Gibberella indica (wilt of pigeon pea)
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- Risk of Introduction
- Hosts/Species Affected
- Host Plants and Other Plants Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Natural enemies
- Seedborne Aspects
- Plant Trade
- Detection and Inspection
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Gibberella indica Rai & Upadhyay
Preferred Common Name
- wilt of pigeon pea
Other Scientific Names
- Fusarium oxysporum f.sp. udum
- Fusarium udum Butler
- Fusarium udum var. cajani
- Gibberella udum
International Common Names
- English: Fusarium wilt of pigeon pea; pigeonpea wilt; wilt of red gram
Local Common Names
- India: wilt of arahar
Taxonomic TreeTop of page
- Domain: Eukaryota
- Kingdom: Fungi
- Phylum: Ascomycota
- Subphylum: Pezizomycotina
- Class: Sordariomycetes
- Subclass: Hypocreomycetidae
- Order: Hypocreales
- Family: Nectriaceae
- Genus: Gibberella
- Species: Gibberella indica
Notes on Taxonomy and NomenclatureTop of page The pigeon pea wilt pathogen was described as Fusarium udum (Butler, 1910). Padwick (1940) found that the fungus produced abundant macroconidia in sporodochia in culture and that these spores were strongly hooked at the apex. He proposed the name F. oxysporum f.sp. cajani. Snyder and Hansen (1940) named the fungus F. oxysporum f.sp. udum. This nomenclature was supported by Chattopadhyay and Sengupta (1967). However, the name F. udum is commonly accepted as the macroconidia of this pathogen have a prominent apical hook which is lacking in F. oxysporum (Booth, 1971).
There is some disagreement on the occurrence of a teleomorph. Rai and Upadhyay (1981) discovered the perfect state of F. udum on wilted and dead pigeon pea plants in Uttar Pradesh, India, and named it Gibberella indica. The perithecia were large and they had two-celled (rarely three-celled) ascospores. Singh (1980) also found the perfect stage of F. udum and named it Gibberella udum. He suspected that cloudy weather, high humidity and a combination of high and low temperatures were responsible for its production. However, Holliday (1980) does not accept the existence of a teleomorph.
DescriptionTop of page The hyphae are hyaline, slender, much branched, usually with little aerial growth (Butler, 1910). The pathogen produces three types of spores. Microconidia are usually aseptate, elliptical, hyaline singly but salmon-pink in mass and measure 6-11 x 2-3 µm in diameter. They are produced on simple or clustered, vertically branched conidiophores (Holliday, 1980). In culture, however, the colour may vary from white to salmon-pink and occasionally orange-red on PSA. Macroconidia are formed on short conidiophores and detach soon after abscission. They are hyaline, three to five septate, 15-15 x 3-5 µm in size, falcate with a distinct foot cell and an apical cell of decreasing diameter towards the tip which may be curved or hooked (Holliday, 1980). The chlamydospores are oval or spherical, single or in chains, thick-walled and measure 5-10 µm in diameter.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|India||Present||Present based on regional distribution.|
|Kenya||Present||Kiprop et al., 2002|
Central America and Caribbean
Risk of IntroductionTop of page Risk criteria Category
Economic importance High
Seedborne incidence Low
Seed transmission Recorded
Seed treatment Yes
Overall risk High
Notes on Phytosanitary Risk
No quarantine restrictions on F. udum are available because of the widespread distribution of the pathogen and the occurrence of pathogenic races. Long-distance dispersal of F. udum into new areas, and also of the spread of virulent races into different areas can occur with infected seed. It is, therefore, essential that the movement of seed from one area to another and from one country to another should only be allowed after treatment with thiram and benomyl.
Hosts/Species AffectedTop of page F. udum is specific to pigeon pea, but it also causes wilt symptoms in Atylosia spp., a wild relative of pigeon pea (Kannaiyan et al., 1985).
