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Moldy Food Toxicity

By Susan Smith, DVM
angell.org/emergency
MSPCA-Angell West
781-902-8400

Ingestion of moldy foods can cause severe and potentially life-threatening systemic poisoning in pets. Several common sources of moldy food exposure in undiscerning dogs include unsecured trashcans, compost, and moldy nuts or fruits that have fallen from trees. The term mycotoxin refers to secondary metabolites produced by several fungal species that grow on various foods. It is interesting to note that molds can grow under a wide range of temperatures from 32°F to 140°F, and different species have different oxygen requirements, but the optimal temperature range for mold growth is 68°F to 86°F, which covers the typical room temperature range.1 This article will focus on two common types of mycotoxins seen in veterinary medicine.

 

 

Tremorgenic mycotoxins are neurotoxins that produce varying degrees of muscle tremors or seizures that can last for hours or days. Approximately 20 mycotoxins have been identified as tremorgens. The most frequently reported tremorgenic mycotoxin to affect dogs is penitrem A, which is produced by Penicillium spp.2 It grows on meat, cereals, nuts, cheese, eggs, fruits, refrigerated food, refuse, and compost.  Affected dogs may have a history of running unsupervised or of ingesting compost, garbage, or moldy foods within two hours before the onset of signs. Clinical signs can be dose-dependent. A small quantity of toxin ingestion can cause fine muscle tremors that may last for several hours or days. With larger exposures, the tremors can be severe, progress to seizures, and may result in disseminated intravascular coagulopathy, multiple organ failure, and death. Vomiting often precedes the earliest tremors, which may help limit the severity of illness. Confirming the diagnosis takes time and is often not feasible because stomach contents or remaining moldy material must be submitted to a diagnostic laboratory for analysis and is not always readily available. Other toxins can cause similar clinical signs; these include strychnine, bromethalin rodenticide, pyrethroids, metaldehyde (slug and snail baits), ethylene glycol, macadamia nuts, cholinesterase inhibitors, methylxanthines, human medications such as pseudoephedrine hydrochloride, and illicit drugs such as amphetamines and cocaine.3 Treatments for tremorgenic mycotoxin toxicity typically involve decontamination when possible and supportive care. Supportive care includes IV fluid therapy, correction of any electrolyte and acid-base abnormalities, thermoregulation, and most importantly, controlling tremors and seizures with muscle relaxants, benzodiazepines, and barbiturates. Patients’ vital signs are monitored closely as hyperthermia (elevated temperature) may occur secondary to muscle tremors/seizures. Decontamination is performed, including emesis induction, gastric lavage, and activated charcoal/cathartic when deemed appropriate. Intravenous lipid emulsion therapy, a newer treatment used for lipid-soluble toxins, has been attempted in mycotoxin cases and has demonstrated beneficial effect.4

Aflatoxins are mycotoxins produced mainly by Aspergillus fungi.  Aflatoxins typically do not produce signs of toxicosis until after they have been absorbed from the gastrointestinal tract, so decontamination is usually futile.  Once absorbed, aflatoxins are rapidly metabolized by the liver. Dose-dependent hepatocellular (liver) injury occurs from the production of free radicals that cause oxidative damage, ultimately resulting in liver failure in many cases. Depending on the aflatoxin concentration, the onset to clinical signs can be variable. Acute exposures can cause depression, weakness, vomiting and diarrhea, icterus and evidence of bleeding (petechiae, melena, epistaxis, and hematemesis).  The most common blood work abnormalities include liver enzyme elevation, low albumin, elevated bilirubin, and elevated ammonia. More severely affected patients display prolongation of bleeding times, elevation in bile acids, thrombocytopenia (low platelet count) and anemia (low red blood cell count). Confirmation of poisoning is best done by either aflatoxin residue testing at a diagnostic laboratory, or via liver biopsy, as aflatoxin produces unique changes in the liver that can be detected on histopathology with liver biopsies. There is not an antidote for aflatoxin; treatment requires aggressive supportive care including IV fluids, plasma/blood transfusions, vitamin K supplementation, and liver protectants. Unfortunately, mortality is high for aflatoxin toxicity. There have been a number of aflatoxin outbreaks in dogs in recent years from contaminated dog food. A timely trip to the veterinarian is recommended if moldy food consumption is noted, or if multiple pets in the same household show any clinical signs mentioned above.

 

[1] Beasley VR: Tremorgenic mycotoxins and various staggers syndromes, in A Systems Affected Approach to Veterinary Toxicology. Urbana, IL, University of Illinois, 1997, pp 137-142.

[2] Schell MM: Tremorgenic mycotoxin intoxication. Vet Med 95(4):283-286, 2000

[3] Lowes, N.R.  et al .: Roquefortine in the stomach contents of dogs suspected of strychnine poisoning in  Alberta.  Can Vet. J. 33:535-538; 1992.

[4] Kormpou, F., O’Sullivan, A., Troth, L. et al: Use of intravenous lipid emulsion in dogs with suspected tremorgenic mycotoxicosis: 53 cases. Vet Evid. 3; 2018.

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