Syndrome; latency | Mechanism of action | Symptoms | Treatment, antidote | Toxins, tests |
Amatoxin / phalloides poisoning 6–12 h (max. 24 h) | Inhibition of RNA polymerase II inhibits the transcription of DNA to mRNA, thus blocking the biosynthesis of many proteins (enzymes, structural proteins, peptide hormones, membrane receptors). | Vomiting, profuse diarrhea, hypotension, acute renal and liver failure, coagulopathy, encephalopathy | Activated charcoal may be given (19), aggressive fluid and electrolyte resuscitation, coagulation factors; other options include hemodialysis/albumin dialysis, with liver transplantation as a last resort. Silibinin is the antidote of first choice; it may be given in combination with N-acetylcysteine (NAC).NAC may be given alone if silibinin is not available | Amatoxins are a group of 10 heat-stable bicyclic oligopeptides. The main active substances, α-amanitin and β-amanitin, are resistant to gastrointestinal peptidases.
Immunoassay (ELISA) and chromatographic techniques to demonstrate α-amanitin in urine are available at several laboratories.*1 Note the window of opportunity: from 6 to a maximum of 36 hours after the mushrooms were ingested) (27– 29) |
Gyromitrin poisoning 6–12 h | Gyromitrin is broken down to monomethylhydrazine (MMH) by a long period of drying, cooking, or by gastric juices. MMH inhibits pyridoxal phosphokinase and leads to reduced production of pyridoxal 5-phosphate (vitamin B6), with neurotoxic effect (vitamin B6 is a key cofactor in the synthesis of GABA). MMH after massive ingestion of gyromitra mushrooms leads to oxidative stress and thus to methemoglobinemia. | If MMH builds up rapidly, the damage caused is mainly to the liver; if it builds up slowly, CNS symptoms are seen (acetylator type) (e12); nausea, vomiting, impaired consciousness, CNS excitation, cerebral seizures, liver and kidney damage (e14); methemoglobinemia may occur | Activated charcoal may be given (19)
Intravenous pyridoxine, or alternatively, e.g., levetiracetam | Gyromitrin, which is metabolized to MMH (e13). MMH is volatile, heat-sensitive, and water-soluble, and these mushrooms were therefore long regarded as edible so long as they were well cooked (in fact, multiple cases are known of severe or even fatal poisoning even when the mushrooms were correctly prepared!) (e12).
No serum or urine tests are available |
Orellanine poisoning 36 h – 17 days | Orellanine, or its metabolite, causes oxidative stress leading to formation of superoxide ions and thus to inhibition of alkaline phosphatase and DNA and RNA polymerases, which in turn results in inhibition of protein biosynthesis in renal tissue (e15– e18) | Thirst, flank pain, weakness, oliguria or even acute renal failure, tubulointerstitial nephritis; there may be irreversible terminal renal failure requiring dialysis | Symptomatic treatment, treatment of renal failure, hemodialysis if indicated*2, steroids | Orellanine
No published serum or urine tests; only testing of renal tissue is available (e19– e21) |