As described above, the protoplasmic poisons are the most likely to be fatal or to cause irreversible organ damage. In the case of poisoning by the deadly Amanitas, important laboratory indicators of liver (elevated LDH, SGOT, and bilirubin levels) and kidney (elevated uric acid, creatinine, and BUN levels) damage will be present. Unfortunately, in the absence of dietary history, these signs could be mistaken for symptoms of liver or kidney impairment as the result of other causes (e.g., viral hepatitis). It is important that this distinction be made as quickly as possible, because the delayed onset of symptoms will generally mean that the organ has already been damaged. The importance of rapid diagnosis is obvious: victims who are hospitalized and given aggressive support therapy almost immediately after ingestion have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50-90% mortality rate. Table 2 provides more accurate diagnoses and appropriate therapeutic measures. A recent report indicates that amanitins are observable in urine well before the onset of any symptoms, but that laboratory tests for liver dysfunction do not appear until well after the organ has been damaged.

Specific cases of mistaken mushroom identity appears frequently. The Early False Morel Gyromitra esculenta is easily confused with the true Morel Morchella esculenta, and poisonings have occurred after consumption of fresh or cooked Gyromitra. Gyromitra poisonings have also occurred after ingestion of commercially available "morels" contaminated with G. esculenta. The commercial sources for these fungi (which have not yet been successfully cultivated on a large scale) are field collection of wild morels by semiprofessionals. Cultivated commercial mushrooms of whatever species are almost never implicated in poisoning outbreaks unless there are associated problems such as improper canning (which lead to bacterial food poisoning). A short list of the mushrooms responsible for serious poisonings and the edible mushrooms with which they are confused is presented in Table 3. Producers of mild gastroenteritis are too numerous to list here, but include members of many of the most abundant genera, including Agaricus, Boletus, Lactarius, Russula, Tricholoma, Coprinus, Pluteus, and others. The Inky Cap Mushroom (Coprinus atrimentarius) is considered both edible and delicious, and only the unwary who consume alcohol after eating this mushroom need be concerned. Some other members of the genus Coprinus (Shaggy Mane, C. comatus; Glistening Inky Cap, C. micaceus, and others) and some of the larger members of the Lepiota family such as the Parasol Mushroom (Leucocoprinus procera) do not contain coprine and do not cause this effect. The potentially deadly Sorrel Webcap Mushroom (Cortinarius orellanus) is not easily distinguished from nonpoisonous webcaps belonging to the same distinctive genus, and all should be avoided.

Most of the psychotropic mushrooms (Inocybe spp., Conocybe spp., Paneolus spp., Pluteus spp.) are in general appearance small, brown, and leathery (the so-called "Little Brown Mushrooms" or LBMs) and relatively unattractive from a culinary standpoint. The Sweat Mushroom (Clitocybe dealbata) and the Smoothcap Mushroom (Psilocybe cubensis) are small, white, and leathery. These small, unattractive mushrooms are distinctive, fairly unappetizing, and not easily confused with the fleshier fungi normally considered edible. Intoxications associated with them are less likely to be accidental, although both C. dealbata and Paneolus foenisicii have been found growing in the same fairy ring area as the edible (and choice) Fairy Ring Mushroom (Marasmius oreades) and the Honey Mushroom (Armillariella mellea), and have been consumed when the picker has not carefully examined every mushroom picked from the ring. Psychotropic mushrooms, which are larger and therefore more easily confused with edible mushrooms, include the Showy Flamecap or Big Laughing Mushroom (Gymnopilus spectabilis), which has been mistaken for Chanterelles (Cantharellus spp.) and for Gymnopilus ventricosus found growing on wood of conifers in western North America. The Fly Agaric (Amanita muscaria) and Panthercap (Amanita pantherina) mushrooms are large, fleshy, and colorful. Yellowish cap colors on some varieties of the Fly Agaric and the Panthercap are similar to the edible Caesar's Mushroom (Amanita caesarea), which is considered a delicacy in Italy. Another edible yellow capped mushroom occasionally confused with yellow A. muscaria and A. pantherina varieties are the Yellow Blusher (Amanita flavorubens). Orange to yellow-orange A. muscaria and A. pantherina may also be confused with the Blusher (Amanita rubescens) and the Honey Mushroom (Armillariella mellea). White to pale forms of A. muscaria may be confused with edible field mushrooms (Agaricus spp.). Young (button stage) specimens of A. muscaria have also been confused with puffballs.

