BB):Disease name:- Bacterial leaf blight
Pathogen:-Xanthomonas oryzae
Seedling wilt (IRRI).
Leaf blight (IRRI).
Symptoms:1) Water-soaked to yellowish stripes on leaf blades or starting at leaf tips
then later increase in length and width with a wavy margin.
2) Appearance of bacterial ooze that looks like a milky or opaque dewdrop
on young lesions early in the morning.
3) Lesions turn yellow to white as the disease advances.
4) Severely infected leaves tend to dry quickly
5) Lesions later become grayish from growth of various saprophytic fungi
6) Seedling wilt or kresek
7) Observed 1-3 weeks after transplanting
8) Green water-soaked layer along the cut portion or leaf tip of leaves as
early symptom
9) Leaves wilt and roll up and become grayish green to yellow
10)Entire plant wilt completely
11)Yellow leaf or pale yellow of mature plants
12)Youngest leaf is uniform pale yellow or has broad yellow stripe
13)Older leaves do not show symptoms
14)Panicles sterile and unfilled but not stunted under severe conditions
Why and where it occurs:The presence of weeds around the field, the rice stubbles, and ratoons of
infected plants sustains survival of the disease. They become sources of initial
inoculum. Likewise, the bacteria in the rice paddy and irrigation canals
encourage new infection on leaves.
Warm temperature (25-30° C), high humidity, rain and deep water favor the
disease. Wetland areas also encourage the presence of the disease. Severe
winds, which cause wounds, and over fertilization are suitable factors for the
development of the disease.
Irrigation water and splashing or windblown rain can disseminate the bacterium
from plant to plant. The use of trimming tools for transplanting and by handling
during transplanting can also trigger new infection. For example, the kresek
symptom is associated with seedling infection, which was damaged during
transplanting operations.
Economic importance
Bacterial blight is reported to have reduced Asia's annual rice production by as
much as 60%. For example, in Japan, about 300,000 to 400,000 hectares of rice
were affected by the disease in recent years. There were 20% to 50% yield
losses reported in severely infected fields. In Indonesia, losses were higher than
those reported in Japan. In India, millions of hectares were severely infected,
causing yield losses from 6% to 60%.
Management principles
Practicing field sanitation such as removing weed hosts, rice straws, ratoons, and
volunteer seedlings is important to avoid infection caused by this disease.
Likewise, maintaining shallow water in nursery beds, providing good drainage
during severe flooding, plowing under rice stubble and straw following harvest
are also management practices that can be followed. Proper application of
fertilizer, especially nitrogen, and proper plant spacing are recommended for the
management of bacterial leaf blight.
The use of resistant varieties is the most effective and the most common
management practices adopted by farmers in most growing countries in Asia.
When different strains of bacteria are present, it is recommended to grow
resistant varieties possessing field resistant genes. Fallow field and allow to dry
thoroughly is recommended.
Seed treatment with bleaching powder (100µg/ml) and zinc sulfate (2%) reduce
bacterial blight. Control of the disease with copper compounds, antibiotics and
other chemicals has not proven highly effective.
2. Rice blast:Disease name:- Rice blast
Pathogen:-Pyricularia grisea
P. oryzae Cavara
Symptoms:1) All aboveground parts of the rice plant (leaves, leaf collar, culm, culm
nodes, neck, and panicle) are attacked by the fungus.
2) Initial symptoms on the leaves are white to grayish green circular lesions
or spots with dark green borders
3) Older lesions on the leaves are elliptical or spindle-shaped and whitish to
gray with brownish or necrotic border
4) Lesions on the leaves may enlarge and coalesce to kill the entire leaves.
5) Lesions on the collar are brown to dark brown and can kill the entire leaf
blade
6) Lesions on the node are blackish to grayish brown and causes the culm to
break at the infected node.
7) Internodal infection of the culm occurs in a banded pattern with a 3-cm
blackened necrotic culm and 3-cm healthy tissue in succession
8) Internodal infection also occurs at the base of the plant which causes
white panicles similar to that induced by yellow stem borer or water deficit
9) Lesions on the neck are grayish brown and causes the girdling of the neck
and the panicle to fall over.
