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Fungal toxicosis in the mink (Mustela vison)

University of British Columbia

The spontaneous occurrence of a liver disease in mink (Mustela vison) prompted an investigation of the animal's environment in the search for a possible aetiological factor. The pathological findings suggested that the disease was diet-induced and possibly resulted from the presence of a toxic factor in the feed. A series of experiments were carried out to ascertain if the condition arose through the action of a transmissible infective agent or from an inadequate supply of some essential nutrient. No evidence was obtained in support of either of these possibilities. Since the pathology noted was suggestive of a hepatotoxic factor or factors and was unlike any of the described intoxications arising from bacterial metabolites, major attention was given to a study of the possible role of the fungi as causative agents. Some fungi, when given the necessary conditions of temperature, moisture and substrate, elaborate toxins that are poisonous to a large number of species. The possibility that a fungal toxin was the cause of the disease in mink was therefore investigated. A literature review covering the mycotoxicoses has been compiled. In order to test the susceptibility of the mink to fungal toxicosis, a model was set up in which mink were fed a ration containing a known fungal toxin, aflatoxin. The mink proved highly susceptible to this toxin. The pathology of aflatoxicosis in the mink has been documented. The fungal population of the mink ration and its cereal ingredients was examined for toxin-producing fungi. A series of toxicity assays were conducted to screen the large number of organisms isolated from mink rations. Toxigenic fungi were isolated from: wheat used in mink ration formulations. The role of cottonseed oil as an agent contributing to this liver condition has been investigated. It is suggested that cottonseed oil either contains a toxic component or contains a specific factor which can be used by a fungus in some phase of its metabolism, and that the by-product of this metabolic pathway may accumulate as a toxic compound.

Text

2011-09-15

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http://hdl.handle.net/2429/37361

Animal Science

University of British Columbia

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