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Amanita phalloides Mushroom Poisoning -- Northern California, January 1997

The popular interest in gathering and eating uncultivated mushrooms has been associated with an increase in incidents of serious mushroom-related poisonings (1). From December 28, 1996, through January 6, 1997, nine persons in northern California required hospitalization after eating Amanita phalloides (i.e., "death cap") mushrooms; two of these persons died. Risks associated with eating these mushrooms result from a potent hepatotoxin. This report describes four cases of A. phalloides poisoning in patients admitted to a regional referral hospital in northern California during January 1997 and underscores that wild mushrooms should not be eaten unless identified as nonpoisonous by a mushroom expert. Case 1. A 32-year-old man gathered and ate wild mushrooms that he believed were similar to other mushrooms he had previously gathered and eaten. Eight hours later, he developed vomiting and profuse diarrhea; he was admitted to a hospital 19 hours after ingestion. On admission, he was dehydrated, and laboratory findings included an aspartate aminotransferase (AST) level of 81 U/L (normal: 0-48 U/L), prothrombin time (PT) of 12.3 seconds (normal: 11.0-12.8 seconds), and bilirubin level of 0.9 mg/dL (normal: 0-0.3 mg/dL). He received intravenous fluids, intravenous penicillin, repeated oral doses of activated charcoal, and oral N-acetylcysteine. Although the diarrhea resolved after 24 hours, his PT and AST and bilirubin levels continued to rise. On the third day after eating the mushrooms, abnormal findings included an AST level of 2400 U/L, alanine aminotransferase (ALT) level of 4100 U/L (normal: 0-53 U/L), PT of greater than 60 seconds, and total bilirubin level of 11 mg/dL. Six days after eating the mushrooms, his bilirubin level was 16 mg/dL, and his AST level had decreased to 355 U/L; he developed metabolic acidosis and hypotension. Seven days after eating the mushrooms, he developed hepatic encephalopathy, oliguric renal failure, and adult respiratory distress syndrome requiring intubation and mechanical ventilation. He died from multiple organ failure 9 days after eating the mushrooms. One mushroom cap remaining after the meal was identified as A. phalloides. Case 2. A 42-year-old man developed vomiting and diarrhea 11 hours after eating wild mushrooms, and he was admitted to a hospital 14 hours after eating the mushrooms. His transaminase levels were elevated 24 hours after ingestion (AST and ALT levels both at 100 U/L); his PT was 12.1 seconds, and his bilirubin level was 0.2 mg/dL. His PT became prolonged the next day and peaked at 35 seconds on the fourth day. His transaminase levels also peaked on the fourth day (AST level of 3000 U/L and ALT level of 6000 U/L); his bilirubin level was 7.8 mg/dL. He was given repeated doses of activated charcoal and oral N-acetylcysteine. His transaminase levels and PT gradually decreased, and he was discharged on the seventh day after eating the mushrooms without sequelae. Case 3. A 30-year-old man used a guidebook to assist in the collection of wild mushrooms. Twelve hours after eating the mushrooms he had gathered, he developed vomiting and severe diarrhea. He was admitted to a hospital 17 hours after ingestion because of orthostatic hypotension and dehydration. Abnormal laboratory findings indicated an AST level of 75 U/L, blood urea nitrogen level of 22 mg/dL (normal: 6-20 mg/dL), and creatinine level of 2.8 mg/dL (normal: 0.6-1.3 mg/dL). He was treated with intravenous fluids. Although renal function indicators were within normal limits 1 day after admission, his liver enzyme and PT levels began to increase; on the fourth day, transaminase levels peaked (AST level of 1900 U/L and ALT level of 2800 U/L), total bilirubin level was 1.6 mg/dL, and PT was 18 seconds. His clinical status continued to improve, and he was discharged 7 days after eating the mushrooms. Case 4. A 68-year-old man ate mushrooms he had collected on a golf course. Two days after eating the mushrooms, he was admitted to a hospital because of diarrhea and weakness. His AST level was 630 U/L, and he had renal failure. On the third day after eating the mushrooms he required hemodialysis, and his transaminase levels and his PT continued to increase; on the fifth day, his AST level was 3500 U/L; ALT level, 4600 U/L; PT, 34 seconds; and bilirubin, 9.7 mg/dL. He developed hepatic encephalopathy and died 6 days after eating the mushrooms.

Reported by: S Zevin, MD, D Dempsey, MD, K Olson MD, California Poison Control System, Div of Clinical Pharmacology and Experimental Therapeutics, Univ of California, San Francisco. Environmental Hazards Epidemiology Section, Health Studies Br, Div of Environmental Hazards and Health Effects, National Center for Environmental Health, CDC.

