page_title: Amanita phalloides
section_title: Treatment
hierarchical_section_title: Amanita phalloides / Toxicity / Treatment
caption_attribution_description: English: Death cap - two young fungal fruiting bodies. Location: Europe, Poland, Mazovian Voivodship, Podkowa Leśna, broadleaf forest/garden. See also other pictures of the same subject.Polski: Muchomor sromotnikowy - dwa młode owocniki. Lokalizacja: Europa, Polska, Województwo Mazowieckie, Podkowa Leśna, las liściasty/ogród. Zobacz też inne zdjęcia tych samych okazów.
context_page_description: Amanita phalloides, commonly known as the death cap, is a deadly poisonous basidiomycete fungus, one of many in the genus Amanita. Widely distributed across Europe, but now sprouting in other parts of the world, A. phalloides forms ectomycorrhizas with various broadleaved trees. In some cases, the death cap has been introduced to new regions with the cultivation of non-native species of oak, chestnut, and pine. The large fruiting bodies appear in summer and autumn; the caps are generally greenish in colour with a white stipe and gills. Cap colour is variable, including white forms, and thus not a reliable identifier.
  These toxic mushrooms resemble several edible species commonly consumed by humans, increasing the risk of accidental poisoning. Amatoxins, the class of toxins found in these mushrooms, are thermostable: they resist changes due to heat, so their toxic effects are not reduced by cooking.
  Amanita phalloides is one of the most poisonous of all known mushrooms. It is estimated that as little as half a mushroom contains enough toxin to kill an adult human.
context_section_description: Consumption of the death cap is a medical emergency requiring hospitalization. The four main categories of therapy for poisoning are preliminary medical care, supportive measures, specific treatments, and liver transplantation.
  Preliminary care consists of gastric decontamination with either activated carbon or gastric lavage; due to the delay between ingestion and the first symptoms of poisoning, it is common for patients to arrive for treatment many hours after ingestion, potentially reducing the efficacy of these interventions. Supportive measures are directed towards treating the dehydration which results from fluid loss during the gastrointestinal phase of intoxication and correction of metabolic acidosis, hypoglycemia, electrolyte imbalances, and impaired coagulation.
  No definitive antidote is available, but some specific treatments have been shown to improve survivability. High-dose continuous intravenous penicillin G has been reported to be of benefit, though the exact mechanism is unknown, and trials with cephalosporins show promise. Some evidence indicates intravenous silibinin, an extract from the blessed milk thistle (Silybum marianum), may be beneficial in reducing the effects of death cap poisoning. A long-term clinical trial of intravenous silibinin began in the US in 2010. Silibinin prevents the uptake of amatoxins by liver cells, thereby protecting undamaged liver tissue; it also stimulates DNA-dependent RNA polymerases, leading to an increase in RNA synthesis. According to one report based on a treatment of 60 patients with silibinin, patients who started the drug within 96 hours of ingesting the mushroom and who still had intact kidney function all survived. As of February 2014 supporting research has not yet been published.
  SLCO1B3 has been identified as the human hepatic uptake transporter for amatoxins; moreover, substrates and inhibitors of that protein—among others rifampicin, penicillin, silibinin, antamanide, paclitaxel, ciclosporin and prednisolone—may be useful for the treatment of human amatoxin poisoning.
  N-Acetylcysteine has shown promise in combination with other therapies. Animal studies indicate the amatoxins deplete hepatic glutathione; N-acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage. None of the antidotes used have undergone prospective, randomized clinical trials, and only anecdotal support is available. Silibinin and N-acetylcysteine appear to be the therapies with the most potential benefit. Repeated doses of activated carbon may be helpful by absorbing any toxins returned to the gastrointestinal tract following enterohepatic circulation. Other methods of enhancing the elimination of the toxins have been trialed; techniques such as hemodialysis, hemoperfusion, plasmapheresis, and peritoneal dialysis have occasionally yielded success, but overall do not appear to improve outcome.
  In patients developing liver failure, a liver transplant is often the only option to prevent death. Liver transplants have become a well-established option in amatoxin poisoning. This is a complicated issue, however, as transplants themselves may have significant complications and mortality; patients require long-term immunosuppression to maintain the transplant. That being the case, the criteria have been reassessed, such as onset of symptoms, prothrombin time (PT), serum bilirubin, and presence of encephalopathy, for determining at what point a transplant becomes necessary for survival. Evidence suggests, although survival rates have improved with modern medical treatment, in patients with moderate to severe poisoning, up to half of those who did recover suffered permanent liver damage. A follow-up study has shown most survivors recover completely without any sequelae if treated within 36 hours of mushroom ingestion.
caption: Young "death cap" mushrooms in Poland, with matchbox for scale
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