ALEUTIAN DISEASE

MARIE-PIERRE RYSER-DEGIORGIS

Centre for Fish and Wildlife Health, Institute of Animal Pathology, Department of Infectious Diseases and Pathobiol- ogy, Vetsuisse Faculty, University of Bern, Bern, Switzerland

Aleutian disease (AD; also known as Aleutian mink disease, mink plasmocytosis or infectious plasmocytosis) was first described in farmed American mink (M ustela vison ) with Aleutian coat colour.

Aleutian mink disease virus (AMDV) is a single-stranded DNA virus in the genus Amdovirus, subfamily Parvoviri- nae, family Parvoviridae. Several strains have been described, ranging from non-pathogenic to highly pathogenic.

The host range of AMDV comprises the mustelids, as well as the raccoon (Procyon lotor), common genet ( Genetta genetta), striped skunk (Mephitis mephitis) and red fox (Vulpes vulpesf¹²°^ιxι. Rare cases of fatal human infections have been reported⁽²²⁾. All mink are susceptible, but in non-Aleutian mink the disease is generally less severe or inapparent.

AD is globally distributed in mink farms. In Europe, it has been reported as important in the Netherlands and Fennoscandia(²3). The occurrence of antibodies to AMDV and/or viral sequences has been documented in free- ranging native European mustelid species and common genets in Spain and France, and in feral American mink in Spain, France and southern England; clinical disease has only rarely been documented/suspected⁽²⁰’^24-26). AMDV infection appears to be particularly widespread in Ameri­can mink, which is thought to be the original host of the virus, supporting the hypothesis that AMDV has been introduced from North America to the rest of the mink­breeding countries.

Transmission occurs horizontally, by direct or indirect contact, and vertically. The virus is shed in urine, faeces and saliva; aerosol spread has also been proposed. AMDV is highly persistent in the environment and resistant to physical and chemical treatments.

Depending on the species, genotype and immune status of the host, and on the virus strain, infected animals may develop: i) a progressive severe disease similar to that in Aleutian mink; ii) a persistent infection with high anti­body titres in the absence of lesions; or iii) a non-persistent infection with low antibody titres, no lesions, and eventual clearance of the virus. While antibodies can have a protec­tive role in AMDV- infected mink kits, and the passive transfer of maternal antibody to kits infected after birth prevents the development of pneumonia, antiviral anti­body exacerbates disease in AMDV-infected adult mink. Following infection with AMDV, antibody binds to virus and forms immune complexes, which are deposited in tissues and cause inflammation and fatal organ failure.

Kits less than 2 weeks old display respiratory distress and die. Clinical signs in adults include apathy, poor pelt, ano­rexia and weight loss, diarrhoea and melaena, infertility, polydipsia, neurological disorders, blood- clotting abnor­malities and, rarely, ocular lesions. Affected animals display anaemia and uraemia, together with hypergammaglobuli- naemia, plasmocytosis, high levels of anti-AMDV anti­body, and viraemia. Susceptibility to other diseases increases. In ferrets (Mustela putorius furo), which are affected by a distinct virus strain, the disease course is milder, and clinical signs include a wasting syndrome or posterior ataxia and paresis, but immune complex disease is not seen(⁶).

Acute interstitial pneumonia in kits is characterized by parenchymal haemorrhages, extensive atelectasis and hyaline membrane formation. Adults with classical AD typically present splenomegaly and lymphadenopathy(²⁷).

Diagnosis of AD in mink is based primarily on the clinical signs and detection of AMDV antibodies. In par­ticular, the presence of hypergammaglobulinaemia with the concurrent presence of AMDV antibodies in American mink or ferret is strongly suggestive of AD⁽²⁸⁾. For detec­tion of anti-AMDV antibodies in serum, counter-current immune electrophoresis (CIE) is the assay of choice and regarded as the ‘gold standard’ for diagnosis of AMDV infection. A recently developed enzyme-linked immuno­sorbent assay (ELISA), with possibly higher sensitivity, was proposed as a suitable alternative¹-²⁹). For screening of tissues by PCR, the spleen should be the first choice; lymph nodes are also appropriate⁽²⁸⁾.

There are no effective vaccines or treatment for AD. The only effective means of control on farms is diligent culling of infected animals. Control of feral American mink populations, prevention of escapes from fur farms and strict protocols for disinfecting equipment during trapping programmes are recommended¹-²⁰’²¹).

AD is a major infectious cause of economical losses in mink farming. Its prevalence and significance in free- ranging carnivores is largely unknown. It has been pro­posed that because of the persistent nature of the disease and the negative effects on reproductive success, AMDV may have negative impacts on wild populations of native susceptible mustelids(^6,20).