SEEDBORNE VIRUS DISEASES OF

ECONOMICALLY IMPORTANT PLANTS

Published By

Muhammad Boota Sarwar

Federal Seed Certification and Registration DepartmentG-9/4, Islamabad

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SEEDBORNE VIRUS DISEASES OF ECONOMICALLY IMPORTANT PLANTS

Seedborne diseases of soybean 1999 cut production

by XB Yang, extension plant pathologist, Department of Plant Pathology

Several seedborne diseases soybean were prevalent in the 1998 growing season and the use of

pathogen-infected seed may have caused the problems.

Low-quality seed is characterized by low germination rate, which often is caused by a high level

of infected seeds in a seedlot. Infected seed can be detected by seed testing. In the 1998

growing season, three pathogens were prevalent in some areas: Phomopsis, soybean mosaic

virus, and bean pod mottle (XB Yang 1999).

Viruses are unique class of pathogens. They are simple in structure, cannot be seen with microscope, yet cause dangerous, diseases in animals (Polio, Rabies, AIDS, Influenza) and plants (mosaics, yellows, stunting/dwarfing, leaf roll/leaf curl, curly top/bunchy top, etc.). Viruses attack wide variety of biological systems including single cell bacteria and highest evolved biological systems, i.e., animals and human being. Approximate number of viruses known is 2000 and about 977 are known to parasitize plants (Agrios, 1997). One pathogenic virus can attack several plant genera, also several viruses attacked same plant species. Viruses behave like parasite inside living cells by utilizing the cell systems and cell resources for their own multiplication this exhausts the animal/plant cells. Outside living cells the viruses behave like chemical molecules (TMV can survive in dried tobacco leaves for decades). In fact viruses have characteristics common to both living and non-living systems. The viruses may spread with seed or vegetative plant parts. If plant cuttings or buds, grafts are used as means of propagation there are fair chances of spread of plant viruses. Important commercial crops (sugarcane, potato and ornamentals) face the problem of quality/disease free seed/planting material. Seed-transmitted viruses are those that are transferred from one place to the other through the agency of the seed and cause infection of the plant produced by germination of such seed. But seed-borne viruses are carried in, on, or otherwise within the seed (Neergaard 1977).

SEEDBORNE PATHOGENS

Seedborne fungi are defined by Ingold 1953 as those which are dispersed in association with some kind of dispersal units of the host. This description embraces all seed types and all associated micro fungi. Baker 1972 limits the description to seedborne pathogens which on or in seeds may or may not show symptoms on the seed and seedborne diseases as those which actively attack seeds and may or may not show symptoms on the seeds. Many of the necrotrophic fungi which are seedborne diseases of emerging seedlings also attack and kill a proportion of the seed e.g ; mycospbaerella pinodes leaf and pod spot with foot rot of peas. The seed “borne” relates to carrying plant pathogens rather than expressing disease or disease symptoms. Diseases which are wholly or mainly expressed on seeds may be better termed seed diseases. The definition of seedborne pathogens applies organisms i.e. fungi, bacteria and

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viruses carried with, on or in seeds, some of which may damage the seed and all of which are transmitted by seeds to infect the crops which grow from them. Table 1 Example of Plant Viruses Transmitted Through Seed and Pollens

Virus Host species True seed transmission (%)

Pollen transmission

Abutilon mosaic Abution spp. 14-24 4Alfalfa mosaic Medicago sativa 10-50 -Barley stripe Hordeum vulgare 15-100 +Bean common mosaic Phaseolus vulgaris 1-93 +Bean yellow mosaic Pisum sativum 10-30 +Black gram mottle Vigna mungo 8 -Cowpea mosaic (common bean) Vigna unguiculata 25-40 -Cowpea mosaic (Banding) V. unguiculata 2.7-19 -Cowpea mosaic (Chavali) V. unguiculata 17-23 -Cucumber mosaic Stellaria media 21-40 -Elm mosaic Ulmus Americana 1-3 +Lettuce mosaic Lactuca sativa 3-10 +Lychnis ring spot Lychnis divaricata 58 +Mungbean and Urdbean mosaic Vigna radiate 20 -Pea early browning P. sativum 37 -Pea enation mosaic P. sativum 1.5 -Pea seed-borne mosaic P. sativum 0-100 -Peanut (groundnut) Indian clump Arachis hypogaea 12 -Peanut mottle A. hypogaea 9 -Peanut stunt A. hypogaea 0.1 -Prune dwarf Prunus cerasus 3-30 +Raspberry ring spot Fragaria spp. 50 +Southern bean mosaic V. unguiculata 3-7 +Soyabean mild mosaic Glycine max 22-70 -Soyabean mosaic G. max 30 +Soyabean stunt G. max 39 +Tobacco ring spot G. max 78-82 +Tomato black ring Rubus spp. 5-19 +Urdbean leaf crinkle Vigna mungo 18 -White clover mosaic Trifolium repens 6 -

VIRUS INDEXINGVirus indexing consists of transmitting the infections agents from a plant in which it may or may not induce symptoms to healthy indicator plants known to show symptoms. The transmission may be based on mechanical or grafted procedures or the insect vector or dodder. Indexing tests may require only days or weeks with herbaceous plants, but may require months or years with woody plants.

