March 2015
Toxicology
Peer Reviewed

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You have asked…

How should mushroom toxicosis be treated in dogs when the mushroom can rarely be identified?

The expert says…

There are thousands of mushroom species in North America, but fewer than 100 are poisonous.1 Mushroom species can be difficult to identify, so treatment, especially in dogs that scavenge, is based on the presumption that the mushroom is toxic.2 The following focuses on types of mushrooms that can result in poisoning in dogs (Tables 1 and 2).

See Table 1. Toxicologic Classification of Toxic Mushrooms

See Table 2. Medications & Dosage Commonly Used to Treat Mushroom Toxicosis

Hepatotoxic Cyclopeptides

Mushroom species are difficult to identify, so treatment—especially in dogs that scavenge—is based on the presumption that the mushroom is toxic.

The most dangerous type of mushrooms contain hepatotoxic cyclopeptides, including amatoxins (most toxic), phallotoxins, and virotoxins. These include Amanita phalloides (death cap or death angel), A ocreata (angel of death), Galerina spp, and Lepiota spp. This class of mushroom results in 95% of mushroom-related fatalities in humans and the most fatalities worldwide.5 When ingested, amatoxins are taken up by hepatocytes via the sodium-dependent transport system and inhibit nuclear RNA polymerase II, which results in decreased protein synthesis and secondary cell death.5 Three phases of toxicosis are seen: severe GI signs (hypersalivation, vomiting, diarrhea, abdominal pain) within 6–24 hours; a false recovery period (12–24 hours); and a hepatorenal phase (36–72 hours postexposure).5,6 Kidney failure can develop as a result of proximal and distal tubular necrosis several days later.5 

Related Article: The Case: Suspected Amanita spp Mushroom Poisoning 

Along with appropriate clinicopathologic monitoring and symptomatic supportive care, treatment includes early decontamination (emesis induction if appropriate, followed by multiple doses of activated charcoal); fluid therapy (crystalloids, colloids); GI support (antiemetics, antacids); treatment for coagulopathy if indicated (vitamin K1 therapy, plasma transfusions); treatment for hepatic encephalopathy (lactulose, neomycin, anticonvulsants); hepatoprotectants (silibinin, S-adenosyl methionine, N-acetylcysteine). Peritoneal dialysis5 and parenteral penicillin G benzathine2,3 have also been reported to yield sucessful results in humans. Acute hepatic failure is more commonly seen in dogs than acute kidney injury; once signs of severe organ injury develop, prognosis is poor to grave.

Mushroom Toxicity Cases

In the past 10 years, the ASPCA Animal Poison Control Center had almost 5000 mushroom cases reported, involving 4561 dogs, 77 cats, 7 birds, 7 goats, 3 ferrets, 3 rabbits, 1 marsupial, and 1 pig.3 Death was reported in 23 animals (0.49%). In the cases where the animal survived, the type of mushroom was unknown at the time of the call (93.3%). In the fatalities, the type of mushroom was unknown 91% of the time.

Top mushrooms identified were: 

  • Psilocybe spp (2.6%)
  • Agaricus bisporus (1.1%)
  • Amanita spp (0.5%)
  • Inocybe spp (0.5%) 
  • Amanita muscaria (0.4%)

 

Muscarinic Agents

Inocybe spp and Clitocybe spp mushrooms contain muscarine, a muscarinic-receptor agonist that results in postganglionic parasympathomimetic effects.4 Clinical signs can be seen within 2 hours and include SLUDGE (salivation, lacrimation, urination, defecation, GI upset, emesis) and neurologic signs.4 Other clinical signs include increased genitourinary muscle tone, miosis, bradycardia, bronchoconstriction, wheezing, dyspnea, vomiting, lethargy, and collapse.4,5

Treatment includes early decontamination (emesis, activated charcoal), fluid therapy, GI support (antiemetics, antidiarrheals), and atropine. Prognosis is fair to good with symptomatic and supportive care.

Isoxazoles

Amanita muscaria (fly agaric) and A pantherina (panther cap) contain isoxazole derivatives muscimol and ibotenic acid, which are potent agonists at GABA receptors that inhibit neuronal and glial GABA uptake.5 These toxins also have psychoactive properties and act as both CNS depressants and stimulants.4,5 Clinical signs, which can be seen within 30 minutes to 12 hours of ingestion, include sedation, ataxia, disorientation, miosis, opisthotonus, paresis, paddling, vestibular signs, tremors, seizures, respiratory depression, coma, and (rarely) death.5

Treatment includes early decontamination if appropriate (emesis and a dose of activated charcoal), fluid therapy, confinement in a quiet area, anxiolytics, and anticonvulsants. Respiratory monitoring and symptomatic supportive care is imperative, as CNS depression and concurrent anticonvulsant therapy can potentially result in apnea.

