Introduction
Background
Mushrooms are the fruiting bodies of a group of higher fungi that have evolved contemporaneously with plants for millions of years. Mushrooms are widely distributed throughout the world, and thousands of species have been identified.
About 100 species of mushrooms are poisonous to humans, and 15-20 mushroom species are lethal when ingested. No simple rule exists for distinguishing edible mushrooms from poisonous mushrooms. In more than 95% of mushroom toxicity (mushroom poisoning) cases, poisoning occurs as a result of misidentification of the mushroom by an amateur mushroom hunter. In fewer than 5% of the cases, poisoning occurs after the mushroom is consumed for its mind-altering properties.
The severity of mushroom poisoning may vary depending on the geographic location where the mushroom is grown, growth conditions, the amount of toxin delivered, and the genetic characteristics of the mushroom. Boiling, cooking, freezing, or processing may not alter the mushroom's toxicity. Variations in clinical effects may depend on an individual's susceptibility and on the presence of confounding factors such as contamination and/or co-ingestion. In general, children, older persons, and persons with disabilities are at a higher risk of developing serious complications with mushroom poisoning than are healthy young adults.
Pathophysiology
Mushroom poisoning occurs after the ingestion of toxins synthesized by the mushrooms themselves. Each poisonous mushroom species contains 1 or more toxins, which may be classified based on the mushroom's physiologic and clinical effects in humans, the target organ toxicity, and the time to symptom onset. The clinical spectrum and toxicity vary with the species consumed, the amount consumed, the season, the geographic location where the mushroom was grown, the preparation method, and an individual's response to the toxins.
Having reviewed the world's scientific literature on mushroom poisoning published from 1951-2002, Diaz classified mushroom poisoning into 3 major categories, depending on the time-to-symptom development.1 These categories include the following:
- Early symptom category: Symptoms generally appear within the first 6 hours of mushroom ingestion and include GI, allergic, and neurologic syndromes.
- Late symptom category: Signs and symptoms begin to appear between 6 and 24 hours after ingestion and may include hepatotoxic, nephrotoxic, and erythromelalgic syndromes.
- Delayed symptom category: Symptoms appear more than 24 hours after ingestion and include mostly nephrotoxic syndromes.
Mushroom toxins include the following:
- Cyclopeptides (ie, amatoxins, phallotoxins, virotoxins)
- Gyromitrins
- Orellanine
- Muscarine
- Psilocybin
- Muscimol/ibotenic acid
- Coprine
- Direct central neurotoxins
- Nephrotoxins
- Myotoxins
- Immunoactive toxins
- Hemolytic toxins
- GI irritants
In Japan, a recent outbreak of acute encephalopathy was noted among patients with renal dysfunction after eating autumn mushrooms.
GI poisons are the most frequently encountered mushroom toxins. Amatoxins, gyromitrins, and orellanine are the most commonly implicated toxins in fatal mushroom poisonings worldwide. The amatoxins and gyromitrins are hepatotoxic. Gyromitrins are also epileptogenic. Orellanine is nephrotoxic. Muscarine, psilocybin, muscimol, and ibotenic acid are nervous system poisons. Coprine causes a disulfiramlike reaction when combined with alcohol.
- Cyclopeptides
- These include amatoxins (high toxicity), phallotoxins (medium toxicity), and virotoxins (no toxicity).
- Amatoxins, which are responsible for more than 95% of mushroom-related fatalities in the United States, are cyclic octapeptides that are synthesized by a number of Amanita species and several of their relatives, including some members of the Galerina, Lepiota, and Conocybe genera.
- At least 5 subtypes of amatoxins are known, the 2 most significant being the alpha-amatoxin, which inhibits RNA polymerase II and protein synthesis, and the beta-amatoxin. Alpha-amatoxin and beta-amatoxin are rapidly absorbed by the GI tract, have limited protein binding, and may undergo enterohepatic recirculation. Both are excreted in the urine and may be detected in the vomitus and feces.