10)If infection of the neck occurs before milk stage, no grain is formed, but if
infection occurs later, grains of poor quality are formed.
11)Lesions on the branches of the panicles and on the spikelet pedicels are
brown to dark brown.
12)The size and shape of the spots vary on different rice varieties.
Why and where it occurs
In the tropics, blast spores are present in the air throughout the year, which
makes the continuous development of the disease possible. The pathogen
infects upland rice more severely than irrigated rice. Growing rice in aerobic soil
in wetlands where drought stress is prevalent also favors infection.
In the temperate countries, the pathogen overseasons in infected crop residues
or in seed.
Cloudy skies, frequent rains and drizzles favor the development of rice blast.
High relative humidity, and extended duration of leaf wetness favor infection. The
rate of sporulation is highest with relative humidity of 90% or higher. The
optimum temperature for germination of the spores of the pathogen is 25-28°C.
Low solar radiation and overcast skies also favor blast. Excess amount of
nitrogen fertilizer like ammonium sulfate, high amount of nitrogen early in the
cropping season have been found to cause severe blast disease.Primary
infection starts where seed is sown densely in seedling boxes for mechanical
transplanting.
Economic importance
Rice blast is one of the most destructive diseases of rice. A 10% neck blast was
reported to cause yield loss of 5-6% and causes chalky kernels. In India, more
than 266,000 tons of rice were lost, which was about 0.8% of their total yield. In
Japan, the disease was reported to occur in about about 865,000 hectares of rice
fields. In the Philippines, yield losses ranging from 50 - 85% were reported before
the introduction of resistant varieties.
Management principles
There are some cultural practices that are recommended against the rice blast.
Early sowing of seeds after the onset of the rainy season is more advisable than
late-sown crops. Early sowing allows escape from the build-up of inoculum
originating from neighboring farms. Excessive use of fertilizer should be avoided
as it increases the intensity of blast, indirectly by promoting luxuriant crop growth
which in turn increases the relative humidity and leaf wetness of the canopy.
Excessive application of nitrogen at the start of the cropping season should be
minimized to avoid luxuriant crop growth which favors the disease. Split
application of nitrogen based on the actual requirements of the crop is
recommended to manage the disease.
Soils known to be low in plant-available silicon should be amended with calcium
silicate slag.
Planting resistant varieties against the rice blast is the most practical and
economical way of controlling rice blast.
Systemic fungicides, such as probenazole, tricyclazole, fthalide, pyroquilon and
tricyclazole, are effective against the disease.
3. Brown spot disease
Pathogen:-Bipolaris oryzae ,
Drechslera oryzae
Helminthosporium oryzae
Cochliobolus miyabeanus
Brown spots on leaves
Symptoms:1. Infected seedlings have small, circular or oval, brown lesions, which may
girdle the coleoptile and cause distortion of the primary and secondary
leaves (symptom is called seedling blight)
2. Infected seedlings become stunted or die
3. Young or underdeveloped lesions on older leaves are small and circular,
dark brown or purplish brown
4. A fully developed lesion on older leaves is oval, brown with gray or whitish
center with reddish brown margin
5. Lesions on older leaves of moderately susceptible cultivars are tiny and
dark
6. When infection is severe, the lesions may coalesce, killing large areas of
affected leaves.
7. Infected glumes with black or dark brown spots
8. Velvety appearance of lesions on infected glumes under severe conditions
9. Infected grains with black discoloration or with brown lesions
10.Infected young roots with black discoloration.
Why and where it occurs:The fungus can survive in the seed for more than 4 years. Infected seeds,
volunteer rice, infected rice debris, and several weeds are the major sources of
inoculums in the field. Infected seeds give rise to infected seedlings. The fungus
can spread from plant to plant and in the field by airborne spores.
The disease is common in nutrient-deficient soils and unflooded soil but rare on
rice grown on fertile soils.
Abnormal soils, which are deficient in nutrient elements, or soils in a muchreduced condition in which toxic substances accumulate favor the development
of the disease.
