What is ergot poisoning?
Ergot is toxic to animals. Animals consume ergot by eating the sclerotia present in contaminated feed. All domestic animals are susceptible, including birds. Cattle seem to be the most susceptible.
Forms of Ergotism
The form of ergotism that is manifested depends on the type of ergot consumed and the ratio of major toxic alkaloids present in the ergot: ergotamine, ergotoxine, and ergometrine. Claviceps purpurea, the common cause of ergot in North Dakota, is usually associated with gangrenous ergotism. Claviceps paspali, an ergot of Paspalum spp. of plants, is most commonly associated with central nervous derangement. Paspalum is a water grass distributed in pastures in southern states, but is not commonly found in North Dakota. The responses of animals consuming ergot are usually quite variable and are dependent on variations in alkaloid content, frequency of ingesting ergot, quantity of ergot ingested, climatic conditions under which ergot grew, the species of ergot involved, and the influence of other impurities in the feed such as histamine and acetylcholine.
Symptoms of convulsive ergotism include hyperexcitability, belligerence, ataxia or staggering, lying down, convulsions and backward arching of the back. Symptoms of gangrenous ergotism involve the extremities of the animal including the nose, ears, tail, and limbs . Early signs usually start in the hind limbs. Lameness may appear from two to six weeks after first ingesting ergot. There may be pain, stamping of the feet, and coolness of the affected areas. If ergot consumption continues, sensation to pain is lost in the affected areas and an indented line appears between normal tissue and gangrenous tissue. This gangrenous tissue is called `dry gangrene.' Eventually all tissue below this line will slough. Besides the limbs, other extremities involved can include the tail and ears. The tips and distal areas of the extremities will also slough. Early signs of gangrenous ergotism usually start in the hind limbs.
Animals fed large amounts of ergot over time lose portions of their hooves, ears, tails, combs, and wattles. Spontaneous abortion and loss of milk has occurred in cows and sows fed even small amounts of ergot. Ergoty feed should not be fed to breeding females. Animals fed large amounts of ergot over time lose portions of their ears or other extremeties.
A diagnosis of ergot poisoning is based on finding the sclerotia in the feed or pasture and whether the animals are exhibiting symptoms of ergotism. Extraction and detection of ergot alkaloids also may be done if ground feed is suspect.
The only treatment for erotism is to remove the ergot-contaminated feed or remove the animals from the contaminated pasture. If nervous signs are present, call your veterinarian for medical advice and supplemental therapy such as pain control. If dry gangrene is present, the affected portion will be sloughed. There is nothing to reverse this process. If secondary infections or open wounds are present, call your veterinarian for appropriate therapy.
Prevention is based on feeding feed and forage that are free of ergot. For pastures, graze the infected fields before seed heads begin to flower. The ergot is contained in the ovary of the flower. Commercially prepared feeds will rarely contain ergot. Non-commercial grain (home grown) should be screened prior to feeding (and planting to prevent contamination of future crops). Special care should be taken in feeding screenings. If feeding ergoty grain is unavoidable, the amount of sclerotia should be reduced to an amount less than 0.1% (by weight) of the feed through mixing with `clean' grain. Again, ergoty feed should not be fed to breeding females.