Hydrazines

A less toxic mushroom is the Gyromitra spp (false morels), which contains hydrazines. Limited information is available about the toxicokinetics of these mushrooms, but the toxin antagonizes pyridoxine (vitamin B6), a cofactor required for the synthesis of GABA.4 Clinical signs are typically seen within 6–8 hours of ingestion, and are generally limited to gastrointestinal signs.4 Rarely, CNS signs (lethargy, seizures, coma) can be seen; with extreme poisonings, hepatic injury has been reported in humans.4

Treatment includes early decontamination, fluid therapy, and antiemetics. If seizures develop, pyridoxine can be used along with diazepam.6 The prognosis is good to excellent with supportive care in most cases.

Related Article: The Case: Metaldehyde Intoxication 

Gastrointestinal Irritants

Numerous mushrooms (eg, Agaricus spp, Boletus spp, Entoloma spp) are GI irritants but are rarely life-threatening when ingested.5 Clinical signs can be seen in several hours, and generally resolve within 1–2 days.5 Treatment typically is not necessary as the signs are self-limiting. With more severe clinical signs, treatment may include fluid therapy and GI support (antiemetics, antidiarrheals).

Psilocin & Psilocybin

Hallucinogenic mushrooms such as Psilocybe spp, Conocybe spp, Gymnopilus spp, and Panaeolus spp contain psilocybin and/or psilocin. Psilocybin is dephosphorylated to psilocin, which crosses the blood-brain-barrier, acting as an LSD (lysergic acid diethylamide)-like compound.5 Clinical signs can develop within 30 minutes to 4 hours in dogs and include anxiety, dysphoria, weakness, mydriasis, ataxia, abnormal mentation, visual hallucinations, tachycardia, howling, aggression, nystagmus, hyperreflexia, hypertension, hyperthermia, and seizures.4,5 This type of mushroom ingestion is typically not life-threatening. Treatment includes early decontamination, anxiolytics or sedation, symptomatic supportive care, and rarely, cooling measures and anticonvulsants. The prognosis for this type of mushroom is good to excellent with symptomatic supportive care.

Related Article: Quiz: Toxicoses and Treatments 

Conclusion

Although rapid identification of mushrooms would be ideal, this is not commonly the case with the emergent dog presenting for mushroom toxicosis. Veterinarians should be aware of the major classes of toxic mushrooms, along with toxicologic classification, methods of toxicity, clinical signs, and treatment. While fatalities are rare, treatment should be aimed at aggressive decontamination and therapy. Typically, hospitalization for 24 hours is warranted. If liver and renal function is normal at 24 hours, patients can be discharged on 1–2 weeks of S-adenosylmethionine. Rechecking a biochemistry panel at 48 hours after discharge is recommended. Ultimately, the prognosis for the majority of mushroom toxicities in dogs is fair to good.

GABA = gamma-aminobutyric acid, SLUDGE = salivation, lacrimation, urination, defecation, GI upset, emesis


JUSTINE A. LEE, DVM, DACVECC, DABT, is CEO and founder of VetGirl (vetgirlontherun.com), a podcast offering RACE-approved CE for veterinary professionals. She has authored and edited several veterinary texts. She also authored reference books and numerous journal articles. Dr. Lee completed her internship at Angell Memorial Hospital in Boston, an emergency fellowship and residency at University of Pennsylvania, and her DVM at Cornell University. She lectures internationally on emergency and critical care and was an NAVC Conference Small Animal Speaker of the Year.

 

References Show
References
  1. Mushrooms. Puschner B. In Osweiler GD, Hovda LR, Brutlag AG, Lee JA (eds). Blackwell’s Five-Minute Veterinary Consult Clinical Companion—Ames: Wiley-Blackwell, 2011, pp 711–719.
  2. Comparative treatment of alpha-amanitin poisoning with N-acetylcysteine, benzylpenicillin, cimetidine, thioctic acid, and silybin in a murine model. Tong TC, Hernandez M, Richardson WH, et al. Annals of Emergency Medicine 50:282–288, 2007.
  3. Personal communication. ASPCA Animal Poison Control Center, Urbana, IL, November 2014.
  4. Mushroom poisoning in dogs. Cope RB. Veterinary Medicine, http://veterinarymedicine.dvm360.com/toxicology-brief-mushroom-poisoning-dogs; accessed February 2015. 
  5. Mushroom toxins. Puschner B. In Gupta RC (ed). Veterinary Toxicology: Basic and Clinical Principles—San Diego: Elsevier Academic Press, 2007, pp 915–925.
  6. Toxic mushrooms. Tegzes JH, Puschner B. Vet Clin North Am Small Anim Pract 32:395–407, 2002.

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