Ergot attacks cereals and both wild and cultivated grasses throughout the world. Only the flowering parts and developing kernels are affected. The disease is favored by periods of prolonged cool, wet weather, which also prolongs the flowering period and the formation of fungal spores.|
Ergot is common on rye but is also found on other small grains such as barley, wheat, and triticale. Oats are the least susceptible of the small grains. More than 200 wild and cultivated grasses may become infected unless seed heads are cut.
Ergot is important because of the presence of numerous potent chemicals in the sclerotia (survival structure). The alkaloids produced within the sclerotia cause a variety of symptoms in animals and humans, including contractions of the smooth muscle fibers and constriction of small blood vessels. Feeding ergot-infested grain to livestock can also lead to reproductive failure. Ergot poisoning is a cumulative process, and proper monitoring of pastures and grain sources can reduce the potential for injury to animals.
Symptoms and Disease Cycle
Ergot is caused by fungi belonging to the genus Claviceps. The ergot bodies are sclerotia produced in place of normal kernels. Grain heads may contain from one to many sclerotia, depending on the grass or grain host and weather conditions. These sclerotia are dark purple to black in color; many are up to four times the length of a normal kernel. Because affected flowers produce ergot sclerotia instead of grain, yields can be reduced as well.
The first sign of ergot infection appears soon after flowering when infected florets exude a sticky slime called "honeydew." This sticky material contains large numbers of spores (conidia) of the fungus and serves as a means of dispersal. Insects are attracted to the rotten odor of the honeydew and pick up and disperse spores as they feed. Splashing rain and contact can also serve to disperse spores. New infections occur as long as the cereal and grass plants bloom and are susceptible.
As infections progress, sclerotia develop in place of kernels. Sclerotia are hard, thick-walled, overwintering fungal structures, which can either be combined with the grain or can fall to the ground. When sowed with the seed or left on the soil surface, sclerotia germinate during the spring to produce fruiting structures called perithecia. The perithecia produce a second type of spore known as an ascospore. Ascospores are forcibly discharged from the perithecia and disseminated by insects, wind, or splashing rain. Spores contacting a flower stigma of a grass or cereal plant germinate and penetrate the ovary within 24 hours. Within 5 days, conidia form on the ovary surface (the "honeydew" stage), completing the disease cycle.
1. Rotate cereals and grasses with nonsusceptible crops such as corn, legumes, or sorghum (plants outside the grass-grain family) for one year or longer. Fortunately, the ergot sclerotia do not remain viable for more than one year.
2. Select and plant only ergot-free seed.
3. Mow wild, escaped, and cultivated grasses before flowering. Eradicate grasses or prevent the heading of grasses in grain fields, fence rows, ditch banks, headlands, roadsides, or other similar areas adjacent to cultivated fields. Heavy grazing of grass pastures before heading also reduces the threat of ergot poisoning among livestock.
4. No commercial varieties of barley, rye, wheat, triticale, or cultivated grasses have been developed that are resistant to ergot. Varieties with exposed florets that remain open for relatively long periods are the most susceptible. The grasses growing in Illinois that are quite susceptible to ergot include various bluegrasses, fescues, bromegrasses, mannagrass, meadow foxtail, orchardgrass, quackgrass, reedgrasses, redtop, ryegrasses, squirrel tail, timothy, wheatgrass, and wild rye.--Joe Toman