- Hepatocellular damage is presumably caused by the formation of free radical intermediates.
- Amanita phalloides (death cap), Amanita virosa (destroying angel), Amanita verna (fool's mushroom), and Galerina autumnalis (autumn skullcap) are the best known and the deadliest amatoxin-containing mushrooms.
Amanita phalloides.
- Gyromitrins
- Gyromitrin is a volatile hydrazine derivative synthesized by certain species of false morel (ie, Gyromitra esculenta, Gyromitra ambigua, Gyromitra gigas, Gyromitra infula) and early false morel (Verpa bohemica). Gyromitrin poisoning typically occurs after ingestion of the toxin-containing mushrooms but may also result from inhalation of the cooking vapors during their preparation.
- In the stomach, gyromitrin is rapidly hydrolyzed into acetaldehyde and N -methyl-N -formyl hydrazine (MFH), which is then slowly converted to N -methylhydrazine (MH). Both MFH and MH are toxic to humans. MFH inhibits a number of hepatic systems, including the cytochrome P-450 and glutathione, and causes hepatic necrosis. Hepatocellular damage is presumably caused by the formation of free radical intermediates. MH inhibits pyridoxine kinase and interferes with all the pyridoxine-requiring enzymes in the body, including those involved in the synthesis of GABA. The reduction of GABA in the brain leads to CNS hyperexcitability and convulsions. Gyromitrin ingestion may also result in methemoglobinemia, hemolysis, and renal failure.
- Orellanine
- Orellanine is a nephrotoxic compound that is synthesized by a number of species of the Cortinarius mushrooms. Orellanine-containing mushrooms include Cortinarius orellanus (webcap) and Cortinarius speciosissimus, both of which are commonly found in Europe and Japan but not in North America. North American Cortinarius species that contain orellanine include Cortinarius gentilis, Cortinarius callisteus, Cortinarius rainierensis, and Cortinarius splendens. The gentilis species is most commonly implicated in orellanine poisoning in the United States.
- Orellanine is colorless and crystalline in nature and may be converted into orelline, which itself may be toxic. Its main effects are on the renal tubular system, where it causes necrosis with relative sparing of the glomerular apparatus. Fatty degeneration of the liver and severe inflammatory changes in the intestine may accompany the renal damage. The Cortinarius mushrooms also may elaborate other compounds, such as cortinarin A, B, and C, which exhibit a nephrotoxic potential in laboratory animals.
Other mushrooms such as Amanita smithiana and Amanita proxima have also been associated with an acute oliguric renal failure that requires temporary hemodialysis. Norleucine has been identified as the nephrotoxin found in A smithiana that causes renal tubular damage.
- Psilocybin: Psilocybin and psilocin are elaborated by a number of mushroom genera, including Psilocybe, Panaeolus, Gymnopilus, Copelandia, Conocybe, Psathyrella, and Pluteu. Psilocybin and psilocin are serotonin (5-HT2) agonists and, when ingested, cause psychedelic effects similar to those of lysergic acid (LSD).
- Ibotenic acid/muscimol: Amanita muscaria (fly agaric) and Amanita pantherina (panthercap) mushrooms synthesize ibotenic acid and muscimol, which are hallucinogenic. Ibotenic acid is structurally similar to glutamic acid and acts as an agonist at the glutamic acid receptors in the CNS. Ibotenic acid may also be decarboxylated in vivo to muscimol, thus increasing the muscimol effect of the mushroom. Muscimol is structurally similar to GABA and acts as a GABA-receptor agonist. These mushrooms also contain significant amounts of anticholinergic substances and small amounts of muscarine.
- Muscarine: Muscarine is a quaternary amine that is elaborated by a number of Inocybe and Clitocybe mushroom species. Muscarine stimulates the peripheral muscarinic nervous system without affecting nicotinic cholinergic activity in the CNS. Ingestion of mushrooms with high concentrations of muscarine, such as Clitocybe dealbata (sweater mushroom) and Inocybe geophylla, results in muscarine poisoning.
