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Page 1: Diseases and Pests in Wheat and Rice

Diseases and Pests in Wheat and Rice

Page 2: Diseases and Pests in Wheat and Rice

WHEAT

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Principal diseasesBarley yellow dwa

rfCommon buntEyespotWheat leaf rust

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Barley Yellow Dwarf

Barley yellow dwarf is a plant disease caused by the barley yellow dwarf virus, and is the most widely distributed viral disease of cereals. It affects the economically important crop species barley, oats, wheat, maize, triticale and rice.

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BiologyBarley yellow dwarf virus (BYDV) is a positive sense single-stranded RNA virus; the viron is not enveloped in a lipid coating. The virus is transmitted by aphids, and the taxonomy of the virus is based on genome organisation, serotype differences and on the primary aphid vector of each isolate.

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PathologyWhen aphids feed on the phloem of the leaf, the virus is transmitted to the phloem cells. Once inside the plant, the virus begins to replicate and assemble new virons. This process requires significant metabolic input from the plant, and causes the symptoms of barley yellow dwarf disease.

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Sources and spreadThere are two main sources by which a cereal crop might be infected

1. By non-migrant wingless aphids already present in the field and which colonise newly-emerging crops. This is known as "green-bridge transfer".

2. By winged aphids migrating into crops from elsewhere. These then reproduce and the offspring spread to neighbouring plants.

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Control"Green bridge" sources must be ploughed in as early as possible. Alternatively, a desiccant herbicide should be applied 10 days prior to cultivation. Insecticide sprays may be used at crop emergence.

Drilling dates prior to mid-October favours attacks from winged migrant aphids. However, yield penalties may be experienced from late drilling. Insecticide sprays in this instance are therefore aimed at killing the aphids before significant spread can occur.

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Common BuntThe bunts and smuts are caused by fungi that affect the seed of wheat and other small grains and grasses. Only loose smut and common bunt occur in Oklahoma. However, Karnal bunt, which does not occur in Oklahoma, is a concern because grain that tests positive for Karnal bunt can not move freely into international markets.

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SymptomsPlants with common bunt may be moderately stunted but infected plants cannot be easily recognized until near maturity and even then it is seldom conspicuous. After initial infection, the entire kernel is converted into a sorus consisting of a dark brown to black mass of teliospores covered by a modified periderm, which is thin and papery.

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The sorus is light to dark brown and is called a bunt ball. The bunt balls resemble wheat kernels but tend to be more spherical. The bunted heads are slender, bluish-green and may stay greener longer than healthy heads.

The bunt balls change to a dull gray-brown at maturity, at which they become conspicuous. The fragile covering of the bunt balls are ruptured at harvest, producing clouds of spores. The spores have a fishy odour. Intact sori can also be found among harvested grain.

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Disease cycleMillions of spores are released at harvest and contaminate healthy kernels or land on other plant parts or the soil. The spores persist on the contaminated kernels or in the soil. The disease is initiated when soil-borne, or in particular seed-borne, teliospores germinate in response to moisture and produce hyphae that infect germinating seeds by penetrating the coleoptile before plants emerge. Cool soil temperatures (5° to 10°C) favour infection.

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The intercellular hyphae become established in the apical meristem and are maintained systemically within the plant. After initial infection, hyphae are sparse in plants. The fungus proliferates in the spikes when ovaries begin to form. Sporulation occurs in endosperm tissue until the entire kernel is converted into a sorus consisting of a dark brown to black mass of teliospores covered by a modified periderm, which is thin and papery.

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ManagementControl of common bunt includes using clean seed, seed treatments chemicals and resistant cultivars. Historically, seed treatment with organomercury fungicides reduced common bunt to manageable levels. Systemic seed treatment fungicides include carboxin, difenoconazole, triadimenol and others and are highly effective. However, in Australia and Greece, strains of T. laevis have developed resistance to polychlorobenzene fungicides.

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Eyespot Eyespot is an important fungal disease of wheat caused by the necrotrophic fungus Tapesia yallundae and Tapesia acuformis. It is also called Strawbreaker. Eyespot is more severe where wheat is grown continuously and when the weather is cool and moist. Treating crops against eyespot with fungicide costs millions to farmers and is complicated by the pathogen becoming resistant to the more commonly used fungicides.

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Symptoms

The eye-shaped elliptical lesions which give eyespot its name form on lower stem bases near to the soil surface. The lesions are straw yellow, often with black pupil-like dots in the centre, and are bordered by greenish-brown to dark-brown rings. In cases of severe infection stems are weakened at the point of infection which makes the host susceptible to lodging

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Development of infection

It is more severe if wheat is grown continuously in same field over the same period. The fungus grows as mycelium which penetrates successive leaf sheaths throughout the growing season. High humidity, cool, and damp weather at the soil surface favours disease development. Whilst dry and hot weather causes the leaf sheaths of the plant to dry and fall off, taking the inoculum with it, thus lessening disease.

