1. Cercospora Leaf Spot
Symptoms
Cercospora leaf spot, caused by Cercospora canescens, manifests as small, circular to irregular brown spots on leaves, typically measuring 2-5 mm in diameter. The spots have dark brown margins with greyish centers and may coalesce to form larger necrotic areas. As the disease progresses, affected leaves turn yellow and drop prematurely, leading to severe defoliation. Spots may also appear on stems and pods in severe infections. The disease is most prominent during flowering and pod formation stages, significantly reducing photosynthetic capacity and yield.
Etiology
The causal agent is Cercospora canescens, a deuteromycete fungus. The pathogen produces olivaceous brown, multiseptate conidia that are obclavate to cylindrical in shape. High humidity (above 80%), moderate temperatures (25-30°C), and prolonged leaf wetness favor disease development. The fungus thrives in warm, humid conditions typical of monsoon seasons. Poor air circulation and dense plant canopies create favorable microenvironments for infection.
Disease Cycle
The pathogen overwinters on infected crop debris and volunteer plants in the soil. Primary infection occurs through wind-borne or rain-splashed conidia from infected residues. The fungus penetrates through stomata or directly through the cuticle. After an incubation period of 7-10 days, secondary sporulation occurs on lesions, producing abundant conidia that serve as secondary inoculum. Multiple disease cycles occur during the crop season through splash dispersal of conidia during rains and irrigation. The disease spreads rapidly under favorable conditions, with secondary infections establishing within 5-7 days.
Management
Integrated management involves cultural, biological, and chemical approaches. Use certified disease-free seeds and resistant varieties where available. Practice crop rotation with non-leguminous crops for at least two years to break the disease cycle. Remove and destroy crop debris after harvest to eliminate primary inoculum sources. Maintain optimal plant spacing to ensure good air circulation and reduce leaf wetness duration. Avoid excessive nitrogen application, which promotes succulent growth susceptible to infection. Apply foliar sprays of mancozeb (0.25%) or chlorothalonil (0.2%) at first disease appearance, repeating at 10-14 day intervals. Carbendazim (0.1%) can be used as a systemic alternative. Biocontrol agents like Trichoderma viride can be incorporated into soil management. Practice balanced fertilization with emphasis on potassium to enhance plant resistance.
2. Web Blight
Symptoms
Web blight, caused by Rhizoctonia solani, initially appears as water-soaked lesions on leaves touching the soil surface. The characteristic feature is the formation of dense, white to greyish-brown mycelial webbing on affected plant parts, particularly on lower leaves and stems. Lesions expand rapidly, becoming irregular, brown, and necrotic with concentric zonation. The webbing connects leaves and stems together, giving the disease its name. In severe cases, entire plants may collapse, and pods become covered with mycelial mats. The disease causes extensive defoliation, stem girdling, and pod rot. Sclerotia (small, dark brown, mustard seed-like structures) may form on infected tissues.
Etiology
The causal organism is Rhizoctonia solani (anastomosis group AG-1), a basidiomycete fungus. The pathogen is a soil-borne organism with a wide host range. It thrives in high humidity (above 90%), warm temperatures (28-32°C), and prolonged wet conditions. Dense canopy, poor drainage, and heavy rainfall create ideal conditions for infection. The fungus is favored by acidic to neutral soil pH (5.5-7.0).
Disease Cycle
The fungus survives as sclerotia or mycelium in soil and crop debris. Sclerotia can remain viable in soil for several years, serving as primary inoculum. Under favorable moisture and temperature conditions, sclerotia germinate and produce mycelium that infects plants through direct penetration or via wounds. Initial infection typically occurs on lower plant parts in contact with soil. The pathogen spreads rapidly through mycelial growth from plant to plant, especially when foliage is wet. Secondary spread occurs through mycelial contact, movement of infested soil, and water splash. The disease progresses rapidly during monsoons, completing multiple cycles within weeks.
