A) Grain Smut / Kernel Smut / Covered Smut / Short Smut in Sorghum

Causal Agent: Sphacelotheca sorghi or Sporisorium sorghi

Economic Importance

• Most destructive smut disease in sorghum, leading to yield losses of up to 25%.
• Widely prevalent in Maharashtra, Uttar Pradesh, Andhra Pradesh, Tamil Nadu, Gujarat, and Karnataka when seeds are not treated with fungicides.
• Susceptible Hosts: Most varieties of Sorghum vulgare. S. halapense and S. sudanens are also affected.
• Recent Decline in Losses: Due to the use of fungicide-treated seeds before sowing.

Symptoms

• Time of Appearance: Becomes apparent during grain formation in the ear.
• Smut Sori Formation: Individual grains are replaced by smut sori. Sori may be localized on parts of the head or occur throughout the inflorescence.
• Appearance of Sori:
  • Dirty white to gray in color, oval or cylindrical.
  • Covered with a tough white cream to light brown peridium (skin).
  • The peridium often remains unbroken until threshing.
• Glumes and Stamens: Glumes remain unaltered but may adhere to the sides of the sorus. In some cases, stamens develop normally and protrude out of the sorus.
• Variation: Size, color, and degree of breakage of sori vary with the race of the fungus and sorghum cultivar. Higher incidence is observed in ratoon crops.

Etiology

• Systemic Fungus: The mycelium occupies the growing point of the seedling and grows along the plant without external symptoms until the earhead appears.
• Chlamydospore Formation: Mycelium aggregates in the immature ovary, forming chlamydospores. Sorus wall forms from the outer mycelium layer and partly by host tissue.
• Sorus Structure: Contains a tough wall with a long, hard, central tissue called columellum. Columellum: Bulbous at the base and narrowed at the tip.
• Smut Spores: Black to dark brown, smooth, thick-walled spores (5-9 µm in diameter). Germinate immediately in the presence of moisture, producing a four-celled promycelium that buds off sporidia.

Disease Cycle

• Externally Seed-borne and Systemic: Spores germinate with the seed, infecting it through the radicle or mesocotyl, leading to systemic infection. Fungal hyphae convert into spores during flowering, replacing the ovary with sori.
• Seed Contamination: Diseased ears, when harvested and threshed with healthy ones, contaminate healthy grains with smut spores. Spores remain dormant on seeds until the next planting season.

Management

1. Cultural Practices: Use disease-free seeds. Follow crop rotation to reduce inoculum buildup. Collect smutted earheads in cloth bags and dip in boiling water to destroy spores.
2. Resistant Varieties: T 29/1, PJ 7K, PJ 23K, Nandyal, and Bilichigan.
3. Chemical Control
   • Seed Treatment: Fine sulphur powder @ 0.5%. Captan or Thiram @ 0.3%.

B) Grain Mold of Sorghum

Causal Agents: Multiple fungi, primarily:

• Fusarium spp. (e.g., Fusarium moniliforme, F. proliferatum)
• Curvularia spp. (e.g., Curvularia lunata)
• Aspergillus spp.
• Alternaria spp.
• Penicillium spp.

Economic Importance

• Major constraint in sorghum production worldwide, especially in humid and semi-humid regions.
• Causes discoloration, deterioration, and reduction in grain quality and yield.
• Reduces seed viability and nutritional value, impacting food and feed safety.
• Mycotoxin contamination (e.g., fumonisins, aflatoxins) poses health risks to humans and livestock.

Symptoms

• Appearance Time: Develops during the grain filling and maturation stages, especially under high humidity and frequent rainfall.
• Discoloration: Affected grains show pink, red, purple, gray, brown, or black discoloration. Discoloration varies with fungal species and sorghum variety.
• Affected Parts: Primarily affects grains, but glumes and panicles may also show mold growth.
• Deterioration: Shriveled grains with reduced size and weight. Reduced germination capacity due to seed embryo damage.
• Mold Growth: Visible mold growth on the grain surface, often with a powdery appearance.