Editorial Note

Editorial Note: Ingestion of A. phalloides may account for approximately 90% of deaths attributable to mushroom ingestion worldwide (1-5); the proportion of cases of mushroom poisoning attributable to A. phalloides in the United States is unknown. In the United States, this species is found primarily in the cool coastal regions of the west coast, but it also grows in several other regions, including the mid-Atlantic coast and in the northeast (1,2). These mushrooms flourish in favorable weather conditions during the fall or the rainy season (2,6). The mature cap usually is metallic green but varies from light yellow to greenish-brown (1-3). A. phalloides, like most mushroom species, is not unique in appearance and can be mistaken for nonpoisonous species; it has no distinct taste or smell, and the toxins are not destroyed by cooking or drying (3,5,6). The principal toxins (amatoxins) are taken up by hepatocytes and interfere with messenger RNA synthesis, suppressing protein synthesis and resulting in severe acute hepatitis and possible liver failure. Radioimmunoassay of amatoxins can be obtained from serum and urine; the tests are performed at referral laboratories (1,2).

Since 1979, A. phalloides has been found in the region from northern California to Washington state, and since 1995, it has appeared in greater numbers because of abundant rainfall during winter months. During the winter of 1995-96, at least 13 persons in northern California were hospitalized for treatment of poisonings after eating A. phalloides; one patient died, and another required a liver transplant. The cluster of mushroom poisoning in northern California described in this report probably occurred because warm, heavy rainfall created optimal conditions for the growth of A. phalloides in unprecedented numbers. In addition, this mushroom grew in places where it had not grown before (e.g., backyards), which increased the likelihood that persons gathering these mushrooms could mistake them for a nonpoisonous species.

Patients may not associate their symptoms with ingestion of wild mushrooms because of the delayed onset. As illustrated by the cases described in this report, symptoms typically occur in a progression through three stages. During the first stage, which occurs 6-24 hours after ingestion, symptoms may include abdominal pain, nausea, vomiting, severe diarrhea, fever, tachycardia, hyperglycemia, hypotension, and electrolyte imbalance. During the second stage, which occurs during the next 24-48 hours, symptoms appear to abate even as hepatic and renal functions deteriorate. During the third stage, which occurs 3-5 days after the ingestion, hepatocellular damage and renal failure may progress, resulting in jaundice and hepatic coma (1-5). Possible sequelae include cardiomyopathy, coagulopathy, and seizures (1,2,5). Death from A. phalloides poisoning usually results from hepatic and/or renal failure and may occur 4-9 days after ingestion. Fatal outcomes are associated with age less than 10 years, a short latency between ingestion and onset of symptoms, and severe coagulopathy (1,4). The fatality rate among persons treated for A. phalloides poisoning is 20%-30% (1,2,4), and the median lethal dose is 0.1 mg to 0.3 mg of the toxin per kg of body weight (1,5).

  1. phalloides poisoning has no specific antidote. The main

treatment is vigorous intravenous fluid replacement and correction of electrolyte disturbances (1-5); correction of coagulopathy, if present, also may be indicated. Physicians should perform gastric lavage and administer repeated doses of activated charcoal to remove any unabsorbed Amanita and to interrupt the enterohepatic circulation of the toxin (2,4,5). Although some therapeutic regimens have included the administration of penicillin, cimetidine, silibinin, or N-acetylcysteine, these treatments have not been confirmed by clinical trials to be effective. Hemodialysis and hemoperfusion may be effective in removing the toxin if initiated within 24 hours of ingestion (7). The only definitive treatment may be liver transplantation once fulminant liver failure occurs (1,2,4).

Unintentional ingestion of A. phalloides can be prevented by ensuring that wild mushrooms are not eaten unless identified as nonpoisonous by a competent mycologist. Education campaigns should be established in areas where A. phalloides is common to educate the public about the potentially lethal consequences associated with eating uncultivated mushrooms. Field guides do not provide sufficient details to differentiate toxic from nontoxic species. Health-care providers should report cases of mushroom poisoning to poison-control centers; these centers can provide expertise in the clinical management of mushroom poisoning.

References

  1. Bryson PD. Mushrooms. In: Bryson PD. Comprehensive review in toxicology for emergency clinicians. 3rd ed. Washington, DC: Taylor and Francis, 1996:685-93.

  2. Klein AS, Hart J, Brems JJ, Goldstein L, Lewin K, Busuttil RW. Amanita poisoning: treatment and the role of liver transplantation. Am J Med 1989;86:187-93.

  3. Lampe KF, McCann MA. AMA handbook of poisonous and injurious plants. Chicago, Illinois: American Medical Association, 1985.

  4. Pinson CW, Daya MR, Benner KG, et al. Liver transplantation for severe Amanita phalloides mushroom poisoning. Am J Surg 1990;159:493-9.

  5. Koppel C. Clinical symptomatology and management of mushroom poisoning. Toxicon 1993; 31:1513-40.

  6. Nicholls DW, Hyne BE, Buchanan P. Death cap mushroom poisoning {Letter}. N Z Med J 1995; 108:234.

  7. Feinfeld DA, Mofenson HC, Caraccio T, Kee M. Poisoning by amatoxin-containing mushrooms in suburban New York -- report of four cases. Clin Toxicol 1994;32;715-21.





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