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Toxicity, Mushrooms - Amatoxin

Author: Douglas S Lee, MD, Attending Physician, Department of Emergency Medicine, Naples Community Hospital
Coauthor(s): Suzanne Bentley, MD, Resident Physician, Department of Emergency Medicine, Mount Sinai School of Medicine; Theodore Bania, MD, Program Director, Assistant Director of Research, Department of Emergency Medicine, Division of Toxicology, Assistant Professor, St Luke's-Roosevelt Hospital Center, Columbia University; Matthew R Denny, MD, MPH, Staff Physician, Department of Emergency Medicine, Mt Sinai Hospital
Contributor Information and Disclosures

Updated: Jun 16, 2009

Introduction

Background

The Greek poet Euripedes recorded the first documented deaths due to mushroom poisoning, or mycetismus, upon describing a family's fatal mushroom ingestion. Today, most reports of deadly mushroom ingestion come from central and Eastern Europe. Almost 50 of the more than 5000 species of mushrooms are poisonous to humans. The Amanita species are reputed to be responsible for 90% of fatal mushroom poisonings worldwide; however, Amanita poisonings are uncommon in North America and were responsible for 2 of 6 deaths caused by mushroom poisoning in a 5-year period in the United States.

<em>Amanita muscaria.</em>

Amanita muscaria.

<em>Amanita muscaria.</em>

Amanita muscaria.


Even experts can mistake Amanita phalloides, also known as the death cap, for similar-looking nontoxic mushrooms.

<em>Amanita phalloides.</em>

Amanita phalloides.

<em>Amanita phalloides.</em>

Amanita phalloides.


The mushroom has no characteristic odor or offensive taste. It is large, with a hemispherical cap 5-15 cm in diameter located on a central stem that is 8-15 cm long and 1-2 cm in diameter. The weight of an average intact mushroom is approximately 25 g. The cap is usually dry and shiny, with a light green-yellow color darkening towards the center. Gills are located under the cap and are not attached to the stem. Incomplete excavation of the entire mushroom may leave behind the vulva, or cup, at the base of the stem.

In the United States, Amanita species most commonly are found in the Pacific Northwest and the Blue Ridge Mountains of the Northeast but are becoming increasingly recognized in Pennsylvania, New Jersey, and Ohio. They tend to grow near filbert (hazelnut), chestnut, or oak trees. Peak season is late summer into fall; however, mushrooms can be found in early winter.

Pathophysiology

The clinical manifestations of an A phalloides ingestion are the result of the cyclopeptide toxins, phalloidin and amatoxin. Phalloidin causes gastroenteritislike effects 6-12 hours after initial ingestion. Phalloidin, a cyclic heptapeptide, interrupts the actin polymerization-depolymerization cycle and impairs cell membrane function. Phalloidin has limited gastrointestinal absorption, and symptoms improve within hours of supportive care.

Amanitins, primarily alpha-amanitin, are responsible for the hepatic, renal, and encephalopathic effects. Amatoxin, an octapeptide, inhibits RNA polymerase II, therefore interfering with DNA and RNA transcription. The toxin mainly affects tissues with high rates of protein synthesis, including the liver, kidneys, brain, pancreas, and testes.

About 60% of absorbed alpha-amanitin is excreted into the bile. The liver is exposed to high concentrations of toxin through the portal system and via the enterohepatic circulation. Hepatocytes are damaged early, with sparing of the hepatic sinusoids. In these cases, fatty degeneration of the hepatic parenchyma and patterns of centrilobular necrosis with hemorrhage are typical.

Amatoxin is eliminated in the urine, gastroduodenal fluids, and feces for several days after ingestion. A single gram of fresh A phalloides can yield approximately 0.2-0.4 mg of alpha-amanitin. The lethal dose is less than 0.1 mg/kg. The toxins of A phalloides are stable to cooking and remain active in dried mushrooms.

Frequency

United States

The 2003 American Association of Poison Control Centers (AAPCC) annual report lists 8,252 mushroom exposures, 60% of which were in children younger than 6 years, and species were only identified in 17% of the cases.1 Forty three of the 8,252 exposures were known to be from cyclopeptides-containing mushrooms. This is likely an underestimation due to underreporting because of the difficulty in identifying the offending agent, delayed patient presentation after ingestion, and difficulty in recognition of the symptoms of mycetismus.2

Mortality/Morbidity

In 1998, no deaths in the United States were attributed to cyclopeptides. Most mortality statistics are from Europe, where the number of victims is larger. With current therapies, mortality from A phalloides is 20-30%. In general, the mortality rate is higher in children than adults. One case series reports mortality of 51% in patients younger than 10 years. This may be due to the lower body weight of children.

