Aflatoxicosis in Dogs

Aflatoxicosis in dogs was first described as hepatitis X in 1952. The disease was experimentally reproduced in 1955 using contaminated feed and again in 1966 using purified aflatoxin B₁. Moldy corn poisoning of swine and turkey X disease were reported in the 1940s. Turkey X disease was linked to aflatoxin in 1961.

Aflatoxins are a group of related compounds produced as secondary metabolites of various fungi, including Aspergillus parasiticus, A. flavus, A. nomius, and some Penicillium spp. Aflatoxins are not produced by all strains of these fungi. The most common aflatoxins in grains are named, in part, for their fluorescent color: aflatoxins B₁ and B₂ fluoresce blue and aflatoxins G₁ and G₂ fluoresce green. Aflatoxin B₁ is the most common and most potent of the aflatoxins.

High-energy and high-protein agricultural crops are most often affected. Corn, peanuts, and cottonseed are frequently implicated; however, rice, wheat, oats, sweet potatoes, potatoes, barley, millet, sesame, sorghum, cacao beans, almonds, soy, coconut, safflower, sunflower, palm kernel, cassava, cowpeas, peas, and various spices have been affected. Ingestion of homemade pet foods, moldy garbage, and improperly stored dog foods also has been implicated in aflatoxicosis.

Mold can grow on crops in the field or during storage. Mycotoxin synthesis depends on factors such as temperature, humidity, drought stress, insect damage, and handling techniques.

Commercial grain is screened routinely for aflatoxins, but contamination of pet food has occasionally resulted from sampling errors. Uneven distribution of mold within a given lot of grain (by analogy, one moldy orange in a large bag of fruit or blue veins in a block of blue cheese) increases the risk of sampling error. A simple black light at 366 nm can be used to detect kojic acid, which fluoresces blue-green and is also produced by many aflatoxin-producing fungi, but its presence does not confirm the presence of aflatoxins, and its absence does not guarantee that aflatoxin is not present. More sensitive analyses that test directly for aflatoxins use enzyme-linked immunosorbent assays, high-performance liquid chromatography (HPLC), and liquid chromatography/mass spectrometry. Many pet food companies currently sample each lot of grain before use and sample postproduction batches of pet food for testing to minimize the problem of sampling error.

Toxicity

Dogs and cats are considered very sensitive to aflatoxin (Newbern and Butler, 1969). The oral median lethal dose (LD₅₀) for aflatoxins in dogs ranges from 0.5 to 1.8 mg/kg. It is difficult to determine the total dose of aflatoxin in field cases when detailed information on the amount ingested and period of exposure is not usually available. Exposure to dog food containing as low as 60 ppb of aflatoxin for 60 or more days has been implicated in aflatoxicosis.

The experimental oral LD₅₀ for aflatoxin in cats is 0.55 mg/kg. There is anecdotal evidence of aflatoxicosis in cats known to have consumed contaminated dog food for approximately 3 months. The cats were lethargic and had vomiting and diarrhea. One of the affected cats died and had liver lesions compatible with aflatoxicosis.

Factors such as dose, genetic predisposition, and concurrent disease influence the course of aflatoxin poisoning. Generally, younger animals, particularly males, seem to be more susceptible. Aflatoxin-related deaths in pups sucking a clinically healthy dam have been reported. Pregnant and whelping bitches also appear to be more susceptible. Early castration decreases mortality in males of some species. Low dietary protein enhances hepatocyte damage, whereas nutritional antioxidants, vitamin A, and carotene decrease it.