Diseases of Pigeonpea | Diseases of Field & Horticultural Crops and their Management-I Notes

1. Phytophthora Blight

Symptoms

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Phytophthora blight, caused by Phytophthora drechsleri f. sp. cajani, manifests as stem blight and leaf blight. Initial symptoms appear as water-soaked lesions on stems, which rapidly expand and turn dark brown to black. Affected stem tissues become soft and rotted, leading to wilting and death of the plant above the infection point. On leaves, symptoms begin as dark green, water-soaked spots that enlarge and turn necrotic. During humid conditions, a white cottony fungal growth may be visible on infected plant parts. The disease progresses rapidly, especially during periods of high moisture and warm temperatures.

Etiology

The causal organism, Phytophthora drechsleri f. sp. cajani, is an oomycete pathogen. It thrives in warm (25-32°C), humid conditions with excessive soil moisture. The pathogen produces both asexual (sporangia and zoospores) and sexual (oospores) structures. Heavy rainfall, poor drainage, and waterlogged conditions favor disease development. The pathogen can survive in soil and plant debris as thick-walled oospores that remain viable for extended periods.

Disease Cycle

The pathogen overwinters in soil as oospores or survives in infected plant debris. During favorable conditions (high moisture and warm temperatures), oospores germinate to produce sporangia. Sporangia release motile zoospores that swim in soil water to reach host roots and lower stems. Zoospores encyst on plant surfaces, germinate, and penetrate through natural openings or directly through the epidermis. Once established, the pathogen colonizes plant tissues and produces new sporangia, which spread through rain splash and irrigation water. The disease spreads rapidly under monsoon conditions, completing multiple infection cycles within a season.

Management

Integrated management strategies are essential for controlling Phytophthora blight. Cultural practices include selecting well-drained fields, avoiding waterlogging, and implementing proper drainage systems. Crop rotation with non-host crops for 2-3 years helps reduce soil inoculum. Use of disease-free seeds and resistant varieties like ICP 8863 and ICPL 87119 provides effective control. Seed treatment with metalaxyl or mefenoxam (6 g/kg seed) protects seedlings during early growth stages. Soil application of Trichoderma harzianum or Pseudomonas fluorescens at 2.5 kg/ha mixed with farmyard manure reduces pathogen populations. Foliar sprays of metalaxyl + mancozeb (0.25%) or dimethomorph (0.05%) at 15-day intervals during disease-favorable periods provide effective protection. Ridge planting and avoiding overhead irrigation minimize disease spread.

2. Wilt Disease

Symptoms

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Wilt disease in pigeonpea, primarily caused by Fusarium udum, is characterized by sudden or gradual wilting of plants. Early symptoms include yellowing of leaves starting from lower branches, followed by drooping and drying of leaves that remain attached to the plant. Vascular discoloration is a diagnostic feature—when infected stems are split longitudinally, dark brown to black streaks are visible in the xylem tissue. Seedlings may show damping-off symptoms, while older plants exhibit gradual yellowing, wilting, and eventual death. Affected plants may wilt unilaterally (one side of the plant) before complete collapse.

Etiology

Fusarium udum is a soil-borne fungal pathogen that colonizes the vascular system of pigeonpea. The fungus thrives in temperatures ranging from 25-30°C with moderate soil moisture. High soil pH (7.0-8.5), presence of root-knot nematodes, and continuous cropping of susceptible varieties increase disease severity. The pathogen produces microconidia, macroconidia, and chlamydospores. Chlamydospores serve as survival structures in soil and can remain viable for several years, making the disease difficult to manage in infested soils.

Disease Cycle

The pathogen survives in soil as chlamydospores and in infected plant debris. When susceptible host roots are present, chlamydospores germinate and produce mycelia that penetrate root tissues through wounds or directly through root hairs. The fungus invades the xylem vessels, colonizes them, and produces toxins and mycelial plugs that block water transport. As the pathogen multiplies, it produces conidia that spread through vascular tissues to above-ground plant parts. Infected plants serve as sources of inoculum, with conidia dispersed through irrigation water, contaminated tools, and soil movement. The pathogen produces chlamydospores in dying tissues, which are released into soil to perpetuate the disease cycle.

