Aleutian Mink Disease Virus and Humans | CDC EID

EID Journal Home > Volume 15, Number 12–December 2009

Volume 15, Number 12–December 2009
Dispatch
Aleutian Mink Disease Virus and Humans
Jørgen R. Jepsen, Francesco d'Amore, Ulrik Baandrup, Michael Roost Clausen, Elisabeth Gottschalck, and Bent Aasted
Author affiliations: Hospital of South-Western Denmark, Esbjerg, Denmark (J.R. Jepsen); Aarhus University Hospital, Aarhus, Denmark (F. d'Amore, M.R. Clausen); Aalborg University, Aalborg, Denmark (U. Baandrup); Gl. Ringstedvej 63 D, Holbæk, Denmark (E. Gottschalck); and University of Copenhagen, Copenhagen, Denmark (B. Aasted)

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Abstract
Reports of a possible relationship between Aleutian mink disease parvovirus (AMDV) and human infection are rare. However, 2 mink farmers with vascular disease and microangiopathy similar to that in mink with Aleutian disease were found to have AMDV-specific antibodies and AMDV DNA. These findings raise the suspicion that AMDV may play a role in human disease.

Autonomous parvoviruses, such as Aleutian mink disease virus (AMDV), cause a broad spectrum of diseases in animals and man. Acute disease manifests itself as a lytic infection of rapidly dividing cells; chronic disease reflects a restricted or abortive infection of specific cell types (1). Aleutian disease (AD) is known to produce clinical signs in mink and ferrets only (2,3), although other mammals have reportedly been antibody positive.

In adult mink, AD is a persistent, slowly progressive AMDV infection in which a dysregulated immune system and a postinfectious antibody response cause an immune complex–mediated vasculitis (2). Perivascular and glomerular immune complexes (2,4,5) can cause membranoproliferative glomerulonephritis (6) and segmental or circumferential arteritis (4) with mononuclear infiltration, fibrinoid necrosis and deposits, and increased intimal cellularity. Mononuclear cells may surround the vessel, and connective tissue proliferation and necrosis in the tunica elastica media narrow the lumen (7). In mink kits, AD causes an acute cytopathic infection of alveolar cells, which leads to respiratory distress and death (8).

Reports of a possible relationship between AMDV and human infection are rare (9). Histopathologic features like those in AMDV-infected mink have been described for 2 patients in the early 1960s (10). Exposed laboratory workers have had persistent anti-AMDV antibodies for up to 18 months; however, injection of their antibody-positive blood into Aleutian mink caused neither lesions nor AMDV-antibody production (11). In vitro studies have demonstrated a permissive infection (production of infectious progeny) of human macrophages with the Utah I strain of AMDV (12). We report finding anti-AMDV antibodies and AMDV genome in tissue from 2 mink farmers with relevant virus exposure and clinical disease similar to that in mink with AD.

The Study
We examined AMDV antibody from each of the 2 patients by countercurrent and line electrophoresis (13). AMDV DNA was identified by standard and nested PCR. DNA was extracted from lymph nodes (patient 1) and from peripheral blood and bone marrow (patient 2) before amplification with AMDV-specific primers. AMDV DNA was identified by 2 different sets of primers in the standard PCR (5–600 bp) and with 2 complete different internal primers in the nested PCR (200 bp). PCR products were cloned, and some clones were sequenced to confirm the presence of AMDV DNA. All PCR reactions were done with appropriate controls.

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