Disease development is favored by high relative humidity (86-100%) and
optimum temperature between 16 and 36°C. Leaves must be wet for 8-24 hours
for infection to occur. Yield losses due to brown spot epidemic in Bengal in 1942
was attributed to continuous temperature of 20-30°C for two months, unusually
cloudy weather, and higher-than-normal temperature and rainfall at the time of
flowering and grain-filling stages.
Economic importance
The disease causes blight on seedlings, which are grown from heavily infected
seeds, and can cause 10-58% seedling mortality. It also affects the quality and
the number of grains per panicle and reduces the kernel weight. The reduction in
yield can be as high as 45% in severe infection and 12% in moderate infection.
There is no loss in yield in light infection. The disease was considered to be the
major factor contributing to the “Great Bengal Famine” in 1942 resulting to yield
losses of 50% to 90% and caused the death of 2 million people. Epidemics in
India have resulted in 14-41% losses in high yielding varieties. Under favorable
environment, yield loss estimates ranging from 16 to 40% in Florida, USA was
reported.
Management principles
The use of resistant varieties is the most economical means of control. There are
cultivars in Thailand, which are found to be resistant to the disease. Proper
management of fertilizer by using silicon fertilizers (e.g., calcium silicate slag) in
poor soil conditions can be used to reduce disease intensity.
Since the fungus is seed transmitted, a hot water seed treatment (53-54°C) for
10-12 minutes may be effective before sowing. This treatment controls primary
infection at the seedling stage. Presoaking the seed in cold water for 8 hours
increases effectivity of the treatment.
Seed treatment with captan, thiram, chitosan, carbendazim, or mancozeb has
been found to reduce seedling infection. Seed treatment with tricyclazole
followed by spraying of mancozeb + tricyclazole at tillering and late booting
stages gave good control of the disease. Application of edifenphos, chitosan,
iprodione, or carbendazim in the field is also advisable.
4.False smut disease
Disease name:- False smut
Pathogen:- Ustilaginoidea virens
Symptoms :1. Individual rice grain transformed into a mass of velvety spores or yellow
fruiting bodies
2. Growth of velvety spores enclose floral parts
3. Immature spores slightly flattened, smooth, yellow, and covered by a
membrane
4. Growth of spores result to broken membrane
5. Mature spores orange and turn yellowish green or greenish black
6. Only few grains in a panicle are usually infected and the rest are normal
Severely infected panicle (IRRI) & Infected grains (on left) (IRRI).
Why and where it occurs
The disease is favored by periods of rain, high humidity, and soils with high
nitrogen content. Wind causes dissemination of the spores from plant to plant.
The fungus overwinters as sclerotia and chlamydospores. The primary infection
of rice plants begins from the ascospores that are produced from sclerotia,
whereas the secondary infection comes from chlamydospores.
Economic importance
The disease causes chalkiness and can reduce 1,000-grain weight. It also
causes a reduction in seed germination of up to 35%. In damp weather, the
disease can be severe and losses can reach 25%. In India, a yield loss of 7-75%
was observed.
Management principles
No special control measures are necessary.
There are varieties that are found to be resistant or tolerant against the disease
in India.
Among the cultural control, destruction of straw and stubble from infected plants
is recommended to reduce the disease.
In areas where the disease may cause yield loss, applying captan, captafol,
fentin hydroxide, and mancozeb can be inhibited conidial germination. At tillering
and preflowering stages, spraying ofcarbendazim fungicide and copper base
fungicide can effectively control the disease.
5.Tungro disease :-
Leaf symptoms of Tungro(IRRI)
Signs and symptoms
1. Discoloration begins from leaf tip and extends down to the blade or the
lower leaf portion
2. Infected leaves may also show mottled or striped appearance – stunting
3. reduced tillering
4. delayed flowering, which may delay maturity - panicles small and not
completely exserted
5. most panicles sterile or partially filled grains and covered with dark brown
blotches.
Why and where it occurs
Tungro incidence depends on the availability of the virus sources, population
and composition of the vector, age and susceptibility of host plants, and
synchronization of the three factors mentioned.
Economic importance
Tungro is one of the most damaging and destructive diseases of rice in countries
in Southeast Asia. Outbreaks of the disease can affect thousands of hectares in
many countries. Plant infected with the virus at the early crop growth stage could
have as high as 100% yield loss in severe cases.
