| Ergotism | |
|---|---|
| Classification and external resources | |
| ICD-10 | T62.2 |
| ICD-9 | 988.2 |
| DiseasesDB | 30715 |
| MeSH | D004881 |
Ergotism is the effect of long-term ergot poisoning, traditionally due to the ingestion of the alkaloids produced by the Claviceps purpurea fungus which infects rye and other cereals, and more recently by the action of a number of ergoline-based drugs. It is also known as ergotoxicosis, ergot poisoning and Saint Anthony's Fire. Ergot poisoning is a proposed explanation of bewitchment.
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The toxic ergoline derivatives are found in ergot-based drugs (such as methylergometrine, ergotamine or, previously, ergotoxine). The deleterious side-effects occur either under high dose or when moderate doses interact with potentiators such as azithromycin.
Historically, eating grain products contaminated with the fungus Claviceps purpurea also caused ergotism.
Finally, the alkaloids can also pass through lactation from mother to child, causing ergotism in infants.
The symptoms can be roughly divided into convulsive symptoms and gangrenous symptoms.
Convulsive symptoms include painful seizures and spasms, diarrhea, paresthesias, itching, mental effects including mania or psychosis, headaches, nausea and vomiting. Usually the gastrointestinal effects precede central nervous system effects. As well as seizures there can be hallucinations resembling those produced by LSD (lysergic acid diethylamide, to which the ergot alkaloid ergotamine is an immediate precursor and therefore shares some structural similarities), although ergot's hallucinations more strongly resemble a delirious and psychotic state, whereas LSD is not psychomimetic. The convulsive symptoms are caused by clavine alkaloids.
The dry gangrene is a result of vasoconstriction induced by the ergotamine-ergocristine alkaloids of the fungus. It affects the more poorly vascularized distal structures, such as the fingers and toes. Symptoms include desquamation or peeling, weak peripheral pulses, loss of peripheral sensation, edema and ultimately the death and loss of affected tissues. Vasoconstriction is treated with vasodilators. [1]
Epidemics of the disease were identified throughout history, though the references in classical writers are inconclusive. Rye, the main vector for transmitting ergotism, was not grown much around the Mediterranean. When Fuchs 1834 separated references to ergotism from erysipelas and other afflictions, he found the earliest reference to ergotism in the Annales Xantenses for the year 857: "a Great plague of swollen blisters consumed the people by a loathsome rot, so that their limbs were loosened and fell off before death."
In the Middle Ages, the gangrenous poisoning was known as ignis sacer ("holy fire") or "Saint Anthony's fire", named after monks of the Order of St. Anthony who were particularly successful at treating this ailment. The 12th century chronicler Geoffroy du Breuil of Vigeois recorded the mysterious outbreaks in the Limousin region of France, where the gangrenous form of ergotism was associated with the local Saint Martial as much as Saint Anthony.
The blight, named from the cock's spur it forms on grasses, was identified and named by Denis Dodart, who reported the relation between ergotized rye and bread poisoning in a letter to the French Royal Academy of Sciences in 1676 (John Ray mentioned ergot for the first time in English the next year), but "ergotism", in this modern sense, was first recorded in 1853.
Notable epidemics of ergotism occurred up into the 19th century. Fewer outbreaks have occurred since then due to rye being carefully monitored in developed countries.
There is evidence[2] of ergot poisoning serving a ritual purpose in the ritual killing of certain bog bodies.[3] Found in peat swamps, Grauballe Man and Tollund Man have been preserved so well that large amounts of rotten cereals and weeds have been extracted from their stomachs, clearly showing force-feeding and primitive sedation.
When milled, the ergot is reduced to a red powder, obvious in lighter grasses but easy to miss in dark rye-flour. In less wealthy countries, ergotism still occurs; an outbreak in Ethiopia occurred in mid-2001 from contaminated barley. Whenever there is a combination of moist weather, cool temperatures, delayed harvest in lowland crops and rye consumption, an outbreak is possible.
Poisonings due to consumption of seeds treated with mercury compounds are sometimes misidentified as ergotism, possibly including the case of mass-poisoning in the French village Pont-Saint-Esprit in 1951.[4] The incident is described in John Grant Fuller's book The Day of St Anthony's Fire.[5]
According to Snorri Sturluson, in his Heimskringla, King Magnus, son of King Harald Sigurtharson, who was the half brother of Saint King Olaf Haraldsson, died from ergotism shortly after the Battle of Hastings.
The convulsive symptoms that can be a result of consuming ergot-tainted rye have also been said to be the cause of accusations of “bewitchment” that spurred the Salem witch trials. This medical explanation for the theory of “bewitchment” is one first propounded by Linnda R. Caporael in 1976 in an article in Science. In her article, Caporael points out that the convulsive symptoms, such as crawling sensations in the skin, tingling in the fingers, vertigo, tinnitus aurium, headaches, disturbances in sensation, hallucination, painful muscular contractions, vomiting and diarrhea, as well as psychological symptoms, such as mania, melancholia, psychosis and delirium, were all symptoms reported in the Salem witchcraft records. Caporael also notes the abundance of rye in the region as well as perfect climate conditions for the tainting of rye.[6] In 1982 historian Mary Matossian revitalized Caporael’s theory in her article in American Scientist. In her article, Matossian builds on Caporael’s theories and also notes that according to English folk tradition all the symptoms of “bewitchment” resemble the ones exhibited in those afflicted with ergot poisoning.[7]
The medical explanation of ergotism causing “bewitchment” has been subject to debate, and has been criticized by several scholars. Within a year of Caporael’s article, the historians Spanos and Gottlieb rebutted Caporael’s theory in the same journal. In Spanos and Gottlieb’s rebuttal to Caporael’s article, they concluded that there are several flaws in the explanation of ergot poisoning as a result of accusations of “bewitchment.” The most notable flaw is that if the food supply was contaminated, the symptoms would have occurred on a house-by-house basis, not just in particular individuals. Spanos and Gottlieb also note the fact that ergot poisoning has additional symptoms not mentioned by those claiming affliction and that the proportion of children afflicted were less than in a typical ergotism epidemic.[8] Other problems have also been raised with Caporael’s theory. The anthropologist H. Sidky noted the problem that ergotism had existed for centuries before the Salem witch trials, and that its symptoms would have been recognizable during the time of the Salem witch trials.[9]
As Dr. Simon Cotton (member of the Chemistry Department of Uppingham School, U.K.) notes, there have been numerous cases of mass-poisoning due to consumption of mercury-treated seeds:
More horrifying than this were epidemics of poisoning, caused by people eating treated seed grains. There was a serious epidemic in Iraq in 1956 and again in 1960, whilst use of seed wheat (which had been treated with a mixture of C2H5HgCl and C6H5HgOCOCH3) for food, caused the poisoning of about 100 people in West Pakistan in 1961. Another outbreak happened in Guatemala in 1965. Most serious was the disaster in Iraq in 1971-2, when according to official figures 459 died. Grain had been treated with methyl mercury compounds as a fungicide and should have been planted. Instead it was sold for milling and made into bread. It had been dyed red as a warning and also had warning labels in English and Spanish that no one could understand.
See Simon Cotton, B.Sc., Ph.D., "Dimethylmercury and Mercury Poisoning", Molecule of the Month (MOTM; published on the School of Chemistry, University of Bristol, U.K. website), October 2003.
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