Pearl millet ergot

Claviceps fusiformis is a fungal pathogen responsible for the disease known as ergot, specifically targeting pearl millet (Pennisetum glaucum). As an ascomycete fungus, it infects the floral tissues of the host plant, disrupting normal grain development and replacing healthy ovaries with dormant survival structures called sclerotia.

The pathogenicity of this fungus lies in its ability to produce toxic alkaloids within the sclerotia. These toxins pose a significant risk to human and animal health if contaminated grain is processed into food or feed. Consequently, Claviceps fusiformis is a major limiting factor for cereal production in regions where environmental conditions favor the fungus.

Early symptoms appear during the flowering stage, characterized by the exudation of a sticky, sugary liquid known as honeydew from infected spikelets. This honeydew is rich in asexual conidia, which facilitate secondary spread via wind, rain splash, or insect vectors. As the disease progresses, dark, elongated, and often curved sclerotia protrude from the florets, replacing the grains.

Environmental conditions are the primary drivers of disease outbreaks. High relative humidity, cloudy weather, and moderate temperatures during the flowering period are highly conducive to fungal infection and spore germination. The sclerotia, which fall to the soil during harvest, serve as the primary source of inoculum for the next growing season after overwintering.

Effective disease management requires an integrated approach. Farmers are encouraged to use clean, pathogen-free seeds and implement cultural practices such as deep tillage to bury sclerotia. Rotation with non-host crops and the use of resistant millet cultivars are also recommended to reduce the overall inoculum density in the field environment.

• Selection of resistant or early-maturing cultivars to avoid peak infection weather.
• Seed cleaning using gravity separators or brine solutions to remove sclerotia.
• Maintaining proper crop rotation cycles.
• Eliminating wild grasses that may serve as alternative hosts for the pathogen.
• Strategic application of protective fungicides during the onset of flowering.