SEED-BORNE VIRUSES REPORTED FORM PAKISTAN

Although the subject of seed-borne viruses and their transmission in seeds has not been studied in detail in Pakistan mainly due to lack of trained manpower and well equipped laboratory

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facilities for the detection of such pathogens however following seed borne viruses have been isolated from different crops at PGRI in Islamabad, Pakistan (Bashir et.al 1999). PEA SEED BORNE MOSAIC VIRUS

Fig 1. Pea seed borne virus disease on pea

It is an important disease where virus is transmitted through seed at high frequency. This

makes exchange of germplasm (seeds) a risky venture from quarantine point of view. The pea

seed borne mosaic virus (PsbMV) is reported from the Czechoslovakia, Yugoslavia, Canada,

Poland, Switzerland, New Zealand, UK, India, Morocco and France (Maury and Khetrapal

1992). The PsbMV infected pea seeds can be recognized by reduced size and necrotic

symptoms on seed coat. The disease is reported to cause 10-35% reduction in yield. The initial

symptoms include chlorosis and stunting of infected plants. The leaflets are narrow and show

downward rolling (Figure 1). The apical malformation observed in late stages of disease

development. The mosaic symptom may or may not be pronounced though vein clearing is

observed. Symptomless pea plants also carry PsbMV. The PsbMV (poty virus) is a flexuous

particle (780 nm) containing ssRNA. It is transmitted through seeds, aphid vectors (pea and

potato aphids) and has a wide host range belonging to legume plants. Comparatively high

temperature (28-32 0C) favour disease progress. The chances of seed transmission are

increased if infection takes place before flowering.

Bean Common Mosaic

Legumes are important group of dicotyledonous plants belongins to family Leguminosae,

subfamily Papilipnoidae has several plants of economic importance used for human food

(vegetable and grain legumes). Phaseolus vulgaris is grown world over. Allen in 1983

described important pathogen and their management of French bean. Bean common mosaic

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virus (BCMV) causes stunting, mottling and leaf malformation. Irregular shades of yellow or

green are observed on infected leaves (Figure2 ).

Fig 2. Bean common mosaic virus

Factors related with host (age), pathogen (strains) and environment might influence symptoms.

BCMV may also produce leaf crinkling, chlorosis and dwarfing. The infected pods have few

seeds of smaller size, which may be malformed or aborted. Virus has very wide host range (44

genera in 9 families). BCMV is flexuous filament (730-750 x 12-15 nm). The BCMV is

transmitted by several species of aphids in non-persistent manner. The incidence of seed

transmission is high (0-93%), which makes this virus an important one.

Management

Chemical (insecticides) control of aphid vectors

Changes in cropping to avoid peak aphid activity periods

Use of virus free healthy seeds

URDBEAN LEAF CRINKLE VIRUS

The ULCV has been reported form Pakistan and could cause 81% yield reduction when infection occurs at early stage of plant development (Bashir et. al., 1991).

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Figure3: Symptoms of urdbean leaf crinkle virus (ULCV) on urdbean plants (b) symptoms of blackeye cowpea mosaic virus (BICMV) on cowpea.

Cowpea Mosaic Comovirus Disease

The disease is common in occurance where the cowpea is grown extensively.It occures chiefly (Vigna unguiculata)and soyabean(Glycine max).Other natural hosts are Phaseolus lathyroides and perennial plant Desmodium canescens.Chenopodium amaranacotol is suitable diagnostic plant reacting only with necrotic local lesions on inoculated leaves.

Symptoms:

Inoculated leaves become necrotic. Vein clearing and chlorotic mottling on leaflets are observed. In advances cases light and dark green mosaic areas are followed by the distortion of the leaves.

Cause: Cowpea mosaic comovirus

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Fig 4. Cowpea mosaic virus

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Fig 5. Cowpea mosaic virus

Disease Cycle: Perennial legume hosts and infected seeds are the natural source of infection perennial hosts represents primary infection.Transmission: Leaf eating beetles chiefly Ceratoma ruficortus transmit virus to the field. Virus is also mechanically transmissable by infected plant sap.

Management: 1. Rogoeing of perennial hosts especially weeds as primary host of infection.

2. Isolation of cultivated crop from infected hosts. 3. Use of healthy and disease free seed is important. 4. Chemical control of vectors should be given priority.

Indian Peanut Clump

Indian peanut clump is also called peanut clump.