- Coprine: A few species of mushrooms, including the Coprinus atramentarius (inky cap) mushroom, produce coprine, an amino acid that is metabolized to 1-aminocyclopropanol in the human body. This metabolite blocks acetaldehyde dehydrogenase, and, in the presence of alcohol, acetaldehyde builds up, resulting in a disulfiram reaction. The effects of 1-aminocyclopropanol may last as long as 72 hours after ingestion of the mushroom.
- Involutin: Ingestion of Paxillus involutus may result in an acute onset of abdominal pain, nausea, vomiting, and diarrhea within 30 minutes to 3 hours of ingestion, followed by an immune complex-mediated hemolytic anemia with hemoglobinuria, oliguria, anuria, and acute renal failure.
- Lycoperdon-associated pneumonitis: An immune reaction is believed to be the cause of the bronchoalveolar allergic syndrome, which is seen after inhalation of spores of some puffball mushroom species.
- GI toxins: Hundreds of mushrooms contain toxins that can cause GI symptoms (eg, nausea, vomiting, diarrhea, abdominal pain) similar to those observed with more dangerous mushrooms. They include Chlorophyllum molybdates (green gill), Omphalotus illudens (jack-o'-lantern), Boletus piperatus (pepper bolete), and Agaricus arvensis (horse mushroom), among many others.
Frequency
United States
Accidental poisonings tend to occur most commonly in the spring and fall, when mushroom species are at the peak of their fruiting stage.
In general, most ingestions result in minor GI illness, with only the most severe requiring medical attention. Because the number of unreported cases is unknown, accurate figures regarding the frequency of mushroom poisoning are difficult to obtain. Cases usually are sporadic, and a few outbreaks have been reported.
In the American Association of Poison Control Centers National Poison Data System 2007 Annual Report, 7351 mushroom exposures were reported in the United States, with 2634 treated in a health care facility and no fatalities.2
International
Mushroom foraging is common in Russia and Europe; however, accurate figures regarding the incidence of mushroom toxicity (mushroom poisoning) are difficult to obtain. Outbreaks of severe mushroom poisoning have occurred in Europe, Russia, the Middle East, and the Far East. In April of 2008, an outbreak of mushroom poisonings in the Upper Assam part of India claimed more than 30 lives.
Mortality/Morbidity
Morbidity and mortality rates depend on the patient's age and general health. Children and elderly persons are at the greatest risk for toxicity. Rapid diagnosis and treatment also significantly alter mortality rates. In the case of amatoxins, the mortality rate, which has been quoted to be 50-60%, may be reduced to well below 10%. Of the 7351 single mushroom exposures reported to US poison control centers in 2007, 35 major outcomes occurred, and no deaths were reported.2
Age
Children and elderly patients are at the greatest risk for toxicity. In a report by the North American Mycological Association (NAMA) Case registry, mushroom toxins may also be transferred to nursing infants through mothers' milk.3 According to the American Association of Poison Control Centers National Poison Data System 2007 Annual Report, 4543 out of 7351 total single mushroom exposures were reported in those younger than 6 years; 1352 mushroom exposures were reported in individuals aged 6-19 years, and 1189 were reported in individuals older than 19 years.2
Clinical
History
Patient history is the most important aspect of the diagnosis. Without eliciting a history of ingestion, the diagnosis of mushroom poisoning cannot be made. Although this may be inconsequential for most mushroom ingestions, it is detrimental for mushrooms containing amatoxin, orellanine, and gyromitrin because the early removal of these toxins from the GI tract drastically alters the outcome of the case. Every effort should be made to identify the mushroom or mushrooms early. If a sample mushroom is available, use of telemedicine and the Internet may prove valuable in identifying the mushroom. If a sample mushroom is not available, questioning patients and their family about the identity of the mushroom they thought they were picking may narrow the list of possibilities.
