Amanita spp

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Amanita muscaria: usually found near conifer trees and hardwood trees (especially oak trees); lives in soil[1]
Massive hepatocellular necrosis with collapse of hepatic cords associated with amantin toxicity in a dog. Preserved bile duct (arrow) in portal area. ‘‘C’’ denotes central vein[2]

Amanita phalloides (death cap or death angel mushroom) are an infrequently ingested highly toxic hallucinogenic mushroom which can cause mycotoxicosis and subsequent hepatopathy in dogs.

The toxic ingredients of these mushrooms are cyclopeptides including the amatoxins, phallotoxins, and virotoxins[3]. Amatoxins are bicyclic octapeptides and include the amanitins (a-, b-, c-, and e-amanitins), amanin, amanullin, and proamanullin. Severe poisonings and lethality are mainly attributable to the amanitins[4].

Acute fulminant liver failure and death can occur within a few days of ingestion and young curious dogs are more prone to ingestion of these mushrooms[5].

Clinically affected dogs usually present within 12 hours following ingestion of mushrooms and show signs of vomiting, diarrhea, lethargy, general body twitching, tremors, ataxia, hepatic encephalopathy and diarrhea. Severe neurological signs such as seizures have also been reported[6][7].

Blood tests usually show marked hypoglycemia, leucocytosis and elevated ALT[2]. Acute renal injury and DIC are possible complication in these cases.

Histological examination of liver biopsies show consist evidence of acute hepatic necrosis due to absorption of amantinin toxins.

A presumptive diagnosis is based on historical evidence of ingestion, identification of amanitin-containing mushrooms in the environment of the animal and presenting clinical signs. In some cases, mushroom pieces may be found in gastric contents and can confirm exposure.

A definitive diagnosis requires enzyme testing of liver samples for presence of toxin.

A differential diagnosis would include other causes of mycotoxicosis, toxin ingestion (e.g. organophosphates and strychnine) and myokymia.

Treatment usually requires aggressive intravenous fluid therapy, N-acetylcysteine and antioxidants such as ascorbic acid.

Dramatic improvements have been reported with use of silibinin when administered at 50 mg/kg in two doses 24 hours apart[8].


  1. Gentle Dr Animal Hospital
  2. 2.0 2.1 Puschner B et al (2007) Diagnosis of Amanita toxicosis in a dog with acute hepatic necrosis. J Vet Diagn Invest 19(3):312-317
  3. Lincoff G &Mitchel DH (1977) Cyclopeptide poisoning. In: Toxic and hallucinogenic mushroom poisoning. A handbook for physicians and mushroom hunters, ed. Lincoff G, Mitchel DH, pp:25–48. Van Nostrand Reinhold Company, New York, NY
  4. Vetter J (1998) Toxins of Amanita phalloides. Toxicon 36:13–24
  5. Tegzes JH& Puschner B (2002) Amanita mushroom poisoning: efficacy of aggressive treatment of two dogs. Vet Hum Toxicol 44(2):96-99
  6. Liggett AD & Weiss R (1989) Liver necrosis caused by mushroom poisoning in dogs. J Vet Diagn Invest 1(3):267-269
  7. Naudé TW & Berry WL (1997) Suspected poisoning of puppies by the mushroom Amanita pantherina. J S Afr Vet Assoc 68(4):154-158
  8. Vogel G et al (1984) Protection by silibinin against Amanita phalloides intoxication in beagles. Toxicol Appl Pharmacol 73(3):355-362