Host Plants and Other Plants AffectedTop of page
|Cajanus cajan (pigeon pea)||Fabaceae||Main|
Growth StagesTop of page Flowering stage, Fruiting stage, Seedling stage, Vegetative growing stage
SymptomsTop of page Pigeon pea plants are susceptible to infection by the wilt pathogen at all stages of development. The main symptom of the disease is wilting characterized by gradual, sometimes sudden, yellowing, withering and drying of leaves followed by drying of entire plant or some of its branches (Singh, 1973). Such plants exhibit loss of leaf turgidity, interveinal clearing and chlorosis before death. Isolated wilted plants may appear about a month after sowing and patches of dead plants in the field, usually at the flowering and podding stage, are the first indication of wilt (Reddy et al., 1990). The characteristic symptom of the disease in the adult plants is a purple band extending upwards from the base of the main stem. The band can clearly be seen in pigeon pea, when the green stems of healthy plants are compared to the diseased stems with coloured lines. Partial wilting is quite common and distinguishes the disease from termite damage, drought and Phytophthora blight, which also kill the plants. Partial wilting is due to infection of lateral roots, while total wilt is a result of tap root infection (Reddy et al., 1990). If an infected plant is split open below the purple band, browning of the stem and brown to black discoloration of xylem vessels is visible. Sometimes lower branches show die-back with the purple band extending from the tip downward and intensive xylem blackening (Reddy et al., 1993b).
List of Symptoms/SignsTop of page
|Leaves / abnormal colours|
|Leaves / wilting|
|Stems / discoloration|
|Stems / internal discoloration|
|Whole plant / wilt|
Biology and EcologyTop of page Transmission
The pathogen is a facultative saprobe, which survives on plant parts left in the soil. Any route by which diseased soil may be transported from infested plot to non-infested plots, including farm implements, irrigation water etc., can potentially transmit the pathogen. Dissemination of the pathogen is also possible through seedborne infection.
After the discovery of the perfect state of the pathogen, two phases of the disease cycle have been suggested: imperfect state (Fusarium udum) and perfect state (G. indica). In both phases of the disease, the pathogen occurs intercellularly, intracellularly and ectotrophically on the collar region as well as on the roots of infected plants. It produces a mass of mycelium and conidia. Both states of the pathogen occur simultaneously on the host. In the case of the imperfect state of the disease cycle, conidia and chlamydospores serve as resting structures for long-term survival. In the perfect state, perithecia are produced on the collar region of infected plants. The longevity of survival of the perfect state is yet to be confirmed (Upadhyay and Rai, 1983). The pathogen is heterothallic. If two opposite mating types come into contact they produce perithecia. Under laboratory conditions, perithecia are produced at 25±2°C. The ascus contains eight ascospores, which are two- to three-celled. The ascospores germinate to produce macro- and microconidia (Reddy et al., 1998). The production of the perfect state of this pathogen and its role in pathogenesis needs further investigation.
The pathogen survives in infected plant parts. The saprobic mycelium produces conidia. These conidia germinate at a wide range of temperatures (15-30°C) under laboratory conditions. When the germtubes come in contact with the roots of pigeon pea plants, they penetrate and colonize the xylem vessels. As the mycelium ages it produces chlamydospores which, after an initial period of dormancy, germinate and infect the roots of the plants. During the cropping season, the ectotrophic growth of the pathogen can also occur on infected roots and the collar.
The fungus is soilborne on diseased plant debris and it survives only on the tissues which it colonizes as a parasite (Subramanian, 1955). McRae (1924) reported that the fungus spreads about 3 m through the soil in one season, apparently along plant roots. The amount of wilt incidence was influenced by the retentive nature of the soil, but not directly by its water content (Mitra, 1925; McRae, 1926). Mundkar (1935) reported that low soil temperature and increasing plant maturity favoured wilt.
Shukla (1975), in a pot experiment, found more wilt inoculum in sand (94%) than in heavy, black soil (18%). Singh and Bhargava (1981) found the fungal population to be highest at 30% soil water-holding capacity and at soil temperatures between 20 and 30°C.
Infected seed may be the primary means of spread of F. udum over long distances and to new areas (Haware and Kannaiyan, 1992). The fungus can survive on infected plant debris in the soil for about 3 years. Disease incidence is more severe on vertisols than on alfisols and ratooning predisposes the plant to wilt (Reddy et al., 1990). Early sowing, weed management and vigorous crop growth favour wilt development. Long- and medium-duration types suffer more from wilt than short- and extra short-duration types (Reddy et al., 1998).
Though infection may occur in the seedling stage, maximum disease occurs at flowering and podding (Reddy et al., 1990) due to the extended time needed by the fungus to colonize the plant. Recent work at ICRISAT has shown that infected plants wilt only after the basal half of the main stem is colonized by the fungus, which takes approximately 3-4 months (Reddy et al., 1993a). This explains why there are low levels of wilt in short-duration types compared to long-duration and ratooned pigeon pea, as the former morphotypes are escaping wilt (Reddy et al., 1998). Any practice which leads to increased plant biomass in pigeon pea was found to increase susceptibility to wilt (Reddy et al., 1994). Higher biomass is produced when the crop is sown early, under weed-free and well-drained conditions, in fertile fields at low plant density and when the rains are well distributed.