The damage caused by the disease depends on the variety used, the plant stage
when infection occurs, the virus particles, and the environmental conditions.
Management principle:- There are three limitations of effective tungro
management:
1) the absence of symptoms at early growth stage of the disease development,
2) lack of resistant varieties to the tungro viruses, and
3) vector adaptation on GLH-resistant variety.
Planting of resistant varieties against tungro virus disease is the most economical
means of managing the disease. There are resistant varieties from the
Philippines, Malaysia, Indonesia, India, and Bangladesh, which are available.
Among the cultural management practices, adjusting the date of planting is
recommended. Likewise, observing a fallow period of at least a month to
eliminate hosts and viruses and vectors of the disease and plowing and
harrowing the field to destroy stubbles right after harvest in order to eradicate
other tungro hosts are also advisable.
Disease of wheat
Rust Disease: Earliest known disease of crop plants
 Three different forms of rust attack on wheat crops.
1. Black or stem rust (Puccinia graminis tritici)
2. Leaf or Brown or orange rust (Puccinia triticina Eriks.)
3. Yellow or stripe rust(Puccinia striiformis)
 Found in all over the world .
6.Stem rust or Black rust disease
Common Disease Name: Stem rust or Black rust.
Pathogen: Puccinia graminis f. sp. tritici.
Symptoms:
1. Oval lesions of uredinia (mass of spores) generally appear on leaves,
sheaths, stem, glumes, spikes and awns.
2. Stems and leaf sheaths are the main tissues affected.
3. On stems, the uredinia are reddish-brown and can be seen to rupture the
host epidermis. On the leaves; uredinia generally penetrate through.
4. Sometimes black lesions are also observed these may indicate the
presence of telia (lesions with resting spores).
5. Uredinia fuse to cover large areas of the host tissue during heavy
infection, releasing a powdery mass of spores.
6. From the seedling stage to the five- or six-leaf stage, stem rust infections
are most obvious on the leaves.
Why and where it occurs:
Presence of mycelium or uredinia on volunteer wheat or barley plants, other
species related to wheat,, wild grasses or berberry plants sustains survival of the
inoculum.
The pathogen (through urediniospores) is effectively dispersed over great
geographical distances by air currents and climatic conditions. Rain or dew is
necessary for effective deposition and germination of uredinospores on
susceptible host plants.
Favorable conditions for infection are hot days (25-30°C) and mild nights (1520°C) with adequate moisture for night time dews.
P. graminis occurs worldwide wherever wheat is grown.
Economic importance:
Stem rust has been largely under control worldwide since the deployment of
resistant varieties. Widespread epidemics are infrequent, but disease within a
region or in individual fields can frequently be severe, resulting in the destruction
of between 50 to 70% of the crop. More recently, a virulent race Ug99 has
evolved in East-Africa that threatens current sources of resistance.
Management principles:
Quarantine of the pathogen is impossible because of the airborne nature of rust
fungal spore dispersal.
Removal of susceptible barberry bushes eliminates local sources of the fungus
and importantly removes the sexual stage of the pathogen’s life cycle, hence
reducing the formation of new races with new combinations of virulence genes.
The use of resistant varieties is the most effective, least expensive and
environmentally friendly means of controlling the disease. Multigenic resistance
(combination of specific or minor resistance genes) may be a more long-term
form of controlling the disease.
Because new rust races can and do arise, global monitoring of new rust races is
not only important for breeding of rust resistance but also in predicting epidemics.
Where possible, a reduced exposure time of wheat to the pathogen by planting
early or through the use of early-maturing cultivars can reduce damage severity
in some areas where inoculum is transported from other areas.
Effective fungicides against rusts are available; however they have not been
widely used mainly because cost-benefit analysis has shown it to be nonprofitable to the farmer.
7. Leaf rust disease
Disease Name: Leaf rust or brown rust.
Pathogen: Puccinia triticina and Puccinia tritici-duri
Symptoms:
1. The fungus forms small reddish-orange pustules (uredinia), which rupture
the upper surface of the leaf blade as the spores mature.
