Aleutian disease is a parvovirus infection 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. Immunoglobulins 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.
Aleutian disease is controlled through a test and slaughter program. Positive mink are identified by blood testing for specific antibody by counterimmunoelectrophoresis or lateral flow ELISA. All positive mink should be culled. Mink 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.
Genetic selection of resistant mink using a quantitative ELISA and/or iodine agglutination test is being used to increase survivability and reproduction. These tests identify mink with hypergammaglobulinemia for culling. The quantitative ELISA identifies overall antibody levels to Aleutian virus, allowing mink with lower antibody levels to be selected for breeding.
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 intranuclear inclusions or distemper antigen in epithelial cells of the bladder, kidneys, bile ducts, intestine, lungs, trachea, and occasionally brain. Recent outbreaks have required PCR confirmation, because immunohistochemistry testing was negative.
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. Ordinarily, adults are vaccinated at the same time.
Mink viral enteritis is a highly contagious disease 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 healthy 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 at least 6–8 wk old with a combination 3-way vaccine containing mink viral enteritis, botulism, and Pseudomonas. Annual vaccination is recommended.
The first case of influenza was identified in the USA in mink in October 2010. Since then, it has become a frequent cause of disease on mink ranches. Influenza usually presents with coughing and sneezing heard in areas of the ranch. Losses usually increase due to secondary bacterial infections. Influenza has also affected newborn kits, presenting as increased respiration and significant death losses. Exposure to influenza can come from multiple sources. Raw pork, poultry products, and sick employees may all be avenues for virus introduction. Treatment consists of treating secondary infections to mitigate losses. Spread across the ranch usually takes 2–6 wk. After the disease runs its course, >90% of mink have been shown to be antibody positive.
Aujeszky disease 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.
Astrovirus infection is a self-limiting neurologic disease seen sporadically in mink kits from mid June to mid July. Usually, the condition is limited to one kit per litter, with an incidence of 0.1%–2%. Higher incidence has been reported on a European ranch. Kits have tremors, and histopathology shows meningoencephalitis. Mortality is low and appears to be caused by inability of the mink to eat or drink because of the shaking. Early in the disease, astrovirus can be identified, but later the mink clear the virus and are negative. Lesions and clinical signs do not improve, and euthanasia of affected mink is warranted for welfare concerns.
Millions of mink have been affected by an agent (most likely a coronavirus) that causes an acute catarrhal gastroenteritis. The disease usually occurs in adult dark mink. Outbreaks occur most frequently during times of stress, eg, 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 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.