Recent work has indicated that the fungus can survive to a depth of 120 cm in soil (Naik, 1993). Limited variation in the fungal population was found between the crop season and the off-season, especially at lower depth. Inoculum placed at a depth of 100 cm was found to infect pigeon pea but did not cause wilt. Only inoculum at 50 cm depth resulted in both infection and wilt (Naik, 1993). The economic threshold level of 20% wilt incidence in a susceptible cultivar was found to vary for vertisols and alfisols, being slightly lower for alfisols (830 c.f.u./g soil) than for vertisols (920 c.f.u./g soil). Threshold levels were higher for tolerant cultivars than for susceptible cultivars. The initial inoculum level in soil was found to be the major factor influencing final wilt incidence compared to soil moisture and temperature.
Many studies have shown the existence of races of the pathogen (Baldev and Amin, 1974; Shit and Gupta, 1978; Reddy and Chaudhary, 1985; Pawar and Mayee, 1986; Gupta et al., 1988; Reddy and Raju, 1992) but a systematic study of the classification and distribution is lacking. This is largely due to the lack of a standardized inoculation technique, a set of differential lines and a rating scale.
Natural enemiesTop of page
Seedborne AspectsTop of page Incidence
The level of seed infection varies with cultivar. Although the pathogen was detected in about 19% of pigeon pea seed, disease transmission was only obtained in up to 4.25% of seedlings grown from infected seeds (Haware and Kannaiyan, 1992).
Effect on Seed Quality
Seedborne infection affects seed quality. Infected seed may become a source of primary infection in new areas or a source of a new race in areas where the disease is already present.
Seed harvested from wilted plants may carry the pathogen in a viable state. Such infected seed yielded F. udum on Nash's medium and could produce diseased seedlings (Haware and Kannaiyan, 1992). Seeds collected from healthy plants do not carry the pathogen. Seed infection differs between varieties.
A mixture of thiram + benomyl can completely eradicate F. udum from infected seed. This combination of fungicides was also effective in controlling disease transmission from infected seed (Haware and Kannaiyan, 1992).
Plant TradeTop of page
|Plant parts liable to carry the pest in trade/transport||Pest stages||Borne internally||Borne externally||Visibility of pest or symptoms|
|Roots||hyphae; spores||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Stems (above ground)/Shoots/Trunks/Branches||hyphae; spores||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|True seeds (inc. grain)||hyphae; spores||Yes||Yes||Pest or symptoms usually invisible|
|Plant parts not known to carry the pest in trade/transport|
ImpactTop of page In an ICRISAT survey conducted from 1975 to 1980, annual losses in grain yield due to wilt were reported to be up to US$ 36 million (Kannaiyan et al., 1984). In eastern Africa, losses were estimated at US$ 5 million (Kannaiyan et al., 1984). Losses caused by the disease are dependent on the stage of wilt occurrence. If wilt occurs prior to podding, loss is total; however, only partial loss may result if wilt occurs at pod filling stage or later (Kannaiyan and Nene, 1981). Long-duration varieties may compensate for loss of early wilted plants. Yield loss in cultivars that are infected but do not show wilt symptoms have not yet been quantified. If wilt occurs during pod filling, the seed may become infected. Such seed may become a source of primary inoculum if not properly treated with fungicides.
DiagnosisTop of page The fungus, as a rule, is confined to the vascular tissues and is both inter- and intracellular. The septate hyphae develop rapidly and the vessels are plugged with the hyphae. Chari et al. (1984) developed a method of detecting wilt before the appearance of symptoms using an electric current; the precision of the method can be up to 94%.
Interaction with other diseases
Wilt incidence is affected by infection with other diseases. Plants affected by sterility mosaic and phyllody were less affected by wilt than unaffected plants of the same genotypes (Chadha and Raychaudhuri, 1966). Similarly, root knot (Meliodogyne sp.) infection increased wilt susceptibility in both susceptible and resistant cultivars (Reddy et al., 1990). However, although infection by cyst nematode (Heterodera cajani) enhanced pathogenicity of F. udum in a wilt-susceptible cultivar, the fungus suppressed the reproduction of the nematode. The reaction of wilt-resistant genotypes was not affected by the presence of the nematode (Sharma and Nene, 1989).
