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Order: Carnivora
Family: Mustelidae
Genus: Mustela
Species: vison
Subspecies no longer considered important and most ranch mink are a composite.
Chromosomes 2n = 30.
The hair coat is genetically controlled. Dark brown color is dominant and the other 90 plus hair coat colors are single, double, triple, or quadruple recessive gene combinations.
9.4.1.1 Rotulism (Clostridium botulinum.)
Toxin is present in contaminated offal. Onset of paralysis occurs 12-96 hrs. post- ingestion. May see incoordination followed by paralysis. Death is due to paralysis of muscles of respiration. Vaccinate weanlings with commercially-prepared toxoid. Feed well preserved or fresh food.
9.4.1.2 Streptococcosis - (alpha-hemolytic streptocci).
May see numerous syndromes:
- A. Subcutaneous abscesses around the head and neck. Lance abscess, flush and begin a penicillin regime (10 to 12,000 IU IM sid for 5-7 days).
- B. Cellulitis of head and throat: Mink are sluggish and anorexic with greatly swollen heads. Syndromes resembles distemper so culture aspirated fluid or tissue. Treat with penicillin.
- C. Septicemia in weanlings. May see acute death of one kit in the litter. Need to necropsy and culture blood or spleen. Treat other kits with penicillin.
9.4.1.3 Salmonellosis
Not well described in mink. Salmonella spp.Known to cause abortions and diarrhea in mink. Culture if organism is suspected. Enforce better husbandry (improved sanitation, isolation of exposed animals, etc.) and examine food source and maintenance.
9.4.1.4 Gray Diarrhea
Etiology is unknown. Disease can occur in mink of all colors, but more prevalent in Aleutian color. Clinically will see gradual increase in food intake with progressive weight loss. The mink become more active and pass gray. foul-smelling, putty stool. Diarrhea may last 3-4 months with eventual death. Evidence points to a malabsorption syndrome. Treatment with antibiotics is unsuccessful.
9.4.1.5 Pasteurellosis - (Pasteurella multocida).
Disease outbreaks occur during spring and fall. Infection of the respiratory tract occurs with clinical signs apparent usually when the lower respiratory tract is involved. May see dyspnea or depression followed by death. Treatment with antibiotics frustrating due to chronicity of infection. May try penicillin or tetracyclines (16 mg/kg g) 8 hr p.o. or 6 mg/kg g 12 hr IV or IM).
9.4.1.6 Pseudomoniasis - (Pseudomonas aeruginosa).
Infection causes explosive outbreaks of pneumonia with source of infection usually traced to a contaminated water supply. Clinical illness of depression and epistaxis may last only 1-2 hrs prior to death. Treatment is difficult. Sulfathiazole is drug of choice but is toxic to mink.
9.4.2.1 Distemper - (Paramyxovirus).
Virus is transmitted by direct contact and infected fomites. As in the canine, mink can exhibit clinical disease followed by death or by remission or can be non-clinical carriers. Clinically, mink may have a serious oculonasal discharge which progressively becomes mucopurelent and crusty. The head and feet become swollen and hyperkaratosis of the footpad is not unusual. CNS signs may or may not occur. Necropsy shows spenomegaly, pneumonia and edema of the subcutis of the head. Diagnosis is made by histopath, virus isolation of ferret inoculation. Quarantine new stock for 50 days before adding to herd. Vaccinate kits at 10 weeks of age (MLV vaccine of chick embryo or mink tissue culture origins). Prevent exposure to dogs.
9.4.2.2 Viral Enteritis - (Same as Panleukopenia in felines - Parvovirus).
Highest mortality is seen in kits. Virus is transmitted by direct contact and infected fomites. Clinical signs include sudden onset of of anorexia with passage of mucoid feces. The animals quickly become dehydrated. On necropsy there are watery intestinal contents with a hemorrhagic mucosa. The lymph nodes and spleen are usually enlarged. Characteristic histopath lesion are the denuded villi of the small intestine with cellular debris in the crypts and lymphoid depletion. Treatment difficult. Prevent by vaccinating kits at 8-10 weeks of age with killed vaccine of mink spleen or mink tissue culture origin.