Cause. Indian peanut clumps virus (IPCV) is in the furovirus group. Two different isolates have been identified: the West African and the Indian. However, the Indian virus is serologically unrelated to the West African virus and is considered by some researchers to cause a separate disease. The soil fungus Polymyxa graminis transmits the West African IPCV and is thought to transmit the Indian isolate also. Both isolates are seed-transmitted. Polymyxa graminis survives in field soil as cystosori. Cysts give rise to zoospores, which “swim” through free soil water until they contact a host root and encyst. Encysted zoospores produce a structure called a satchel through which zoosporic cytoplasm enters the host cell and becomes a plasmodium. Only primary root tissue of young roots is infected; optimum infection occurs at a temperature of about 25°C. The host cell then becomes infected with IPCV if P.graminis is viruliferous. After a period of time, the plasmodium develops into a zoosporangium, which releases additional zoospores that repeat the infection cycle. However, some plasmodia develop into cysts and often nearly every cell in the small feeder roots will contain a cyst. As root cells senesce, cysts are eventually released into the soil, where they can remain viable for years without loss of virulence. IPCV in condidered by some researchers to cause a different disease than peanut clump virus.

Distribution. India and West AfricaSymptoms. Symptoms are areas of diseased plants within fields that enlarge in succeeding years. Diseased plants are stunted and quadrifoliates are small initially and have mosaic mottling and chlorotic rings but subsequently become dark green and have faint mottling. Plants eventually become bushy and have small, dark green leaves. Several flowers are produced on erect petioles. The number and size of pods is reduced, resulting in smaller-sized seeds. Root systems are small and diseased roots darken with an epidermal layer that easily peels off. However, Isolates from different locations in India caused different symptoms on five different host range plants.

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Fig 6: Peanut Clump Virus (a)

Fig 7: Pea nut Clump Virus (b)

Management

1. Sow virus-free seed. 2. Grow resistant cultivars in India.

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Peanut Mottle

Cause. Peanut mottle virus (PmoV) is a potyvirus that is disseminated mechanically and in a nonpersistent manner by several aphid species. Another important means of dissemination is by seed. PMoV is found at a low rate in embryos but not in seed coats or cotyledons. Wild peanut, Arachis chacoense, serves as a reservoir for PMoV. Different strains of PMoV exist.

Distribution Worldwide

Symptoms. Diseased plants have a leaf mottling, leaflets that curt upward,and depressed interveinal tissue. A mild mottle that occurs on the youngest leaves is best observed by transmitted light. Symptoms tend to become obscure during hot, dry weather as diseased plants mature. Seeds are discolored, and diseased pods are smaller than healthy pods and have gray to brown patches. Yield and nodulation is reduced.

Symptom expression varies with the strains of Rhizobium that produce nodules on the diseased plant. Plants harboring an ineffective Rhizobium strain show more severe symptoms than plants harboring an effective strain.

Fig 8:

Management. Grow the most tolerant cultivar

Peanut Stripe

Cause. Peanut stripe virus (PStV) is in the potyvirus group. Two symptom variants of peanut stripe virus occur: stripe (PStV-S) and blotch (PStV-B). It has been proposed that the virus producing mild mottle, peanut mild mottle virus, and peanut chlorotic ring mottle virus, a virus found on peanut in Thailand, should also be considered as PStV. Two different strains of PStV have also been identified in Taiwan and identified as PStV-Ts and PStV-Tc. The tow strains are indistinguishable serologically.

Peptide profile data suggest that that PStV is a strain of bean common mosaic virus. PStV is transmitted mechanically, in a nonpersistent manner by aphids, and is seedborne in cotyledons and embryos.

Distribution. China, India, Indonesia, Malaysia, the Philippines, Taiwan, Thailand, and the United States, primarily in research areas of Florida, Georgia, North Carolina, Oklahoma, Texas, and Virginia.

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Symptoms. PStV-S causes dark green stripes along the lateral leaf veins. Initially, there is a discontinuous dark striping or banding along lateral veins of diseased leaves that resembles a sergeant’s stripes. Later on older leaves, the striping fades and a mild oak-leaf pattern occurs and becomes the predominat symptom expression.PStV-Ts induces severe mosaic and systemic necrotic symptoms. PStV-Tc causes stripe symptoms.

Fig 9:

Management. The University of Georgia has issued the following guidelines for managing PStV in Georgia.

1. Only Georgia-certified seed shall be sown in research plots with the exception of breeding and variety performance tests.

2. Seed from research plots shall not be processed through commercial cleanining and shelling operations.

3. Peanuts form experimental plots shall be processed or sold for processing only and are not to be sued for seed except in breeding tests.

4. All residual peanut seed and debris shall be removed form harvesting handling, and transporting equipment before such items are removed form areas contaminated with PStV to clean areas.

5. All research plots containing plants inoculated with virus shall be grown under screen cages with proper precautions to prevent spread and shall be planted only on experiment station land.

