1. Phomopsis Blight
Symptoms
Phomopsis blight, also known as fruit rot or collar rot, affects all above-ground parts of the brinjal plant. On seedlings, circular gray spots with light brown centers appear on leaves, often leading to damping-off. The most characteristic symptom is the appearance of numerous small, circular lesions on fruits that enlarge and become sunken with concentric rings. These spots turn brown to black and may cover the entire fruit surface. Infected fruits become shriveled and mummified. On stems, elongated brown to black lesions develop, particularly near the soil line, causing wilting and plant death. Leaf spots are circular to irregular, ash-gray with dark margins.
Etiology
The causal organism is Phomopsis vexans (syn. Diaporthe vexans), a fungal pathogen belonging to the family Diaporthaceae. The fungus produces pycnidia containing alpha and beta conidia. Alpha conidia are hyaline, one-celled, and oval to ellipsoidal (5-9 × 2-3 μm), while beta conidia are filiform and curved. The pathogen thrives in warm, humid conditions with optimal temperatures between 25-30°C and relative humidity above 80%.
Disease Cycle
The fungus overwinters in infected plant debris, mummified fruits, and seeds. Primary infection occurs through seed-borne inoculum or soil-borne mycelium from crop residues. Spores are disseminated by rain splash, wind, and irrigation water. The pathogen enters through wounds, natural openings, or directly penetrates the epidermis. Secondary spread occurs rapidly during monsoon season through conidia produced in pycnidia on infected tissues. The disease cycle is continuous in regions where brinjal is grown year-round.
Management
Cultural Practices: Use disease-free seeds or treat seeds with hot water (50°C for 30 minutes) or thiram (3 g/kg). Practice crop rotation with non-solanaceous crops for 2-3 years. Remove and destroy infected plant debris and mummified fruits. Ensure proper drainage and avoid overhead irrigation. Maintain optimum plant spacing for good air circulation.
Resistant Varieties: Grow resistant or tolerant varieties such as Pusa Purple Long, Pusa Purple Cluster, Arka Shirish, and Arka Anand.
Chemical Control: Spray with mancozeb (0.25%) or carbendazim (0.1%) at 10-15 day intervals, beginning at the first sign of disease. Pre-harvest interval must be observed. Drench nursery beds with copper oxychloride (0.3%) before sowing.
Biological Control: Seed treatment and foliar sprays with Trichoderma viride or Pseudomonas fluorescens can reduce disease incidence.
2. Sclerotinia Rot
Symptoms
Sclerotinia rot primarily affects stems and fruits of brinjal plants. Initial symptoms appear as water-soaked lesions on stems near the soil line or at branch junctions. These lesions enlarge rapidly and turn brown. A characteristic white, cottony mycelial growth develops on infected tissues, particularly under humid conditions. As the disease progresses, the stem becomes soft and girdled, causing wilting and collapse of the entire plant or affected branches. Inside hollow stems and on fruit surfaces, hard, black, irregularly shaped sclerotia (2-10 mm) form within the white mycelium. Infected fruits show soft, watery rot covered with white fluffy growth.
Etiology
The causal agent is Sclerotinia sclerotiorum, a fungal pathogen with a wide host range. The fungus produces abundant white mycelium and characteristic black sclerotia, which are survival structures. Under favorable conditions, sclerotia germinate to produce apothecia (cup-shaped structures) that release ascospores. The pathogen prefers cool, moist conditions with optimal temperature of 15-20°C and high relative humidity (>85%). It can survive in soil for several years as sclerotia.
Disease Cycle
The pathogen overwinters as sclerotia in soil or plant debris. In cool, moist conditions, sclerotia germinate either myceliogenically (producing mycelium) or carpogenically (producing apothecia). Apothecia release millions of ascospores that are wind-dispersed and infect senescent flowers, leaves, or wounded tissues. Mycelial growth from sclerotia can directly infect stems in contact with soil. The fungus produces oxalic acid, which lowers tissue pH and facilitates infection. Infected tissues develop new sclerotia, completing the cycle. Dense crop canopy and cool temperatures favor disease development.
