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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Ergotism [Old French: argot, cock spur] It was known as an obstetric remedy to the Chinese around 1000 BC. The use of barley in many ancient remedies suggests that the ergot fungus was unknowingly used by the ancients in childbirth and other conditions. The poisonous properties of molds growing on grain were described by Galen (129–200) who was probably the first physician to recognize the fungus. A reference to it in midwifery was made by Adam Lonicer or Lornicerus, a German botanist, in 1582. Casper Bauhin (1560–1624) described and illustrated the fungus. Epidemics of ergot poisoning due to infected rye or barley have been recorded since the Middle Ages. The first recorded outbreak occurred in France, at Limoges in AD 591. The symptoms of intense irritation and burning which led to dancing were interpreted as demonic possession. In 1085 Pope Urban II designated St Anthony as the saint against the disease and it came to be known as ignus sacer (holy fire) or St Anthony’s fire. The first suggestion that it was due to contamination of rye by biological agents was made by the Parisian herbal physician Denis Dodart in 1676. In his letter to the Royal Academy of Sciences Paris, he pointed out that degenerating rye contained an external agent. One of the last outbreaks in England occurred in Manchester in 1927. The fungus was named Claviceps purpurea.
Biosensors for the detection of mycotoxins
Published in Toxin Reviews, 2022
Akansha Shrivastava, Rakesh Kumar Sharma
Ergot alkaloids are the secondary metabolites of fungi and these are produced by various species of Claviceps. The effect of this group of alkaloids has been shown in the middle ages called "Holy Fire" or "St. Anthony’s Fire", also known as the disease ergotism. Other alkaloids include ergometrine, ergotamine, and ergotoxine (Crews 2015, Miedaner and Geiger 2015). There are two forms of ergotism: Gangrenous, which affects the blood supply to extremities and convulsive, and ultimately affects the central nervous system. The fungal species which produce these alkaloids include Claviceps purpurea (rye and other cereals), Claviceps paspali (forage grass), Claviceps fusiformis, Claviceps gigantea, and Sphacelia sorghi (an anamorphic form of Claviceps). The clinical symptoms of ergotism are a manifestation in the form of gangrene, abortion, convulsions, suppression of lactation, and hypersensitivity (Berthiller et al. 2017). The ingestion of ergot occurs through infected cereals, commonly in the form of bread produced from contaminated flour. A recently reported another alkaloid from the same class, purpurolic acid from plant-parasitic sclerotia of Claviceps purpurea has been reported and considered as highly toxic for animal feed (Roberts et al. 2016). Ergot alkaloids contamination has been reported in rye food, wheat food, multigrain food, rye feed, wheat feed, and triticale feed. Among these samples, rye feed contained the highest amount of ergot alkaloids, i.e. 12,340 µg/kg (Malysheva et al. 2014).
The discovery and development of inhaled therapeutics for migraine
Published in Expert Opinion on Drug Discovery, 2019
Nicolas Vandenbussche, Peter J Goadsby
The alkaloid analgesic ergotamine was first extracted from Claviceps purpurea, a parasitic fungus well-known as the cause of St. Anthony’s Fire (a form of ergotism) in the Middle Ages attracted from eating moldy bread [17,18]. Its use in migraine was established in the early twentieth century and is renowned as one of the first successful migraine specific therapies. Sadly, the drug is also known for its difficult use in clinical practice in terms of drug delivery, unfavorable side effects, and tolerability profile. Ergotism, vasoconstriction, and nausea are a few of the most prominent and feared side effects. Ergotamine has several pharmacokinetic disadvantages through the classical oral or nasal routes including poor oral bioavailability, first pass metabolism, and unpredictable pharmacokinetics [19,20].
A cluster of lysergic acid diethylamide (LSD) poisonings following insufflation of a white powder sold as cocaine
Published in Clinical Toxicology, 2021
Darren M. Roberts, Kulanka H. Premachandra, Betty S. Chan, Robin Auld, Thanjira Jiranantakan, Christopher Ewers, Catherine McDonald, Vanessa Shaw, Jared A. Brown
LSD, a semisynthetic product of lysergic acid which is a natural substance from the parasitic rye fungus Claviceps purpurea, was first synthesised in 1938. Its psychoactive effects were discovered in 1943 and it became an illegal drug of abuse from the mid-1960s [12]. LSD potently binds to human serotonin 5-HT2A, as well as 5-HT1A, 5-HT2C, dopamine D2 and α2 adrenergic receptors, and less potently to α1 adrenergic, D1 and D3 receptors. Its agonistic effects on 5-HT2A receptors are responsible for the hallucinogenic effects [12–17].