The history also should include (1) the time of ingestion, (2) time to onset of symptoms, (3) the amount of mushrooms ingested, (4) whether other people ingested the same mushrooms, and (5) whether the meal included other mushroom species. Because patients often mix mushrooms, symptoms from one type of mushroom may mask or overlap with symptoms from another type of mushroom, thus making identification even more difficult.
Mushrooms are best classified by the physiologic and clinical effects of their poisons. The traditional time-based classification of mushrooms into an early/low toxicity group and a delayed/high toxicity group may be inadequate. Additionally, many mushroom syndromes develop soon after ingestion. For example, most of the neurotoxic syndromes, the Coprinus syndrome (ie, concomitant ingestion of alcohol and coprine), the immunoallergic and immunohemolytic syndromes, and most of the GI intoxications occur within the first 6 hours after ingestion.
Ingestions most likely to require intensive medical care involve mushrooms that contain cytotoxic substances such as amatoxin, gyromitrin, and orellanine. Mushrooms that contain involutin may cause a life-threatening immune-mediated hemolysis with hemoglobinuria and renal failure. Inhalation of spores of Lycoperdon species may result in bronchoalveolitis and respiratory failure that requires mechanical ventilation.
Mushrooms that contain the GI irritants psilocybin, ibotenic acid, muscimol, and muscarine may cause critical illness in specific groups of people (eg, young persons, elderly persons). Hallucinogenic mushrooms may also result in major trauma and require care in an intensive care setting. Lastly, coprine-containing mushrooms cause severe illness only when combined with alcohol (ie, Coprinus syndrome).
- Amanita poisoning
- Poisoning is characterized by a latent period of 6-12 hours after ingestion (range 6-48 h), during which the patient is asymptomatic.
- At the end of this latent period, a sudden and severe gastroenteritislike illness phase occurs. The patient experiences abdominal pain, vomiting, and profuse watery diarrhea, which may lead to severe dehydration, electrolyte abnormalities, and, rarely, circulatory collapse in young and elderly persons. This phase, which may last as long as 2-3 days, is followed by an apparent recovery phase characterized by an apparent clinical improvement; however, an asymptomatic rise in hepatic enzyme levels signifies the onset of hepatic necrosis.
- The third phase of amanita poisoning, ie, the hepatorenal syndrome, is characterized by jaundice, hypoglycemia, coma, and multiorgan and system failure followed by death in 50-90% of patients. With therapy, mortality may be well below 10%. The course of amatoxin poisoning typically lasts 6-8 days in adults and 4-6 days in children.
- Gyromitrin poisoning
- The initial phases of poisoning resemble those of amatoxin poisoning and are characterized by a latent period of 6-10 hours after ingestion (range 3-48 h).
- At the end of this latent period, the patient experiences a sudden onset of headache, abdominal cramping, vomiting, and diarrhea, which are generally self-limited. In patients who are young, elderly, or who are undergoing isoniazid therapy, this phase may be followed by monomethylhydrazine-related CNS symptoms such as vertigo, delirium, convulsions, and coma. If the toxin has been inhaled, the first phases are usually bypassed and the patient may exhibit CNS toxicity within 2 hours of the exposure. Hematologic, renal, and hepatic toxicities may also occur, followed by recovery. Hepatotoxicity is heralded by an elevation of transaminase levels, followed by signs and symptoms of hepatic insufficiency, and, rarely, death.
- Recovery typically begins 2 days after the onset of symptoms but may last as long as 5 days. In a small number of patients, the course may be fulminant, accounting for a 2-4% mortality rate.
- Orellanine poisoning: Poisoning begins with a seemingly minor GI illness characterized by mild nausea, vomiting, and, sometimes, diarrhea lasting 24-48 hours after ingestion. This phase is followed by a prolonged latent period lasting from 3 days to 3 weeks. An intense thirst and polyuria herald renal failure. The patient also may experience headaches, myalgias, muscle cramps, loss of consciousness, and convulsions. Dialysis may be required in as many as 50% of the patients, and death may occur in 15% of the cases.