Management
Cultural Practices: Deep plowing to bury sclerotia (>5 cm depth) reduces their viability. Practice crop rotation with non-susceptible crops like cereals or grasses for 3-4 years. Remove and destroy infected plants immediately. Maintain proper plant spacing and prune lower branches to improve air circulation. Avoid excessive irrigation and ensure good drainage. Use drip irrigation instead of flood irrigation.
Sanitation: Remove crop residues and weeds that may harbor the pathogen. Solarize soil during hot months by covering with transparent plastic for 4-6 weeks to kill sclerotia.
Chemical Control: Apply carbendazim (0.1%) or thiophanate-methyl (0.1%) as soil drench and foliar spray. Preventive applications are more effective than curative treatments.
Biological Control: Trichoderma harzianum and Coniothyrium minitans are mycoparasites that attack sclerotia. Incorporate these biocontrol agents into soil or apply as foliar sprays.
3. Little Leaf Disease
Symptoms
Little leaf is a phytoplasma disease characterized by severe stunting and malformation. Infected plants show reduced leaf size with leaves becoming small, narrow, and thickened. Internodes are shortened, resulting in a bushy, stunted appearance. Leaves exhibit yellowing (chlorosis) and upward curling of margins. The most diagnostic symptom is excessive proliferation of axillary shoots, giving a "witches' broom" appearance. Flowers become green (phyllody), with floral parts transforming into leaf-like structures. Fruits, if formed, are small, malformed, and unmarketable. Affected plants rarely produce viable fruits. Symptoms typically appear 30-45 days after infection and progress gradually.
Etiology
Little leaf disease is caused by phytoplasmas, which are cell wall-less, prokaryotic organisms belonging to the class Mollicutes. The specific phytoplasma associated with brinjal little leaf belongs to the 16SrI or 16SrVI group. These obligate parasites inhabit the phloem tissue of plants and cannot be cultured on artificial media. Phytoplasmas disrupt normal phloem function and hormone balance, particularly affecting auxin and cytokinin levels, leading to characteristic symptoms. They are transmitted by phloem-feeding insect vectors.
Disease Cycle
The disease is transmitted primarily by leafhoppers, particularly Hishimonus phycitis and Orosius albicinctus. The phytoplasma multiplies in both the plant host and insect vector. When an insect feeds on infected plants, it acquires the phytoplasma, which then multiplies in the insect's body. After a latent period of 10-45 days, the insect becomes infective for life and can transmit the pathogen to healthy plants during feeding. The phytoplasma cannot survive outside living hosts. Weeds and alternative hosts serve as reservoirs. Disease incidence is higher during periods of high vector populations, typically in warm, humid seasons.
Management
Vector Control: Control of leafhopper vectors is the primary management strategy. Use yellow sticky traps to monitor and reduce vector populations. Apply systemic insecticides such as dimethoate (0.03%) or imidacloprid (0.005%) at regular intervals to control vectors. Begin applications early in the crop season.
Cultural Practices: Remove and destroy infected plants immediately upon detection to eliminate inoculum sources. Control weeds in and around the field that serve as alternative hosts for both phytoplasma and vectors. Use barrier crops like maize or sorghum around brinjal fields to reduce vector immigration. Avoid planting near infected fields.
Use of Healthy Planting Material: Raise seedlings in insect-proof nurseries covered with fine mesh (40-60 mesh) to prevent vector access. Use disease-free transplants.
Resistant Varieties: While no completely resistant varieties exist, some cultivars show field tolerance. Local screening trials can identify relatively tolerant varieties.
Chemical Treatment: Tetracycline antibiotics can suppress phytoplasma, but their use is generally not recommended due to development of resistance and environmental concerns. Root and stem injection of oxytetracycline (500 ppm) has shown suppression of symptoms in experimental conditions.
Integrated Approach: Combine early planting to avoid peak vector periods, regular field monitoring, prompt removal of diseased plants, vector control, and maintenance of field sanitation for effective disease management.