6. Breeders shall release only seed that is free from PStV.7. Virus-free seed to be retained for future seed production shall not sown in areas where

PStV-infected peanuts have been frown previously.8. Virus-free seed shall not be sown in proximity to leguminous crops or other hosts, and

rigid weed control shall be practiced in and around virus-free plots.9. Researchers shall not import peanuts unless they are either tested for PStV before

sowing or grown in screened isolation for one growing season to allow for visual inspection and serological assay if necessary.

10. Peanut breeding plots shall be isolated form other research plots.11. The Uniform Peanut Performance Trial shall be sown exclusively at one university

farm.12. Other legume crop-breeding nurseries shall be separated from peanut research plots.13. All seed shall be removed from PStV-infected research plots and plots shall be

fumigated.

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14. Infected seed, except breeders seed, shall be destroyed.15. Some wild peanut accessions are resistant.

SOYBEAN MOSAIC VIRUS

Natural infection of SMV has been reported in soybean in Pakistan and SMV is a serious disease of soybean in NWFP (Ali and Hassan, 1992). Soybean mosaic (also known as soybean crinkle), caused by soybean mosaic virus (SMV), is world wide in distribution. Other potyviruses closely related to SMV may also be involved. The disease was first observed in the United States in the early 1900s and is believed to have been introduced with the first soybeans brought from Asia. Soybean mosaic is regarded as an important disease in some areas of the world. Yield may be reduced by 50 percent in any one field. Yield reduction as high as 93 percent have been recorded in experimentally inoculated plants. Infected plants produce fewer, smaller, lighter-weight seeds, which may have mottled seed coat. Infection by SMV can predispose some cultivars to infection by Phomopsis longicolla. Cobbs resulting in a loss of seed germinability.

SYMPTOMS

SMV can be seedborne infected seeds may fail to germinate or may produce disease seedlings. Infected seedlings are spindly, with crinkled unifoliolate leaves, which may be shaped normally but be mottled. Subsequent trifoliolate leaves become prematurely chlorotic & some severely stunted, mottled, and rugose than the unifoliolate leaves.

A plant’s reaction to SMV infection depends on the genotype of host, the strain of the virus plant age at the time of infection & environmental conditions. Plants infected early in the seasons are stunted, with shortened petioles & internodes. Leaves are reduced in size & generally misshapen puckered, occasionally with dark green enations along the veins. Affected leaflets are generally asymmetric and curl down at the margin. The youngest and most rapidly growing leaves show the most severe symptoms. Typically SMV infected plants mature later than uninfected plants but infected plants from certain soybean lines mature earlier.

The symptoms associated with necrosis include a brown discoloration of leaf veins; yellowing of leaves; browning of petioles and stems bud blight and defoliation, leading plant to death. Symptoms are less severe at 24 – 25’C & are largely massed above 30’c.

Expression of pod symptoms depend on cultivar susceptibility, time of infection, viral strain & temperature. Diseased pods are often stunted & flattened with less pubescence. They are curved more acutely than pods on healthy plants.

Viable seeds produced in diseased pods may be mottled brown or black. They are usually smaller than seeds from healthy plants and germination may be inhibited.

HOST RANGE SMV can infect several host species, mostly in the Fabaceae. It causes local lesions on Chenopodium album L., C, quinoa Willd., cyamopsis tetragonoloba(L.) Taub., Dolichos biflorus L. Indigofera hirsutaL., Lbalab purpureus (L.) Urban, Phaseolus lunatus L. and Vigna unguiculata (L.)Walpers.The virus induces systemic symptoms in soybeans and Glycine soja Sieb. & Zucc. Amd in Canavalia ensiforms(L). Crotalaria spectabills Roth, Cyamopsis tetragonoloba (L).

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Latent infections occur in Hipppocrepis multisiliquosa L., Lotus tetragonolobus L., Lupinus angustifolius L., phaseolus speciosas Kunth in H.B.K., some cultivars of P. vulgaris L., and Scorpiurus sulcata L.

Fig 10. Soybean mosaic virus

TRANSMISSION

SMV is readily sap-transmitted with or without the use of abrasives. The virus is graft-transmissible but is not transmitted by dodder.

A percentage of seeds from infected plants carry the virus, which may remain viable in seeds for at least 2years. The extent of seed transmission depends on the virus strain and host genotype. In certain areas that lack vectors that can retain SMV for long periods and host in which the virus can over winter, seed transmission plays an important role in the epidemiology of Soybean mosaic.

At least 31 aphid species transmit the virus efficiently in a nonpersistent manner. Aphids become viruliferous by feeding on infected stems, stem tip, and old or young leaves.

MULTIPLICATION

Viruses must multiply in infected cells for translocation and systemic infection to take place. SMV moves both up and down in plants and can be detected in all parts of systemically infected plants. Multiplication and movement occur most rapidly at 26’C; no movement is detectable at 10’C. SMV moves slowly from infected cells. In systemically infected plants, virus content is correlated with the severity of symptoms.