Etiology

• Polyetic Disease: Caused by multiple fungal species thriving in warm, humid environments.
• Favorable Conditions: High humidity (above 90%) and frequent rainfall during grain filling and maturation stages. Susceptibility increases with delayed harvest and mechanical injuries to grains.
• Sources of Inoculum: Airborne spores and contaminated seeds. Crop residues and alternate hosts (e.g., grasses).

Disease Cycle

• Primary Inoculum: Airborne conidia from infected residues, alternate hosts, or seed-borne spores.
• Secondary Spread: By wind, rain splash, and insects.
• Infection and Colonization: Spores germinate on the grain surface under favorable moisture and temperature conditions. Mycelium penetrates the grain, leading to discoloration and deterioration.
• Survival and Perpetuation: Fungi survive in plant debris, seeds, and soil. Continuous cropping and residue retention increase inoculum potential.

Management

• Cultural Practices Early planting to escape high humidity during grain maturation.
• • Timely harvesting to avoid overexposure to humid conditions.
  • Field sanitation: Remove crop residues and alternate hosts to reduce inoculum.
  • Proper spacing to enhance aeration and reduce humidity within the crop canopy.
• Resistant Varieties Grow mold-resistant cultivars with hard, pigmented pericarps and tight glumes. Examples: CSH 16, CSH 14, M 35-1, CSV 15, and Hybrid 7078.
• Chemical Control Seed Treatment: Captan, Thiram, or Carbendazim to reduce seed-borne inoculum. Fungicidal Sprays: Propiconazole, Carbendazim, or Mancozeb during flowering and grain filling stages.
• Post-Harvest Management Drying grains to moisture levels below 12% to inhibit mold growth. Proper storage in well-ventilated, dry conditions to prevent moisture accumulation.

C) Anthracnose or Red Leaf Spot of Sorghum

Causal Agent: Colletotrichum graminicola

Economic Importance

• Widespread disease in all sorghum-growing areas worldwide.
• In India, it is severe in Andhra Pradesh, Madhya Pradesh, Rajasthan, Tamil Nadu, and Delhi.
• Causes significant yield loss and reduction in grain quality.
• Affects leaves, stalks, and inflorescences, leading to leaf blight, stalk rot, and reduced photosynthesis.

Symptoms

• Affects both leaves and stalks: Causes anthracnose (leaf spot) and stalk rot (red rot).
• Leaf Spot (Anthracnose):
  • Small, red-colored spots appear on both surfaces of the leaf.
  • White center surrounded by a red, purple, or brown margin.
  • Numerous small black dots (acervuli – fruiting bodies) are visible on the white surface of the lesions.
  • Lesions coalesce, leading to large necrotic areas and leaf blight.
  • In the midrib region, elongate elliptical red or purple lesions with black acervuli are observed.
• Stalk Rot (Red Rot):
  • Circular cankers develop externally on stalks and inflorescences.
  • When the stem is split open, it shows discoloration (either continuous or marbled).
  • Stem lesions also exhibit black acervuli.

Etiology

• Mycelium is localized within the leaf spots.
• Acervuli with long dark setae emerge through the epidermis.
• Conidiophores are short, single-celled, and colorless.
• Conidia are:
  • Short, hyaline, single-celled, and vacuolate.
  • Falcate (curved) in shape.

Disease Cycle

• Wide host range, including Johnson grass, Sudan grass, maize, barley, and wheat.
• Primary Inoculum: Survives on infected plant debris and seed.
• Primary Infection: Conidia produced on infected debris and seeds initiate the primary infection.
• Secondary Spread: Airborne conidia produced on first infected plants spread the disease within the season.

Favourable Conditions

• Continuous rain and high humidity.
• Temperature range of 28-30°C.
• Dense plant canopy that retains moisture.

Management

1. Cultural Practices: Destruction of infected plant debris and collateral hosts. Crop rotation with non-host crops to reduce inoculum build-up.
2. Resistant Varieties
   • Grow resistant varieties such as: SPV 162, CSV 17, Texas Milo, Tift Sudan
3. Seed Treatment Captan or Thiram at 3 g/kg of seed to reduce seed-borne inoculum.
4. Chemical Control: Fungicidal Sprays: Mancozeb @ 0.25% or Carbendazim @ 0.1% during early stages of disease appearance.