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 ALEUTIAN DISEASE

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Hei865
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Registration date : 2006-09-07

PostSubject: ALEUTIAN DISEASE   Tue Sep 26, 2006 10:12 am

by Dr. Elizabeth Hillyer

Aleutian disease, or AD, is caused by a parvovirus. It was first reported in ranch-bred mink in the 1950's and was named after mink homozygous for the aleutian gene, which typically develop the most severe forms of the disease. Ferrets can be infected with mink strains of the AD virus and there is at least one ferret-specific strain of the AD virus. The infection in both ferrets and mink is characterized by viral persistence associated with non-neutralizing antibody. However, ferrets infected as adults usually do not develop AD virus-associated disease.

The classic form of AD in mink is in immune complex-mediated disease. Affected mink show severe hypergammaglobulinemia, glomerulonephritis, arteritis, plasmacytosis, and progressive wasting. Death occurs within 5 months of infection in Aleutian mink, which are susceptible to all strains of the virus. Depending on the viral strain and host genotype and immune status, non-Aleutian mink may clear the AD virus, become inapparent carriers, or develop progressive disease similar to that seen in Aleutian mink. Decreased fertility, abortion, and neonatal interstitial pneumonitis may also be associated with AD virus infection in this species. Ranch mink are regularly screened for AD, there is no vaccine for the disease.

Ferrets that are experimentally infected with mink strains of AD virus develop virus-specific antibody and show evidence of persistent infection for up to 180 days. however, they do not usually develop the severe disease seen in mink when they are inoculated with either ferret or mink strains fo AD virus. In clinical practice, ferrets can be seropositive for AD virus without ever developing signs of the disease. S. Brown screened over 500 shelter ferrets in Illinios during the 1980's and found that approximately 10% tested seropositive on counterimmunoelectrophoresis. Only two of these animals went on to develop signs of disease consistent with AD.

AD typically manifests as a wasting disease in ferrets. Weight loss, lethargy, pallor, hepatomegaly, splenomegaly, melena, rear leg or generalized weakness, and neurologic signs are all possible findings. A presumptive diagnosis of AD in ferrets is based on the presence of the typical clinical signs in conjunction with hypergammaglobulinemia and a positive antibody titer. Hypergammaglobulinemia is usually pronounced, with gamma globulins representing more than 20% of total protein, and serum protein electrophoresis shows a monoclonal spike.

The two most common tests for AD virus antibody are counterimmunoelectrophoresis and immunofluorescent antibody tests. Counterimmunoelectrophoresis is used for screening mink and is rapid, highly specific, and inexpensive (there is a footnote here to contact United Vaccines, 1-608-277-2030) The immunofluorescent antibody test may be more sensitive than counterimmunoelectrophosesis.

Two case reports describe naturally occurring AD in ferrets. In one report, four ferrets aged 2 years or older developed a chronic, wasting disease; mild hepatomegaly and splenomegaly were present at necropsy. Histologic findings varied in severity but included splenic reticuloendothelial cell hyperplasia, lymphocytic-plasmacytic infiltration in hepatic portal areas, periportal fibrosis, bile duct hyperplasia, and membranous glomerulonephritis. The second case reports AD in two 2 yo castrated male ferrets, both of which had positive AD virus antibody titers on both counterimmunofluorescent antibody testing. Clinical and necropsy findings in these two animals illustrate the spectrum of disease possible in association with AD virus. The first ferret showed anorexia, cachexia, hypochromic microcytic anemia, progressively increasing hyperglobulinemia, and tarry feces. Histologic evaluation at necropsy revealed a mild-to-severe inflammatory infiltrate composed mostly of plasma cells interspersed with lymphocytes in multiple organs, including the meninges, choroid plexus, liver, thyroid gland, heart, salivary glands, common bile duct, pancreas, kidneys, lungs, and lymph nodes. The second ferret tested positive for posterior pareseis;laboratory testing revealed hypoalbuminemia and hypergammaglobulinemia. Clinical signs that developed in this animal included intermittent head tremor, diarrhea, and fecal/urinary incontinence. On histopathologic exam, infiltrations of plasma cells and lymphocytes were found in the doudenum, stomach, salivary gland, liver, thyroid gland, lungs and right atrium; disseminated, nonsuppurative, lymphoplasmacytic encephalomyelitis was present.

There is no specific treatment for ferrets with AD. Instruct the owner how to provide supportive care and be sure that the ferret is on a good diet. The course of the disease is typically chronic. Remember that infected animals can serve as a potential source of infection for other ferrets. There is no vaccine for the disease.
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