Mushroom Toxicity Clinical Presentation

Updated: May 12, 2022
  • Author: B Zane Horowitz, MD, FACMT; Chief Editor: Sage W Wiener, MD  more...
  • Print


A careful patient history is the most important aspect of the diagnostic process. Without a history of ingestion, the diagnosis of mushroom poisoning is difficult, but must be considered in the differential diagnosis of liver failure and kidney failure. Although failing to obtain such a history may be inconsequential for most mushroom ingestions, it is detrimental for patients who have ingested mushrooms containing amatoxin, orellanine, or gyromitrin because the early removal of these toxins from the gastrointestinal (GI) tract may alter 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 it. If a sample mushroom is not available, questioning patients and their family about the identity of the mushroom they thought they were picking or purchasing may narrow the list of possibilities. An attempt to use an experienced mycologist to identify the mushroom directly or through photos of the mushroom should be considered in symptomatic patients.

Obtain a history of the exposure that includes the following:

  • Quantity of mushrooms ingested - Typically, the amount consumed at a meal or a single whole mushroom is sufficient to cause symptoms [13]

  • Preparation of the mushroom (eg, raw or cooked) - The effects of mushrooms vary greatly, and cooking may not alter toxicity

  • Source of the mushroom (eg, gathered outdoors or purchased via the Internet)

  • Time of ingestion

  • Any other people who may have ingested the same mushrooms

  • Symptoms noted and time to onset of symptoms after ingestion

  • Any other types of mushrooms that may have been ingested at the same meal - Since patients may mix mushrooms, symptoms from one type of mushroom may mask or overlap with symptoms from another type, thus making identification even more difficult

  • Prehospital treatment, including home remedies

  • Medications regularly taken

  • Past medical history, with a focus on arrhythmias, asthma, prostatic hypertrophy, and gastric outlet obstruction

The timing of symptom onset has long been considered crucial for differentiating life-threatening or severe mushroom poisonings from less serious ones. Milder poisonings (eg, from muscarine-containing mushrooms) typically become symptomatic early, well within 5 hours of ingestion. [3, 4, 5, 6, 24] In contrast, mushrooms from the cyclopeptide (A phalloides) or orellanine (Cortinarius) groups, which can produce hepatic and renal failure, respectively, typically do not produce symptoms until later, 6-24 hours after ingestion.

There is, however, a growing sense that mushrooms are best classified by the physiologic and clinical effects of their poisons rather than by the timing of symptom onset. The traditional time-based classification may be inadequate. Some serious mushroom syndromes develop soon after ingestion. For example, most of the neurotoxic syndromes, the Coprinus syndrome (ie, concomitant ingestion of alcohol with coprine, and most of the GI intoxications occur within the first 6 hours after ingestion. Amanita smithiana may cause vomiting in as few as 2-4 hours after ingestion and may lead to severe renal toxicity.

Ingestions most likely to require intensive medical care involve mushrooms that contain cytotoxic substances such as amatoxin, gyromitrin, norleucine, 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 necessitates 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. Finally, coprine-containing mushrooms cause severe illness only when combined with alcohol (ie, Coprinus syndrome).

Identification of mushroom

Although identification of the actual mushroom consumed is important, it is often impossible, because the mushroom in question has already been digested. Nevertheless, the attempt should be made, and to this end, descriptions of the physical characteristics of the mushroom (if available) and the circumstances in which it was obtained are valuable. Clinicians should be careful to not make decisions based on rough descriptions; involve the local Poison Center (800-222-1222), which can identify a local mycologist for identification.

When no specimen is brought in by a patient with a suspected mushroom ingestion, sending an experienced forager to the site to collect any mushrooms growing in the area might be helpful. Different types of mushrooms can be found in the same location, however, and a single sample can lead to false identification of the mushroom that was ingested. Accordingly, all possible mushrooms in the immediate vicinity of where the ingestion occurred must be considered.

