A) Blast Disease of Rice (Oryza sativa):

Causal Organism:

• Pathogen: Pyricularia oryzae (Syn: P. grisea)
• Sexual Stage: Magnaporthe grisea

History and Economic Importance:

• First recorded in China (1637) and Japan (1704). Reported in Italy (1828), USA (1876), and Tamil Nadu, India (1918).
• Causes yield loss of 30-61%, and up to 70-80% in severe cases.

Symptoms:

1. Leaf Blast: Small, water-soaked bluish-green specks develop into spindle-shaped spots with a grey center and dark brown margin. Severely affected leaves dry up and wither, giving a burnt appearance.
2. Node Blast: Irregular black areas encircle nodes, causing breakage and death of plant parts above the affected nodes.
3. Neck Blast: Infected peduncle turns brownish-black, causing “rotten neck” or “panicle blast.”
   • Early Infection: No grain filling; panicle remains erect.
   • Late Infection: Partial grain filling; small brown to black spots on glumes.

Etiology:

• Mycelium: Hyaline to olivaceous, septate, highly branched.
• Conidia: Pyriform, 3-celled, hyaline to pale olive green, produced on slender conidiophores.
• Perfect Stage: Magnaporthe grisea producing perithecia and 4-celled hyaline ascospores.
• Toxins Produced: α-picolinic acid, Pyricularin, and Pyriculol.

Disease Cycle:

• Primary Inoculum: Mycelium and conidia in infected straw and seeds.
• Survival: On collateral hosts (e.g., Panicum repens, Echinochloa crusgalli) and in straw piles.
• Dissemination: Airborne conidia dispersed during dew or rain, causing secondary infections.

Favourable Conditions:

• Excess nitrogenous fertilizers, intermittent drizzles, cloudy weather.
• High Relative Humidity: 93-99%
• Low Night Temperature: 15-20°C or < 26°C
• Longer dew duration, cloudy weather, slow wind movement.

Forecasting Models:

• BLAST (Japan’s first model)
• PYRICULARIA, PYRIVIEW, BLASTAM, P BLAST
• Epi-Bla (Developed in India)
• Conditions for Forecasting:
  • Minimum night temperature: 20-26°C
  • High relative humidity: 90%+ for a week
  • Critical stages: Seedling, post-transplanting tillering, and neck emergence.

Management Practices:

i) Cultural Practices:

• • Use disease-free seeds.
  • Grow resistant varieties: Simhapuri, Tikkana, Sriranga, Phalguna, IR 64, IR 36, Jaya, Vijaya, MTU series (e.g., MTU 9992, MTU 1005).
  • Destroy weed hosts.
  • Split application of nitrogen and judicious use of fertilizers.
  • Avoid close spacing in the main field.

ii) Seed Treatment:

• • Chemical: Captan, Thiram, Carbendazim, Carboxin, or Tricyclazole (2 g/kg of seed).
  • Biocontrol: Trichoderma viride (4g/kg) or Pseudomonas fluorescens (10g/kg).

iii) Chemical Control:

• • Nursery Spray: Carbendazim (25 g) or Edifenphos (25 ml) for 8 cent nursery.
  • Field Spray:
    • Edifenphos @ 0.1%
    • Carbendazim @ 0.1%
    • Tricyclazole @ 0.06%
    • Thiophanate Methyl @ 0.1%

B) Brown Spot or Sesame Leaf Spot or Helminthosporiose

Pathogen: Helminthosporium oryzae (Syn: Drechslera oryzae)
Sexual Stage: Cochliobolus miyabeanus

Historical Importance

• This disease was the principal cause of the Bengal famine of 1942-43 in India.
• First reported by Sundararaman from Madras in 1919.
• Now present in all rice-growing states in India.
• Under highly favorable conditions, it can cause up to 90% yield loss.

Symptoms

• The fungus attacks rice crops from the seedling stage in nurseries to the milk stage in the main field.
• Symptoms appear as lesions (spots) on the coleoptile, leaf blade, leaf sheath, and glumes, most prominently on the leaf blade and glumes.
• Initial symptoms are minute brown dots that later become cylindrical, oval, or circular spots.
• Multiple spots coalesce, causing leaf drying.
• Seedlings may die, giving nurseries a brownish scorched appearance.
• Dark brown or black spots appear on glumes, containing conidiophores and conidia of the fungus.
• The disease causes:
  • Failure of seed germination.
  • Seedling mortality.
  • Reduced grain quality and weight.
• Associated with a physiological disorder called akiochi in Japan.
• Abnormal soil conditions, especially potassium deficiency, predispose plants to heavy infection.

