Steatitis or myositis
(yellow fat disease, see Yellow Fat Disease) occurs in young, rapidly growing mink as a result of excessive, rancid, unsaturated fatty acids and a deficiency of vitamin E in the diet. Affected mink may be found dead, or they may exhibit slight locomotor disturbances followed by death. Necropsy findings include yellow, edematous internal or subcutaneous fat that contains an acid-fast pigment. It is more common to find myoglobinuria and dark red bladders (resembling plum bladder). Histopathology shows myositis and cardiomyopathy. Hepatic vitamin E levels <15 mcg/g can lead to acute death. Control consists of removal of the source of the rancid fats and polyunsaturated oils and proper storage of feed. Stabilized vitamin E may be administered in the feed (15 mg/mink) for 4 wk, and affected kits should be injected parenterally with 10–20 mg of vitamin E for several days. Feeding a nutritionally sound diet with added vitamin E is preventive.
(thiamine deficiency) results from feeding certain raw fish that contain the enzyme thiaminase. These include whitefish, freshwater smelt, carp, goldfish, creek chub, fathead minnow, buckeye shiner, sucker, channel catfish, bullhead, minnow, white bass, sauger pike, burbot, and saltwater herring. Affected mink gradually become anorectic, lose weight, and die after terminal convulsions and paralysis. Fish that contain high levels of thiaminase should be thoroughly cooked at 181°F (83°C) for ≥5 min, or fed raw as a portion of the diet only on alternate days. Mink injected with thiamine hydrochloride, 50 mg, SC, recover rapidly. Adequate thiamine (brewer's yeast) should be included in the ration.
Rickets occurs due to the rapid growth rate of kits when rations are deficient in vitamin D, calcium, or phosphorus. Affected kits usually crawl unsteadily in a frog-like posture, have rubbery bones, and are smaller than normal. The diet should be supplemented as required, and severely affected kits may be treated individually. (see Rickets.)
Nursing disease is a metabolic disease that affects lactating mink ~40 days after whelping. It is characterized by rapid dehydration, serum electrolyte imbalances, renal shutdown, and death. Treatment can be successful if affected females are identified as soon as they begin refusing feed and rehydrated with IP or SC sterile fluids. The disease is multifactorial; although there appears to be a genetic predisposition in certain light color mutations, it is more severe in females with large litters and during hot weather. Often, affected females have concurrent subclinical mastitis. Adequate water, environmental cooling systems, fostering kits from large litters to make litter size more manageable for the female, and early weaning help prevent this condition.
Cotton underfur usually indicates anemia and may be caused by feeding certain fish (Pacific hake, coalfish, whiting) that interfere with iron metabolism in mink, which affects melanin pigment formation. Thoroughly cooking the offending fish at 181°F (83°C) for ≥5 min or feeding it on alternate days prevents the condition.
Biotin deficiency, which can cause gray underfur and loss of guard hair, is seen when high levels of uncooked eggs, particularly turkey eggs, are fed. Avidin, a factor present in eggs, inactivates biotin, a vitamin required for pigmentation and hair growth. Affected mink may be injected with 1 mg biotin twice weekly for 4 wk, and biotin may be added to the ration. Biotin deficiency can be prevented by cooking eggs at 196°F (91°C) for 5 min.
Last full review/revision October 2014 by Hugh Hildebrandt, DVM