The term mycotoxin generally refers to secondary metabolites of molds growing on foodstuffs, and the synthesis of many mycotoxins
is genetically controlled. In addition, mycotoxin production [and subsequent concentrations produced] can be modulated by
the substrate composition and texture, pre-existing plant pathology, humidity, temperature and oxygen levels.
Aflatoxins are mycotoxins produced mainly by Aspergillus fungi that potentially can be found in food items [e.g., pet food, moldy cheese and bread]. Most, if not all, of the confirmed
cases of aflatoxicosis reported in the literature have been documented in dogs, though cats are known to be susceptible via
experimental studies. Aflatoxins are metabolized extensively by the liver following intestinal uptake, and the majority of
the toxic effects are observed in the liver. The reactive epoxide causes severe hepatocellular necrosis, which leads to decreased
Exposures can be acute, or last several days to a weeks; depending on the aflatoxin concentration, the onset to clinical signs
can be quite variable. Acute exposures can cause abrupt onset of depression, weakness, severe vomiting and diarrhea, icterus
and evidence of bleeding.
The most commonly reported aberrations observed on a complete blood count and serum chemistries include increases in serum
hepatic enzyme activity [ALT, AP, AST], hypoalbuminemia, hyperbilirubinemia [hyperbilirubinuria], and elevated ammonia levels.
More severely affected patients display prolongation of bleeding times, elevation in bile acids, thrombocytopenia and anemia.
Confirmation of poisoning is best done by aflatoxin residue testing of any remaining suspect food items, or possibly liver.
Histopathological examination of the liver can reveal areas of necrosis and fatty change with biliary hyperplasia, varying
degrees of inflammatory changes, megalocytosis and areas of nodular hyperplasia.
There is no specific treatment of aflatoxicosis - a successful outcome requires aggressive therapy directed to the problems
observed. Some treatment options include IV fluids, electrolytes, vitamins B12 and K1, plasma/blood transfusions, silymarin, SAMe, actigall and parenteral nutrition.
Vomitoxin [deoxynivalenol, DON] has been an infrequent cause of poisoning in pets. This trichothecene mycotoxin has been detected in
dog food, where the toxin was produced by Fusarium mold growing on grains [wheat, corn, barley oats] that had been added to
the food. Vomitoxin appears to be heat stable and levels of 4 to 7.5 ppm in the diet have caused feed refusal in dogs and
cats, respectively. Vomiting in dogs and cats has been observed at dietary concentrations of 8 to 10 ppm. In other species,
vomitoxin has been linked to skin irritation, cardiotoxicity and immune system abnormalities. In addition to feed refusal
and vomiting, diarrhea and abdominal tenderness have also been reported. Confirmation of poisoning is best done by vomitoxin
testing of the remaining suspect feed. Recovery is rapid and generally uneventful following removal of the contaminated
feed from the diet.
The tremorgenic mycotoxin penitrem A can be produced by a few Penicillium molds which commonly grow on moldy food items [cheese, bread and nuts are favorite substrates] and in garbage and compost
piles. Poisonings in dogs is frequent, and though cats are considered sensitive to the toxic effects of this mycotoxin, poisonings
are rarely reported. Poisonings have been observed following ingestion of as little as a single slice of moldy bread. Roquefortine
is another compound commonly isolated along with penitrem A; though it is questionable whether this is responsible for any
of the clinical problems observed and may be useful as a diagnostic marker.
Clinically, one generally sees an abrupt onset of salivation, muscle tremors and seizures. Poisoned patients often display
hyperresponsiveness to external stimuli, so this clinical disease is very similar to pets exposed to strychnine, metaldehyde,
bromethalin or chlorinated hydrocarbons. No pathognomonic or consistent abnormalities are observed on a complete blood count,
serum chemistry panel or urinalysis, and confirmation of poisonings is generally obtained by residue testing of the vomitus/stomach
contents, lavage washings, and in some cases, urine, bile and serum.
Treatment plans should include aggressive decontamination procedures [e.g., emesis, gastric lavage, activated charcoal, cathartic]
if deemed appropriate. The toxin is thought to be excreted by the bile, so repeated doses of activated charcoal may be of
benefit. The tremors and seizures are generally controlled with diazepam or methocarbamol [barbiturates can be used for longer
seizure control]. Supportive care should include IV fluid therapy, correction of any electrolyte and acid-base abnormalities,
proper thermoregulation and parenteral nutrition. Signs may persist up to 5 days depending on exposure dose.
Acute pulmonary hemorrhage during isoflurane anesthesia in two cats undergoing a routine dental cleaning was recently associated
with exposure to the toxic black mold Stachybotrys chartarum. One of the cats died, and the other cat responded to supportive
care. The house where the cats lived had been severely contaminated with mold as a result of weather damage several months
previous to the illness. Satratoxin G, a biomarker for the mold, was detected in serum from both cats.
Mader DR et al. Acute pulmonary hemorrhage during isoflurane anesthesia in two cats exposed to toxic black mold (Stachybotrys chartarum). JAVMA 231(5):731-735.
Hooser SB and Talcott PA. 2006. Mycotoxins. In Small Animal Toxicology, Eds. ME Peterson and PA Talcott, Elsevier Inc., pp.