Ergot alkaloids: extent of human and animal exposure

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.

Development and validation of a new LC–MS/MS method for the simultaneous determination of six major ergot alkaloids and their corresponding epimers. Application to some food and feed commodities

“…The alkaloid pattern and individual alkaloid contents in sclerotia vary largely, due to differences in the maturity of the sclerotia and to other factors such as the fungal strain, the host plant, the geographical region and the prevailing weather conditions (Lombaert, 2001;Storm, Rasmussen, Strobel, & Hansen, 2008). Similarly, data from the literature indicate that the total alkaloid content in sclerotia can vary between 0.01% and 1% (w/w) (Burk, Hobel, & Richt, 2006;Lauber, Schnaufer, Gredziak, & Kiesswetter, 2005;Lombaert, 2001;Scott, 2009). …”

IAG ring test visual detection of ergot sclerotia in rye 2015

“…Other relevant limits are 200-500 mg/kg in cereals depending on purpose (Switzerland), 10 mg/kg for feed grains and zero tolerance for other grains (UK), and 100-3300 mg/kg depending on cereal species and grade (Canada). Krska and Crews (2008) and Scott (2009) . The frequency of occurrence ranged from a few samples to a share of 25-50% positive samples (van Raamsdonk et al, 2009).…”

“…The ergot alkaloids are principally produced in the sclerotia, but ergot alkaloids were occasionally detected in visually non-detectable infestations of cereal samples, and sclerotia were found without any detectable level of ergot alkaloids (Mulder et al, 2012). Ergot content in individual sclerotia can vary considerably (Lorenz and Hoseney, 1979;EFSA, 2005;Krska and Crews, 2008;Scott, 2009). …”

“…and in New England in the late 17th Century (Woolf, 2000), among other cases (Scott, 2009). The intoxication symptoms were already known as Saint Anthony's fire from the Middle Ages (Lee, 2009a).…”

“…The intoxication symptoms were already known as Saint Anthony's fire from the Middle Ages (Lee, 2009a). After an outbreak in France (Pont St. Esprit; Lorenz and Hoseney, 1979;Scott, 2009) …”