Age

Mycetismus commonly is due to amateur mushroom picking or accidental ingestions by unsupervised children.

Clinical

History

Collect important information about the ingestion of wild mushrooms in patients with suspected amatoxin poisoning, which generally occurs at least 6 hours before the onset of symptoms. Attempt to determine the following:

  • Time of ingestion
  • Time of onset of symptoms
    • Phalloidin causes GI symptoms about 6-12 hours after ingestion.
    • Renal and liver toxicity caused by amanitin is evident 24-48 hours after ingestion. A recent pattern of delayed-onset renal toxic mushroom ingestion is emerging in Western North America.3
  • Description of mushrooms
  • Location at which mushrooms were obtained
  • Other mushrooms and co-ingestants: GI symptoms may occur earlier than 6 hours due to other mushrooms ingested at the same time; however, symptoms from isolated A phalloides usually begin at least 6-12 hours after the ingestion. Make efforts to identify other toxins ingested during an attempted suicide.

Toxicity from A phalloides occurs over several days and is usually divided into the following stages:

  • Stage I: Sudden onset of nausea, vomiting, watery diarrhea, and cramping abdominal pain occurs 6-12 hours after ingestion. Patients may become dehydrated and hypotensive during this episode. Patients often present during this stage, and, if misdiagnosed, may be erroneously discharged without further care.
  • Stage II: Clinical improvement occurs with supportive care. Despite the resolution of symptoms, hepatic and renal damage is ongoing, which is evident by rising laboratory test values.
  • Stage III: If discharged, patients may return to the hospital 2-6 days later with severe coagulopathy, renal failure, and encephalopathy.

Physical

The examination depends on the stage of the poisoning. Due to profuse vomiting and watery diarrhea, the patient may present in hypovolemic shock during the GI phase.

  • Vital signs
    • Tachycardia
    • Hypotension
  • Head, ears, eyes, nose, and throat: Epistaxis or scleral icterus that is related to hepatic failure may appear in a patient with delayed presentation.
  • Abdominal: The patient can have mild diffuse tenderness, and a rectal examination reveals occult bloody stool. Hepatomegaly results from hepatitis late in the course of the disease.
  • Neurologic: Effects are related to hepatic failure. Depending on the time that elapses after ingestion, the examination findings may vary from normal to agitation, somnolence, seizures, or coma.

Causes

  • Causes include ingestion by any of the following:
    • Amateur mushroom hunters seeking a fresh picked meal
    • Adults and adolescents seeking psychotropic mushrooms
    • Unsupervised children in suburban or rural areas

More on Toxicity, Mushrooms - Amatoxin

Overview: Toxicity, Mushrooms - Amatoxin
Differential Diagnoses & Workup: Toxicity, Mushrooms - Amatoxin
Treatment & Medication: Toxicity, Mushrooms - Amatoxin
Follow-up: Toxicity, Mushrooms - Amatoxin
Multimedia: Toxicity, Mushrooms - Amatoxin
References

References

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Further Reading

Keywords

amatoxin, death angel, death cap, mushroom poisoning, Amanita, Amanita species, Amanita poisoning, Amanita phalloides, A phalloides, amanitin, alpha-amanitin, mycetismus, treatment, diagnosis

Contributor Information and Disclosures

Author

Douglas S Lee, MD, Attending Physician, Department of Emergency Medicine, Naples Community Hospital
Douglas S Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Suzanne Bentley, MD, Resident Physician, Department of Emergency Medicine, Mount Sinai School of Medicine
Disclosure: Nothing to disclose.

Theodore Bania, MD, Program Director, Assistant Director of Research, Department of Emergency Medicine, Division of Toxicology, Assistant Professor, St Luke's-Roosevelt Hospital Center, Columbia University
Theodore Bania, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, New Mexico Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Matthew R Denny, MD, MPH, Staff Physician, Department of Emergency Medicine, Mt Sinai Hospital
Matthew R Denny, MD, MPH is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Michael E Mullins, MD, Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine
Michael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Emergency Physicians
Disclosure: Johnson & Johnson stock ownership None; Savient Pharmaceuticals stock ownership None

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center
Jeffrey R Tucker, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, and Massachusetts Medical Society
Disclosure: Merck Salary Employment

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

 
 
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