Disease of Mustard

A) Alternaria Leaf Spot

Causal Organism:

• Alternaria brassicae and Alternaria brassicola
• Sub-division: Deuteromycotina

Symptoms:

• Small, dark-colored spots initially appear on leaves.
• Spots enlarge and become circular (about 1 mm in diameter).
• Concentric rings develop within the spots, giving a “target-like” appearance.
• Under humid conditions, conidiophores form within the spots.
• Spots may coalesce, leading to blighting and premature defoliation of leaves.
• Affected pods show black spots, reducing seed quality and germination.

Etiology:

• The fungus produces conidia (asexual spores) on conidiophores.
• Conidia are multicellular, dark, and have both transverse and longitudinal septa.
• Spread mainly by wind, rain splash, and infected plant debris.
• The pathogen can survive as dormant mycelium or conidia on crop residues.

Disease Cycle:

• Primary Infection: The fungus survives on infected crop debris as dormant mycelium.
• Secondary Infection: Spread occurs mainly through wind-borne conidia, which infect healthy leaves and pods.

Favourable Conditions:

• High humidity (above 90%) and temperatures between 20-25°C.
• Frequent dew or rain favors spore germination and infection.

Management:

• Cultural Practices: Removal and destruction of infected plant debris. Crop rotation with non-host crops.
• Seed Treatment: Use disease-free or treated seeds with Carboxin + Thiram at 2 g/kg of seed.
• Chemical Control: Spray Mancozeb at 0.25% or Carbendazim at 0.1% at 10-day intervals.
• Biological Control: Use antagonistic fungi such as Trichoderma harzianum.

B) Downy Mildew

Causal Organism:

• Peronospora parasitica
• Sub-division: Mastigomycotina

Symptoms:

• Symptoms appear on all aerial parts, especially leaves and inflorescence.
• Greyish-white, irregular, necrotic patches on the lower surface of leaves.
• Yellowing on the upper leaf surface corresponding to the necrotic patches below.
• Severely infected leaves curl, deform, and eventually die.
• Affected inflorescences exhibit hypertrophy (abnormal growth) known as “Stag head.”
• Infected inflorescences fail to produce siliqua or seeds.

Etiology:

• The fungus produces sporangia on branched sporangiophores emerging from stomata.
• Sporangia are spread by wind and rain splashes.
• Infection occurs through stomata, leading to systemic colonization.
• The pathogen survives as oospores in plant debris or soil.

Disease Cycle:

• Primary Infection: The fungus survives as oospores in affected host tissues or on weed hosts. Oospores germinate to produce sporangia, which initiate primary infection.
• Secondary Infection: Spread occurs through wind-borne sporangia, leading to secondary infections on healthy plants.

Favourable Conditions: Cool, moist weather conditions (15-20°C) with high humidity. Dense crop canopy promoting prolonged leaf wetness.

Management:

• Cultural Practices: Collect and destroy infected plant debris. Practice crop rotation with non-cruciferous crops to break the disease cycle.
• Seed Treatment: Seed dressing with Metalaxyl (Apron 35SD) at 6 g/kg of seed.
• Chemical Control: Single spray of Metalaxyl + Mancozeb (Ridomil Gold) at 0.2%. Spray Mancozeb at 0.25% or Copper oxychloride at 0.3% at the first appearance of symptoms.
• Resistant Varieties: Use resistant or tolerant mustard cultivars (if available).

C) White Rust

Causal Organism:

• Albugo candida or Albugo cruciferarum
• Sub-division: Mastigomycotina

Symptoms:

• Local Infection: Isolated white or creamy-yellow raised pustules appear on the underside of leaves. Pustules may coalesce to form larger patches.
• Systemic Infection:
  • Causes hypertrophy (abnormal enlargement) and hyperplasia (increased cell production).
  • Malformation and distortion of floral parts.
  • Entire inflorescence can be replaced by swollen, sterile structures known as “Stag head.”
  • Severe systemic infection in the stem leads to maximum damage.

Etiology:

• The fungus produces sporangia that release motile zoospores under moist conditions.
• Zoospores infect host tissues, leading to pustule formation.
• Pathogen survives as oospores in infected plant debris and soil.

Disease Cycle:

• Primary Infection: The fungus survives through oospores in affected host tissues.
• Secondary Infection: Spread occurs through zoospores disseminated by rain splash or irrigation water.

Favourable Conditions: Cool and moist weather. High humidity and dense crop canopy.

Management:

• Cultural Practices: Collect and destroy infected plant debris. Practice crop rotation with non-cruciferous crops.
• Seed Treatment: Metalaxyl at 6 g/kg of seed.
• Chemical Control: Metalaxyl + Mancozeb (Ridomil Gold) at 0.2%.
• Resistant Varieties: Use resistant mustard cultivars (if available).

D) Downy Mildew

Causal Organism:

• Peronospora parasitica
• Sub-division: Mastigomycotina

Symptoms:

• Affects all aerial parts, mainly leaves and inflorescence.
• Greyish white irregular necrotic patches on the lower leaf surface.
• Upper surface shows yellowing corresponding to the necrotic patches below.
• Severe infection causes hypertrophy of the inflorescence (Stag head).
• Infected inflorescences are malformed and do not produce siliqua or seeds.

Etiology:

• Produces sporangia that release zoospores, which infect the host under humid conditions.
• Survives as oospores in infected plant debris and on alternate hosts.

Disease Cycle:

• Primary Infection: Survives through oospores in plant debris and alternate hosts.
• Secondary Infection: Spread through wind-borne sporangia and zoospores.

Favourable Conditions:

• Cool, moist weather conditions.
• High humidity and dense crop canopy.

Management:

• Cultural Practices: Collect and destroy infected plant debris. Crop rotation with non-cruciferous crops.
• Seed Treatment: Metalaxyl (Apron 35SD) at 6 g/kg seed.
• Chemical Control: Metalaxyl + Mancozeb (Ridomil Gold) at 0.2%.
• Resistant Varieties: Use resistant cultivars, if available.

D) Sclerotinia Stem Rot

Causal Organism:

• Sclerotinia sclerotiorum
• Sub-division: Deuteromycotina

Symptoms:

• Water-soaked spots on stems, later covered with cottony white mycelial growth.
• Affected stems become bleached and shred over time.
• Girdling of the stem leads to premature ripening and lodging of plants.
• Hard black sclerotia form inside and occasionally on the stem surface.
• Basal stalk infections are rare but possible.

Etiology:

• Produces sclerotia, which are hard, black resting structures surviving in soil for years.
• Under favorable conditions, sclerotia produce apothecia, releasing ascospores.
• Ascospores infect host plants, causing disease.

Disease Cycle:

• Primary Infection: Sclerotia survive in soil and produce apothecia, releasing ascospores.
• Secondary Infection: Spread through irrigation water or rain splash carrying spores to healthy plants.

Favourable Conditions:

• High humidity (90-95%) and moderate temperatures (18-25°C).
• Wind currents aid ascospore dispersal.

Management:

• Cultural Practices:
  • Crop rotation, avoiding susceptible crops (e.g., sunflowers, mustard) for at least four years.
  • Avoid planting next to fields with a history of Sclerotinia.
  • Control broad-leaved weeds, which can be alternate hosts.
• Seed Treatment: Use thoroughly cleaned seeds.
• Cultural Control: Avoid dense stands to reduce humidity.
• Chemical Control: Foliar fungicides like Carbendazim, Tebuconazole, or Thiophanate-methyl.
• Biological Control: Use Coniothyrium minitans, a mycoparasite of sclerotia.