CONTROL

Resistance to SMV is conditioned by a pair of alleles. Allele Rsv (from PI 96983) controls a high level of resistance. Allele rsv (from Tokyo via Ogden) controls a lower level of resistance. Use of SMV free seeds and rouging of infected plants in field used to produce planting seed.

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GARLIC YELLOW STREAK POTYVIRUS

The local garlic variety was found free of virus infection (Bashir et. at. 1997b).

First found in Allium sativum in New Zealand also found in Australia & New Zealand but spread world wide.

SYMPTOMSAllium sativum chlorotic streaks mottling and mosaic symptoms

TRANSMISSIONTransmitted in nature by insect vector belonging to the aphidae: Myzus persicae. Transmitted in a non-persistance manner. Non-vector transmission is by mechanical inoculation.Diagonastic host species & symptoms Chenopodium amaranticolor C. quinoa;Allium cepa,A.porrumThermal inactivation point 60-65 °C longevity in vitro 2-3 days at °C dilution end point 10(-4). Particles found in all parts of the host plant in the cytoplasm. e

Cucumber Mosaic Virus

Cause. A strain of cucumber mosaic virus (CMV-CA). CMV is in the cucumovirus group and is transmitted by seed and by the aphid Macrosiphum euphorbiae. CMV infects 31 species of plants in six families.

Distribution. China , Europe and the United States.

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Symptoms. Chlorotic spots occur on young expanded leaves that are small, rolled, and generally chlorotic. A mosaic or mottling occurs on some leaves. Diseased plants are stunted to one-half to two-thirds the size of a healthy plant.CMV in exotic fig plant were imported form Syria. When these were planted under controlled conditions, all the plants expressed virus-like symptoms (fig). Based on ELISA results, CMV was detected in all the plants.

Management. Not reported.

Fig 12 ; Cucumber mosaic

Sugarcane MosaicCause. Sugarcane mosaic virus (SCMV) is in the potyvirus group. SCMV is transmitted by several aphid species in a nonpresistent manner and by sap inoculation. SCMV is seedborne at a low rate in sweet maize seed but not in seed of other types of maize. SCMV does not normally cause severe disease in maize except for sweet maize.

Distribution. Tropical and subtropical areas.

Symptoms. Initially, a mild mottle occurs in interveinal areas of diseased leaves. Chlorotic patterns soon occur and elongate to produce streaks or stripes with irregular margins. Plants may become severely stunted, are lighter in appearance than healthy plants, and produce ears with few or no kernels.

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Fig 13 ; Sugarcane Mosaic Virus

Management

1. Do not grow maize near sugarcane.2. Control grassy weeds. 3. Grow resistant hybrids, especially for sweet maize.

Clover Yellow Mosaic

Cause. Clover yellow mosaic virus (CIYMV) is in the potexvirus group CIYMV is seedborne.

Distribution. Canada and probably other red clover-growing areas.

Symptoms. Diseased plant frequently stunted and bushy. Leaves have a mosaic appearance and the veins are yellowed.

Fig 14: Clover Yellow Mosaic

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Management. Sow disease-free seed. Other general managemnt measures may be useful.

Lettuce mosaic virus (LMV)

Cause: LMVcan infect all lettuce types. LMV is seedborne in all lettuce types and infected seed probably serves as the chief source of inoculum, although weed hosts are also recognized.

Symptoms: Plants infected through seed are referred to as seedborne "mother" plants because they can serve as virus reservoirs from which aphids can spread the virus to surrounding healthy plants. The mother plants show early mosaic symptoms, stunted and never develop marketable heads. Secondary infected plants show mosaic, leaf puckering, and deep or accentuated serration of the leaf margins in most lettuce types (fig. 1).

Fig 15. Lettuce mosaic virusControl:

Two methods for controlling LMV are currently in use. First, because of the prevalence of seedborne virus, lettuce seed is tested by three methods (direct reading of lettuce seedlings, inoculation of ground-up seed with a sensitive indexing host, or, more recently, a serological technique) to ensure that each lettuce seed lot contains no infected seeds in a sample of 30,000 seeds. A more successful control measure is the incorporation of virus resistance into the principal lettuce types grown on both mineral and organic soils.

Tomato mosaic. It is most common viral disease of tomato caused by Tomato mosaic virus

(TMV) belonging to genus Tobamo virus. It is reported to reduce yields upto 23%.

Symptoms:

The characteristic symptoms are mottled areas of light and dark green colour on leaves. Some strains may cause yellow mottling also. Leaves may be reduced in size and may be curled. Severe infection may cause necrosis of leaf and stem. The fruits before ripening also show symptoms on the surface as well as internal browning and collapse of cells.