9.4.2.3 Transmissible Encephalopathy - (Mink scrapie - slow virus).
Disease has 9 months incubation with no apparent stimulation the animal's immune response. Infected mink will gradually show dysphagia followed by hyperexitability. Prior to death, the animal becomes progressively more somnolent. The virus is believed to be food-borne. There is no treatment to vaccine.
9.4.3.1 Dermatophytosis - (Michrosporium canis primarily).
Mink are relatively resistant. Kits may show patchy alopecia on head and feet with spontaneous regression when kit matures.
9.4.4.1 Fleas (Ceratophyllus vision)
9.4.4.2 Lice (Trichodectes refuses)
9.4.4.3 Mites (Sarcoptes spp., Tyroglyphus spp., Cheyletiera spp.)
9.4.4.4 Coccidia (Eimeria spp.)
See mortality in weaned kits (summer and early fall). Can occur in herds housed on solid or wire floors. Adults mink are source of infection. See mucoid feces, anorexia and weight loss lasting 4-10 weeks. Immunity develops following infection. Sulfapyrimadines (merazine, methazine, etc.) 50 mg/kg g 12 h p.o. or sulfaquinoxaline 3.5 gm/L water for 2 weeks, improve sanitation.
9.4.5.1 Urinary Calculi
Magnesium ammonium phosphate.
9.4.5.2 Steatitis
Seen in weanling kits on high unsaturated fat diet with low vitamin E. (stored horse meat or fish scrap). See sudden death or incoordination prior to death. Supplement with 5 IU vitamin E/day/mink for prevention, for affected animals, administer 15-20 IV vitamin E IM/Mink plus feed fresh meat or liver to which 15 IU vitamin E has been added.
9.4.5.3 Rickets
9.4.5.4 Chastek's Paralysis
Thiamine deficiency. Caused by feeding raw fish containing thiaminase (carp, suckers, goldfish, white bass, burbot, whitefish, ocean herring, bullhead and channel catfish). Add brewer's yeast to diet, cook fish or feed raw fish on alternate days.
Urinary Incontinence - ("wet belly"). Etiology is unknown. Can affect up to 10% of males in herd. Some ranchers found that increasing the carbohydrate concentration of the ration successfully treated the condition. Some associated condition with Proteus spp. Infection and/or calculi and treated mink with ammonium chloride or acid phosphate salts to acidify the urine.
Two major diseases attributed to genetic makeup;
AD was found to affect mink that are homogeneous for the autosomal recessive gene (a) for gray coat color. All mink are susceptible to the disease, but only (aa) mink died before pelting age (7 mos). Disease is caused by an unidentified virus which causes a chronic viral infection. Transmission is thought to occur via oral and aerosol routs. Also researchers have demonstrated vertical transmission. Several body tissues have been found to be infective (urine, saliva, blood, and bone marrow). Principle lesions consist of plasma cell proliferation and
infiltration of all viscera, marked hypergammaglobulinemia, bile duct proliferation with hepatic periportal fibrosis and fibrinoid degeneration of arteries, especially in periportal fibrosis and fibrinoid degeneration of arteries, especially in the renal glomeruli. AD is thought to be related to plasma cell myeloma.
In mink, animals affected with CHS are homozygous recessive for Aleutian gene (a). Studies show all (aa) mink examined have CHS and may explain genotypic susceptibility of (aa) mink to AD virus. In experimental and natural infections, CHS mink infected with AD virus had a higher, faster mortality than non-CHS, AD-infected mink. CHS is characterized by the presence of inclusions (giant lysosomes) in circulating leukocytes, partial albinism and histiocytic infiltration of multiple organs.
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