2. Affects primarily the leaves and leaf sheaths.
3. As the leaves age, the pustules begin to produce dark black spores.
These glossy, black pustules (telia) are mostly seen on the lower leaf
surface and leaf sheaths covered by epidermal tissue. Teliospores do not
infect wheat. Telia may not develop when plants become infected near
maturity.
4. Individual pustules are circular to oval with a diameter of 1.5 mm.
5. On resistant wheat cultivars pustules may appear as small, necrotic spots
which does not develop spores or have tiny pustules with little sporulation.
On moderately resistant wheat cultivars, the uredinium is surrounded by a
halo of pale green or yellow host plant tissue, limiting the extent of
infection.
Why and where it occurs:
Occurs worldwide wherever wheat is grown, excellent conditions for disease
development are cool nights, high atmospheric moisture combined with warm
days (15 to 25°C).
Urediniospores of the pathogen germinate and infect susceptible or moderately
susceptible wheat plants and produce more spores under ideal conditions.
During ideal conditions the pathogen life cycle may take 7-10 days to complete.
A minimum of 7-9 cycles would be required to cause an epidemic.
The leaf rust pathogen survives the period between wheat harvest and sowing by
infecting volunteers (self-sown) of wheat or wild grasses which provide a ‘green
bridge’ for survival of the pathogen across seasons.
Leaf rust pathogen which has survived on volunteers, initiate disease from the
lower leaves whereas the disease initiated from upper leaves are due to wind
dispersed spores.
Economic importance:
The disease causes more damage worldwide than other wheat rusts. On
average losses range from 5 to 20%, however in severe cases can reach 50%.
Management principles:
The use of resistant varieties is the most effective, least expensive and
environmentally friendly means of controlling disease. Multigenic resistance
(combinations of major or minor resistance genes) is be the most long-term form
of controlling the disease.
New leaf rust races do arise, thus monitoring of new races is not only important
for breeding of leaf rust resistance but also in predicting epidemics.
Prior removal of volunteer plants which support disease growth between wheat
cropping seasons will reduce the amount of rust inoculum. However, disease can
still occur from wind dispersed spores from distant sources.
Where possible damage severity can be reduce by minimizing exposure time of
wheat to the pathogen by planting early or through the use of early-maturing
cultivars.
Fungicide application is only recommended if; the wheat variety is susceptible to
leaf rust, the yield potential of the crop is high or the disease started early and
the flag leaf is in danger of becoming infected.
8.Stripe rust disease
Common Disease Name: Stripe rust or yellow rust.
Pathogen: P. striiformis West. f. sp. tritici Eriks. & E. Henn.
Symptoms:
1. The fungus forms clusters of tiny yellow- to orange-colored pustules,
called uredinia. On young plants the pustules appear as blotches covering
large areas of affected leaves. In older plants pustules appear in linear
2.
3.
4.
5.
6.
rows on the leaf forming narrow stripes along the length of the wheat leaf,
which eventually merge and whole leaf can be covered with uredinia in
susceptible cultivars. Resistant cultivars can show from small necrotic
stripes to blotches carrying uredinia that have little or moderate
sporulation.
Affects leaves, spikes and occasionally leaf sheaths.
During infection of the wheat spikes pustules appear on the inner surface
of the glumes and lemmas.
Individual pustules are oval and about 0.5-1 mm in diameter.
Stunting of plants is common with severe early infections.
Narrow black stripes form on the leaves later on in the season during
reproductive development and are called telia.
Why and where it occurs:
Disease usually is more important when wheat grown in cooler climates (2 to
20°C). Stripe rust is mainly an important disease of wheat either grown in
highlands, mountainous regions or during the winter or early spring in cool
lowland locations.Urediniospores of the pathogen germinate, penetrate, infect
and produce more wind-dispersed spores on susceptible wheat plants that are
capable of causing epidemics when conditions are favourable, i.e. cooler
temperatures with dew or free moisture on the plants.
Under ideal conditions the pathogen life cycle may take as little as 7 days to
complete.
During late summer, telia may form which give rise to teliospores.
The pathogen survives the period between wheat harvest and sowing on
volunteers (self-sown) of wheat, barley or wild grasses which provide a ‘green
bridge’ for stripe rust to survive across seasons.