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Fig 16: Tomato Mosaic Virus (Leaf Symptoms)

Fig 17: Tomato Mosaic Virus (Fruit Symptoms )

Cause: Tomato mosaic was earlier supposed to be caused by TMV, CMV, PVX or PVY. Now, Tomato mosaic virus (ToMV) is a separate virus closely related with CMV (both are Tobamo virus). ToMV is a RNA containing straight rod particle (about 300 x 18 nm). The virus remains active in extracted host plant juice upto 50 years. The virus can survive in soil (dry or wet) and

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plant debris for more than two years. Seed borne ToMV is considered to be main source of primary inoculum, in addition to root debris left in soil. It is contagious and can spread in field easily by sap or contact/mechanical transmission. Operations during transplanting and training are chief means of spread.

Tomato spotted wilt Symptoms:

The disease caused by Tomato spotted wilt virus (TSWV) is characterized by bronze coloured marking on upper side of young leaves. Leaves may also show slight downwards curling. Stiffening of leaflets, formation of small circular necrotic spots on leaves with upward marginal rolling are other symptoms. The necrosis on stem near tips may cause wilting of infected plants. The fruits on infected plant show pale red or yellow or sometimes white areas on normal red skin.

Fig 18: Purple flecking of young leaves caused by tomato spotted wilt.

Fig 19: Fruit symptoms of tomato spotted wilt.

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CAUSE:, TSWV (tospo virus) is a RNA virus with membrane envelope surrounding protein

coat. It has very wide host range (300 plant species belonging to mono and dicots). Weeds and

perennial ornamentals are reservoirs of virus. The virus is transmitted by thrips (Thirips tabaci)

in persistent manner. It is also transmitted by tomato seeds.

Management of tomato viral diseases.

Tomato viruses have wide host range and weeds/volunteer plants serve as reservoirs, these

should be eradicated to reduce load of initial inoculum. Several practices have been

recommended for management of vectors (aphids, thrips, etc.). Barrier crops (corn, non-

susceptible, tall crops) break the flight of insects. Reflective mulches on earth repel insect

vector from the fields (yellow sticky polythene) and reduces TSWV upto 64% (Sharma 1999).

Use of insecticides thimet, phorate, malathion, pyrethrum, demelon, parathion and disulfolon

has been recommended (Azam et al., 1997).

Host resistance is the most important component of management strategy. Transgenic plants

resistant to ToMV have been released (Asakawa et at., 1993). Kim and others in 1994

developed genetically engineered tomato plant resistant to TSWV (expressing the antisense

RNA and coat protein gene).

ALFALFA LATENT VIRUS

Alfalfa latent virus is also called pea streak virus.

Cause

Alfalfa latent virus (ALV) is in the carlavirus group. ALV is transmitted in a nonpersistent manner by the pea aphid, Acyrthosiphon pisum. ALV is also seed transmitted at a low rate and sap transmitted by machinery during harvesting.

Distribution

Hungary and the United States (Arizona, Nebraska, and the northwestern Unites States); however, ALV is presumed to be widespread in most alfalfa-growing areas.

Symptoms

Diseased plants are apparently symptomless.

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Fig 20: Alfalfa Latent Virus

Management

Grow alfalfa cultivars resistant to the peas aphid to prevent spread of ALV to food legume crops.

ALFALFA MOSAIC VIRUS

Cause

Alfalfa mosaic virus, (AMV), overwinters in alfalfa and other perennial host plants. AMV is disseminated from diseased to healthy plants primarily by the pea aphid, Acyrthosiphon pisum, although other aphids may also be involved. AMV is also seedborne and is transmitted through pollen and occasionally the ovules. Infected seed is the most likely source of inoculum in new alfalfa-growing areas.

Distribution

Wherever alfalfa is grown.

Symptoms

Older stands have the highest number of diseased plants. Symptoms are most obvious during cool weather in the spring and autumn. The most common symptoms are yellow streaks parallel to the leaf veins and yellow or light green mottling that is often accompanied by a distortion of the leaves. Stunting often occurs, and infrequently, plants die. Infected plants may also be symptomless.

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Fig 21 : Symptoms of alfalfa mosaic virus

Management

1. Sow virus-free seed.2. Control aphids where possible.3. Grow the most resistant cultivar.

BARLEY MOSAIC

Cause Barley mosaic virus (BMV) is seedborne and is transmitted both by the corn leaf aphid, Rhopalosiphum maidis, and mechanically. Oat and wheat are also hosts.Distribution India

Symptoms Diseased plants are generally stunted. Initially, leaves are chlorotic but later develop mosaic symptoms. Diseased seeds, which are small and shriveled, have poor germination.

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Fig 22: Maize Mosaic Virus

Management Grow resistant cultivars.

BARLEY STRIPE MOSAIC

Barley stripe mosaic is also known as barley false stripe, false stripe, lantern head, and stripe mosaic.

Cause

Barley stripe mosaic virus (BSMV) can remain viable in seed for up to 8 years and ovewinters in wild oat, Avena fatua. When infected seed germinates, the highest numbers of resulting seedlings become diseased at temperatures of 20° to 24°C. BSMV is spread when injured leaves rub against each other and by infected pollen, but it is not known to be transmitted by insects or other means. BSMV is spread further in barley sown in the spring than in the autumn.