When mushrooms are obtained for identification, the entire mushroom should be dug up to preserve the architecture of the bulb, stem, and cap. Individual mushrooms should be carefully placed in a dry paper bag, not a plastic or cloth bag; transporting the mushrooms in this manner minimizes destruction of their natural architecture, discoloration of their caps or gills, and premature release of their spores. The mushrooms must not be refrigerated or crushed.

Collecting the patient’s gastric contents after emesis may yield identifiable spores, but this is rarely a viable means to identification.

Remote viewing of digital images of the mushroom sent over the Internet may facilitate the identification of unknown mushrooms by mycologists. [25]

Amatoxin poisoning

Amatoxin poisoning is characterized by a latent period of 6-12 hours after ingestion (range, 6-48 hours), during which the patient is asymptomatic. However, occasional case reports have shown that some patients may present with GI symptoms earlier than 6 hours, making the differentiation between amatoxin poisoning and other benign mushroom exposure difficult. [26]

At the end of the postingestion 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 either followed by an apparent recovery phase characterized by apparent clinical improvement or rapid deterioration to fulminant liver failure.

The third phase of amanita poisoning (ie, the hepatorenal syndrome) is characterized by jaundice, coagulopathy, hypoglycemia, coma, and multiple organ dysfunction syndrome (MODS) followed by death. With early therapy, mortality may be well below 5%; however, liver transplantation has been necessary in severe liver injury. The course of amatoxin poisoning typically lasts 6-8 days in adults and 4-6 days in children in those that recover without transplantation.

Gyromitrin poisoning

The initial phases of gyromitrin poisoning resemble those of amatoxin poisoning and are characterized by a latent period of 6-10 hours after ingestion (range, 3-48 hours).

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. 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 exposure.

Hematologic, renal, and hepatic toxicities may also occur, followed by recovery. Hepatotoxicity is heralded by an elevation of transaminase concentrations, 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 patients, and death may occur in 15% of cases.

Norleucine poisoning

Amanita smithiana, a mushroom found in the northwestern region of the United States, is nephrotoxic, but it typically causes GI distress within 2-12 hours. [26] It is almost always mistaken by foragers for the edible nontoxic matsutake pine mushroom (Tricholoma magnivalere), which it closely resembles. These 2 mushrooms usually grow in the same region and are foraged for in the fall. For mushroom ingestions in the Pacific Northwest, patients who have early-onset symptoms (< 3 hours after ingestion) and remain symptomatic should be fully evaluated in a hospital with serial chemistries and renal function tests, until the mushroom identity is confirmed to be nontoxic or the patient’s condition improves. [24]

Patients with Amanita smithiana poisoning present with nausea and vomiting as early as 2-4 hours post ingestion and may demonstrate with early elevations in liver enzymes, making these cases difficult to distinguish clinically from toxicity due to the amatoxin-containing mushrooms. The liver function abnormalities typically resolve over 48 hours, while the creatinine climbs at a linear rate of approximately 2 mg/dL/day.

Other mushrooms that contain norleucine toxin are Amanita proxima (France and Spain), Amanita abrupta, Amanita solitaria, and Amanita pseudoporphyria (Japan). Amanita 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 ingestion.

Psilocybin poisoning

After ingestion of psilocybin-containing mushrooms, 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

Muscarine 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 and muscimol poisoning

Symptoms of ibotenic acid and muscimol poisoning generally occur within 1-2 hours of mushroom ingestion. In children, ibotenic-acid (glutaminergic) effects may predominate, including hyperactivity, excitability, illusions, delirium, and convulsions. In adults, muscimol (gamma-aminobutyric acid [GABA]-ergic) effects may predominate, including drowsiness, dysphoria, and vertigo (sometimes accompanied by sleep).

Periods of drowsiness may be interspersed 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. Patients may develop symptoms if an alcoholic beverage is consumed within hours of ingestion of the mushroom. Rarely, symptoms may develop upon drinking ethanol up to 48-72 hours after the mushroom is eaten. Symptoms that develop within 0.5-2 hours after ingesting ethanol include headache, nausea, vomiting, flushing, chest pain, and diaphoresis (as is typical of the disulfiram syndrome) and may last for 2-3 hours.