The fungus is inhibited by high temperatures. Urediniospores of stripe rust are
susceptible to ultraviolet light hence viable spores are generally not thought to
travel on air-currents over large distances.
Economic importance:
In most wheat-producing areas, yield losses caused by stripe rust range from
10% to 70% if resistant varieties are not grown.
Management principles:
Prior removal of volunteer wheat plants which support disease growth between
wheat cropping seasons will reduce the amount of rust inoculum in the new
season crop.
The use of resistant varieties is the most effective, least expensive and
environmentally friendly means of controlling the disease. Multigenic resistance
(combination of major or minor resistance genes) may be a more long-term form
of controlling the disease. New stripe rust races can and do arise, thus
monitoring of new races is not only important for breeding of stripe rust
resistance but also in predicting epidemics.
Avoid planting of very susceptible and susceptible varieties and select more
resistant varieties. Widespread cultivation of resistant varieties minimizes the
level of stripe rust inoculum in the environment and reduces the occurrence of
new races.
If susceptible varieties are grown then seeds should be treated with fungicides
which suppress early infections by stripe rusts.
Crop monitoring during the growing season is important as early application of
foliar fungicide is effective in the control of stripe rust. The number of applications
and timing of fungicide treatments required is dependent on the progress of the
disease and the level of resistance within the variety.
9.Loose Smut disease
Pathogen:-Ustilago tritici (Pers.) Rostr.
Symptoms:
The entire inflorescence, except the rachis, is replaced by masses of smut
spores (picture on left). These black teliospores often are blown away by the
wind, leaving only the bare rachis and remnants of other floral structures (picture
on right).
Development:
Wind blown teliospores that land on the flowers of wheat plants can germinate
and infect the developing embryo of the kernel. The mycelium of the loose smut
fungus remains dormant in the embryonic tissues of the kernel until the kernel
begins to germinate. The mycelium then develops along with the growing point of
the plant, and at flowering time replaces the floral parts of the spike with masses
of black spores. Infection and disease development are favored by cool, humid
conditions, which prolong the flowering period of the host plant.
Hosts/Distribution: The disease can occur wherever wheat is grown.
Importance: Yield losses depend on the number of spikes affected by the
disease; incidence is usually less than one percent and rarely exceeds thirty
percent of the spikes in any given location.
10. Karnal Bunt disease
Also known as Partial bunt
Pathogens :-Tilletia indica, syn. Neovossia indica
Symptoms:
Karnal bunt is not easily detected prior to harvest, since it is usual for only a few
kernels per spike to be affected by the disease. Following harvest, diseased
kernels can be easily detected by visual inspection: a mass of black teliospores
replaces a portion of the endosperm, and the pericarp may be intact or ruptured.
Diseased kernels give off a fetid or fishy odor when crushed.
Development: Karnal bunt is a seed- or soil-borne, floral infecting disease.
lnoculum (teliospores) on or near the soil surface germinates, producing sporidia,
which are carried by wind to the floral structures. These sporidia in turn
germinate and penetrate the glumes, rachis, or the ovary itself. The fungus
enters the newly formed kernel and develops in the intercellular space between
the endosperm and seed coat. The degree of disease establishment and
development depends on environmental conditions from spike emergence
through grain filling.
Hosts/Distribution: Karnal bunt can affect wheat, triticale, rye, and several
other related grasses, but not barley. The disease is endemic in the Asian
Subcontinent and now in Mexico.
Importance: Karnal bunt is a relatively minor disease. Actual losses in yield
are minimal, but the disease is on the quarantine lists of many countries and
therefore of importance in world grain trade.
11.Powdery Mildew disease
Pathogen :-Blumeria graminis sp. Tritici [teleomorph]
Oidium monilioides (Nees) Link [anamorph]
Symptoms: On all hosts, the first visible symptoms of this disease are white to
pale gray, fuzzy or powdery colonies of mycelia, and conidia on the upper
surfaces of leaves and leaf sheaths (especially on lower leaves) (picture on left),
and sometimes on the spikes. Older fungal tissue is yellowish gray (picture on
right). This superficial fungal material can be rubbed off easily with the fingers.