Detection and InspectionTop of page Symptoms of the disease are distinct as described under Symptoms and can be identified in the field.
Prevention and ControlTop of page Resistant Crop Cultivars
There has been considerable research on the control of this disease. The major emphasis has been on the identification of resistance and the production of wilt-resistant cultivars (Deshpande et al., 1963). Pot and field screening techniques have been developed for the identification of resistance (Nene et al., 1981a; Haware and Nene, 1994). For a pot-screening technique, autoclaved pigeon pea stem pieces are mixed with non-autoclaved alfisol in pots (Reddy et al., 1998). The soil is inoculated with a F. udum culture multiplied on sand-pigeon pea flour (9:1) medium. A susceptible cultivar is sown and the wilted plant material is re-incorporated in the pots for three cycles.
Wilt-diseased plots have been used to screen crops against several vascular wilts. At ICRISAT Centre (Patancheru, India), it was found that the wilt disease develops more quickly in alfisols than in vertisols and shows up earlier in alfisols (Nene et al., 1980). The best way to develop the disease is to incorporate stubble from diseased plants into the soil and to grow wilt-susceptible cultivars in intermittent rows all over the field (Reddy et al., 1998). The search for sources of resistance to wilt in pigeon pea began as early as 1905 at Pune, India (Butler 1908, 1910). Many sources of resistance were identified at locations throughout India (Alam, 1931; Reddy et al., 1998). Despite the availability of large number of sources of resistance, only a few cultivars were popular with the farmers.
Multilocation tests conducted in India and eastern Africa helped to identify several lines resistant to wilt at several locations. Moderately resistant lines are available in all maturity groups. Some of these lines also show resistance across locations and seasons (Nene et al., 1981b, 1989; Amin et al., 1993). These lines includes ICP 8863 (Maruti), ICP 9145, ICP 9174, ICP 12745, ICPL 333, ICPL 8363, ICPL 88047, BWR 37. DPPA 85-2, DPPA 85-3, DPPA 85-8, DPPA 85-13, DPPA 85-14, Bandpalera, ICP 47769, ICP 9168, ICP 10958, ICP 11299, C11 (ICP 7118), BDN1 (ICP 7182). ICP 8864 and ICP 9145 have been released for commercial cultivation in Malawi and have become very popular (Reddy et al., 1995). The lines that showed resistance in Kenya were ICP 8869, ICP 9145 and ICP 10960. The lines that were resistant in Malawi are ICP 7855, ICP 9145, ICP 9154, ICP 9174, ICP 9177, ICP 10958, ICP 11297, ICP 11299 and ICP 12738. Maruti (ICP 8863), which has been released for commercial cultivation in India (Konda et al., 1986), has become very popular in peninsular India. Lines which combine wilt resistance and resistance to other diseases have been identified. For example, ICPL 87 and C11 possess resistance to wilt, sterility mosaic and Phytophthora blight; ICP 7667, ICP 8861, ICP 8662 (Hy3C) to wilt, sterility mosaic and powdery mildew; ICPL 81 to wilt and halo blight; BDN1 to wilt, Phytophthora blight and halo blight; ICP 8661, ICP 8662, ICP 8867, ICP 8869, ICP 10962 to wilt and Alternaria blight.
Inheritance of resistance
Limited information is available on the inheritance of resistance to the disease. In a cross between one resistant (ICP 8863) and two susceptible (ICP 2376 and LRG 3C) lines, resistance was found to be controlled by a single recessive gene. The gene was designated pwr1 (Jain and Reddy, 1995).
Nature of resistance
The nature of resistance was analysed in cultivars that were resistant and susceptible to wilt. The extract from a resistant cultivar (C-11-6) inhibited spore germination and the growth of the germtube. The inhibitory compounds in the resistant cultivar were identified as chlorogenic acid and caffeic acid (Murthy and Bagyaraj, 1983).
Pigeon pea is generally grown in inter- and mixed-cropping systems in rotation with other crops. However, since the fungus survives on deep-seated roots of the host, below the depth of ordinary cultivation, the success of rotation will depend upon the field sanitation (removal of affected plants with their roots), hot weather cultivation etc. A 4-5-year rotation has been found to free the field completely of the wilt pathogen (Singh, 1973). Field studies conducted at ICRISAT Centre (Patancheru, India) have shown that crops such as sorghum, castor, maize and groundnut inhibit the soil population of F. udum (Himani Bhatnagar, 1995). One-year breaks with either sorghum or fallow reduced wilt in the following pigeon pea crop from 60-90% to 16 and 31%, respectively (Natarajan et al., 1985). Pigeon pea rotation with tobacco has been recommended as a possible means of control because of the adverse effect of tobacco root exudates on the pathogen (Bose, 1938). Wilt incidence was increased with increasing pigeon pea biomass (Reddy et al., 1994).