- Psilocybin poisoning: The onset of hallucinations is usually rapid, and the effects generally subside within 2 hours. Poisoning by these mushrooms is 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, in whom large doses may cause hallucinations accompanied by fever, convulsions, coma, and death.
- Muscarine poisoning: Poisoning is characterized by increased salivation, perspiration, and lacrimation within 15-30 minutes of mushroom ingestion. With large doses, patients may experience abdominal pain, severe nausea, diarrhea, blurred vision, and labored breathing. Intoxication generally subsides within 2 hours. Death is rare but may result from cardiac or respiratory failure in severe cases.
- Ibotenic acid/muscimol poisoning: Symptoms generally occur within 1-2 hours of mushroom ingestion. In children, ibotenic-acid effects (glutaminergic) may predominate. These effects include hyperactivity, excitability, illusions, delirium, and convulsions. In adults, muscimol GABAergic effects may predominate and include drowsiness, dysphoria, and vertigo (sometimes accompanied by sleep). Periods of drowsiness may alternate between periods of hyperactivity and periods of delirium. Symptoms generally last for 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 as long as 12 hours.
- Coprine poisoning: The digestion of coprine-containing mushrooms generates a metabolite that inhibits acetaldehyde dehydrogenase. Therefore, these mushrooms cause symptoms to occur only when alcoholic beverages are consumed within 2 hours of ingestion. Symptoms include headache, nausea, vomiting, flushing, chest pain, and diaphoresis typical of the disulfiram syndrome and may last for 2-3 hours.
- Miscellaneous GI poisons: Many toxic mushrooms (poisonous mushrooms) produce symptoms that are similar to those caused by the deadly protoplasmic poisons. Some mushrooms may cause vomiting, diarrhea, or both that last for several days. Fatalities caused by these mushrooms are rare and are due to dehydration and electrolyte imbalances caused by diarrhea and vomiting; fatalities occur especially in debilitated, very young, or very old patients. Replacement of fluids and other appropriate supportive therapy prevents death in these cases.
- Paxillus syndrome may occur following the ingestion of P involutus. This syndrome begins with gastroenteritislike symptoms within 3 hours of ingestion, followed by an acute hemolytic anemia with hemoglobinuria and renal failure.
- Bronchoalveolar allergic syndrome may follow the inhalation of spores of puffball mushroom species. This syndrome begins with a nasopharyngitis, which is followed by worsening respiratory symptoms, including dyspnea, cough, fever, and malaise, which may progress to respiratory failure.
- A proxima toxicity is characterized by a latent phase that lasts 12-24 hours, followed by an initial gastroenteritislike illness, with nausea, vomiting, and diarrhea. Oliguric renal failure occurs several days after the ingestion.
- A smithiana toxicity, which begins 30 minutes to 12 hours after the ingestion, is characterized by nausea, vomiting, diarrhea, malaise, and dizziness and is followed by oliguric renal failure. This mushroom has also been associated with hepatotoxicity.
Physical
The physical findings depend on the type of mushroom ingested.
- Cyanosis may be secondary to hypoxia from any cause but may occur with gyromitrin poisoning. Gyromitrin poisoning causes methemoglobinemia and, occasionally, may occur after an intravenous injection of psilocybin.
- Facial flushing may be a manifestation of anticholinergic poisoning and may be noted in a patient's coprine-related disulfiram (Antabuse) reaction.
- Jaundice may be observed in patients with liver failure due to gyromitrin and amatoxin poisoning. Jaundice may also be a manifestation of hemolysis, rarely seen with Paxillus ingestion.
- Fever may be seen with psilocybin and muscimol poisonings.
- Tachycardia is nonspecific, may be seen with any of the mushrooms, or may be a manifestation of hypoxia or hypovolemia from any cause.