Host tissue beneath the fungal material becomes chlorotic or necrotic and, with
severe infections, the leaves may die. Eventually, black spherical fruiting
structures (cleistothecia) may develop in the mvcelia and can be seen without
magnification.
Development: The development of powdery mildew is favored by cool (1522ºC), cloudy, and humid (75-100% relative humidity) conditions.
Hosts/Distribution: The fungus has a high degree of host specificity. Isolates
infecting wheat do so exclusively; the same appears to be true for isolates
infecting barley, oats, and rye. Further specialization exists in the form of races.
Powdery mildew occurs worldwide in cool, humid, and semiarid areas where
cereals are grown.
Importance: Powdery mildew can cause major yield losses if infection occurs
early in the crop cycle and conditions remain favorable for development so that
high infection levels are reached before heading.
Disease in maize (corn)
12.Head smut disease:-
Head smut is a systemic disease of maize caused by Sphacelotheca reiliana.
The pathogen affects the tassels and the ears, causing characteristic symptoms
that are easily recognized. Head smut can cause extensive economic damage in
areas where maize is cultivated frequently and the growing season is
characterized by dry and hot conditions. Incidence of head smut as high as 80%
has been documented.
Pathogen: Sphacelotheca reiliana (syn. Sorosporium reilianum, Ustilago
reiliana)
Symptoms
Characteristic symptoms of head smut are visible once the maize plant has
reached the tasseling and reproductive growth stages. Tassels and ears are
typically malformed, overgrown, and replaced by smut sori. Smut sori are usually
covered by a thin tissue, which ruptures to revela masses of dry, black spores
(teliospores) that are wind disseminated. A tangled mass of vascular threads are
often observed in ruptured sori. Sori can infect a few spikelets in the tassel or can
infect the entire tassel leading to abnormal growth and structures. Infected ears
are round, lacking in silks, and the ear is replaced by masses of teliospores that
leave the vascular bundles exposed and shredded. Under less severe infection,
only partial sections of the ear may be smutted and some normal kernels may
still form. Occasionally sori can form on leaves where they develop as narrow
stripes. Infected plants are also frequently dwarfed and may tiller.
Management principles
Host resistance
Resistant varieties are available and should be cultivated in regions where head
smut is a problem. Both qualitative and quantitative resistance has been
documented.
Varieties with rapid seedling emergence may escape disease infection.
Cultural methods
As teliospores can survive for several years in the soil, crop rotation is of limited
use.
Planting maize during seasons that are unfavorable to teliospore germination will
reduce infection.
Ensuring that the soil is well-fertilized can reduce disease severity, as head smut
is reported to be more serious under nitrogen stress.Removing and destroying
sori before they rupture can limit the spread of inoculum.
Fungicides
Foliar application of fungicide has not been effective for the control of head smut.
Seed treatment with systemic fungicides and in-furrow treatments with fungicides
have been used to effectively control head smut.
Fungicide treatment in-furrow may not be economical under low disease
pressure or for grain production.
13.Fusarium ear rot disease:-
Gibberella and Fusarium ear rot occur widely throughout maize growing regions
of the world. They are of particular concern as the causal pathogens produce
mycotoxins that are harmful to humans and livestock. The causal pathogens of
Gibberella and Fusarium ear rot also cause stalk and seedling blights of maize.
Pathogen:- Fusarium graminearum
Fusarium verticilioides syn.& Fusarium moniliforme .
F. proliferatum and F. subglutinans
Symptoms:-
Fusarium ear rot. Fusarium ear rot is characterized by cottony mycelium growth
that typically occurs on a few kernels or is limited to certain parts of the ear,
unlike Gibberella ear rot. Mycelium is generally white, pale pink or pale lavender.
Infected kernels typically display white streaking (also known as ‘starburst’
symptoms) on the pericarp and often germinate on the cob. Typically, infection
occurs close to ear tips and is commonly associated with damage and injury
caused by ear borers. Under severe infestation, the entire ear appears withered
and is characterized by mycelium growth between kernels.
Why and where it occurs
Gibberella ear rot is more prevalent in cool and humid maize growing regions.
The disease is favored by cool, wet weather immediately following silking.