PROTOPLASMIC POISONS

Amatoxins:

Several mushroom species, including the Death Cap or Destroying Angel (Amanita phalloides, A. virosa), the Fool's Mushroom (A. verna) and several of their relatives, along with the Autumn Skullcap (Galerina autumnalis) and some of its relatives, produce a family of cyclic octapeptides called amanitins. Poisoning by the amanitins is characterized by a long latent period (range 6-48 hours, average 6-15 hours) during which the patient shows no symptoms. Symptoms appear at the end of the latent period in the form of sudden, severe seizures of abdominal pain, persistent vomiting and watery diarrhea, extreme thirst, and lack of urine production. If this early phase is survived, the patient may appear to recover for a short time, but this period will generally be followed by a rapid and severe loss of strength, prostration, and pain-caused restlessness. Death in 50-90% of the cases from progressive and irreversible liver, kidney, cardiac, and skeletal muscle damage may follow within 48 hours (large dose), but the disease more typically lasts 6 to 8 days in adults and 4 to 6 days in children. Two or three days after the onset of the later phase, jaundice, cyanosis, and coldness of the skin occur. Death usually follows a period of coma and occasionally convulsions. If recovery occurs, it generally requires at least a month and is accompanied by enlargement of the liver. Autopsy will usually reveal fatty degeneration and necrosis of the liver and kidney.

Hydrazines:

Certain species of False Morel (Gyromitra esculenta and G. gigas) contain the protoplasmic poison gyromitrin, a volatile hydrazine derivative. Poisoning by this toxin superficially resembles Amanita poisoning but is less severe. There is generally a latent period of 6 - 10 hours after ingestion during which no symptoms are evident, followed by sudden onset of abdominal discomfort (a feeling of fullness), severe headache, vomiting, and sometimes diarrhea. The toxin affects primarily the liver, but there are additional disturbances to blood cells and the central nervous system. The mortality rate is relatively low (2-4%). Poisonings with symptoms almost identical to those produced by Gyromitra have also been reported after ingestion of the Early False Morel (Verpa bohemica). The toxin is presumed to be related to gyromitrin but has not yet been identified.

Orellanine:

The final type of protoplasmic poisoning is caused by the Sorrel Webcap mushroom (Cortinarius orellanus) and some of its relatives. This mushroom produces orellanine, which causes a type of poisoning characterized by an extremely long asymptomatic latent period of 3 to 14 days. An intense, burning thirst (polydipsia) and excessive urination (polyuria) are the first symptoms. This may be followed by nausea, headache, muscular pains, chills, spasms, and loss of consciousness. In severe cases, severe renal tubular necrosis and kidney failure may result in death (15%) several weeks after the poisoning. Fatty degeneration of the liver and severe inflammatory changes in the intestine accompany the renal damage, and recovery in less severe cases may require several months.

NEUROTOXINS

Poisonings by mushrooms that cause neurological problems may be divided into three groups, based on the type of symptoms produced, and named for the substances responsible for these symptoms.

Muscarine Poisoning:

Ingestion of any number of Inocybe or Clitocybe species (e.g., Inocybe geophylla, Clitocybe dealbata) results in an illness characterized primarily by profuse sweating. This effect is caused by the presence in these mushrooms of high levels (3- 4%) of muscarine. Muscarine poisoning is characterized by increased salivation, perspiration, and lacrimation within 15 to 30 minutes after ingestion of the mushroom. With large doses, these symptoms may be followed by abdominal pain, severe nausea, diarrhea, blurred vision, and labored breathing. Intoxication generally subsides within 2 hours. Deaths are rare, but may result from cardiac or respiratory failure in severe cases.

Ibotenic acid/Muscimol Poisoning:

The Fly Agaric (Amanita muscaria) and Panthercap (Amanita pantherina) mushrooms both produce ibotenic acid and muscimol. Both substances produce the same effects, but muscimol is approximately 5 times more potent than ibotenic acid. Symptoms of poisoning generally occur within 1 - 2 hours after ingestion of the mushrooms. An initial abdominal discomfort may be present or absent, but the chief symptoms are drowsiness and dizziness (sometimes accompanied by sleep), followed by a period of hyperactivity, excitability, illusions, and delirium. Periods of drowsiness may alternate with periods of excitement, but symptoms generally fade within a few hours. Fatalities rarely occur in adults, but in children, accidental consumption of large quantities of these mushrooms may cause convulsions, coma, and other neurologic problems for up to 12 hours.

