ALEUTIAN DISEASE.
Formally considered a disease of mink, the parvovirus that causes Aleutian disease is becoming increasingly prevalent in ferrets. A fulminant lethal infection in mink, the Aleutian disease virus appears to be a chronic latent infection in ferrets (often referred to as "hypergammaglobulinemia" of ferrets), which causes clinical disease over a period of one to two years. While the parvovirus itself causes little or no harm to the ferret host, the marked inflammatory response generated by the ferret may cause life-threatening hematopoietic and urinary derangement. The large number of antigen-antibody complexes associated with the humoral response to the presence of the virus results in a systemic vasculitis (with the most prominent lesions being in the glomerular capillaries, resulting in eventual renal failure and death). The marked lymphoplasmacytic response interferes with bone marrow hematopoiesis, and local accumulations of plasma cells may result in organ derangement.

In 1997, a rescue facility in San Antonio, Texas experienced an epizootic of AD which was unlike any previously documented. In contrast to the 40% or less morbidity seen in other facilities, 61/65 animals tested positive on CIEP testing for AD virus antibodies. Early signs of infection noted in a number of animals were an ascending paralysis and respiratory signs such as sneezing or coughing. Post-mortem on one of these animals showed characteristic plasmacytic infiltrates in the spinal cord and other organs. Similarly affected animals who received supporting treatment recovered from the paralysis, but have since gone on to succumb two years later of more characteristic disease (glomerulonephritis, hypergammaglobulinemia, etc.) Similar facility outbreaks have been reported in Wisconsin, Alabama, Maryland, and Virginia.

Clinical signs. Most infected ferrets remain asymptomatic until shortly before death. Non-specific signs include lethargy, anorexia. Ataxia and paraparesis may be seen classically in chronic cases (but occasionally in very acute cases as a premonitory sign) due to accumulations of inflammatory cells within the spinal cord.. Anemia, thrombocytopenia, and/or leukopenia, cutaneous hemorrhages, and secondary infections may be seen in various combinations in end stage disease.

Diagnosis. An elevated globulin (defined as >20% of the total protein) is strongly indicative of this disease. Ferrets with total proteins over 7.5, especially those with mildly decreased albumins should be immediately suspect. Additionally, a CIEP test is commercially available from United Vaccines, and may be run on a hematocrit tube of blood. Biopsy or necropsy specimens from infected ferrets (particularly kidney, spleen, and liver) often yield a presumptive diagnosis.

Gross lesions. Gross lesions are seen only late in the course of disease. Splenomegaly and lymphadenopathy are the most common gross lesions with this disease; splenic infarction as a result of marked splenomegaly may complicate the clinical and pathologic picture.. Enlarged, brown-tan kidneys may be present. In terminal cases, clotting abnormalities resulting from vasculitis and the marked hypergammaglobulinemia may result in petechial hemorrhage and hematuria.

Microscopic lesions. Several characteristic microscopic findings are seen in ferret AD as well as in the mink disease. Prominent plasmacytic infiltrates are seen in numerous organs, most prominently in the renal interstitium, hepatic portal areas, and in the splenic red pulp, where an almost pure population of plasma cells expands the red pulp. Additionally, there may be marked plasmacytosis of numerous lymph nodes and the bone marrow. In most cases, there will be marked membranous glomerulonephritis and numerous ectatic protein-filled tubules as a result. (Note: Glomerulosclerosis is commonly seen in chronic interstitial nephritis in this species - but there is little evidence of tubular protein casts or plasmacytic infiltrate in uncomplicated CIN). Vasculitis may be seen in almost any organ.

Treatment. There is no current treatment for Aleutian disease in the ferret, nor is there a vaccine for this disease. Supportive therapy may prolong life; however most cases are not diagnosed until late in the course of disease, and infected animals may serve as a source of infection for other ferrets.

References.

Alexandersen S et al. Acute interstitial pneumonia in mink kits inoculated with defined isolates of Aleutian mink disease parvovirus. Vet Pathol 31:216-228, 1994.

Daoust PY, Hunter DB. Spontaneous Aleutian disease in ferrets. Can Vet J 19:133-135, 1978.

Ohshima K et al. Comparison of the lesions of Aleutian disease in mink and hypergammaglobulinemia in ferrets. Am J Vet Res 39:653-657, 1978.

Oxenham M. Aleutian disease in the ferret. Vet Rec 126:585, 1990.

Palley LS et al. Parvovirus-associated syndrome (Aleutian disease) in two ferrets. JAVMA 201:100-106, 1992.

Porter HG et al. Aleutian disease in ferrets. Infect Immun 36:379-386, 1982.

Welchman E, et al. Aleutian disease in domestic ferrets: diagnostic findings and survey results. Vet Rec 132:479-484, 1993.

Une Y et al. Spontaneous Aleutian diseases in a ferret. J Vet Med Sci 62(5): 553-555, 2000.

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