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).
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
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Klein AS, Hart J, Brems JJ, Goldstein L, Lewin K, Busuttil RW.
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Lampe KF, McCann MA. AMA handbook of poisonous and injurious
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Pinson CW, Daya MR, Benner KG, et al. Liver transplantation for
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Koppel C. Clinical symptomatology and management of mushroom
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