Distribution

Southern Asia, Australia, Europe, Japan, mexico, western North America, and Russia.

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Symptoms

Symptoms vary with the mode of infection and temperature. Leaf symptoms that result from seedborne infection are a mottling or spots that are either narrow or wide, numerous or few, and continuous or broken. The color of the mottling or spots may be light green, tan, yellowish, or bleached white, which contrasts to the rest of the green leaf. Infrequently, entire diseased leaves may be nearly white.

Virulent strains of BSMV cause brown stripes, which are continuous or broken and have irregular margins, often form a V- or Chevron-shape on leaves. Sometimes plans are severely stunted and florets, which are sterile, may have no heads or poorly developed heads and kernels. Protein synthesis is affected.

Fig 23: barley stripe mosaic virus (a)

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Fig.24 Barley strpe mosaic virus (b)

Management

Grow Resistant Cultivars. Sow disease-free seed.

Rotate barley with non grass crops.

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PEANUT MOTTLE

Cause

Peanut mottle virus (PMV) is in the poryvirus group. PMV is transmitted mechanically and in a nonpesistent manner by several species of aphids. Infected peanut seed provides primary inoculum.

Distribution Australia and the United State (New York and Texas)

Symptoms

Three types of symptoms occur: one in susceptible genotypes and the other two in resistant genotypes. Susceptible genotypes display necrotic lesions and vein necrosis of inoculated unifoliate leaves. Uninoculated trifoliate leaves in the field develop a mosaic, followed by chlorosis and necrosis of veins, petioles, and stems. Plants frequently die.Resistant genotypes react with necrotic lesions and vein necrosis or with chlorotic lesions that eventually coalesce. In both reactions, the virus remains localized in inoculated leaves. Few or no seeds are produced on diseased plans.

Fig 25: Peanut mottle virusManagement

1. Grow resistant cultivars2. Separate bean fields from peanut fields.

SOUTHERN BEAN MOSAIC

Cause

Southern bean mosaic virus (SBMV), which is in the sobemovirus group, consists of different strains. SBMV is seedborne; the incidence of infection is higher in seeds with cracked coats

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than in seeds with intact coats. SBMV is also transmitted mechanically, by growing plants in virus infested soil, and by several beetles.

Distribution South America

Symptoms

Either circular (1-3 mm in diameter), brownish-red local lesions or systemic mottling and vein banding symptoms occur on diseased leaves. Leaves also may be blistered and malformed or crumpled.

Pods have dark green, water-soaked, irregular-shaped blotches. The number and weight of seed may be reduced; however, the number of pods may be greater in diseased that in healthy plans.

Fig 26: Southern Bean Mosaic Virus

Management

1. Sow virus-free seed.2. Grow resistant cultivars

MAIZE CHLOROTIC MOTTLE

Cause

Maize chlorotic ottle virus (MCMV) is in the sobemovirus group. MCMV survives in corn residue and is transmitted by six species of beetles: the cereal leaf beetle, Oulema melanopa;

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the corn flea beetle, Chaetocnema pulicaria; the flea beetle, Systema frontalis; the southern corn rootworm, Diabrotica undecimpunctata; the northern corn rootworm, D. longicornis; and the western corn rootworm, D. virgifera. MCMV is also transmitted by seed, by thrips (Frankliniella williamsi), mechanically, and possibly by soil. In the absence of fresh maize roots, newly hatched larvae of vectors forage on infested crop residues and acquire MCMV, which is transmitted later by larvae feeding on developing maize roots.

MCMV survival in maize tissues, and perhaps viability of beetle eggs in soil, may occur only in soils with high water-holding capacities. Such soils can maintain infected crop residues in a”proper” state of hydration and preserve virus particles. Continuous maize production greatly increases the incidence of MCMV. Other hosts of MCMV include barley, johnsongrass, rye, sorghum, and wheat.

MCMV, together with either maize dwarf mosaic virus strain B or wheat streak mosaic virus, is one of the viruses that causes corn lethal necrosis. At least two strains of MMV exist: the Peru Strain, MCMV-P; and the Kansas strain, MCMV-K.

Distribution

Brazil, Peru, and the United States (Hawaii, Kansas, Nebraska, and Texas).

Symptoms

Initially, fine, chlorotic stripes are parallel to the veins of the youngest diseased leaves. Stripes coalesce and produce elongated, chlorotic blotches that eventually become necrotic. Eventually, leaves curl downward and plant death follows. Diseased plants are stunted, have distorted tassels, and form fewer ears. Significant yield losses may occur from infection by MCMV alone.

