Among the hundreds of thousands of fungal species and the tens of thousands of those recognizable as gilled mushrooms, only about 100 would qualify as poisonous of which only about 10 are deadly. Nonetheless, poisonous mushrooms cast pallor on the consumption of fungi as food; the epithet toadstool elicits emotions that inappropriately and unfortunately associate the innocent mushroom with loathsome warty uncleanliness and therefore promotes mycophobia, the fear of fungi. The word toadstool itself has an etymology that is suggestive of Stygian origins; it is a calque word of German provenance. “Todesstuhl” means “death stool.” One reason for mycophobia is identification since many of the deadly variants are similar in appearance to those that are edible; in many cases only an expert can tell them apart and even they can make mistakes. Another reason is indication; there are no sine qua non proofs of mushroom toxicity, poisonous mushrooms do not all blacken silver spoons and do not all taste bitter, popular nostrums aside.
History has impugned the mushroom as the source of the poison that has dispatched any number of notables, among them Claudius, the fourth Roman Emperor. The perpetrator is alleged to have been his fourth wife Agrippina who wanted her son Nero to succeed to the throne in lieu of Britannicus, the son of Claudius by his third wife Messalina (who had incidentally been put to death for her part in a previous assassination attempt). The death is recounted by the philosopher Seneca the Younger in December 54, only two months after the event occurred. According to his account, it happened quite quickly, the onset of illness and death being separated only by about an hour. The idea that mushrooms were the cause is perpetrated in later writings by Tacitus, Suetonius and Dio Cassius, the latter adding a description of Agrippina serving Claudius a plate of mushrooms. The mushroom death of Claudius is almost certainly apocryphal, as deadly mushrooms are relatively slow to act; those that act rapidly generally cause gastrointestinal distress that is rarely if ever fatal.
It is more likely the case that mushroom poisoning occurs as a result of volition, the decision to consume a mushroom of dubious identification resting with the victim. There have been occasions where arrogant decisiveness has overridden caution. The most notable case is that of Johann Schobert, a composer who was employed by the Prince of Conti in Paris in the latter half of the 17th Century. He wrote harpsichord concertos, opera and sonatas that purportedly served as the basis for some of the later work by Mozart, his contemporary. Schobert may have had a talent equal to that of Mozart; we shall never know, as he succumbed to mushroom poisoning. According to the historical account, he had gathered some mushrooms in Pré-Saint-Gervais near Paris with his family and proceeded to a restaurant to have the chef prepare them. When he was told that they were poisonous, he proceeded to a second restaurant with like result. Undeterred, he went home to Paris and made mushroom soup for dinner. He was joined in death by his wife, one of his children, and a friend, a doctor; fittingly, it was the doctor who had proffered the mushroom identification in the first place.
Mushroom poisoning is generally categorized into four types according to the symptoms that result. It is not practical to use the type of toxin as a basis for classification, since there is a paucity of knowledge about the nature and chemistry of fungal toxins in general; this is particularly true for fungi whose consumption may yield an unpleasant though not fatal result. In addition, for all practical purposes, the identification of the mushroom that caused the condition under evaluation is usually a matter of conjecture since the victim has succumbed to the condition after having eaten the evidence. The four types are protoplasmic poisons, neurotoxins, gastrointestinal irritants, and those that are toxic only in combination with other substances, notably alcohol.
The protoplasmic poisons are those that destroy cells that can lead to the failure of major organs. These are the deadly mushrooms. They are mostly of one genus, the Amanita, though there are some deadly species in the genera Lepiota and Galerina. The common names of the most prominent of the Amanitas are grim evidence of their virulence: the Death Cap (A. phalloides) and the Destroying Angel (A. virosa). The common names of the mushroom of the other genera are equally foreboding: Deadly Lepiota (L. josserandii) and Deadly Galerina (G. autumnalis). The so-called Amatoxin is called amanitin, reflecting the primary generic provenance – Amanita. It is a bicyclic octapeptide, which essentially means that it is comprised of ring-shaped structures with eight peptides, compounds of amino acids. Cell destruction is incident to the inhibition of RNA polymerase; the lack of messenger RNA precludes protein synthesis. Since the liver is one of the primary areas of protein synthesis in the body, it is particularly susceptible to amanitin.
Amanitin poisoning is characterized by a long latency period ranging from about 6 to 15 hours during which there are no adverse symptoms (it is for this reason that the rapid death of Claudius is not likely of mycological origin). This is followed by symptoms that are typical of a gastrointestinal irritant: abdominal pain, vomiting, diarrhea, and dehydration. A period of apparent recovery ensues, only to be followed about a day later by a gradual deterioration that includes a loss of strength, restlessness, and jaundice, the result of irreversible liver damage. The mortality rate ranges from about 30 to 90 percent according to the amount of toxin consumed and on the age and general health of the victim.
Treatment follows diagnosis which usually depends on an evaluation of the symptoms and a knowledge of dietary history. Although there is a commercially available radioimmunoassay (RIA) test kit available, it takes about two hours to get a result; since the timeliness of treatment following poisoning is crucial, it is rarely used for initial diagnosis. If immediate and determined remedial action is taken, the mortality rate is reduced to as low as 5 percent. Inserting a stomach pump to evacuate the bile from the duodenum is crucial to the treatment, as the impairment of the kidneys causes the amanitin to be recirculated to the liver where the bile carries to the intestines, a vicious cycle. There are two other types of protoplasmic poisons that are found in mushrooms: hydrazines and orellanines. Methylhydrazine is found in the False Morel, Gyromitra esculenta; its chemistry is very similar to rocket fuel. Orellanine is found in the Sorrel webcap mushroom, Cortinarius orellanus. The symptoms of both toxins are similar to but less severe than that of amanitin.
