Abstract

Ergot alkaloids are formed by Claviceps spp. on grains and grasses and by fungal endophytes such as Neotyphodium spp. in grasses, notably tall fescue and perennial ryegrass. Ergots from grains and grasses show a wide variation in alkaloid composition. The main ergot alkaloids are pharmacologically active lysergic acid derivatives – e.g. ergometrine (ergonovine), ergotamine, ergosine, ergocornine, α-ergocryptine, ergocristine, and ergovaline; derivatives of isolysergic acid, e.g. ergotaminine; and clavine alkaloids, e.g. agroclavine. Other structurally unrelated toxic alkaloids such as lolitrems are formed by fungal endophytes in grasses. The present review focuses more on how man and animals are exposed to ergot alkaloids than on toxicology and methods of analysis. Ergot poisoning in humans, well known in the Middle Ages, can be of two types: convulsive ergotism and gangrenous ergotism. Since the beginning of the last century there have been outbreaks in Russia, England, India, France and Ethiopia. The principal route of human exposure to ergot alkaloids is by consumption of contaminated food; another route is inhalation of grain dust. Toxicoses in animals due to ergot alkaloids are more common, particularly poisoning of livestock grazing on endophyte infected grasses. Analyses in Canada, Germany, Switzerland, Sweden and Denmark found ergot alkaloids in human foods such as wheat and rye flours, bread, and other grain foods, often at levels greater than 1000 µg/kg. Processing studies have confirmed that the alkaloids survive baking; they also remain to some extent after brewing of beer. There is little evidence for carryover of ergot alkaloids into animal tissue and milk. As an indication of the importance of controlling ergot for the health of animals and people, Canada, the European Union, Switzerland, USA, Japan, Australia and New Zealand have regulations for ergot in grains but only Uruguay and Canada have regulations for the actual ergot alkaloids in feed.

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