| Ergotism | |
|---|---|
| Other names | Saint Anthony's fire, ergotoxicosis |
 | |
| Advanced ergotism withgangrene | |
| Specialty | Emergency medicine  |
| Symptoms |
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| Types | Convulsive, gangrenous |
| Causes | Long-termergot poisoning |
Ergotism (pronounced/ˈɜːrɡətˌɪzəm/UR-gət-iz-əm) is the effect of long-termergot poisoning, traditionally due to theingestion of thealkaloids produced by theClaviceps purpurea fungus—from the Latinclava "club" or clavus "nail" and-ceps for "head", i.e. the purple club-headed fungus—that infectsrye and othercereals, and more recently by the action of a number ofergoline-based drugs. It is also known asergotoxicosis,ergot poisoning, andSaint Anthony's fire.
Ergotism is the effect of long-termergot poisoning.[1] The symptoms can be roughly divided intoconvulsive symptoms andgangrenous symptoms.[1]
Ergot alkaloids, the active compounds produced by the ergot fungus, can cause severevasoconstriction, leading to symptoms like gangrene and convulsions. Additionally, ergot alkaloids can mimicneurotransmitters and hormones in the human body, causing hallucinations and affecting hormonal balance. Chronic exposure to some ergot alkaloids has been linked to reproductive issues, such as spontaneous abortions and infertility, due to their action on the pituitary gland.[1]
Convulsive symptoms include painful seizures andspasms,diarrhea,paresthesias, itching, mental effects includingmania orpsychosis, headaches,nausea, and vomiting. Usually the gastrointestinal effects precedecentral nervous system effects.[citation needed]
The drygangrene is a result ofvasoconstriction induced by theergotamine-ergocristine alkaloids of the fungus.[citation needed] It affects the more poorly vascularizeddistal structures, such as the fingers and toes. Symptoms includedesquamation or peeling, weak peripheralpulses, loss of peripheral sensation,edema and ultimately the death and loss of affectedtissues. Vasoconstriction is treated withvasodilators.[2]
Historically, eatinggrain products, particularlyrye, contaminated with the fungusClaviceps purpurea was the cause of ergotism.[3]
The toxic ergolinederivatives are found in ergot-baseddrugs (such asmethylergometrine,ergotamine or, previously,ergotoxine). The deleteriousside effects occur either under highdose or when moderate doses interact withpotentiators such aserythromycin.[citation needed]
The alkaloids can pass throughlactation from mother to child, causing ergotism in infants.[citation needed]
Dark-purple or black grain kernels, known as ergot bodies, can be identifiable in the heads ofcereal or grass just before harvest. In most plants the ergot bodies are larger than normal grain kernels, but can be smaller if the grain is a type of wheat.[citation needed]
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Removal of ergot bodies is done by placing the yield in abrine solution; the ergot bodies float, while the healthy grains sink.[4] Infested fields must be deep-ploughed; ergot cannot germinate if buried more than one inch (2.5 cm) in soil and therefore will not release its spores into the air.Crop rotation with non-susceptible plants helps reduce infestations, since ergot spores live only one year. Wild and escaped grasses and pastures can be mown before they flower to help limit spread of the fungus.
Chemical controls can also be used but are not considered economical, especially in commercial operations, and germination of ergot spores can still occur under favourable conditions even with the use of such controls.
Throughout history, at least 83 outbreaks of ergotism have been documented, particularly in Europe.[5] One of the most notable incidents occurred in 944 AD in France, where ergot poisoning led to widespread hallucinations, gangrene, and convulsions. Another possible case is associated with the Salem witch trials in 1692, where some historians believe ergotism may have contributed to the symptoms reported by the accusers.[6]
Epidemics of the disease were identified throughout history, though the references in classical writings are inconclusive. Rye, the mainvector (route) for transmitting ergotism, was not grown much around theMediterranean. When Fuchs separated references to ergotism fromerysipelas and other conditions in 1834, he found the earliest reference to ergotism in theAnnales 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".[citation needed]
In the Middle Ages the gangrenous poisoning was known as "holy fire" or "Saint Anthony's fire", named after monks of theOrder of St. Anthony, who dedicated themselves to treating this ailment. According toSnorri Sturluson in hisHeimskringla, KingMagnus II of Norway, son ofKing Harald Sigurtharson, who was the half-brother of Saint KingOlaf Haraldsson, died from ergotism shortly after theBattle of Hastings. The 12th-century chroniclerGeoffroy du Breuil of Vigeois recorded the mysterious outbreaks in theLimousin region of France, where the gangrenous form of ergotism was associated with the localSaint Martial. Likewise, an outbreak in Paris around 1129 was reported to be cured by the relics of SaintGenevieve, a miracle commemorated in the26 November "Feast of the Burning Ones."[7] The French physician Tessier observed a huge epidemic in the year 1778 in Sologne (France), during which more than 8000 people died, and was hence persuaded to recommend drainage of fields, compulsory cleaning of grain and replacement of infected grain with potatoes.
