Bacterial Diseases of Mink
Botulism (see Botulism) occasionally causes heavy losses in unvaccinated mink that consume feed containing type C toxin. Usually, many mink are found dead within 24 hr of exposure to the toxin, while others show varying degrees of paralysis and dyspnea. Necropsy findings are nonspecific and related to death from respiratory paralysis. Diagnosis is confirmed by inoculation of serum or filtered tissue from affected mink into mice. The immunotype of the botulism toxin is type C in almost all outbreaks.
Toxic feed should be removed and sampled for testing, and stored feed or ingredients tested for the toxin. Recovered mink are not immune to further challenge. Annual vaccination of kits (at 6–8 wk) and breeders with vaccines containing type C botulism toxoid, Pseudomonas bacterin, distemper, and mink virus enteritis vaccines is highly recommended.
Pseudomonas aeruginosa may result in serious losses. Mink of all ages are affected, particularly during the stress of fall molt. Mink are usually found dead with no prodromal signs. A bloody nasal exudate may be seen at the time of death. Gross lesions include a severe hemorrhagic pneumonia with swelling and consolidation of one or more lung lobes. Treatment involves immediate vaccination of the entire herd. A Pseudomonas bacterin is included in the recommended 3-way vaccine (see above).
Escherichia coli has become the more common cause of hemorrhagic pneumonia in mink as a result of vaccination against Pseudomonas. Gross and clinical signs are indistinguishable from those of Pseudomonas. Bacterial culture is the only way to determine which pathogen is present. Exposure to E coli most frequently comes from contaminated water, but it may also be feedborne. Underlying viral infections such as influenza, Aleutian disease, and distemper must be excluded. Antibiotic sensitivities are a must to assist with treatment selection, because sensitivity patterns for E coli in mink vary greatly.
Urinary tract infections, commonly called “plum bladders,” cause serious losses in females in late spring (during pregnancy and lactation) and in males in late summer and autumn (during the rapid growth and furring period). Several predisposing factors have been suggested, including contamination of food, cages, or nest boxes by pathogenic bacteria; decreased water intake; or increased ash intake.
Mink may die without showing signs, but a large, distended bladder can be palpated grossly, or they may have difficulty in urinating or dribble urine. Occasionally, hematuria may be seen. Necropsy findings include acute hemorrhagic cystitis or pyelonephritis, usually associated with calculi (magnesium ammonium phosphate) in the bladder or kidneys. Various organisms, including staphylococci, coliforms, and Proteus sp, have been isolated.
In severe outbreaks, culture and antibiotic sensitivity tests should be done, and medication added to the feed. Good sanitation to reduce environmental contamination and increasing the water supply help prevent the condition. When a continual problem exists (with magnesium ammonium phosphate calculi), feed-grade (75%) phosphoric acid may be added to the feed (0.8 lb/100 lb [8 g/kg] of wet mixed feed), from March to early June and from mid-July to October, to reduce the urine pH. Feed and urine pH should be monitored to keep urine pH at ≤6. Feed pH should not be <5.1.
A variety of bacteria, mainly staphylococci, streptococci, and Escherichia coli, are involved in mastitis in mink. Staphylococcal mastitis typically results in abscessation of affected glands or subclinical disease evidenced only by mild diarrhea in the kits. E coli causes a peracute, necrotizing mastitis similar to that seen in dairy cattle. Predisposing factors include poor nest box and cage sanitation, rough or sharp edges to the entrance of nestboxes, and high bacterial contamination of feed. Treatment and prevention involve improving management and treating individual animals or the herd with appropriate antibiotics based on sensitivity testing.
Various diseases or signs of disease, including septicemia, pneumonia, purulent pleuritis, abortions, abscesses, cellulitis, and enteritis, occur sporadically; occasionally, they may become herd problems. Many bacteria, including Proteus, Klebsiella, and Campylobacter spp, coliforms, streptococci, staphylococci, and salmonellae, have been isolated.
Treatment should be based on antibacterial sensitivity tests. Drugs may be administered parenterally or in the feed or water. Dosage can be estimated on the basis of body wt; female mink weigh ~2–3 lb (0.9–1.4 kg), and males ~5–6 lb (2.3–2.8 kg). Dosages recommended for cats should be used and adjusted for weight. However, some sulfonamides (eg, sulfaquinoxaline and sulfamethazine) and streptomycin should not be used in mink. Trimethoprim/sulfadiazine causes abortions in pregnant female mink.
The source of infection should be determined and eliminated. Enteritis often is caused by contaminated or spoiled feed and dirty nest boxes. Abscesses are often caused by injury from wire or splintered wood in the pens, awns in hay or straw used for bedding, or spicules of bone in the feed. Outbreaks of tularemia, anthrax, brucellosis, tuberculosis, and clostridial infections have been caused by feed contaminated with tissue of animals that have died or are carriers of these infections. Careful selection of feed ingredients and disinfection of equipment and pens are important in prevention and control of many infections. Dead stock should not be used as mink feed.