Nutritional muscle degeneration and steatitis (yellow fat disease) may occur in large, rapidly growing male mink as a result of feeding rancid or excessive, unsaturated fatty acids, together with a deficiency of vitamin E or selenium in the diet. Morbidity and mortality are variable on farms; however, without treatment, mortality may be up to 75%. Affected mink may be found dead, or they may exhibit mild hind end ataxia followed by death. Postmortem findings include serosanguinous effusion within the pericardial sac or thorax, red or white epicardial streaks (similar to white muscle disease in other species), dark urine in the bladder (due to myoglobinuria), and sometimes yellow, edematous internal or subcutaneous fat.
Degenerative cardiomyopathy with fibrosis may be seen microscopically. Hepatic vitamin E concentrations <15 mcg/g can lead to quick death in mink. Control can be achieved through removal of the source of the rancid fats and proper storage of feed. Stabilized vitamin E may be administered in the feed (15 mg/mink, PO, every 24 hours for 4 weeks), and affected kits should be injected parenterally with vitamin E (10–20 mg, SC, every 24 hours for several days), in addition to a single injection of selenium (not to exceed 0.06 mg/kg, SC, once). Feeding a nutritionally sound diet with added vitamin E is preventive.
Fatty liver disease (hepatic lipidosis) has been reported in mink receiving melatonin implants. The implants are administered in the early fall and are used to encourage accelerated growth of the winter pelage so that pelting can begin earlier in the season. Affected animals in good body condition may die without premonitory signs. Gross lesions include marked hepatomegaly and lipidosis and pale, mildly enlarged kidneys with or without digested blood in the stomach and intestines. Microscopically, marked hepatic and moderate renal lipidosis occur. Treatment recommendations for affected animals include addition of choline chloride to the feed and a series of vitamin B injections (0.5 mL, SC, every 48 hours for 3 doses) for mink with melatonin implants. Increased dietary protein may prevent development in melatonin-implanted animals.
Fatty liver disease with sporadic death also may occur when dietary energy is disproportionately derived from fat, during periods of high growth and excessive feed intake in the fall, as well as when mink are excessively diet restricted in the winter or after mobilization of fat reserves in late pregnancy (similar to pregnancy toxemia in other species) or during peak lactation. In general, fatty liver disease results from nutritional imbalances in animals with overweight or obese body condition.
Thiamine deficiency (Chastek paralysis) occurs sporadically in mink and results from ingestion of raw fish containing thiaminase, which results in a vitamin B1 (thiamine) deficiency. Fish containing thiaminase 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 develop anorexia, weakness, and diarrhea and die 2–3 days later after terminal seizures and paralysis. Grossly, bilaterally symmetrical hemorrhage and malacia may occur in the lateral and medial vestibular nuclei. Fish that contain high amounts of thiaminase should be thoroughly cooked (83°C) for ≥5 minutes or fed raw as a portion of the diet only on alternate days. Mink in early stages rapidly recover after injection with thiamine hydrochloride (50 mg/mink, SC, once). Adequate thiamine (brewer’s yeast) should be included in the ration.
Rickets may occur in rapidly growing kits when diets are deficient in vitamin D, calcium, or phosphorus. Affected kits usually crawl unsteadily in a frog-like posture, have soft, defective bones, and are smaller than normal. The once common disorder is rare on mink farms due to modern feeding practices with vitamin and mineral supplementation.
Nursing disease is a complex metabolic disease affecting lactating mink, typically occurring in late lactation (ie, ~40 days after whelping). It is characterized by anorexia, weight loss, lethargy, rapid dehydration, serum electrolyte imbalances, insulin resistance, renal shutdown, and death. The disease is multifactorial, and there may be a genetic predisposition to the disease in animals with certain pale coat color mutations. It is more severe in older females with large litters and during hot weather. Often, affected female mink have concurrent subclinical mastitis. Treatment can be successful if affected females are identified as soon as they begin refusing feed and are rehydrated with sterile balanced electrolyte solutions administered orally or subcutaneously. Female mink may be coaxed to eat raw liver, egg yolks, or canned cat food and should be treated daily until they start eating spontaneously again. Adequate water, environmental cooling systems, fostering kits from large litters to balance litter sizes, better management of feeding practices throughout the year to maintain optimal body condition of breeding females, and early weaning of kits may help to prevent nursing disease. Sodium chloride may be added to the feed (0.42–0.50 NaCl/100 kcal) of nursing females to encourage more fluid intake and reduce the incidence of nursing sickness.
Cotton underfur is characterized by abnormal gray to white undercoat, pale carcass, and poor growth. It usually indicates anemia. It may be caused by consuming certain fish (eg, Pacific hake, coalfish, or whiting) that interfere with iron metabolism and melanin pigment formation in mink. Thoroughly cooking fish (83°C) for ≥5 minutes or feeding it on alternate days is preventive.
Biotin deficiency can cause gray underfur and loss of guard hair as well as exudation and crusting around the eyes, nose, and mouth. It may occur when high levels of uncooked eggs, particularly turkey eggs, are ingested. Avidin, a factor present in eggs, inactivates biotin, a vitamin required for normal pigmentation and hair growth. Affected mink may be administered biotin (1 mg, PO, twice weekly for 4 weeks), and biotin may be added to the ration. Biotin deficiency can be prevented by cooking eggs (91°C) for 5 minutes prior to feeding.