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Invasion of fungiInvasion of Pseudocercosporella herpotrichoides'" in wheat initiates with release of enzyme for breaking the plant cell wall. A specific sequence of enzymes is employed; without these enzymes the fungus would not be able to invade the plant cell. The fungus is present in the plant stem, it causes disease by affecting nutrient and water supply to upper parts of the plant, weakening the plant stem.

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Plant defencesWheat cells release hydroxyproline glycoprotein (HRGP) in their cell walls. Secretion of HRGP is dependent on the signal induced by the fungal elicitors stimulating the transcription of genes encoding HRGP accumulation in the cell wall. In the case of wheat HRGP is less accumulated allowing for more easy invasion by the fungus.

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Method of control

I. The best method of control for eyespot disease is breeding for resistance. Currently the gene conferring resistance to eyespot is the Pch1 gene. To generate resistant culitvars plants containing this gene are bred with others to pass the gene to their offspring

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II. Crop rotation is also important in reducing the extent of disease because eyespot fungi live on debris of the previous crop. Cropping the wheat with alternate non-host crops and with set-aside periods of at least one year helps to lessen disease.

III. Use of fungicide can be effective in the short term but is not a long term solution as the pathogen can develop resistance to fungicides. Application of chemicals is also costly.

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Wheat Leaf RustWheat leaf rust, is fungal disease that affects wheat, barley and rye stems, leaves and grains. In temperate zones it is destructive on winter wheat because the pathogen overwinters. Infections can lead up to 20% yield loss - exacerbated by dying leaves which fertilize the fungus. The pathogen is Puccinia rust fungus. Puccinia triticina causes 'black rust', P.recondita causes 'brown rust' and P.sriiformis causes 'Yellow rust'. It is the most prevalent of all the wheat rust diseases, occurring in most wheat growing regions.

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SymptomsSmall brown pustules develop on the leaf blades in a random scatter distribution. They may group into patches in serious cases. Infectious spores are transmitted via the soil. Onset of the disease is slow but accelerated in temperatures above 15°C, making it a disease of the mature cereal plant in summer, usually too late to cause significant damage in temperate areas. Losses of between 5 and 20% are normal but may reach 50% in severe cases.

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Control

Varietal resistance is important. Chemical control with triazole fungicides may be useful for control of infections up to ear emergence but is difficult to justify economically in attacks after this stage.

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RICE

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Common Types of Diseases

Rice BlastSheath BlightStem RotTungro

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Rice BlastMagnaporthe grisea, also known as rice blast fungus, rice rotten neck, rice seedling blight, blast of rice, oval leaf spot of graminea, pitting disease, ryegrass blast, and Johnson spot is a plant-pathogenic fungus that causes a serious disease affecting rice. It is now known that M. grisea consists of a cryptic species complex containing at least two biological species that have clear genetic differences and do not interbreed.

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A Rice Leaf with Rice Blast

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SymptomsInitial symptoms white to gray-green lesions or spots with darker borders produced on all parts of shoot

Older lesions elliptical or spindle-shaped and whitish to gray with necrotic borders

Lesions wide in the centre and pointed toward either end

Lesions may enlarge and coalesce to kill the entire leaves

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Causal agent or factorA fungus causes rice blast. Its conidiophores are produced in clusters from each stoma. They are rarely solitary with 2-4 septa. The basal area of the conidiophores is swollen and tapers toward the lighter apex.

The conidia of the fungus measure 20-22 x 10-12 µm. The conidia are 2-septate, translucent, and slightly darkened. They are obclavate and tapering at the apex. They are truncate or extended into a short tooth at the base.

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Mechanism of damageConidia are produced on lesions on the rice plant about 6 days after inoculation. The production of spores increases with increase in the relative humidity. Infection tubes are formed from the appressoria and later the penetration through the cuticle and epidermis. After entering the cell, the infection tube forms a vesicle to give rise to hyphae. In the cell, the hyphae grew freely.

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ManagementManipulation of planting time and fertilizer and water management is advised.

Early sowing of seeds after the onset of the rainy season is more advisable than late-sown crops.

Excessive use of fertilizer should be avoided as it increases the incidence of blast.

Water management practices in rain fed areas lessen the likelihood of stress, which also aid in blast control.

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Planting resistant varieties against the rice blast is the most practical and economical way of controlling rice blast.

Systemic fungicides such as pyroquilon and tricyclazone are possible chemicals for controlling the disease.

Nitrogen should be applied in small increments at any time.

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Sheath BlightThe pathogen involved in this disease is Rhizoctonia solani Kunh (anamorph), Thanatephorus cucumeris (Frank) Donk (teleomorph).

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SymptomsInitial lesions are small, ellipsoidal or ovoid, greenish-gray and water-soaked and usually develop near the water line in lowland fields.

Older lesions are elliptical or ovoid with a grayish white centre and light brown to dark brown margin.

Lesions may reach the uppermost leaf under favourable conditions.

