* Damage in commercial grain crops may occur in pollen-limiting environments, such as those caused by low night temperatures or in plants under stress, and in late flowering forage sorghums.

* A disease of the ovary, ergot reduces grain yield because infected flowers do not produce grain.

* The disease lowers grain/seed quality, makes threshing difficult, reduces germination and seedling emergence, and predisposes seedlings to other disease.

Ergot only attacks unfertilized ovaries. Few or all flowers in an inflorescence may be infected. The most obvious external sign of the disease is the exudation from the infected flowers of honeydew, a thin-to-viscous, sweet, sticky fluid that gives the name 'sugary' or 'honeydew' disease to the malady.

The ergot pathogen is a fungus that infects the ovary, following nearly the same path the pollen takes for fertilization. Normally, pollen requires only a few hours for fertilization while it takes 2-3 days for the fungus to colonize the ovary. Once fertilized, on ovary can usually resist infection. Thus, flowers are susceptible when their stigmas become receptive, but not after their ovaries are fertilized.

Factors that ensure rapid fertilization reduce the chances of ergot attack while factors that increase the time between stigma emergence and fertilization enhance the risk and severity of ergot. Such factors include;

* Poor timing of pollen production in seed-production plots. (The better hybrid seed parents produce pollen in relation to stigma emergence, the lower their chances of being infected.)

* Low night temperatures, high relative humidity (>90%), cloudiness, and/or wetness following stigma emergence. These factors not only favor infection, they also reduce anther emergence, anther dehiscence, and pollen deposition.

After honeydew production, high relative humidity (>90%) and/or wetness favor the production of secondary conidia which are efficiently spread by wind.

Primary infection in the field is possibly established by ascospores from germinating sclerotia, spachelial conidia, and conidia from collateral grass weed hosts (e.g., Cenchrus spp, Panicum spp, Ischaemum pilosum, Dicanthium spp), wild sorghums (including johnson grass and shatter cane), volunteer plants, and infected panicle debris in soil. After infection, millions of conidia are released in the honeydew, and are spread by rain splash and probably by insects. Secondary conidia are spread by wind and cause new infections both near to and far from the initial infections. The pathogen can also be dispersed on clothing, footwear, and farm implements. Several cycles of infection can occur in the same growing season if susceptible sorghum hosts are available.

Survival between seasons can be via infected panicles left in the field after harvesting, or as sclerotia mixed with seed during threshing and seed processing. Conidia remain viable in panicle debris for at least 9 months, whilst sclerotia can survive for several years.

Planting fungicide treated seed is highly recommended as a control measure.

Toxicity to animals. Evidence to date suggests that sclerotia-contaminated sorghum grain has little, if any, implication for animal health. On the contrary, honeydew-smeared leaves are more palatable to animals, but further studies are required to confirm these observations.