Miscellaneous GI poisons

Many toxic mushrooms produce symptoms that are similar to those caused by the deadly protoplasmic poisons. Some 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; they are especially likely to occur in debilitated, very young, or very old patients. Replacement of fluids and other appropriate supportive measures prevent death in these cases.

Paxillus syndrome may occur after the ingestion of Paxillus 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 (eg, Lycoperdon). 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.

Erythromelalgia syndrome is characterized by onset of painful allodynia in the hands about 3-7 days after ingestion and may persist for months. The mushroom Clitocybe acromelalga (Poison Dwarf Bamboo Mushroom) in Japan and the mushroom Clitocybe amoenolens in Alpine areas of Europe cause this syndrome through acromelic acid, which stimulates glutamergic receptors. [20]


Physical Examination

The physical findings depend on the type of mushroom ingested.

Gyromitrin poisoning may cause cyanosis due to methemoglobinemia and occasionally may occur after an intravenous (IV) injection of psilocybin.

Facial flushing may be a manifestation of anticholinergic poisoning and may be noted in a patient’s coprine-related disulfiramlike reaction. Profuse sweating and facial flushing are prominent features of muscarinic poisoning and should raise suspicion of this condition. [13, 14]

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 observed 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; reflex tachycardia has also been observed in this setting, though less commonly.

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.


A few of the toxic mushrooms may exhibit a known toxidrome, the recognition of which permits early diagnosis and treatment.

Patients with muscarine poisoning may present early with a characteristic cholinergic toxidrome. The acronyms SLUDGE (salivation, lacrimation [with blurred vision and miosis], urinary frequency, diarrhea, GI distress, and emesis) and DUMBBELS (diarrhea, urinary frequency, miosis, bradycardia, bronchorrhea, emesis, lacrimation, and salivation) are potentially useful memory aids for this syndrome.

An anticholinergic syndrome may occur with the ingestion of hallucinogenic mushrooms. Such a syndrome is characterized by fever, tachycardia, agitation, hallucination, hypertension, skin flushing, dry mucous membranes, mydriasis, and blurred vision.

Patients with muscimol-induced GABA-ergic 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. Muscarine does not directly cause central nervous system (CNS) symptoms, because it is an ionized quaternary amine and is incapable of crossing the blood-brain barrier. The dizziness and headache occasionally experienced by patients poisoned with muscarine are the consequence of the peripheral cardiovascular and respiratory effects of the toxin.

GI symptoms and hepatotoxicity

Early onset of GI symptoms (eg, cramps, vomiting, and increased bowel activity) and diarrhea (rarely) leading to dehydration commonly occurs with the ingestion of nonlethal toxic mushrooms (eg, those containing muscarine).

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.



Complications of mushroom toxicity include the following:

  • Respiratory – Aspiration pneumonia may occur with mushroom poisonings and involves loss of airway protective reflexes

  • Neurologic – Convulsions are common in gyromitrin poisoning, but they also may be due to hypoxia, acidosis, and metabolic abnormalities; cerebral edema may be a complication of hypoxia, acidosis, trauma, and hepatic failure

  • Hepatic – Fulminant hepatic failure (FHF) is a complication of amatoxin and gyromitrin poisonings; hypoglycemia, in turn, is a common complication of hepatic failure caused by poisoning with gyromitrin or amatoxin

  • Renal – Kidney failure is a common complication of norleucine and orellanine poisoning but also may be due to hypoperfusion and shock and may be part of the hepatorenal syndrome

  • Hematologic – Methemoglobinemia may complicate gyromitrin poisoning; hemolysis may complicate gyromitrin poisoning

  • Trauma may complicate hallucinogenic mushroom poisoning

  • Hypovolemia and electrolyte disturbances may complicate any mushroom poisoning