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Toxicity, Mushroom - Amatoxin

Author: Andrew K Chang, MD, Associate Professor, Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center
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Updated: Nov 9, 2009

Introduction

Background

Of more than 5000 species of mushrooms in the United States, approximately 100 are poisonous, and less than a dozen are deadly.

Most fatalities resulting from mushroom ingestion are associated with amatoxins within the mushrooms. Amatoxins (cyclic octapeptides) represent 1 of 3 major groups of cyclopeptides (in addition to phallotoxins and virotoxins) and are heat-stable, insoluble in water, and not destroyed by drying. At least 5 subtypes of amatoxins exist; alpha and beta amatoxins are the most significant subtypes.

Alpha amatoxin inactivates RNA polymerase II and inhibits protein synthesis, which ultimately leads to cell death. Amanita toxins are found in several Amanita species (A phalloides, A bisporigera, A hygroscopia, A ocreata, A suballiacea, A tenuifolia, A verna, A virosa) and some members of the genera Galerina (G autumnalis, G marginata, G venenata) and Lepiota (L brunneoincarnata, L chlorophyllum, L helveola, L josserandii). Even experienced mushroom pickers may mistake death cap (Amanita phalloides), which is generally considered the most toxic of the world's cyclopeptide-containing mushrooms, for one of its benign cousins.

Pathophysiology

Amatoxin poisoning can be divided into 3 stages.

• Amatoxin poisoning has a characteristic latent period of 6-12 hours postingestion before onset of clinical symptoms. After this asymptomatic period, abdominal cramping, vomiting, and profuse watery diarrhea (rice water, choleralike) occur. Fluid losses may be severe enough to cause profound dehydration and even circulatory collapse.
• Once this acute gastrointestinal phase is over (usually after 24 h), the second stage begins. Although the patient appears to have improved clinically, ongoing liver damage is occurring as indicated by laboratory abnormalities (elevation of serum aminotransferase levels, prothrombin time). This stage may last as long as 2-3 days.
• Hepatic and renal injury become clinically apparent and may progress to fulminant hepatic failure in the third phase. Death may occur in 3-7 days.

Frequency

United States

In 2007, 7351 single exposures to mushrooms were reported to the American Association of Poison Control Centers.¹

In 1996, 10,584 mushroom exposures were reported to the American Association of Poison Control Centers.² Eighty-eight percent of reported mushroom exposures were unidentified. Only 54 were identified as amatoxin exposures; however, this number is undoubtedly an underestimation given the number of unknown mushroom exposures.

One author estimates incidence of mushroom exposures at 5 exposures per 100,000 population per year.

International

No adequate database exists to estimate worldwide exposures.

• Mushroom foraging is more common in parts of Europe and Russia than in other parts of the world.
• From mid-July to September of 1998, 9 people died and 180 were poisoned from mushrooms in Russia.
• In July and August of 1997, 34 people died of mushroom poisoning across Russia.

Mortality/Morbidity

Ninety-five percent of all mushroom fatalities in North America are associated with cyclopeptide-containing species (amatoxins). Worldwide, most mushroom fatalities are ascribed to amatoxins. Amatoxins are associated with mortality rates ranging from 10-60%.

Ingestion of a single Amanita phalloides mushroom can be lethal.

No deaths due to mushroom exposures were reported in the 2007 American Association of Poison Control Centers National Poison Data System annual report.¹

Age

• Most unintentional mushroom exposures occur in children younger than 6 years.
• Mortality is higher in children because they absorb a larger dose of toxins per body weight.

Clinical

History

With amatoxin ingestion, onset of GI symptoms typically is delayed 6-12 hours or more. An earlier onset of symptoms suggests that another mushroom is responsible for symptomatology. However, if the patient's meal included several different mushrooms, an earlier onset of symptomatology does not rule out concomitant amatoxin ingestion.

• Presenting complaints include severe abdominal pain, cramping, nausea and vomiting, profuse diarrhea, and weakness.
• With delayed presentation, complaints may include symptoms attributable to hepatic dysfunction, such as jaundice, lethargy, or bruising.
• If a mushroom sample is available, place it in a dry paper bag (do not moisten or refrigerate).

Physical

Assessing the patient's volume status is an important component of the initial evaluation. With delayed presentations, look for signs of hepatic or CNS dysfunction.

• Vital signs
  • Tachycardia
  • Hypotension
• Skin
  • Poor turgor
  • Jaundice, bruising (with hepatic failure)
• Abdomen
  • Mild tenderness
  • Diarrhea, may have a positive result on a Hemoccult test (guaiac positive)
• Neurologic (if hepatic failure or hypoglycemia)
  • Confusion
  • Lethargy
  • Coma

Causes

• Unintentional childhood ingestions
• Misidentification of mushroom by forager
• Deliberate seeking of psychotropic mushrooms

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