Management
Management requires an integrated approach combining cultural and chemical methods. Use healthy, fungicide-treated seeds and avoid heavily infested fields. Implement crop rotation with cereals or other non-susceptible crops for 2-3 years. Ensure proper field drainage to prevent waterlogging and reduce soil moisture. Maintain wider row spacing (45 cm) to improve air circulation and reduce canopy humidity. Practice clean cultivation by removing infected plant debris and deep ploughing to bury sclerotia. Apply well-decomposed organic amendments to promote beneficial microbial activity. Seed treatment with Trichoderma harzianum or Pseudomonas fluorescens provides biological protection. For chemical control, apply validamycin (0.2%) or hexaconazole (0.1%) at early disease stages, followed by subsequent sprays at 10-day intervals. Carbendazim (0.1%) can be used as a soil drench for managing soil-borne inoculum. Avoid overhead irrigation during humid conditions.
3. Yellow Mosaic Disease
Symptoms
Mungbean yellow mosaic disease (MYMD) is characterized by bright yellow irregular patches or mottling on leaves, alternating with green areas, creating a distinct mosaic pattern. Symptoms first appear on younger leaves as small yellow spots that gradually enlarge and coalesce. Severely affected leaves become entirely yellow with only veins remaining green. Plants show stunted growth, reduced leaf size, shortened internodes, and overall bushy appearance. Flowering is significantly reduced or delayed, and pods formed are fewer, smaller, and often malformed with reduced seed set. Early infection results in severe yield losses up to 85%. The disease is most severe during warm, dry weather when whitefly populations are high.
Etiology
The disease is caused by Mungbean yellow mosaic virus (MYMV) or Mungbean yellow mosaic India virus (MYMIV), both belonging to the genus Begomovirus, family Geminiviridae. These are single-stranded DNA viruses transmitted exclusively by the whitefly Bemisia tabaci (biotype B) in a persistent, circulative manner. The virus requires 15-30 minutes for acquisition and 8-24 hours for transmission. Whiteflies remain viruliferous for their entire lifespan. High temperatures (30-35°C), low humidity, and bright sunshine favor both virus replication and vector multiplication. The disease is most prevalent during summer and early kharif seasons.
Disease Cycle
The virus survives in infected perennial hosts, alternative weed hosts (such as Parthenium, Euphorbia, and other malvaceous weeds), and volunteer legume plants. The primary source of inoculum is viruliferous whiteflies migrating from infected hosts. When whiteflies feed on infected plants, they acquire the virus through phloem sap ingestion. After a latent period within the vector, infective whiteflies transmit the virus to healthy green gram plants during feeding. The virus multiplies systemically within the plant through phloem tissues. Secondary spread occurs through the large whitefly population that builds up on infected crops. The disease spreads rapidly when conditions favor vector multiplication and movement. There is no seed transmission of the virus.
Management
Effective management focuses on controlling the whitefly vector and using resistant varieties. Plant resistant or tolerant varieties such as PDM-139, SML-668, and IPM-02-3, which show field resistance to MYMD. Adjust sowing time to avoid peak whitefly populations—early sowing in kharif season helps escape severe infection. Remove and destroy infected plants immediately to reduce inoculum sources. Control alternative hosts and weed populations in and around fields that harbor both virus and vectors. Use yellow sticky traps (@ 8-10 per acre) to monitor and trap adult whiteflies. Apply neem oil (0.5%) or neem seed kernel extract (5%) as a deterrent to whiteflies. For chemical vector control, spray imidacloprid (0.005%) or thiamethoxam (0.005%) at 15 and 30 days after sowing. Dimethoate (0.03%) can be used for managing high whitefly populations. Apply mulches with reflective materials to repel whiteflies. Practice barrier cropping with maize or sorghum around fields to intercept migrating whiteflies. Maintain field sanitation by removing crop residues after harvest. Avoid mixed cropping with other susceptible legumes or hosts that may serve as reservoirs.