Etiology

• Mycelium: Greyish-brown to dark brown, septate.
• Conidiophores: Arise singly or in small groups, straight or geniculate, pale to brown.
• Conidia: Usually curved with a bulge in the center, tapering towards the ends. Occasionally straight, pale olive green to golden brown, and 6-14 septate.
• Perfect Stage: C. miyabeanus Produces perithecia with asci containing 6-15 septate ascospores. Ascospores are filamentous or long cylindrical, hyaline to pale olive green.
• Toxins Produced: C25 terpenoid phytotoxins, including: Ophiobolin A (most toxic). Ophiobolin B. Ophiobolin I, These toxins disrupt the protein fragments of cell walls, affecting cell integrity.

Disease Cycle

• Overwinters in infected plant parts, not soil-borne.
• Primary Source of Infection: Infected seeds (externally seed-borne). Infected seeds cause seedling blight, with pale yellowish-brown spots on coleoptiles.
• Dissemination: Through air currents from infected spots.
• Collateral Hosts:
  • Digitaria sanguinalis
  • Leersia hexandra
  • Echinochloa colonum
  • Pennisetum typhoides
  • Setaria italica
  • Cynodon dactylon
• Note: Symptoms of potassium deficiency can be similar to brown spot symptoms, leading to diagnostic confusion.

Favourable Conditions

• Temperature: 25-30°C
• Relative Humidity: Above 80%
• Excess nitrogen aggravates disease incidence.

Management

Cultural Practices:

• • Use disease-free seeds.
  • Field sanitation: Remove collateral hosts and infected debris.
  • Crop rotation and adjustment of planting time.
  • Proper fertilization with slow-release nitrogenous fertilizers.
  • Good water management.
  • Use of soil amendments.
• Resistant Varieties: Bala, BAM 10, IR-20, Jaya, Ratna, Tellahamsa, Kakatiya

Chemical Control: Seed treatment with Thiram or Captan @ 4 g/kg. Mancozeb spray @ 0.2% twice: First spray after flowering. Second spray at the milky stage.

C) Sheath Blight of Rice

Pathogen: Rhizoctonia solani
Sexual Stage: Thanetophorus cucumeris

Symptoms

• Growth Stage Affected: From tillering to heading stage.
• Initial Symptoms: Noticed on leaf sheaths near the water level. Formation of oval, elliptical, or irregular greenish-grey spots on leaf sheaths.
• Lesion Development: Spots enlarge and the center becomes greyish-white with an irregular blackish-brown or purple-brown border. Lesions coalesce and cover entire tillers from the water line to the flag leaf.

• Impact on Plant:
  • Presence of large lesions causes death of the whole leaf.
  • In severe cases, all leaves of the plant may be blighted.
  • Infection extends to inner sheaths, leading to death of the entire plant.
  • Older plants and 5 to 6-week-old leaf sheaths are highly susceptible.
  • Early heading and grain filling stages result in poorly filled grain, particularly in the lower panicle.

Pathogen Characteristics

• Mycelium: Septate and long cells. Hyaline when young, turning yellowish-brown when old.
• Sclerotia: Globose in shape. Initially white, turning brown or purplish-brown as they mature.

Disease Cycle

• Survival: The pathogen survives as sclerotia or mycelium in dry soil for up to 20 months. In moist soil, survival is limited to 5-8 months.
• Host Range: Infects over 188 crop species across 32 plant families.
• Dispersal: Sclerotia spread through irrigation water, causing new infections.

Favourable Conditions

• High Relative Humidity: 96-97%.
• Temperature: 30-32°C.
• Cultural Practices: Closer planting and heavy nitrogen fertilization increase disease severity.

