Conditions · Emergency medicine and toxicology
Mushroom poisoning (Amanita) !
Poisoning from eating wild mushrooms. Death cap (Amanita) toxins cause late vomiting and diarrhoea, followed by liver failure days later.
Updated 2026-11-01
Structures involved
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Why it happens
- Chemical (toxic) cell injury: direct and after metabolism
- α-Amanitin
- RNA polymerases I, II and III
- Liver: lobule, acinus, hepatocytes, sinusoids, Kupffer cells
What it is
Poisoning from eating toxic wild mushrooms. The most dangerous are amatoxin-containing species, mainly Amanita phalloides (death cap) and related Amanita, Galerina and Lepiota species, which destroy liver cells and can cause fulminant liver failure. Other mushrooms cause early, usually self-limited syndromes such as gastrointestinal upset, cholinergic (muscarinic) effects or hallucinations.
Who gets it
Most deaths from mushroom poisoning worldwide are caused by amatoxins. Cases cluster among foragers and migrants who confuse toxic species with edible ones they know from home. In Colombia, wild mushroom poisonings are reported to national toxicological surveillance; species such as Amanita muscaria grow in pine and eucalyptus plantations in the Andean region.
Causes
- Amatoxins (Amanita phalloides and similar species, Galerina, Lepiota): liver failure
- Muscarine (Clitocybe, Inocybe): cholinergic syndrome
- Ibotenic acid and muscimol (Amanita muscaria): agitation, delirium, hallucinations
- Psilocybin: hallucinogenic effects
- Gastrointestinal irritants: early vomiting and diarrhoea
- Orellanine (Cortinarius): delayed kidney failure
Risk factors
- Foraging and eating wild mushrooms
- Confusing toxic species with familiar edible ones
- Several people sharing the same meal
- Children eating mushrooms from gardens or fields
- Delay in seeking care because early symptoms look like gastroenteritis
Pathophysiology
Amatoxins (alpha-amanitin) are absorbed by the gut and taken up by hepatocytes, where they inhibit RNA polymerase II, stopping protein synthesis and causing cell death, mainly in the area around the central vein. They undergo enterohepatic circulation, re-exposing the liver, and are excreted by the kidneys, which can also be injured. Cooking does not destroy them. The result is a typical three-phase course: delayed gastroenteritis, a deceptive latent period, then liver failure.
Classification
- Early onset (under 6 hours): usually gastrointestinal irritants, muscarinic or hallucinogenic species; generally benign
- Late onset (over 6 hours): suggests amatoxins or orellanine; potentially lethal
- Amatoxin phases: gastrointestinal (6–24 h), latent apparent improvement (24–48 h), hepatic and renal failure (2–6 days)
Symptoms and signs
- Severe watery diarrhoea, vomiting and cramping abdominal pain starting 6 or more hours after eating
- Dehydration and low blood pressure
- Apparent improvement on the second day despite rising liver enzymes
- Jaundice, bleeding, confusion and drowsiness (liver failure)
- Reduced urine output (kidney injury)
- Muscarinic species: sweating, salivation, tearing, slow heart rate
Diagnosis
- Clinical
- Detailed history: wild mushroom ingestion, time to symptom onset, who else ate; keep leftover mushrooms or photos for identification by a mycologist. Contact the poison centre.
- Tests
- Liver enzymes, bilirubin, INR, glucose, creatinine and electrolytes every 12 hours or so; blood gas and lactate; urine amatoxin testing where available.
- Imaging
- Not needed for diagnosis; liver ultrasound only to exclude other causes.
Differential diagnosis
- Viral or bacterial gastroenteritis
- Acetaminophen toxicity
- Viral hepatitis
- Ischaemic hepatitis
- Organophosphate poisoning (for cholinergic presentations)
Goal of treatment
Restore fluid losses, reduce absorption and enterohepatic recirculation of toxin, support the liver and kidneys and refer early for transplantation if liver failure progresses.
Treatment
- Acute
- Aggressive intravenous fluids and electrolyte replacement; activated charcoal, sometimes repeated, when the patient can tolerate it.
- Medical
- Toxin-blocking therapies with limited evidence: silibinin, N-acetylcysteine and high-dose penicillin G; atropine for marked muscarinic symptoms; correction of glucose and coagulation.
- Follow-up
- Serial liver, kidney and coagulation tests and glucose; strict fluid balance. Nursing: hourly urine output, neurological checks for encephalopathy, bleeding precautions.
- Procedure
- Biliary drainage in selected cases to interrupt toxin recirculation; renal replacement therapy for kidney failure.
- Surgical
- Urgent liver transplantation for fulminant hepatic failure; early contact with a transplant centre.
Drugs for this condition
Complications
- Fulminant hepatic failure with encephalopathy and cerebral oedema
- Coagulopathy and bleeding
- Acute kidney injury
- Hypoglycaemia
- Multiorgan failure and death
Prognosis
Most patients recover with early supportive care, but amatoxin poisoning still causes deaths and some patients need liver transplantation. Delay in presentation, young age and severe coagulopathy predict a worse outcome.
Prevention
- Do not eat wild mushrooms unless identified by an expert
- No home test or folk method reliably separates toxic from edible species, and cooking does not inactivate amatoxins
Test yourself
Think of the answer, then tap the question to see it.
What timing clue suggests a deadly amatoxin mushroom poisoning?
Gastrointestinal symptoms starting more than 6 hours after eating; early-onset symptoms are usually benign.
How do amatoxins kill liver cells?
They inhibit RNA polymerase II, blocking mRNA and protein synthesis.
What is the deceptive phase of amatoxin poisoning?
A latent period on day 2 when symptoms improve while liver enzymes keep rising.
Which therapies are used for amatoxin poisoning?
Fluids, activated charcoal, silibinin, N-acetylcysteine, high-dose penicillin and, if liver failure progresses, transplantation.
Which mushroom toxin causes a cholinergic syndrome and what is its treatment?
Muscarine (Clitocybe, Inocybe), treated with atropine for marked symptoms.
Related conditions
- Acute liver failure
- Acute (viral) gastroenteritis
- Acute kidney injury
- Hepatorenal syndrome
- Acetaminophen toxicity
- Viral hepatitis
- Hypoglycaemia (including insulin-induced)
- Anticholinergic toxicity (incl. scopolamine «burundanga»)
- Organophosphate and carbamate poisoning
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Amanita Species Mushroom Poisonings — Northern California, November 2025–March 2026 (Morbidity and Mortality Weekly Report (MMWR), Centers for Disease Control and Prevention, 2026); Amanita phalloides Mushroom Poisonings — Northern California, December 2016 (Morbidity and Mortality Weekly Report (MMWR), Centers for Disease Control and Prevention, 2017).
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