56 Fungus Poisoning
Two categories of fungus poisoning may be distinguished: (1) mycetism, the result of eating poisonous fungi mistaken for the edible variety (which has a long history and a worldwide incidence), and (2) my cotoxicoses, the result of inadvertent ingestion of food containing toxins produced by fungi.
The latter, although also of worldwide incidence, has (with the exception of ergotism) been generally recognized only during the twentieth century.Mycetism
Calamities tend to impress, and the first reference to fungi in the Greek classics is an epigram by Euripides writing about 450 B.C. He was commemorating the death of a woman and her two children, in one day, after eating poisonous fungi. During Roman times, edible fungi were a delicacy, and diverse advice regarding them was offered by several authors such as Horace, Celsus, Dioscorides, Galen, and Pliny. The advice consisted of how to avoid poisonous species, how to render poisonous forms harmless, and how to treat fungus poisoning.
Much of this ancient folklore on precautions to ensure edibility was compiled by the authors of the first printed herbals in the fourteenth and fifteenth centuries, and some has even survived to the present day. It is, however, invariably unreliable because the distribution of poisonous and edible species seems to be random. For example, the esteemed esculents Amanita caesarea (“Caesar’s mushroom,” a Roman favorite) and Amanita rubescens (“the blusher”) are congeneric with Amanita phalloides (“death cap”) and several related species {Amanita pantherina, Amanita υerna, Amanita υirosa) that have been, and still are, responsible for most fatalities from fungus poisoning in north temperate regions. The only reliable guide is correct identification.
The most frequent effect of fungus poisoning is gastroenteric disturbance of greater or lesser severity.
Amanita phalloides toxins, symptoms of which occur 4 to 6 hours or more after ingestion, also cause severe damage to the liver and kidneys. Other Amanita toxins have a hemolytic effect, whereas hallucinogenic species cause psychosomatic symptoms. Fever is unusual.The chemistry of toxic fungi has been under investigation since muscarine was isolated in Germany in 1869. That name came from the “fly agaric” (Amanita muscaria) which has been equated by R. G. Wasson (1971) with the Indian soma. T. Wieland (1986), together with his father, brother, and other collaborators, has made extensive studies of the Amanita toxins (amatoxins, phallotoxins, virotoxins).
As already indicated, mycetism is of worldwide distribution, the species of fungi implicated depending on the locality, but there are variations in its reported incidence. In western Europe, for example, there are more published records of mycetism in France, where edible forms of fungi are widely collected from the wild for sale, than in the United Kingdom, where eating wild forms is still regarded with suspicion. Most poisonous fungi are larger basidiomycetes, but a few ascomycetes with large fruit bodies are poisonous (e.g., Gynmitra esculenta, which is, however, edible if dried or if the cooking water is discarded).
A recent development that has led to increased incidence of fungus poisoning originated from the ethnomycological studies of Wasson (1971). These studies drew attention to the hallucinogenic properties of some larger fungi, particularly species of Psilocybe containing the compound psilocin - which is able to induce psychotropic effects similar to lysergic acid and mescalin. Collection of such forms in the wild for self-administration or illegal sale has resulted in misidentifications or overdoses and the need for medical attention.
Mycotoxicoses
Until the twentieth century, the only mycotoxicosis of human beings generally recognized in the West was ergotism, although serious outbreaks of human mycotoxicoses had occurred in Russia and Japan.
Kaschin-Beck (or Urov) disease of children is characterized by generalized osteoarthritis caused by eating moldy grain. It was prevalent among the Cossacks and endemic in both Asiatic and European Russia and in northern Korea and China in the 1860s. A similar mycotoxicosis (the “drunken [or intoxicating] bread syndrome”) was also prevalent in Russia. But the most extensively documented mycotoxicosis in Russia is alimentary toxic aleukia (or septic angina); it was known before World War I and became epidemic during World War II in the Russian grain belt, when some 10 percent of the population was affected and suffered high death rates (Mayer 1953). The problem was that in affected districts it was the practice to allow the ripe cereal crop to go through the winter under the snow. When the snow cover was so heavy that the underly-737 ing soil did not freeze deeply, and the spring was mild with frequent thawing and freezing, the grain was molded by Fusarium species and other fungi that produced toxins (mostly trichothecines).
Known in Japan from the seventeenth century, a form of cardiac beriberi (Shoshin-Kakke) was shown in 1891 to be caused by eating moldy rice. In 1940 the toxin involved was identified as Citreoviridin, produced by Penicillium citreo-υiride. After World War II, a severe outbreak of a similar but different mycotoxicosis due to eating rice that had deteriorated in storage (“yellowed rice”) was recorded in Japan.
Several major mycotoxicoses of farm animals have been documented in Russia, and a few more have been reported elsewhere. Significant attention was focused on mycotoxicoses after the summer of 1960, when more than 100,000 young turkeys and other poultry died in the United Kingdom after being fed a ration containing ground peanut (Arachis hypogea) meal imported from Brazil. Cattle and pigs were also affected, and feeding experiments induced cancer of the liver in the rat. The toxin, found to be produced by strains of Aspergillus flavus, was designated aflatoxin.
At first, testing for aflatoxin was limited to animal tests using 1-day-old ducklings, which are Particularlly sensitive to the toxin, but a sensitive chemical test was soon developed.Aflatoxin was shown to be widespread in foods containing peanuts, and in parts of Africa and Asia the incidence of human liver cancer has been correlated with the intake of aflatoxin. It has not been possible, however, to legislate for aflatoxin-free peanut products because the methods of harvest and storage of peanuts in the primary peanut-producing countries are such that the introduction of the necessary changes could be effected only in the long term. The U.S. Food and Drug Administration, therefore, has set an aflatoxin tolerance of 20 parts per billion (ppb) for finished peanuts products. Interest in aflatoxicosis, because of its carcinogenic potential, is still intense. The literature on this subject is very extensive, and includes two major monographs (Goldblatt 1969; Heathcote and Hibbert 1978) and numerous reviews.
Geoffrey C. Ainsworth
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