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Lesions may coalesce forming bigger lesions with irregular outline and may cause the death of the whole leaf.

Severely infected plants produced poorly filled or empty grains, especially those on the lower portion of the panicles.

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ConfirmationThe disease is easily distinguished by the irregular lesions, which are initially water-soaked to greenish gray and later becomes grayish white with brown margin. These lesions are usually found on the leaf sheaths near the waterline and on the leaves. The disease can be confirmed by the presence of sclerotia.

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Mechanism of damageThe sclerotia germinate and initiate infection once they get in contact with the rice plant.

The fungus penetrates through the cuticle or the stomatal slit. Infection pegs are formed from each lobe of the lobate appressorium of infection cushion.

The mycelium grows from the outer surface of the sheath going through the sheath edge and finally through the inner surface.

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Economic importanceRice sheath blight is an increasing concern for rice production especially in intensified production systems. In Japan, the disease caused a yield loss of as high as 20% and affected about 120,000-190,000 hectares.

Studies at IRRI showed that sheath blight causes a yield loss of 6% in tropical Asia.

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Management principlesSanitation, specifically removing of weeds, can help control sheath blight considering that the pathogen also attacks weeds which are commonly found in rice fields.

Removal of infected stubbles or crop residues from the field is also recommended to reduce the amount of inoculum for the succeeding cropping season.

Spraying infected plants with fungicides, such as benomyl and iprodione, and antibiotics, such as validamycin and polyoxin, is effective against the disease.

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Stem RotThe pathogen involved in this disease is Sclerotium oryzae Cattaneo (anamorph), Magnaporthe salvinii (Cattaneo) R.A. Krause & R. K. Webster (teleomorph)

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SymptomsInitial symptoms are small, irregular black lesions on the outer leaf sheath near water level.

Lesions expand as the disease advances.

Visible numerous tiny white and black sclerotia and mycelium inside the infected culms.

Infected culm lodges and caused unfilled panicles and chalky grain.

Severe infection causes tiller death.

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ConfirmationBlackish, dark, irregular lesions are visible on the outer leaf sheath. The lesion later expands and affects the inner culm. If infected culm is dissected, it reveals dark gray masses of fungi and small white and black sclerotia or infection bodies.

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Why and where it occursThe infection bodies or sclerotia are found in the upper soil layer. They survive in air-dry soil, buried moist rice soil, and in tap water. They can also survive on straw, which is buried in the soil. The sclerotia float on irrigation water and infect newly planted rice during land preparation.

Infection is high on plants with wounds as a result of lodging or insect attack. The panicle moisture content and nitrogen fertilizer also influence disease development.

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Economic importanceThe infection is seen on the rice crop during early heading and grain filling. The leaf sheaths decay and cause lodging and lower grain filling. It can cause heavy losses in many countries. For example, in Japan, there are 51,000 to 122,000 hectares infected and estimated annual losses of 16,000-35,000 due to this disease.

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Management principlesA balanced use of fertilizer or split application with high potash and lime to increase soil pH reduces stem rot infection and increases yield.

The use of resistant cultivars may be the best control measure for stem rot.

Chemicals such as fentin hydroxide sprayed at the mid-tillering stage, thiophanate-methyl sprayed at the time of disease initiation can reduce stem rot incidence in the rice field.

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Tungro

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Signs and symptomsdiscoloration begins from leaf tip and extends down to the blade or the lower leaf portion.

infected leaves may also show mottled or striped appearance – stunting.

delayed flowering, which may delay maturity - panicles small and not completely exserted.

most panicles sterile or partially filled grains and covered with dark brown blotches.

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Factors favouring disease developmentpresence of the virus sources

presence of the vectorage and susceptibility of host plants

synchronization of the three above factors

all growth stages of the rice plant specifically the vegetative stage

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ConfirmationThere are some serological tools to detect tungro viruses. These are Latex agglutination test, Enzyme Linked Immunosorbent Assay or ELISA, and Rapid Immunofilter Paper Assay or RIPA. The presence of the vector Nephotettix spp. is indicative of the disease.

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Causal agent or factorTungro virus disease is transmitted by leafhoppers, wherein the most efficient vector is the green leafhopper, Nephotettix virescens (Distant). The disease complex is associated with rice tungro baciliform virus (RTBV) and rice tungro spherical virus (RTSV).

Insects could acquire the virus from any part of the infected plant. After acquiring the virus, the vector can immediately transmit to the plants.

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Mechanism of damageThe insect acquires the virus by feeding on the plant for a short time in an 8-hr acquisition access period (minimum of 30 minutes). It can transmit the virus immediately after feeding. Either or both viruses can be transmitted during a 1 hour inoculation access period (minimum of 7 minutes).

After feeding on a diseased plant, the insect can transmit the virus for about 5 days and the longest is about a week.

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Economic importanceTungro 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.

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Management principlesThere 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,

3. vector adaptation on GLH-resistant variety.

Planting of resistant varieties against tungro virus disease is the most economical means of managing the disease.

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