Damage in commercial grain crops is often significant in pollen-limiting environments and in 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 diseases.
Ergot has implications for quarantine and the seed trade because seed harvested from infected fields is often rejected.
The pathogen has extraordinary capacity to spread rapidly. In Brazil, an epidemic of the disease in 1995 covered 800,000 km2 (308,880 square miles) in a week, and in Queensland it spread over 60,000 km2 (23,166 square miles) in 3 weeks in 1996.
First reported in India in 1917 and in Kenya in 1924, sorghum ergot was initially restricted to Asia and Africa. In 1995, a widespread ergot epidemic caused serious losses in Brazil, and it is now known to occur in Argentina, Bolivia, Colombia, and Paraguay. In spite of strict quarantine precautions, in April 1996, the disease was first noticed in Australia where it is now endemic throughout Queensland. The disease has not yet been reported in USA.
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 as 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, an ovary can usually resist infection. Thus, flowers are susceptible when their stigmas become receptive, and not after their ovaries are fertilized.
The ovary is infected much before the initiation of honeydew exudation. In fact, the earliest symptoms of infection can be seen on the ovary if flowers are dissected 3-4 days after infection. The infected ovary (left) appears dull green and smaller or larger than the healthy, fertilized ovary (right) which is dark green and
Superficial, white mycelial growth initially appears at the basal end of the ovary and extends upward as the pathogen colonizes ovary tissues both internally and externally. Finally, the complete ovary is converted into a white, fungal mass, or sphacelium, that is visible between the glumes. Honeydew exudation then begins.
Newly formed honeydew droplets are colorless and transparent, and become progressively opaque.
Honeydew can be uniformly yellow-brown to pink, or superficially matt white.
Continued production of honeydew causes droplets to lengthen, smearing seeds and leaves, and falling to the ground. When infection is severe, affected panicles can be recognized from a distance. They may be white with fresh honeydew, or black if the honeydew is saprophytically colonized.
During wet or humid periods at relative humidities above 90%, the ergot fungus produces secondary condia on the surface of the honeydew which appear as a white scum or powdery growth. This white growth covers the surface of the honeydew wherever it is present including the particle, leaves, and soil. If moist conditions persist, several saprophytes grow on the honeydew. One of these, Cerebella sp produces a large, black convoluted matted mass that conceals the sphacelium.
If conditions are warm and dry after the honeydew is formed, it desiccates, forming a brittle, hard, white crust on panicles and leaf surfaces. Under warm dry conditions, sphacelia gradually harden to form solid dense sclerotia. But, in moist conditions, the sphacelia shrivel, become fibrous, and fail to develop into sclerotia.
Ergot can be caused by two fungal pathogens; Indian and African. The sexual stage of the Indian pathogen is Claviceps sorghi (left) while that of the African pathogen is C. africana (right). The asexual stage of both fungi is Sphacelia sorghi. The alkaloid content, and to a less extent, the morphology, of the sclerotia determine the identity of the two species.
Toxicity to animals. Evidence to date suggest 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.
Primary infection in the field is possibly established by ascospores from germinating sclerotia, sphacelial conidia, and conidia from collateral grass weed hosts (e.g., Cenchrus spp, Panicum spp, Ischaemum pilosum, Dicanthium spp), wild sorghums, 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 particle debris for at least 9 months, whilst sclerotia can survive for several years.
Factors that ensure rapid fertilization reduce the chances of ergot attack.
Factors that increase the time between stigma emergence and fertilization enhances the risk and severity of ergot. Such factors include;
CautionErgot is not the only cause of honeydew exudation in sorghum. Insects, such as aphids, also secrete sticky honeydew that is often interspersed with the white molts of the insects. Leaves can also exude honeydew at temperatures below 20 degrees C (68 F) due to a physiological disorder called 'leaf sugary disease'. Honeydew from insects and leaf sugary disease do not contain spores of the ergot fungus.
Several options can be integrated;
SICNA International Sorghum and Millets Newsletter