- Most potentially life-threatening mushrooms will cause symptoms more than 6 to 8 hours, or even longer, after ingestion.
- Cyclopeptide (Amanita phalloides), Monomethylhydrazine (Gyromitra spp.) mushrooms can cause life-threatening hepatotoxicity.
- The majority of toxic mushrooms taken belong to the gastrointestinal irritant group.
- A. muscaria mushrooms do not cause significant muscarinic symptoms. They belong to the Ibotenic acid/muscimol group, and the name is a misnomer.
Most toxic mushroom species fall into one of nine distinct classifications or groups. These groups contain specific chemical toxins that give rise to distinct clinical syndromes that are characterized by the time to onset after ingestion, and the nature of the symptoms.
The more severely toxic and potentially life-threatening species generally have a delayed onset of symptoms. For Groups I and II, symptoms usually begin 6 to 24 hours after ingestion; Group VIII can cause symptoms 24 hours to 2 weeks after ingestion. Less toxic species, comprising Groups III to VII, usually cause symptoms within 30 minutes to 3 hours after ingestion (Fig. 129–1). When identification of a particular mushroom is necessary, an expert mycologist can be located by contacting a regional poison center.1
Timeline algorithm after ingestion.
Group I: Cyclopeptide-Containing Mushrooms
This is one of the major groups of mushrooms that can lead to life-threatening toxicity. Some examples of mushrooms in this group include A. phalloides (Fig. 129–2), A. verna, A. virosa, and certain species of Galerina and Lepiota. These mushrooms contain amatoxins, phallatoxins, and virotoxins. Only the amatoxins are considered significant in human poisoning. Amatoxins are felt to cause toxicity by interfering with RNA polymerase reactions.
Amanita phalloides, the “death cap” produces amatoxins and accounts for most of the fatalities due to mushroom ingestion. (With permission from Knoop et al. Atlas of Emergency Medicine, 2nd ed. McGraw-Hill; 2002.)
Initial toxic effects primarily include nausea, vomiting, and abdominal pain; they are characteristically delayed 6 to 24 hours postingestion. This is an important clinical distinction from the very large group of GI irritants (Group VII). Other clinical effects include fluid and electrolyte derangement, hypotension, CNS depression, seizures (rare), fulminant hepatic failure, and coagulopathy. After the period of initial GI distress, the patient may seem to improve clinically while having a subclinical deterioration in hepatic status. Fulminant hepatic failure is the most important consequence of cyclopeptide toxicity, and is seen approximately 3 days postingestion.2
Treatment generally centers on supportive care and replacement of fluid and electrolytes. Activated charcoal is generally recommended. There are a number of interventions that have been attempted for cyclopeptide poisoning, including hemoperfusion, high-dose penicillin, high-dose cimetidine, N-acetylcysteine, silibinin, and thioctic acid. None of these therapies ...