Aleutian Disease (Plasmacytosis)
This parvovirus infection is characterized by poor reproduction, gradual weight loss, oral and GI bleeding, renal failure and uremia, and high mortality. All color phases of mink may be infected, but light color phases genetically derived from the Aleutian color phase are most susceptible. The causative parvovirus is not related to mink viral enteritis (see Mink Viral Enteritis). Transmission occurs in utero and by direct or indirect contact with infected mink.
After infection, immunoglobulin levels frequently increase markedly. Immuno-globulins are unable to neutralize the virus; immune complexes form and deposit in various tissues, resulting in immune-complex glomerulonephritis and arteritis. Gross pathologic changes include splenomegaly, renal changes (varying from swelling and petechiation to atrophy and pitting), and enlargement of mesenteric lymph nodes. Histologic lesions include plasma cell infiltration in the kidneys, liver, spleen, lymph nodes, and bone marrow; bile duct proliferation; membranous glomerulonephritis; and fibrinoid arteritis. Kits from dams negative for Aleutian disease virus may die from acute interstitial pneumonia.
The disease is controlled through a test and slaughter program. Positive mink are identified by blood testing for specific antibody by counterimmunoelectrophoresis. All positive mink should be culled. Mink that are to be kept for breeding stock should be tested in late fall (before selection of breeding stock and pelting) and in January or February (before breeding). New introductions to the herd should be tested.
There is no vaccination or effective treatment. The virus is present in the saliva, urine, feces, and blood of infected mink. Pens should be steam cleaned and dipped in or sprayed with 2% sodium hydroxide. Equipment should be disinfected after handling, vaccinating, or testing mink on infected farms. Raccoons and flies may serve as vectors, and their control is essential.
Mink of all ages are susceptible to canine distemper virus (see Canine Distemper). The incubation period is 9–14 days. The virus may be recovered from infected mink 5 days before clinical signs appear. Recovered mink may continue to shed the virus for several weeks. Transmission may be direct (through contact or aerosol) or indirect.
Clinical signs include nasal and ocular discharge; hyperemia, thickening, and crustiness of the skin on the muzzle, feet, and ventral abdominal wall; neurologic signs (convulsions and “screaming fits”); or a combination of these. Histologic ELISA, immunohistochemistry, or fluorescent antibody examination may reveal intracytoplasmic or intra-nuclear inclusions or distemper antigen in epithelial cells of the bladder, kidneys, bile ducts, intestine, lungs, trachea, and occasionally brain.
In outbreaks, affected mink should be culled, and the balance of the herd vaccinated as soon as possible. Deaths from neurotropic distemper may occur until 12 wk after vaccination. Kits should be vaccinated prophylactically when 11–12 wk old with a modified live vaccine contained in a recommended 4-way vaccine. Ordinarily, adults are vaccinated at the same time.
Mink Viral Enteritis
This highly contagious disease is caused by a parvovirus related to, but not identical with, that of feline panleukopenia (see Feline Panleukopenia). All ages are susceptible, but the disease is most serious in kits. Transmission usually occurs by the fecal/oral route; the incubation period is 4–8 days.
Clinical signs include sudden anorexia; depression; watery, mucoid, blood-tinged diarrhea; dehydration; and death. Characteristic gross lesions include a flaccid, dilated, hyperemic small intestine with liquid fetid contents. Some mink may die suddenly with no gross lesions. Intestinal lesions are characterized by erosion of surface mucosa, blunting and attenuation of villi, and dilation of crypts. Ballooned epithelial cells may contain inclusion bodies similar to those of feline panleukopenia. A fluorescent antibody procedure is used to confirm the diagnosis. Splenic and lymph node lesions include lymphoid depletion and necrosis.
Early in an outbreak, all mink showing signs should be culled or isolated, and all clinically normal mink should be vaccinated immediately. Affected mink can be treated PO with a mixture of kaolin, pectin, and neomycin. Mink viral enteritis can be prevented by vaccination. All mink should be vaccinated when they reach 11–12 wk old with a combination 4-way vaccine containing mink viral enteritis, distemper, botulism, and Pseudomonas. Annual vaccination is recommended.
Aujeszky's Disease (Pseudorabies)
This occurs occasionally in mink fed pork products contaminated with pseudorabies virus (see Pseudorabies). Mortality may be high and clinical signs are referable to the CNS (tonic and clonic convulsions, excitement alternating with depression, and self-mutilation in some cases). Diagnosis is confirmed by virus isolation or serology. Because contaminated pork is the usual source of infection, all pork products should be cooked before being fed to mink.
Epizootic Catarrhal Gastroenteritis
Millions of mink have been affected by an agent (most likely a virus) that causes an acute catarrhal gastroenteritis. The disease usually occurs in adult dark mink. Outbreaks occur most frequently during times of stress, eg, during early fall molting, spring mating, and whelping seasons. Clinical signs (mucus in the feces and partial anorexia) rarely last longer than 5–6 days. Death may occur if the affected mink are immunosuppressed by the Aleutian disease virus. There are no commercially available vaccines. Treatment is symptomatic and of questionable value. It is important to differentiate this condition from mink viral enteritis.
Last full review/revision April 2012 by John R. Gorham, DVM, PhD