Gibberella ear rot can be particularly serious when water collects between husks
and kernels at the base of the plant following heavy rainfall. Gibberella ear rot is
typically more prevalent where infected crop debris is allowed to overwinter.
Fusarium ear rot is one of the most common ear rots of maize. Fusarium ear rot
is more prevalent where dry and hot weather occurs during flowering. The
disease is commonly associated with injury to ears caused by borers.
Economic importance:
Contamination of grain with mycotoxins can render stored grain unsuitable for
human and livestock consumption which can result in serious economic losses.
Management principles
Host resistance
Cultivation of varieties that are resistant to ear rots is the most practical and costeffective means of ear rot management.
Varieties with tight husks appear to be more vulnerable to Gibberella ear rot.
Chemical control
As ear rot typically develops late in the season and in storage, use of fungicide is
not appropriate.
Where the crop is infected systemically with Fusarium species, application of
fungicide early in the season can limit ear infection.
Management of insect pests (ear borers) will reduce infection of the ear through
injury sites caused by insect feeding.
Proper storage
Storing grain at low moisture (below 15%) reduces the incidence of Gibberella
zeae and Fusarium species in storage.
Cultural control
Management of infected crop debris will reduce the amount of disease inoculum
in subsequent season.
14.Common rust disease
Common rust is caused by the funghi Puccinia sorghi and is found in most
subtropical, temperate, and highland environments with high humidity. Epidemics
of common rust can cause substantial yield loss. Yield losses in excess of 50%
have been recorded under severe disease pressure.
Pathogen: Puccinia sorghi
Symptoms:Circular to elongate (0.2 to 2 mm long), with dark brown pustule (uredinia)
scattered over both leaf surfaces giving the leaf a rusty appearance. Pustules
may emerge in circular bands due to infection that occurred in the whorl.
Pustules break through the leaf epidermis and release powdery reddish-brown
spores (urediospores). As pustules mature they release brownish-black spores
(teliospores) which are the overwintering spores. Under severe disease pressure,
leaves may turn chlorotic and senesce prematurely.
Why and where it occurs
Common rust is a cool weather disease and occurs worldwide in subtropical and
temperate environments where the growing season is characterized by mild
temperatures, high relative humidity, and high moisture. Optimum temperatures
for urediospore germination and formation of infection structures are between 15
and 17°C. Common rust outbreaks are common during the ear filling period and
can spread rapidly in favorable environmental conditions.
Leaves in the whorl are particularly vulnerable to rust due to high moisture
content and relative humidity. Young leaves appear more susceptible than older
leaves. Continuous cultivation of susceptible maize ensures that the pathogen
has a continuous host and results in build up of disease inoculum.
Economic importance:
Yield losses as high as 50% have been recorded due to common rust. Sweet
corn varieties are particularly susceptible to common rust compared to dent
maize varieties.
Management principles
Host resistance
Cultivation of resistant varieties is the most cost-effective and practical means of
disease management.
Varieties with both quantitative and qualitative resistance are available.
Qualitative resistance is determined by the presence of Rp genes. Several Rp
genes have been documented. However, it has been reported that pathotypes
have emerged in various regions worldwide that are virulent against each of the
Rp genes.
Fungicides
Application of fungicides is cost-effective if applied when levels of secondary
inoculum are low (i.e. when pustules are first observed on leaves).
Scouting for rust should be conducted 2 weeks prior to tasseling.
If wet weather is not expected, rust is unlikely to increase in severity.
Cultivate early maturing varieties that limit secondary cycles of disease and can
avoid periods of heavy disease pressure later in the season.
References:
 Agrios, George N. ,Plant Pathology. 5th ed.
Burlington, MA: Elsevier Academic Press,
2005.
 Pandey b.p.,plant pathology pathogen
&plant disease(2010),page no (147214).s.chand &co.ltd new Delhi.
 http://www.knowledgebank.irri.org/RiceDoct
or/index.php/information-sheets-mainmenu2730
 http://wheatdoctor.cimmyt.org/en/pests-adiseases/list/122?task=view
 http://en.wikipedia.org/wiki/Bright's_disease
#Symptoms.
 http://maizedoctor.cimmyt.org/en/pests-anddiseases/list/218