Notable epidemics of ergotism occurred into the first half of the 20th century, as in the Italian island ofAlicudi,[9] although fewer outbreaks have occurred in modern times owing to rye being carefully monitored in developed countries. However,a severe outbreak of something akin to ergot poisoning occurred in the French village ofPont-Saint-Esprit in 1951, resulting in nearly 250 people affected and seven deaths.[10] The outbreak and the diagnostic confusion surrounding it are vividly described inJohn Grant Fuller's bookThe Day of St Anthony's Fire.[11]
Ergotsclerotiums were found in the gut of theGrauballe Man, abog body dated the late 3rd century BC.[12]
Poisonings due to consumption of seeds treated withmercury compounds are sometimes misidentified as ergotism.[13][14] There have been numerous cases of mass-poisoning due to consumption of mercury-treated seeds.[15]
Theconvulsive symptoms from ergot-tainted rye may have been the source of accusations ofbewitchment that spurred theSalem witch trials. This medical explanation for the theory of "bewitchment" was first propounded byLinnda R. Caporael in 1976 in an article inScience.[16] In her article, Caporael argues that the convulsive symptoms such ascrawling sensations in the skin,tingling in the fingers,vertigo,tinnitus aurium,headaches, disturbances in sensation,hallucination, painfulmuscular contractions,vomiting, anddiarrhea, as well as psychological symptoms such asmania,melancholia,psychosis, anddelirium, were all symptoms reported in the Salem witchcraft records. Caporael also states that there was an abundance of rye in the region, as well as climate conditions that could support the tainting of rye.[16] In 1982, historianMary Matossian raised Caporael's theory in an article inAmerican Scientist, in which she argued that symptoms of "bewitchment" resemble the ones exhibited in those affected by ergot poisoning.[17]
The hypothesis that ergotism could explain cases of bewitchment has been subject to significant debate and has been criticized by several scholars. Within a year of Caporael's article, historians Nicholas Spanos and Jack Gottlieb refuted the idea in the same journal.[18] In Spanos and Gottlieb's rebuttal to Caporael's article, they concluded that there are several flaws in the explanation. They noted that if ergotism was present in Salem, the symptoms would have occurred by household, not individual. Whole families, and particularly all the young children in a household, would have shown symptoms, but this was not the case. In general, the proportion of children affected was significantly less than in a typical ergotism epidemic. Spanos and Gottlieb also state that most of ergot poisoning's symptoms, like crawling and tingling sensations, vertigo, tinnitus, vomiting, and diarrhea, do not appear in the records of events in Salem. Lastly, they note that convulsive ergotism epidemics only take place in communities suffering from vitamin A deficiencies; they argued that residents of Salem, living in a farming community with ample access todairy, would have had no reason to bedeficient invitamin A. Therefore, an outbreak of ergotism as the cause of the Salem epidemic was unlikely. Historians published in the early 21st century continue to stand by Spanos and Gottlieb's conclusion.[19]
Historian Leon Harrier has argued that only some members of a household might have shown symptoms because they had underlying conditions. Being chemically similar tolysergic acid diethylamide (LSD), ergot would not survive in the acidic environment of a typical human's stomach, especially in properly cooked food.[citation needed] But if some residents of a household were malnourished and had bleeding stomach ulcers, those individuals would have had a heightened risk of absorbing the toxin (even with properly cooked food items) through the stomach lining, offering a direct route to the bloodstream. Only those with these preexisting conditions would have been affected by ingesting contaminated grains, leaving the majority unaffected.
Anthropologist H. Sidky noted that ergotism had been known for centuries before the Salem witch trials and argued that its symptoms would have been recognizable during the time of the Salem witch trials.[20]
In 2003 it was pointed out that ergots produced by different strains ofClaviceps purpurea, as well as those growing in different soils, may produce different ergot alkaloid compositions. This may explain the different manifestations of ergotism in different outbreaks. For example, an alkaloid present in high concentrations in ergots from Europe east of theRhine may have caused convulsive ergotism, while ergot from the west caused epidemics of gangrenous ergotism.[21]
In medieval Europe, outbreaks of ergotism were sometimes interpreted as divine punishment or witchcraft. The condition's symptoms, particularly hallucinations and convulsions, often led to accusations of demonic possession. The disease's association with St. Anthony's Fire is linked to the Order of St. Anthony, a medieval Christian order that provided care for ergotism sufferers.[22]
The prevalence of ergotism was closely linked to environmental conditions, such as cold, damp weather, which promoted the growth of the ergot fungus. Poor storage of grain also contributed to the risk of contamination. Changes in agricultural practices and the introduction of disease-resistant crop varieties have largely eliminated ergotism in modern times.[23]
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..
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