- Bradycardia may be a manifestation of muscarine poisoning.
- Mydriasis is commonly observed with ingestion of mushrooms that contain psilocybin and muscimol (because they also contain anticholinergic substances).
- Miosis is observed with toxicity caused by muscarine-containing mushrooms.
- Toxidromes
- A few of the toxic mushrooms may exhibit a known toxidrome, permitting early diagnosis and treatment. A cholinergic toxidrome may occur with mushrooms that contain muscarine. Patients present early with a so-called SLUDGE (salivation, lacrimation [with blurred vision and miosis], increased urinary frequency, diarrhea, GI distress, emesis) reaction. Severe poisoning may also result in cardiotoxicity manifested as bradycardia and hypotension. In addition, severe bronchorrhea may lead to respiratory failure.
- An anticholinergic syndrome may occur with the ingestion of hallucinogenic mushrooms. An anticholinergic syndrome is characterized by fever, tachycardia, agitation, hallucination, hypertension, skin flushing, dry mucous membranes, mydriasis, and blurred vision.
- Patients with muscimol-induced GABAergic syndrome present with lethargy, ataxia, dysarthria, sleep, and coma.
- A glutaminergic syndrome may be seen with ibotenic acid poisoning and presents with hallucinations, hyperactivity, ataxia, myoclonic jerks, and convulsions.
- Because several mushrooms contain both muscimol and ibotenic acid, their ingestion generally results in alternating excitatory and inhibitory symptoms.
- Central nervous system
- Hallucinations may be caused by poisoning from mushrooms that contain muscimol, ibotenic acid, psilocybin, and psilocin.
- Convulsions may be secondary to hypoxia and shock but may also be caused by poisoning from mushrooms that contain gyromitrin, psilocybin, and isoxazole.
- Coma may be secondary to hypoxia, hypoglycemia, and hypovolemia but may also be caused by hepatic encephalopathy due to poisoning with amatoxin and gyromitrin.
- Muscle fasciculations are commonly observed in poisoning from mushrooms that contain muscarine.
- Gastrointestinal symptoms and hepatotoxicity
- Early onset of GI symptoms and diarrhea (rarely) leading to dehydration commonly occurs with the ingestion of nonlethal toxic mushrooms.
- Delayed GI symptoms, with vomiting and profuse diarrhea leading to shock, may occur with the ingestion of mushrooms that contain amatoxins and gyromitrins. These mushrooms are also hepatotoxic and may result in fulminant hepatic failure. Hepatomegaly and hepatic tenderness may signal the onset of hepatic failure and may be followed by encephalopathy, coma, bleeding, diatheses, cerebral edema, hepatorenal syndrome, and death.
Causes
Accidental poisoning accounts for more than 95% of the cases of mushroom intoxications and generally is due to the ingestion of a misidentified species of mushroom. Misidentification occurs despite significant variations between the species because they exhibit enough similarities to confuse the inexperienced mushroom hunter. The remaining cases are due to the intentional ingestion of the mushrooms for their mind-altering properties.
- Cyclopeptide poisoning commonly is due to Amanita species (ie, bisporigera, ocreata, phalloides, tenuifolia, virosa, verna) and Galerina species (ie, autumnalis, marginata, venenata). Less commonly, poisoning is due to Amanita species (ie, hygroscopica, suballiacea, verum), Clitocybe species (ie, cerrusata, dealbata, illudens), Galerina species (ie, badipes, beinrothii, fasciculata, micolor, sulciceps), Lepiota species (ie, brunneoincartata, citrophylla, clypeolarioides, heimii, helveola, josserandii, pseudohelveola, rufescens, subincarnata), Omphalotus olearius, and Pholiotina filaris.
- Monomethylhydrazine poisoning commonly is due to Gyromitra species (ie, ambigua, esculenta, infula). Also included in this group are the following Gyromitra species: brunnea, californica, caroliniana, fastigiata, and gigas.
