Introduction Toxic mushrooms found in the us may are associated with 3 major clinical syndromes: (1) early onset gastroenteritis,



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Mushroom Toxicity



Allen Repp, M.D. October 22, 2002




  1. Introduction

    • Toxic mushrooms found in the US may are associated with 3 major clinical syndromes: (1) early onset gastroenteritis, (2) delayed onset gastroenteritis and multisystem organ dysfunction, and (3) central nervous system manifestations

    • Identification of the type of mushroom ingested is often difficult or impossible, so treatment based on presenting symptomatology is advocated by many toxicologists




  1. Epidemiology

    • Approximately 10,500 mushroom exposures were reported to poison control centers in 1997, with 0.3% of cases complicated by major toxicity and only 2 deaths

      • 90% of toxic ingestions were inadvertent

      • 85% occurred in children

      • Other common scenarios included mushroom foragers mistakenly consuming toxic mushrooms, persons attempting suicide or homicide, and persons intentionally consuming mushrooms for hallucinogenic effects




  1. Early Gastroenteritis Syndromes

    • Most common manifestation of toxic mushroom ingestion

    • Mushrooms implicated:

      • Chlorophyllum molybdites (aka green-spored parasol) – common mushroom in summer in eastern and southern North America (and lawns in southern California)

      • Jack-O-Lantern – bright orange-yellow mushroom with luminescence that grows in clusters at the base or stumps of deciduous trees

      • Agaricus bisporus – common supermarket mushroom (!) can induce gastroenteritis in some susceptible individuals

    • Clinical presentation:

      • Onset of abdominal pain, cramping, diarrhea, vomiting within 2 hours of ingestion

      • Self-limited, and usually resolves within 12 hours, although may persist up to 48 hours

      • Wide variability in response to ingestion  consumption of the same meal may affect some people severely while not affecting others at all

    • Basic pathophysiology: production of heat-stable and heat-labile toxins

    • Differential diagnosis: food-borne gastroenteritis (especially with pre-formed bacterial toxins such as Staphylococcal food poisoning). Prolonged or worsening sx should raise concern for mixed mushroom ingestion

    • Treatment: Oral or IV fluid hydration with short term hospitalization required only if patient unable to tolerate oral rehydration




  1. Delayed Gastroenteritis Syndromes

    • Two major mushroom families implicated – Amanita and Gyromitra

    • Amanita species (A. phalloides, A. virosa, A. verna), aka death cap, death angel, destroying angel

      • Account for 95% of deaths due to mushrooms

      • Grow in fall throughout North America and Europe

      • Caps are usually white or green with similarly colored free gills (ending before the stem begins); stalk has a ring and becomes thicker toward the ground; the stalk terminates in a volva (a cup at the end of the stalk in the soil)

      • Pathophysiology:

        • Amatoxins = heat stable, cyclic octapeptides contained in the mushrooms

        • Absorbed through intestinal mucosa and actively transported into hepatocytes

        • In hepatocytes, alpha-amantin binds to RNA polymerase II and inhibits protein synthesis, leading to hepatocyte death

        • Undergoes enterohepatic circulation and is cleared from serum in 36 hours via biliary and renal excretion

      • Clinical Presentation: 3 Stages

        • Stage 1 (days 1-2) -- Abdominal cramping, vomiting, profuse watery diarrhea (cholera-like) starting 5-12 hours after ingestion

        • Stage 2 (days 3-5) – Symptomatic improvement, but ongoing liver damage marked by increasing transaminases and PT. Most adults recover by day 5, but up to 40% may progress to stage 3.

        • Stage 3 (days 6-) – Clinically apparent hepatic and renal injury that may progress to fulminant hepatic failure

      • Diagnosis:

        • Based on suggestive clinical and laboratory data

        • Maixner Test – to test mushroom for presence of amatoxin by applying HCl to a paper with dried juice from the mushroom in question  blue color indicates amatoxins

        • Thin-layer chromatography can be used to assay urine for amatoxin levels

        • Liver biopsy show extensive hepatic necrosis with yellow atrophy and marked fatty degeneration

      • Treament

        • Reduce absorption – gastric lavage if < 1 hour from ingestion; activated charcoal if < 24 hours after ingestion

        • Aggressive rehydration, repletion of electrolytes, and glucose (as hypoglycemia is a potentially serious complication)

        • Decrease amatoxin uptake into hepatocytes

          • High dose penicillin thought to compete for active uptake sites

          • Silibinin (silybinin) – water soluble milk thistle extract (not available in the US)

          • Charcoal hemoperfusion, if instituted within 24 hours of ingestion

        • Anti-oxidants: n-acetylcysteine and vitamin C

        • Orthotopic liver transplant

    • Gyromitra esculenta, aka false morel

      • Description: Mushroom with brown, convoluted cap and no gills that grows in spring throughout North America

      • Pathophysiology: Heat labile toxin, gyromitrin, is converted to monomethylhydrazine, a water soluble toxin identical to a form of rocket fuel

      • Clinical Presentation:

        • Abdominal pain, bloating, vomiting, diarrhea at 6-10 hours after ingestion closely followed neurologic symptoms such as weakness, dizziness, headache, confusion, seizures, muscle cramps, and lack of coordination

        • May resolve without sequelae or may progress to acute hepatic failure and renal failure

        • Hemolysis and methemoglobinemia are also classically reported

      • Diagnosis

        • Identification of mushroom by experienced mycologist

        • Gas-liquid chromatography can be used to measure hydrazines

        • Liver biopsy shows diffuse hepatocellular necrosis

        • Kidney biopsy shows severe interstitial nephritis

      • Treatment

        • Reduction of absorption, aggressive rehydration, and electrolyte and glucose repletion

        • For patients with neurologic symptoms  high dose pyridoxine (up to 25 gm/day) has been used with anecdotal success

        • For patients with methemoglobinemia  methylene blue




  1. Neurologic Syndromes

    • Mushrooms of Psilocybe family contain hallucinogen psylocybin, which inhibits serotonin activity and may quickly induce mild euphoria to frank hallucinosis

    • Inobybe and Clitocybe mushrooms contain muscarine and rapidly produces symptoms of cholinergic excess (salivation, lacrimation, diaphoresis, abdominal discomfort, vomiting)

    • Amanita muscaria contains a mixture of psychoactive and muscarinic substances




  1. Other Mushroom Syndromes

    • Disulfiram-like reactions have been reported after consumption of cooked Coprinus mushrooms

    • Delayed interstitial nephritis and renal failure from the toxin orellanine in Cortinarius orellanus

    • Rhabdomyolyis due to mycotoxin in Russula subnigricans

Beth Israel Deaconess Medical Center Residents’ Report


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