Management Strategies

i) Cultural Practices:

• • Optimum Fertilizer Application: Avoid excess nitrogen.
  • Optimum Plant Spacing: Prevents high humidity and reduces disease incidence.
  • Weed Control: Eliminate alternate weed hosts.
  • Organic Amendments: Improve soil health and reduce pathogen load.
  • Irrigation Management: Prevent flow of water from infected to healthy fields.
  • Field Sanitation:
    • Deep ploughing in summer and burning stubbles to destroy sclerotia.

ii) Resistant Varieties: Grow tolerant varieties like Shiva (WGL 3943).

iii) Chemical Control: Propiconazole @ 0.1% or Hexaconazole @ 0.2%. Validamycin @ 0.2% for effective control. Spray Schedule: Start at 45 days after transplanting and repeat at 10-day intervals (3 sprays depending on disease severity).

iv) Biological Control:

• • Seed Treatment:Use Pseudomonas fluorescens @ 10 g/kg of seed. Seedling Dip: 2.5 kg/ha in 100 liters of water for 30 minutes.
  • Soil Application: P. fluorescens @ 2.5 kg/ha after 30 days of transplanting. Mix with 50 kg of FYM/Sand before application.

D) Bacterial Leaf Blight (BLB) of Rice

Pathogen: Xanthomonas oryzae pv. oryzae

Economic Importance

• First Reported:
  • Japan (1884).
  • In Indonesia, Kresek disease killed young seedlings completely in 1950.
  • India: First reported in 1959. Severe outbreaks in Bihar and Uttar Pradesh (1963).

• Yield Losses:
  • In severely affected fields, yield losses range from 20-30%, occasionally reaching 50%.
  • In India, millions of hectares are infected yearly, with losses as high as 60% in certain states and the Godavari district of Andhra Pradesh.
• Susceptible Varieties: Taichung Native 1 is highly susceptible.

Symptoms

1. Kresek (Wilt Syndrome):

• • Occurs in seedlings within 3-4 weeks after transplanting.
  • Results in either death of the entire plant or wilting of a few leaves.
  • The bacterium enters through hydathodes and cut wounds at leaf tips, becoming systemic and leading to seedling death.

2. Leaf Blight in Mature Plants:

• • Noticed typically at the heading stage, but severe cases occur earlier.
  • Water-soaked, translucent lesions appear near leaf margins.
  • Lesions enlarge with wavy margins, turn straw yellow, and eventually cover the entire leaf blade, which may turn white or straw-colored.
  • Leaf sheaths may also show lesions in susceptible varieties.
  • Milky or opaque dew drops with bacterial masses appear on young lesions in the early morning, which dry to leave a white encrustation.
  • Discolored spots with water-soaked margins are visible on affected grains.
  • Bacterial Ooze Test: If the cut end of an infected leaf is dipped in water, the water becomes turbid due to bacterial ooze.

Etiology

• Bacterium Characteristics:
  • Aerobic, Gram-negative, non-spore forming, rod-shaped with a monotrichous polar flagellum at one end.
  • Capsulated cells form aggregate masses.
  • Colony Appearance: Circular, convex with entire margins, whitish yellow to straw yellow, and opaque.
  • Strains: Multiple strains exist with varying virulence. Tropical strains are generally more virulent than those in temperate areas (e.g., Japan).

Disease Cycle

• Entry:
  • Through water pores (hydathodes) on leaf edges or through injuries in roots or leaves.
  • Does not enter through stomata.
  • Primarily a vascular (systemic) disease, where bacterial cells move through vascular tissues, causing wilting.
• Dissemination: Rain storms, typhoons, and irrigation water help in spreading the pathogen from field to field.
• Primary Source of Infection:
  • Overwintering in seeds (husk and endosperm).
  • Survives in soil, plant stubbles, and debris.
  • Collateral Hosts: Leersia hexandra, Leersia oryzoides, Zizania latifolia, Cyperus rotundus, Cyperus deformis, Phalaris arundinacea, Cynodon dactylon, etc.
  • Secondary Infection: Caused by bacterial ooze which serves as secondary inoculum.

Favourable Conditions

• Cultural Practices: Clipping of seedling tips at transplanting. Flooding and deep irrigation water. Severe winds.
• Weather Conditions: Heavy rain and dew. Temperature: 25-30°C.
• Nutrient Management: Excessive nitrogen application, especially late top dressing.

