Description

The Phalloides Syndrome is produced by Amanita phalloides and related mushrooms that produce a toxin that can result in multi-organ failure and death.


 

Mushroom species involved:

(1) Amanita phalloides ("death cap")

(2) Amanita verna ("destroying angel")

(3) Amanita virosa

(4) other Amanita species

(5) Galerina species

(6) Imocybe species

(7) Omphalotus olearius

(8) Clitocybe dealbata and other species

(9) Lepiota species

 

Toxin: amanitins, also called amatoxins (cyclic oligopeptides designated alpha, beta, gamma and delta). The toxin inhibits RNA polymerase 2, with failure to transcribe mRNA. Symptoms occur when protein stores are exhausted.

 

Features of the toxin: thermostable

 

History: ingestion of wild mushrooms during the summer or autumn

 

Stage

Descriptor

Features

1

incubation period

Asymptomatic for the first 8 to 12 hours (range 6 to 16 hours) after ingestion

2

gastrointestinal stage

Recurring episodes of abdominal pain with vomiting and severe watery diarrhea. Gastrointestinal hemorrhage may occur. Severe electrolyte imbalances and dehydration may occur. The patient may develop shock with or without acute renal failure.

 

temporary lull

Clinical improvement with resolution of GI symptoms (false recovery)

3

cytotoxic stage

Onset of hepatocellular damage which may be rapidly progressive 24 to 48 hours after ingestion

4

comatose stage

Multi-organ failure with coma, coagulopathy and liver failure

 

Late clinical findings:

(1) jaundice and hepatomegaly

(2) hemorrhage with petechiae

(3) oligouria or anuria

(4) cerebral involvement with coma

(5) pulmonary congestion

 

Laboratory findings:

(1) markedly elevated liver transaminase levels

(2) aminoacidemia

(3) markedly prolonged PT and PTT

(4) elevated BUN and creatinine

(5) demonstration of amanitin (multiple types) or other toxins (phallotoxins, viroisin, viroidin)

(6) usually negative tests for viral hepatitis

 

Histologic findings:

(1) liver – massive centrolobular hepatocellular necrosis

(2) kidneys – acute tubular necrosis

 

Clinical outcomes:

(1) slow resolution of symptoms with recovery

(2) death from progressive multi-organ failure

(3) liver transplantation

 


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