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CDC Morbidity and Mortality Weekly Report
Vol. 46, No. 22, June 6, 1997.

Amanita phalloides  Mushroom Poisoning --
Northern California, January 1997 Mushroom Poisoning

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 require d 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 p atients 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 in gestion. 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 thir d 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
>60 seconds, and total b ilirubin 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 a fter
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 t ransaminase levels and
PT gradually decreased, and he was dischar ged on the seventh day after
eating the mushrooms without sequelae. 

Case 3. A 30-year-old man used a guidebook to assist in the col lection 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 o f 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
intraveno us fluids. Although renal function indicators were within normal
limits 1 day after adm ission, 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 biliru bin 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 eat ing 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, Divof Clinical Pharmacology and Experimental Therapeutics,
Univ of California, San Francisco.Environmental Hazards Epidemiology
Section, Health Studies Br, Div of Environmental Hazardsand Health
Effects, National Center for Environmental Health, CDC. 

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 con
ditions 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 nonpoisonou s 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 result ing
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
n umbers 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 thr ough 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, sympt
oms 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 cardiomyop
athy, coagulopathy, and s eizures (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 < 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). 

A. phalloides poisoning has no specific antidote. The main treatment is
vigorous intravenous fluid replacement and correction of electrol yte
disturbances ( 1-5 ); correction of coagulopathy, if present, also may be
indicated. Physicians should perform g astric 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, c imetidine, 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 definit ive 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 ed ucate the public about the potentially
lethal conseque nces 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 p
oisoning 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

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