Mushrooms are a rich source of toxins; mushroom poisoning has increased as the result of the popularity of hunting wild mushrooms. High concentrations of muscarine are present in various species of Inocybe and Clitocybe. The symptoms of muscarine intoxication (salivation, lacrima-tion, nausea, vomiting, headache, visual disturbances, abdominal colic, diarrhea, bronchospasm, bradycardia, hypotension, shock) develop within 30-60 minutes of ingestion. Treatment with atropine (]-2 mg intramuscularly every 30 minutes) effectively blocks these effects.
Intoxication produced by Amanita muscaria and related Amanita species arises from the neurologic and hallucinogenic properties of muscimol, ibotenic acid, and other isoxazole derivatives that stimulate excitatory and inhibitory amino acid receptors. Symptoms range from irritability, restlessness, ataxia, hallucinations, and delirium to drowsiness and sedation. Treatment is mainly supportive; benzodiazepines are indicated when excitation predominates; atropine often exacerbates the delirium.
Mushrooms from Psilocybe and Panaeolus species contain psilocybin and related derivatives of tryptamine that cause short-lasting hallucinations. Gyromitra species (false morels) produce GI disorders and a delayed hepatotoxicity. The toxic substance, acetaldehyde methylformylhydra-zone, is converted in the body to reactive hydrazines. Although fatalities from liver and kidney failure have been reported, they are far less frequent than with amatoxin-containing mushrooms.
The most serious form of mycetism is produced by Amanita phalloides, other Amanita species, Lepiota, and Galerina species. These species account for >90% of fatal cases. Ingestion of as little as 50 g of A. phalloides (deadly nightcap) can be fatal. The principal toxins are the amatoxins (a- and ¡3-amanitin), a group of cyclic octapeptides that inhibit RNA polymerase II and hence block messenger RNA (mRNA) synthesis. This causes cell death, particularly in the GI mucosa, liver, and kidneys. Initial symptoms include diarrhea and abdominal cramps. A symptom-free period lasting up to 24 hours is followed by hepatic and renal malfunction. Death occurs in 4—7 days from renal and hepatic failure. Treatment is largely supportive; penicillin, thioctic acid, and silibinin may be effective antidotes, but the evidence is anecdotal.
Because the toxicity and treatment strategies for mushroom poisoning depend on the species ingested, their identification is key. Regional poison control centers in the U.S. maintain up-to-date information on the incidence of poisoning in the region and treatment procedures.
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