- Orellanine poisoning is commonly due to C orellanus, Cortinarius speciosissimus, C gentilis, Cortinarius splendens, Cortinarius venenosus, and C rainierensis. Amanita Smithiana was once thought to contain orellanine, but the nephrotoxin in this species is in fact not known.
- Psilocybin and psilocin poisoning commonly are due to many Psilocybe species (ie, pelliculosa, semilenciata, caerulipes, cubensis), among others, but it also may be due to the ingestion of many Panaeolus species, some Amanita species, some Gymnopilus species (ie, spectabilis), and some Stropharia species. Psathyrella foenisecii and Psathyrella sepulchlaris are also common causes of psilocybin intoxication.
- Ibotenic acid and muscimol poisonings are commonly due to Amanita species (ie, A gemmata, A muscaria, A pantherina, A cokeri). Panaeolus campanulatus and Tricholoma muscarium also contain isoxazole derivatives.
- Muscarine poisoning is commonly due to Clitocybe species (ie, dealbata, dilatata, illudens, nebulens). Most Inocybe species also contain muscarine and may result in muscarinelike symptoms. Additionally, some Amanita species (ie, A muscaria, A gemmata, A pantherina, A parcivolvata) and some Boletus species contain muscarine, along with other toxins.
- Coprine poisoning is commonly due to ingestion of Coprinus mushrooms, including C atramentarius (inky cap), Coprine comatus, Coprine insignis, and Coprine micacius. Clitocybe clavipes may also contain coprine and cause a disulfiramlike reaction if ingested with alcohol.
- Immunoallergic reactions resulting in hemolysis, hemoglobinuria, and immune-complex mediated renal failure have occurred after the ingestion of P involutus.
- A large number of mushrooms cause GI symptoms when ingested by humans. These include species of most of the "little brown mushrooms," ie, from the genera Agaricus, Entoloma, Gomphus, Hebeloma, Lactarius, Lepiota, Lycoperdon, Pholiota, Polyporus, Ramaria, Russula, and Tricholoma. Additionally Chlorophyllum species (ie, esculentum, molybdates), Clitocybe nebularis, Laetarius species, P involutus, and many Amanita species cause GI irritation only. In Europe, P involutus has been reported to cause severe illness and death due to a Paxillus syndrome, which is characterized by abdominal cramps, diaphoresis, icy cold extremities, weakness, loss of consciousness, and circulatory collapse.
- Allergic bronchoalveolar syndrome results from the inhalation of spores of many Lycoperdon (puffball) species.
- Rhabdomyolysis with renal failure has been reported after the ingestion of Tricholoma species in France and Russula subnigricans in Taiwan.
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Further Reading
Keywords
mushroom toxicity, mushroom poisoning, mycetism, toadstool poisoning, amatoxins, gyromitrins, orellanine, muscarine, psilocybin, muscimol/ibotenic acid, coprine, general GI irritants, neurotoxins, nephrotoxins, myotoxins, phallotoxins, virotoxins, destroying angel, autumn skullcap, Amanita phalloides, Amanita virosa, Amanita verna, Galerina autumnalis, false morel, Gyromitra esculenta, Gyromitra ambigua, Gyromitra gigas, Gyromitra infula, early false morel, Verpa bohemica, webcap, Cortinarius orellanus, Cortinarius speciosissimus, Cortinarius gentilis, Cortinarius callisteus, Cortinarius rainierensis, Cortinarius splendens, Amanita proxima, fly agaric, panthercap, Amanita muscaria, Amanita pantherine, Psilocybe, Panaeolus, Gymnopilus, Copelandia, Conocybe, Psathyrella Pluteus, sweater mushroom, Clitocybe dealbata, Paxillus involutus, green gill, Chlorophyllum molybdates, jack-o'-lantern, Omphalotus illudens, pepper bolete, Boletus piperatus, horse mushroom, Agaricus arvensis