The neurotoxins, as the name suggests, cause neurological problems which can produce symptoms that range from convulsions, hallucinations, anxiety, depression, and coma to profuse sweating and spastic colon. The most well known of the mushrooms that produce neurotoxins is the Amanita muscaria, commonly known as the Fly Agaric for its traditional use as an effective pesticide against the insect. In Eurasia, it is bright red with white cottony patches on the cap, the epitome of the forest fungus. In North America, it is less conspicuous, typically with a yellow-orange hue. It has long been noted for its mind-altering properties, having been ostensibly used for this purpose by the Koryak tribesmen of the Kamchatka peninsula and by the Norse warriors known as the berserkers. The active ingredient is ibotenic acid and its derivative muscimol, the latter having about five times the potency of the former. Ibotenic acid is an excitatory amino acid; it simulates the effects of natural transmitters on neurons in the central nervous system. The symptoms occur about an hour after ingestion and are characterized by an initial period of dizziness that may succeed to drowsiness followed by intense activity, excitement, hallucinations, and delirium. The depression-mania sequence may repeat several times in cyclic fashion before abating in a few hours. It is almost never fatal unless large quantities are ingested, as may be the case with young children infatuated with its aesthetic appeal.
The Amanita muscaria also lends its name to the other major neurotoxin, muscarine; it was first discovered incident to investigations into the chemical constituency of its namesake mushroom. Muscarine is found at levels as much as one hundred times the level in the Fly Agaric in mushrooms from the genera Inocybe (e.g. I. geophylla, or White Fiber Head) and Clitocybe (e.g. C. dealbata, or Sweating Mushroom that often grows near the edible Fairy Ring Mushroom – Marasmius oreades – and is mistakenly consumed with it). The initial symptoms of muscarine poisoning are fluid related, manifest in increased perspiration, salivation, lacrimation and urination about 15 minutes after ingestion. Follow-on symptoms include vomiting and diarrhea that continue for up to 24 hours; the administration of the antidote atropine results in rapid remission and complete recovery. Though fatalities are rare, severe cases can cause cardiac and/or respiratory arrest.
The gastrointestinal irritants are the least defined and most widespread of the mushroom toxins. Their virulence ranges from mild, short-lived stomach discomfort to vomiting and diarrhea that can last for several days. Fatalities are very rare and are usually associated with desiccation of otherwise debilitated individuals, the very young or the very old. The specific toxins are generally unknown as the need for detailed chemical analysis is mitigated by the ubiquity of the potential causes and the by the non-fatal nature of the affliction. What is known is largely anecdotal, as few cases that are traced to mushroom poisoning are reported relative to the numbers that occur. This is exacerbated by the degree to which susceptibility to specific toxins varies from one individual to the next; some people become mildly ill after eating almost any wild mushroom. Therefore, the mushrooms that are unequivocally identified with gastrointestinal distress are those that are relatively widespread and which resemble an edible species; they are therefore mistakenly consumed with some regularity. Examples include the Jack-O-Lantern (Omphalotus illudens) that closely resembles the Chanterelle (Cantharellus cibarius) and the Green-spored Lepiota (Chlorophyllum molybdites) that closely resembles the Parasol Mushroom (Macrolepiota procera).
The most peculiar of the mushroom toxins is coprine, an amino acid produced by mushrooms of the genus Coprinus, notably C. atramenarius, the Alcohol Inky. Coprine is converted to cyclopropanone hydrate in the human body. This compound interferes with the breakdown of alcohol; because of its similarity to Antabuse in blocking the oxidation of alcohol in the acetaldehyde stage, it is sometimes called a disulfiram-like toxin. The symptoms are generally mild, consisting of flushing of the head and neck, tingling of the extremities, cardiovascular disturbances such as heart palpitations, headache and nausea. It is listed in field guides as edible, with caution; it has no adverse side effects if alcohol is not consumed for about three days.
Mushroom poisoning is a complex phenomenon, the complexity a result of the variation in fungi according to geography, genetics and local environmental fluctuations; the toxic content of individual mushroom species can vary from non-existent to virulent. A contributing and no less perplexing dilemma is the variability of susceptibility; the idiosyncratic response of different individuals who consume the same mushroom can range from gustatory pleasure to violent purging. The more extreme reactions do not tend to follow the typical vectors of age or general health of the victim, but seem rather to correlate to something syllogistic to an allergic reaction; this is thought to be attributable to certain constituents of wild mushrooms that are not found in other foods, such as the sugar trehalose.
The only safeguard against mushroom poisoning is knowledge and caution; the only other option is abstinence. In order to safely eat wild mushrooms, it is necessary to be able to recognize those which are edible. But this knowledge is not sufficient to prevent a potentially unpleasant, if not life-threatening event. One must also be able to recognize the poisonous species and have the knowledge of the subtleties of taxonomy that can lead to improper identification (as was the case the composer Schobert). Michael Pollan writes of his identification problems with his first wild chanterelle. His conclusion is that: “I didn’t realize it at the time, but I had impaled myself that afternoon on the horn’s of the omnivore’s dilemma” which is that eating can be dangerous and that “when it comes to figuring out which of those things are safe to eat, he’s pretty much on his own.” One may therefore conclude that eating wild mushrooms is the quintessential Omnivore’s Dilemma (which is of course the title of the book). Caution is necessary in consumption; only a small portion should be eaten on the first occasion of any individual’s sampling of a wild mushroom. Since an adverse reaction is always possible, a smaller dose will yield a less harmful result. It is both safe and rewarding to eat wild mushrooms, if only a little care is exercised.