Mushroom poisoning of companion animals, particularly dogs, is a potentially underestimated problem in North America. Because
of their wandering and scavenging nature, dogs seem particularly prone to mushroom poisoning.1-8 While there have been sporadic reports of mushroom poisoning in dogs in the veterinary literature,1-8 anecdotal experience in the Pacific Northwest suggests it is more prevalent than the literature indicates.
This article summarizes the clinical effects of the toxicologically important mushrooms in North America. Spring, summer,
and fall are the principal seasons for mushroom poisoning in most of North America.9
IDENTIFICATION AND TREATMENT
Table 1. Toxicologic Classification of Toxic Mushrooms
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Toxic mushrooms are divisible into eight groups based on their toxin type (Table 1).9 Six of these groups are of potential veterinary significance, and representative members of these groups are common throughout
North America.9 In line with the adage, "There are old mushroom hunters, there are bold mushroom hunters, but there are no old, bold mushroom
hunters," all wild-growing mushrooms should be regarded as toxic until proven otherwise.
Ideally, samples of the ingested mushrooms should be brought in to the clinic along with the affected animal. Do not place
mushrooms for identification in a plastic bag; instead, wrap them in a moist paper towel or wax paper or place them in a paper
bag. Identifying mushroom species is often complex, so consult a human poison information center with experience in mushroom
identification (e.g. the Oregon Poison Center [(800) 222-1222]) or a mycologist as needed.9,10
Cyclopeptides
Amanita phalloides, the death cap mushroom, is the most common cause of potentially fatal mushroom poisoning in people and
dogs.
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Amanita, Galerina, and Lepiota species mushrooms contain toxic cyclopeptides. Amanita species are the most commonly documented cause of fatal mushroom poisoning in dogs,1,2,4-8 and they account for 95% of mushroom-related fatalities in people.9Amanita phalloides, the death cap mushroom (Figure 1), accounts for more than 50% of all mushroom-associated deaths in people and most of the reported fatal cases in dogs.1,2,6,9The toxic cyclopeptides in these mushrooms are amatoxins, phallotoxins, and virotoxins.8,9 These peptides are rapidly absorbed from the gut, and their duration of action is increased by enterohepatic circulation
and active resorption of amatoxins from the renal glomerular filtrate. Amatoxins and phallotoxins are responsible for most
of the pathologic effects.9 Amatoxins interfere with DNA and RNA transcription and, thus, selectively affect the rapidly replicating cells of the gastrointestinal
(GI) and renal tubular epithelium and liver. Phallotoxins irreversibly polymerize hepatic actin filaments, triggering hepatic
cholestasis.9
Typically, 10 to 12 hours pass between consumption and the onset of clinical signs.9 This delay is an important differential diagnostic feature of cyclopeptide ingestion and is probably due to the time required
for amatoxins to bind to intranuclear RNA polymerase II.9
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