Flora and fauna: Hazardous biotoxins for pets (Proceedings)


Flora and fauna: Hazardous biotoxins for pets (Proceedings)

Aug 01, 2008


While scores of potentially toxic plants may be ingested, relatively few plants account for the majority of exposures. In cases of plant exposure, plants should be positively identified in order to determine their potential toxicity. Whole plant samples are preferred for identification, but it may be possible to identify a plant based upon examination of plant parts either from the environment of the animal or from vomitus. With few exceptions, treatment of toxic plant ingestions involves symptomatic and supportive care.

Recently, ingestion of grapes or raisins by dogs has been associated with acute renal failure (ARF). The proximate toxin has not been identified and not all dogs that ingest grapes or raisins are affected. In addition, there is no apparent relationship between the number of grapes or raisins ingested and the occurrence of ARF. Clinical signs of intoxication include anorexia, emesis, diarrhea, lethargy, abdominal pain, and oliguria followed by anuria. Histopathologic lesions include proximal renal tubule degeneration and necrosis. Diagnosis of intoxication relies on a history of recent ingestion of grapes or raisins. Treatment includes early GI decontamination and symptomatic and supportive care. Hemodialysis should be considered if available. The prognosis is poor based upon reported cases to date.


A variety of mushrooms are toxic. However, the most poisonous mushrooms contain cyclopeptide toxins, especially amanitin. Several genera of mushrooms contain amanitin, but ingestion of Amanita spp. and Galerina spp. are most often involved in intoxication. Ingestion of amanitin-containing mushrooms results in fulminant liver failure. Renal failure and coagulopathy can also occur. Amanitin toxins inhibit protein synthesis by ribosomes within hepatocytes. Following mushroom ingestion, there can be a latent period before the onset of clinical signs. Clinical signs include hyperglycaemia following by hypoglycaemia, coagulation abnormalities, ataxia, listlessness, bradycardia and shock. Antemortem diagnosis of Amanita intoxication relies on a history of recent mushroom ingestion and, if testing is available, detection of amanitin in serum, urine or GI contents. Whether amatoxin testing is available or not, an attempt should be made to identify the genus and species of mushroom ingested. Unfortunately, mushroom identification often requires specialized expertise that may or may not be readily available and fresh samples are necessary.

Once liver damage has occurred, treatment is often unrewarding. GI decontamination is warranted if early after an ingestion. Multiple doses of activated charcoal are indicated due to enterohepatic recirculation of the toxins. Penicillin G and silymarin (derived from Silybum marianum or milk thistle) have been used, but their efficacy is uncertain. Silymarin at a total dose of 1.4 to 4.2 g per day can be given orally for 4 to 5 days. Alternatively, N-acetylcysteine at doses similar to those for treating acetaminophen intoxication can be administered. Silymarin and N-acetylcysteine are hepatoprotective. Vitamin K1 and blood transfusions are indicated in cases with coagulopathy.


Mycotoxins are secondary fungal metabolites that can intoxicate humans and animals. There are a number of mycotoxins that have been characterized and cause animal disease. However, two major classes of mycotoxins are responsible for the majority of small animal intoxications: aflatoxins and tremorgenic mycotoxins.

Aflatoxins are produced by certain fungal species in the genus Aspergillus in corn, peanuts and other agricultural products during warm and humid conditions. Four major aflatoxins are produced (aflatoxins B1, B2, G1 and G2) under natural conditions, with aflatoxin B1 being both the most prevalent and toxic. Aflatoxins are metabolized by the liver to reactive epoxides which bind covalently with cellular macromolecules such as DNA, RNA and proteins. Such binding results in damage to hepatocytes leading to impaired liver function, bile duct proliferation, bile stasis and liver fibrosis. Cases have occurred in dogs but have not been reported in cats.