Root exudates from a range of crops, which are frequently intercropped with pigeon pea, and green manuring reduce wilt incidence either by reducing population of F. udum or by increasing the antagonistic activity of the microbial population in the soil. A higher incidence of wilt in sterilized soil than in unsterilized soil was attributed to the action of antagonistic organisms such as Aspergillus niger, Rhizopus nigricans and Bacillus subtilis (Vasudeva and Roy, 1950; Vasudeva and Govindaswami, 1953). In later studies, Singh (1973) reported the production of 'bulbiformin' by B. subtilis, which inhibits the growth of F. udum. The antibiotic remains active in soil for 35 days. It was also found that the rhizosphere of resistant cultivars contains a greater population of Streptomyces spp., which are antagonistic to F. udum, than the rhizosphere of susceptible cultivars. The soil composition and certain cultural practices can affect wilt incidence (Shukla, 1975; Upadhyay and Rai, 1981). These findings indicate that the disease can be kept under control if conditions can be created in the soil that are suitable for the development of antagonistic organisms through organic amendments.
Seedborne infection can be eliminated by seed dressing with a mixture of benomyl and thiram.
ReferencesTop of page
Alam M, 1931. Several reports on the sources of resistance to wilt. Administration Report of the Botanical Section 1930-31. Bihar and Orissa, India: Department of Agriculture, 42-65.
Amin KS; Reddy MV; Raju TN; Nene YL; Singh RA; Zote KK; Bendre NJ; Jha DK; Bidari VB; Naphade SD; Arjunan G; Agarwal SC; Sinha BK; Mahendra Pal; Grewal JS; Anilkumar TB, 1993. Multilocational evaluation of pigeonpea for broad-based resistance to Fusarium wilt in India. Indian Journal of Plant Protection, 21(1):28-30; 6 ref.
Baldev N; Amin KS, 1974. Studies on the existence of races in Fusarium udum causing wilt of Cajanus cajan. SABRAO Journal, 6:201-205.
Butler EJ, 1908. Selection of pigeonpea for wilt disease. Agricultural Journal of India, 3:182-183.
Butler EJ, 1910. The wilt disease of pigeonpea and the parasitism of Neocosmospora vasinfecta Smith. Memoirs of the Department of Agriculture in India. Botanical Series, 2:1-64.
Chadha KC; Raychaudhuri SP, 1966. Interaction between sterility mosaic virus and Fusarium udum Butl. in pigeonpea. Indian Journal of Agricultural Sciences, 36:133-139.
Chattopadhyay SB; Sengupta PK, 1967. Studies on wilt diseases of pulses 1. Variation and taxonomy of Fusarium sp. associated with wilt diseases of pulses. Indian Journal of Mycological Research, 5:45-53.
Deshpande RB; Jeswani LM; and Joshi AB, 1963. Breeding wilt resistant varieties of pigeonpea. Indian Journal of Genetics and Plant Breeding, 23:58-63.
Himani Bhatnagar, 1995. Influence of Agricultural Production Systems on Plant Diseases. Crop Protection Division Progress Report. Patancheru, India: ICRISAT Asia Center.
Jain KC; Reddy MV, 1995. Inheritance of resistance to fusarium wilt in pigeonpea (Cajanus cajan (L.) Millsp.). Indian Journal of Genetics, 55:436-439.
Kannaiayan J; Nene YL; Reddy MV, 1981. Survival of pigeonpea wilt Fusarium in Vertisols and Alfisols. In: Proceedings of the International Workshop on Pigeonpeas, volume 2, 15-19 December 1980, ICRISAT Center, India. Patancheru, A.P., India: ICRISAT, 291-295.
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McRae W; Shaw FJF, 1933. Influence of manures on the wilt disease of Cajanus indicus Spreng. and isolation of types resistant to the disease. Part II. The isolation of resistant types. Scientific Monograph, Imperial Council of Agricultural Research, 7, Pusa, India, 37-68.
Mitra M, 1925. Report of the Imperial Mycologist. Scientific Report of the Agricultural Research Institute, Pusa, 1924-25. Pusa, India, 45-57.