Management Strategies

i) Cultural Control:

• • Grow resistant cultivars such as: MTU 9992, Swarna, Ajaya, IR 20, IR 42, IR 50, IR 54, TKM 6, Mashuri, IET 4141, IET 1444, IET 2508, Chinsura Boro, etc.
  • Resistant Donors: Tetep, Tadukan, Zenith, etc.
  • Destroy affected stubbles by burning or ploughing.
  • Judicious use of nitrogenous fertilizers.
  • Avoid clipping seedling tips during transplanting.
  • Avoid flooded conditions and water flow from infected to healthy fields.
  • Remove and destroy weed hosts.

ii) Seed Treatment: Soaking seeds for 8 hours in Agrimycin (0.025%) followed by hot water treatment for 10 minutes at 52-54°C to eradicate seed-borne bacteria.

iii) Chemical Control: Spray Streptocycline (250 ppm) with Copper Oxychloride (0.3%).

E) Bacterial Leaf Streak (Xanthomonas campestris pv. oryzicola)

Economic Importance:

• First found in the Philippines (1918). Common in tropical Asia but absent in Japan and other regions.
• In India, reported in Uttar Pradesh, Madhya Pradesh, Andhra Pradesh, Maharashtra, Karnataka, Odisha, Haryana, and West Bengal.
• Highly susceptible varieties: IR 8, Jaya, and Padma.

Symptoms:

• Fine translucent streaks appear between the leaf veins.
• Lesions enlarge lengthwise and laterally, turning brown with a yellow halo around them on highly susceptible varieties.
• Yellow band-like exudates form on lesions under humid conditions.
• In severe cases, leaves may dry up completely.

Etiology:

• Short rod-shaped, gram-negative bacterium (1.2 µm x 0.3 to 0.5 µm).
• Strains vary in pathogenicity, with virulent strains causing longer streaks.

Disease Cycle:

• Survives in infected seeds but not in crop debris.
• Enters through stomata and wounds, infecting parenchymatic cells without entering vascular systems.
• Spread facilitated by wet leaf surfaces, rain storms, and typhoons.

Favorable Conditions: High relative humidity (83-93%) or morning dew for 2-3 hours.

Management:

• Grow resistant varieties: IR 20, Krishna, and Jagannath.
• Destroy affected stubbles by burning or plowing.
• Judicious use of nitrogen fertilizers.
• Avoid clipping of seedlings and prevent irrigation water flow from infected to healthy fields.
• Seed treatment: Soak seeds in Streptocycline (250 ppm) followed by hot water treatment at 52°C for 30 minutes.
• Spray Streptocycline (250 ppm) with copper oxychloride (0.3%).

F) False Smut of Rice

Pathogen: Ustilaginoidea virens
Previous Synonym: Claviceps oryzae-sativa

Economic Importance

• Geographical Distribution: Found in Asia, Latin America, and Africa.
• Historical Epidemic: Severe outbreak in Burma (1935).
• Cultural Belief: In Southeast Asia, its occurrence is traditionally considered a sign of a good crop year.

Symptoms

• Affected Part: Individual grains in the rice panicle.
• Appearance:
  • Grains transform into yellow or greenish spore balls with a velvety texture.
  • Initially small, but can grow up to 1 cm or larger.
  • At the early stage, spore balls are covered by a membrane which later bursts as they enlarge.
  • Ovaries are converted into large velvety green masses due to fungal fructification.
  • Usually, only a few spikelets in a panicle are affected.

Etiology

• Chlamydospores:
  • Formed on spore balls.
  • Shape: Spherical to elliptical.
  • Appearance: Waxy and olivaceous (greenish-brown).

Disease Cycle

• Survival: In temperate regions, the fungus overwinters as sclerotia and chlamydospores.
• Primary Infection: Ascospores produced on overwintered sclerotia initiate primary infection.
• Secondary Infection: Chlamydospores play a major role in secondary infection, which significantly contributes to disease spread. Infection generally occurs at the booting stage of rice plants.
• Spore Ball Characteristics: Chlamydospores are present on spore balls but are not easily detached due to sticky material.

Favourable Conditions Weather: Rainfall and cloudy weather during the flowering and maturity stages of rice.