Psilocybin Poisoning:

A number of mushrooms belonging to the genera Psilocybe, Panaeolus, Copelandia, Gymnopilus, Conocybe, and Pluteus, when ingested, produce a syndrome similar to alcohol intoxication (sometimes accompanied by hallucinations). Several of these mushrooms (e.g., Psilocybe cubensis, P. mexicana, Conocybe cyanopus) are eaten for their psychotropic effects in religious ceremonies of certain native American tribes, a practice which dates to the pre- Columbian era. The toxic effects are caused by psilocin and psilocybin. Onset of symptoms is usually rapid and the effects generally subside within 2 hours. Poisonings by these mushrooms are rarely fatal in adults and may be distinguished from ibotenic acid poisoning by the absence of drowsiness or coma. The most severe cases of psilocybin poisoning occur in small children, where large doses may cause the hallucinations accompanied by fever, convulsions, coma, and death. These mushrooms are generally small, brown, nondescript, and not particularly fleshy; they are seldom mistaken for food fungi by innocent hunters of wild mushrooms. Poisonings caused by intentional ingestion of these mushrooms by people with no legitimate religious justification must be handled with care, since the only cases likely to be seen by the physician are overdoses or intoxications caused by a combination of the mushroom and some added psychotropic substance (such as PCP).

GASTROINTESTINAL IRRITANTS

Numerous mushrooms, including the Green Gill (Chlorophyllum molybdites), Gray Pinkgill (Entoloma lividum), Tigertop (Tricholoma pardinum), Jack O'Lantern (Omphalotus illudens), Naked Brimcap (Paxillus involutus), Sickener (Russula emetica), Early False Morel (Verpa bohemica), Horse mushroom (Agaricus arvensis) and Pepper bolete (Boletus piperatus), contain toxins that can cause gastrointestinal distress, including but not limited to nausea, vomiting, diarrhea, and abdominal cramps. In many ways these symptoms are similar to those caused by the deadly protoplasmic poisons. The chief and diagnostic difference is that poisonings caused by these mushrooms have a rapid onset, rather than the delayed onset seen in protoplasmic poisonings. Some mushrooms (including the first five species mentioned above) may cause vomiting and/or diarrhea which lasts for several days. Fatalities caused by these mushrooms are relatively rare and are associated with dehydration and electrolyte imbalances caused by diarrhea and vomiting, especially in debilitated, very young, or very old patients. Replacement of fluids and other appropriate supportive therapy will prevent death in these cases. The chemistry of the toxins responsible for this type of poisoning is virtually unknown, but may be related to the presence in some mushrooms of unusual sugars, amino acids, peptides, resins, and other compounds.

DISULFIRAM-LIKE POISONING

The Inky Cap Mushroom (Coprinus atramentarius) is most commonly responsible for this poisoning, although a few other species have also been implicated. A complicating factor in this type of intoxication is that this species is generally considered edible (i.e., no illness results when eaten in the absence of alcoholic beverages). The mushroom produces an unusual amino acid, coprine, which is converted to cyclopropanone hydrate in the human body. This compound interferes with the breakdown of alcohol, and consumption of alcoholic beverages within 72 hours after eating it will cause headache, nausea and vomiting, flushing, and cardiovascular disturbances that last for 2 - 3 hours.

MISCELLANEOUS POISONINGS

Young fruiting bodies of the sulfur shelf fungus Laetiporus sulphureus are considered edible. However, ingestion of this shelf fungus has caused digestive upset and other symptoms in adults and visual hallucinations and ataxia in a child.

Many idiosyncratic adverse reactions to mushrooms have been reported. Some mushrooms cause certain people to become violently ill, while not affecting others who consumed part of the same mushroom cap. Factors such as age, sex, and general health of the consumer do not seem to be reliable predictors of these reactions, and they have been attributed to allergic or hypersensitivity reactions and to inherited inability of the unfortunate victim to metabolize certain unusual fungal constituents (such as the uncommon sugar, trehalose). These reactions are probably not true poisonings as the general population does not seem to be affected.