Management

Wilt management requires a comprehensive approach combining resistant varieties, cultural practices, and biological control. Cultivation of resistant varieties such as ICP 8863, Maruti, Asha, and BDN 711 is the most effective strategy. Long crop rotations (3-4 years) with cereals or non-host crops reduce soil inoculum. Deep summer plowing exposes chlamydospores to solar heat, reducing their viability. Seed treatment with Trichoderma viride or T. harzianum (4 g/kg seed) along with carbendazim (2 g/kg seed) provides early protection. Soil application of Trichoderma spp. or Pseudomonas fluorescens (2.5 kg/ha) enriched with farmyard manure at sowing reduces pathogen populations. Avoiding excessive nitrogen fertilization and maintaining balanced nutrition improves plant resistance. Using raised beds, ensuring proper drainage, and practicing timely sowing help minimize disease incidence. Rogueing and destruction of infected plants prevent further spread within the field.

3. Sterility Mosaic Disease (SMD)

Symptoms

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Sterility Mosaic Disease is one of the most devastating viral diseases of pigeonpea. Symptoms vary depending on the plant growth stage at infection. Early infection results in severe stunting with excessive vegetative growth, producing a bushy appearance due to proliferation of secondary and tertiary branches. Leaves show prominent mosaic patterns with light and dark green patches, reduced leaf size (leaf enation), and distorted shapes. Affected leaves become chlorotic and brittle. Most characteristic is complete or partial sterility—infected plants fail to flower or produce only a few sterile flowers that do not set pods. Late-infected plants show milder symptoms with partial sterility and reduced pod setting. The disease significantly reduces yield, with early-infected plants producing virtually no grain.

Etiology

Sterility Mosaic Disease is caused by Pigeonpea Sterility Mosaic Emaravirus (PPSMEaV), a member of the genus Emaravirus. The virus is transmitted exclusively by the eriophyid mite Aceria cajani in a persistent manner. The mite vector is extremely small (0.15-0.20 mm), wedge-shaped, and barely visible to the naked eye. Both nymphs and adults can acquire and transmit the virus. The mite feeds on the undersurface of young leaves, creating entry points for the virus. Virus transmission occurs within 3-4 hours of mite feeding on infected plants, and infected mites remain viruliferous throughout their life. There are multiple strains of the virus with varying virulence and geographical distribution.

Disease Cycle

The disease cycle is closely linked to the biology and activity of the eriophyid mite vector. The virus survives in infected pigeonpea plants (main source) and alternate hosts like Cajanus platycarpus and C. scarabaeoides. Eriophyid mites acquire the virus while feeding on infected plants. The virus has a latent period in both the vector (3-4 days) and the plant (12-21 days). Viruliferous mites migrate to healthy plants through wind currents, where they feed and transmit the virus. Mite populations and disease spread are favored by high humidity (70-80%) and moderate temperatures (20-30°C). Peak mite activity and disease spread occur during monsoon months. The virus multiplies in infected plants, which serve as continuous sources of inoculum for mite acquisition and further spread. Volunteer plants, ratoon crops, and perennial hosts serve as off-season reservoirs.

Management

Management of Sterility Mosaic Disease requires integration of multiple strategies focused on reducing virus sources and vector populations. Growing resistant or tolerant varieties is the primary control measure—varieties like ICPL 87119 (Asha), ICP 8863, BDN 2, PRG 176, and TS 3R show good resistance. Controlling volunteer plants and alternate weed hosts within and around fields eliminates off-season virus reservoirs. Early sowing (June-July in India) before peak mite populations reduces disease incidence. Border rows of maize or sorghum act as barrier crops, reducing mite migration into fields. Rouging and removal of diseased plants during early growth stages prevents them from serving as virus sources. Seed treatment with imidacloprid (5 g/kg seed) provides early protection against mites. Foliar sprays of dicofol (0.05%) or spiromesifen (0.04%) at 30 and 45 days after sowing control mite populations. Spray application of neem oil (3%) is an eco-friendly alternative. Intercropping pigeonpea with cereals like sorghum or pearl millet reduces disease incidence by disrupting mite movement. Maintaining field sanitation, avoiding late planting, and ensuring adequate spacing reduce disease pressure. In endemic areas, replacing susceptible varieties with resistant ones provides long-term sustainable management.

About the author

M.S. Chaudhary
I'm an ordinary student of agriculture.

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