Mundkar BB, 1935. Influence of temperature and maturity on the incidence of sunnhemp and pigeonpea wilt at Pusa. Indian Journal of Agricultural Sciences, 5:606-618.
Naik MK, 1993. Ecology and integrated disease management of fusarium wilt of pigeonpea. Legumes Pathology Progress Report No. 19. Patancheru, India: ICRISAT.
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Nene YL; Kannaiyan J; Reddy MV, 1981. Pigeonpea diseases. Resistance-screening techniques. ICRISAT Information Bulletin No. 9.
Nene YL; Kannaiyan J; Reddy MV; Zote KK; Mahmood M; Hiremath RV; Shukla P; Kotasthane SR; Sengupta K; Jha DK; Haque MF; Grewal JS; Mahendra Pal, 1989. Multilocational testing of pigeonpea for broad-based resistance to Fusarium wilt in India. Indian Phytopathology, 42(3):449-453; 2 ref.
Raut NK; Bhombe BB, 1971. A review of the work of selections of tur varieties resistant to Fusarium wilt at College of Agriculture, Parbhani (Maharashtra). College of Agriculture Magazine, Parbhani, 12:37-42.
Ravishanker, 1936. Isolation of wilt-resistant tur. Nagpur Agriculture College Magazine, 10:162-167.
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Reddy MV; Raju TN; Naik MK, 1993. Infection and colonization of Fusarium udum in pigeonpea. Indian Phytopathology, 46:268 (Abstr.).
Reddy MV; Raju TN; Sharma SB; Nene YL; McDonald D, 1993. Handbook of pigeonpea diseases. ICRISAT Information Bulletin Patancheru, India; International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), No. 42:61 pp.
Singh KP, 1980. The association of Giberella udum with the wilted arhar plants recorded again. Indian Phytopathology, 33:161.
Singh RS, 1973. Plant Diseases. G.B. Pant University of Agriculture & Technology, Pantnagar.
Snyder WC; Hansen HN, 1940. The species concept in Fusarium. American Journal of Botany, 27:64-67.
Subramanian CV, 1955. The ecological and the taxonomic problems in Fusaria. Proceedings of the Indian Academy of Sciences, Section B41:102-109.
Upadhyay RS; Rai B, 1981. Effect of cultural practices and soil treatments on incidence of wilt disease of pigeonpea. Plant and Soil, 62:309-312.
Upadhyay RS; Rai B, 1983. A new disease cycle of wilt of pigeonpea. Current Science, 52:978-981.
Vaheeduddin S, 1956. Selection of tur (Cajanus cajan L.) resistant varieties against wilt (Fusarium udum Butler). Agricultural College Journal of Osmania University, 3:12-13.
Vaheeduddin S; Nanjundiah SM, 1956. Evolving wilt resistant strains in tur (Cajanus cajan L.). Proceedings of the Indian Science Congress, 43(4):20.
Vasudeva RS, 1952. Investigation on the inhibitory action of Bacillus subtilis on Fusarium udum Butl., the fungus causing wilt of pigeonpea (Cajanus cajan). Annals of Applied Biology 39:229-238.
Vasudeva RS; Chakrabarty BP, 1954. The antibiotic action of Bacillus subtilis in relation to certain parasitic fungi with special reference to Alternaria solani. Annals of Applied Biology 41:612-618.
Vasudeva RS; Govindaswami GV, 1953. Studies on the effect of associated soil microflora on Fusarium udum Butl., the fungus causing wilt of pigeonpea with special reference to its pathogenicity. Annals of Applied Biology 40:573-583.
Vasudeva RS; Roy TC, 1950. The effect of associated microflora on Fusarium udum Butl, the fungus causing wilt of pigeonpea (Cajanus cajan). Annals of Applied Biology 37:166-177.
Williams FJ; Grewal JS; Amin KS, 1968. Serious and new diseases of pulse crops in India in 1966. Plant Disease Reporter, 52:300-304.
Zaveri PP; Shah RM; Pathak AR; Patel JA; Kher HR; Patel RS; Tikka SBS, 1986. BDN 2 a wilt tolerant superior cultivar of pigeonpea for Gujarat. International Pigeonpea Newsletter, 5:38-39.
Zote KK; Thombre PG; Khalikar PV; Dandnaik BP; Chavan GV; Olekar SS, 1983. Breeding pigeonpea for resistance to wilt and sterility mosaic. International Pigeonpea Newsletter, 2:43-44.
Distribution MapsTop of page
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