Coprine

The last specific rapid-acting toxin, coprine, is found in many Coprinus sp. of mushrooms. The mushrooms are also known as “inky caps” because of the substance they produce when picked. Ingested alone, little effect is noted, but subsequent ingestion of alcohol produces a disulfiram-like reaction, with intense vomiting, tachycardia, and flushing. This is caused by inhibition of acetaldehyde dehydrogenase.⁶ Care, once again, is symptomatic, and vomiting tends to resolve in a matter of hours.

These mushroom classes have the similarity that clinical effects present rapidly following ingestion, within 3 hours in almost all cases. This important distinction led to the early syndromic classification schemes, which have been modified significantly with increasing complexity.^7,8 The following ingestions, if identified, can produce serious clinical effects, including hepatic and renal failure, seizures, and rhabdomyolysis.

Cyclopeptides

More than 90% of fatalities associated with toxic mushroom ingestion have been attributed to amatoxin-containing species such as Amanita phalloides.⁹ Gallerina sp. and Lepiota sp. are also included in this classification. Gastrointestinal effects such as nausea and vomiting are common, but tend to be delayed until 6-24 hours after ingestion, which is a subtle differentiation from the other five classifications. Unfortunately, it is not uncommon to miss or be unable to obtain this history, and thus discharge patients with this highly dangerous ingestion after their symptoms are controlled. A quiescent phase, occurring at 12–36 hours after ingestion, may falsely lead patients and physicians alike to believe that a more benign species has been consumed. However, 2-6 days after ingestion, some patients experience hepatic and renal toxicity that can lead to death.

These toxicities are caused primarily by alpha-amanitin, a cyclopeptide that is one of the deadliest naturally occurring compounds. As little as 0.1 mg/kg can be fatal, a dose that is often present in a single mushroom.⁶ The mechanism of toxicity relates to interference with RNA polymerase II, which prevents DNA transcription. While elevation of liver enzymes may begin in the quiescent phase, fulminant hepatic failure with elevated transaminases and bilirubin and coagulopathy are not present until the third stage of poisoning.

Evidence-based recommendations are difficult to find for amatoxin poisoning, but multiple recommendations do exist in the literature.

Transfer to a center capable of performing liver transplantation is mandatory if advanced poisoning with evidence of liver failure is present. Multiple studies have attempted to delineate criteria that would merit transplantation, including two of the following: grade 2 hepatic encephalopathy or higher, prothrombin time of more than twice normal despite therapy, bilirubin level greater than 25 mg/dL, and hypoglycemia requiring infusion therapy.¹⁰