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Fig 27: Maize Chlorotic Mottle Virus

Management

1. Grow tolerant hybrids.2. Rotate maize with soybean.

MAIZE DWARF MOSAIC

Cause

Maize dwarf mosaic virus (MDMV) now consists of format MDMV stains A, D, E, and F. MDMV is transmitted mechanically from the mouthparts of several aphids, and is sedborne in sweet maize. Disease appearance and spread are related to aphid numbers. Plants infected when young are more severely diseased than old plants. However, late sowings of sweet maize are more severely diseased than early sowing. Soil moisture and nitrogen availability are associated with virus infection.Several wild and cultivated grasses are susceptible to MDMV. In Mississippi, 70% of all grass species are susceptible in various degrees to MDMV.

Distribution

Wherever maize is grown

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Symptoms

Symptoms are variable and most severe on plans infected when young; those infected at the pollination stage of plant growth or later may appear normal. Initially, plants have stippled mottle or mosaic of light and dark green that develops in to narrow streaks on the youngest diseased chlorotic background. Symptoms may occur on all leaves, leaf sheaths, and husks that develop into narrow streaks on the youngest deseased leaves. Sometimes the mosaic appears as dark green “islands” on a chlorotic background. Symptoms may occur on all leaves, leaf sheaths, and husks that develop after infection. As diseased plants mature, the mosaic disappears and leaves become yellowish green and frequently show red streaks that are generally observed after periods of cool night temperatures of 15.5°C and below.

Severely diseased plants are barren. Plants are predisposed to root rot, and stalk strength is reduced because diseased stalks become smaller in diameter than those of healthy plants. Upper internodes may be shortened, giving a “feather duster” appearance to diseased plants.

Fig 28: Maize Chlorotic Dwarf Virus

Management

1. Grow resistant hybrids.2. Destroy overwintering hosts.3. Plant sweet maize early.

MAIZE RING MOTTLE

Cause

Maize ring mottle virus is transmitted by seed.

Distribution

Bulgaria.

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Symptoms

Chlorotic spots and rings occur on diseased leaves.

Management

Not reported.

REFERENCES

Agrios, G.N., 1997. Plant pathology, 4th ed., Academic press, New York.

Ali, A. and S. Hassan. 1992. Biological characterization of soybean mosaic virus. Sarhad J. Agri. 8 : 555-569.

Allen, D.J., 1983. The pathology of tropical food legumes, Disease resistance in crops improvement, John Wiley and Sons. Chichester p. 413.

Asakawa, Y. 1993. Evaluation of the impact of the release of transgenic tomato plants with TMV resistance on the environment, Jpn. Agric. Res. Quart. 27 :126-136.

Azam, K.M., Razvil, S.A., Zouba A. and Al- Raeesi, A.A., 1997. Management of whitefly (Bemisia tabaci) and Tomato leaf curl virus in tomato crop, Arab. Near East Plant Prot. Newsl. :25-27.

Bashir, M., Hanif, M. and Z. Ahmad. 1997. Detection of garlic yellow streak potyvirus from field collected garlic samples by enzyme linked immunosorbent assay In: Ann. Rept. Pl. Genetic Resou. Inst. NARC.Islamabad Pakistan p. 36-37. Bashir. M., S.M. Mughal B.A. Malik. 1991. Assessment of yield losses due to urdbean leaf crinkle virus in urdbean, Vigna mungo (l) Hepper. Pak. J. Botany. 23: 140-142.

Carroll, T.W., P.L. Gossel and E.A. Hockett. 1979. Inheritanc of resistance to seed transmission of Barley stripe mosaic virus in barley. Phytopathology, 69: 431-433.

Cooper, V.C. 1976. The seed transmission of cherry leaf roll virus. Ph.D. thesis University of Brimingham. p. 184.

Hampton, R.O. 1983. Seed borne viruses in crop germplasm resources : disease dissemination risks and germplasm reclamation technology. Seed Sci. & Technology. 11: 535-546.

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Hemmati, K. and D.L. McLean, 1977. Gamete seed transmission of alfalfa mosaic virus and its effects on germination and yield in alfalfa plants. Phyopathology. 67: 576-579.

Kim, J.W., Sun, S.S.M. and T.L. German.1994. Disease resistance in tobacco and tomato plants transformed with tomato spotted with virus nucleocapsid gen. Plant Dis. 78 : 615-621.

Maury, Y. and R.K. Khetrapal. 1992. Pea seed borne mosaic virus, In: Plant diseases of international importance, vol 2, H.S. Chaube and U.S. Singh (Eds), Prentice Hall, New Jersey p.337.

Neergaard, p. 1977. Seed borne viruses. In: Seed pathology .1 Macmillan press. London and Madras, p. 839.

Sharma, P.K. 1999. Identification and management of viruses infecting Tomato in himachal Pradesh, Ph.D thesis, UHF, Solan, India p.129 Shepherd, R.J. and Q.L. Holdeman. 1965. Seed transmission of the Jhonsongrass strain of he sugarcane mosaic virus in corn. Plant. Dis. Rept.49: 468-469.

d/bhutta/book seed path/seedborne virus diseases of plants final

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