Management Strategies

1. Chemical Control:
   • Copper Oxychloride @ 0.3%.
   • Carbendazim @ 0.1%.
   • Spray Timing: At the panicle emergence stage for effective control.

G) Tungro Disease 

Economic Importance

• Known as Penyakitmerah in Malaysia (since 1938) and identified as Tungro in 1965.
• Found in tropical Asia, especially in Bangladesh, India (West Bengal, Kerala), Indonesia, and the Philippines.
• It is highly destructive, with historical losses of 30% or 1.4 million hectares annually.
• Severe epidemics occurred in Thailand (1966) and the Philippines (1971).

Symptoms

• Affects plants in both nursery and main fields.
• Stunting is severe in susceptible varieties and mild in resistant ones.
• Leaf Discoloration: Yellow to orange (common in Japonica varieties) and interveinal chlorosis.
• Mottling on young leaves (pale green to whitish stripes); rusty streaks on older leaves.
• Reduced Tillering and poor root systems.
• Small Panicles with discolored grains.
• Iodine Test: Infected leaves show dark blue streaks when dipped in iodine-potassium iodide solution.

Etiology

• Caused by two viruses:
  1. Rice Tungro Bacilliform Virus (RTBV) – Bacilliform particles (130 x 30 nm) with circular ds DNA (8.3 KbP).
  2. Rice Tungro Spherical Virus (RTSV) – Isometric particles (30 nm) with ss RNA (10 KbP).
• RTBV is responsible for most symptoms, while RTSV aids in transmission by green leafhoppers.

Disease Cycle

• Severe damage in regions with year-round host plants and insect vectors.
• Sources of Inoculum: Infected stubbles from previous seasons and wild rice as collateral hosts.
• Vector Transmission: By leafhoppers – Nephotettix virescens, N. nigropictus, N. parvus, N. malayanus, and Recilia dorsalis.
• Mode of Transmission: Non-persistent manner.

Management

1. Cultural Practices Deep summer ploughing and burning of stubbles. Destroy weed hosts of viruses and vectors.
2. Resistant Varieties Grow disease-tolerant cultivars like MTU 9992, 1002, 1003, 1005, Suraksha, Vikramarya, Bharani, IR 36, IET 2508, RP 4-14, IET 1444, IR50, and Co45.
3. Chemical Control In Nursery: Apply Carbofuran granules @ 170 g/cent, 10 days after sowing. In Main Field: Apply Carbofuran @ 10 kg/ac.
   • Sprays:
     • Monocrotophos @ 2.2 ml/L
     • Phosphamidon @ 1 ml/L
     • Ethophenphos @ 1.5 ml/L
     • Neem Oil @ 3% (15 and 30 days after transplanting) This integrated approach helps in effectively managing Tungro Disease in rice crops.

H) Khaira Disease of Rice

Economic Importance

• First reported in Tarai region of Uttar Pradesh, India.
• Commonly occurs in zinc-deficient soils, especially in areas with high pH, calcareous soils, and soils with low organic matter.
• Affects yield and grain quality, leading to significant economic losses.

Symptoms

• Chlorosis: Yellowing of leaves, especially on young leaves.
• Brown Spots: Appearance of rusty brown spots on the lower leaves.
• Poor Tillering and Stunted Growth.
• Delayed Maturity and reduced grain filling.
• White Panicles may appear in severe cases.

Etiology

• Caused by Zinc Deficiency in soil.
• High phosphorus levels and high soil pH (>7.0) aggravate the problem.

Disease Cycle

• Zinc becomes unavailable to the rice plants due to:
  • High pH or alkaline soils.
  • Calcareous soils with high calcium carbonate content.
  • Waterlogged conditions and poor drainage.
  • Excessive phosphorus fertilization.

Management

1. Soil Amendment and Fertilization Apply Zinc Sulphate (ZnSO₄) @ 20-25 kg/ha as basal or 5 kg/ha as foliar spray.Apply organic manure to improve soil structure and nutrient availability.
2. Water Management Proper water management to avoid waterlogging.
3. Cultural Practices Use of Zinc-efficient rice varieties. Balanced fertilization, avoiding excessive phosphorus application.
4. Foliar Spray 0.5% Zinc Sulphate with 0.25% Lime spray at early stages. Repeat the spray after 15 days if necessary.