Lead poisoning may occur in mink that have ingested lead paint from wire, feed or waterer devices, or other equipment. Affected mink gradually lose weight and die within 1–2 months with clinical signs consistent with gastroenteritis, muscular incoordination, stiffness, trembling, seizures, and death disturbance. Individual mink may be treated with calcium EDTA as a chelating agent. All sources of lead should be removed.
Insecticides other than pyrethrum, piperonyl butoxide, and rotenone may be highly toxic to mink of all ages. All insecticides may be toxic to kits < 8 weeks old, and application on or near nest boxes should be avoided.
Wood preservatives (chlorinated phenols and cresols) can cause mortality in kits in the first 3 weeks of life and occasionally in older mink. These preservatives should not be used where mink can readily access and chew materials (eg, pens, nest boxes, or nest litter). Shavings used as nest box litter should not contain wood preservatives.
Diethylstilbestrol causes reproductive failure and a high incidence of urinary tract infections in mink and should not be included in the ration. Similarly, thyroid and parathyroid glands included in meat trimmings fed to mink may result in reproductive failure if present at high levels.
Chlorinated hydrocarbons and polychlorinated biphenyls contained in the ration can cause reproductive failure. Mink are exquisitely sensitive to the effects of polybrominated biphenyls; 1 ppm in the ration has resulted in reduced litter sizes and decreased kit viability. ( See also Persistent Halogenated Aromatic Poisoning.)
Dimethylnitrosamine (DMNA), found in fish meal preserved with sodium nitrate, sodium benzoate, or formalin, is hepatotoxic to mink. The chemical causes hepatic degeneration, ascites, and extensive internal hemorrhage when consumed by mink.
Sulfaquinoxaline can disrupt normal coagulation in mink, leading to extensive internal hemorrhage.
Streptomycin may cause dyspnea and CNS depression in mink and should be avoided.
Salt toxicosis may be seen in young kits starting on solid food. Affected kits become dehydrated and, after rehydration, show classic CNS signs of salt toxicosis, including tremors, seizures, and death. The most common inciting factor is increased salt concentrations in feedstuffs. By-products from the cheese, poultry, fish, and processed sandwich meat industries often contain high salt concentrations. Kits eating feed supplemented with high amounts of sodium chloride to prevent nursing sickness in the dam may also die from salt toxicosis if access to water is limited.
