ACUTE INTERSTITIAL PNEUMONIA IN MINK KITS INOCULATED WITH DEFINED ISOLATES OF ALEUTIAN MINK DISEASE PARVOVIRUS

The present study addressed the causal role of Aleutian mink disease p arvovirus (ADV) in acute interstitial pneumonia in mink kits. All the examined isolates of ADV caused interstitial pneumonia in newborn kits , although the severity of disease and the mortality varied. These fin dings indicate that ADV is the direct causal agent of this disease in mink kits and that cofactors, which could have been present in the ori ginal ADV-K isolate, do not play a role. Acute interstitial pneumonia characterized by hypertrophy and hyperplasia of alveolar type II cells , intranuclear viral inclusions, interstitial edema, and hyaline membr ane formation was experimentally reproduced in mink kits infected as n ewborns with live different isolates of ADV. Four hundred forty-nine n ewborn mink kits were included in the study, of which 247 were necrops ied. The lesions caused by the different isolates were indistinguishab le by histopathologic examination, but the incidence (50-100%) and sev erity (mortality of 30-100%, n = 218) of disease among the mink kits v aried. Also, the content of ADV antigens in the lungs of infected kits varied among the groups. According to these features, the examined is olates could be placed in groups of high and low virulence. ADV-K, ADV -Utah I, and ADV-DK were in a highly virulent group producing a mortal ity of 90-100% (n = 110) in mink inoculated as newborns. ADV-GL and AD V-Pullman belonged to a group of low virulence, with an incidence of c linical disease of 50-70% and a mortality of approximately 30-50% (n = 118) in kits inoculated as newborns. The mortality in the control gro up receiving a mock inoculum was around 12% (n = 34). The period from infection to development of fatal disease varied from approximately 12 days for the highly virulent isolates up to around 20 days for the is olates of low virulence. The 107 mink kits that survived inoculation w ith ADV as newborns developed lesions typical of classical Aleutian di sease irrespective of the ADV isolate used. The lesions consisted of c hronic immune complex-mediated glomerulonephritis and infiltrations wi th mononuclear cells, including plasma cells in lung, liver, spleen, k idney, mesenteric lymph node, and intestine. Surviving kits also had h ypertrophy of the bronchus-associated lymphoid tissue and focal subple ural, intraalveolar accumulations of large cells with foamy cytoplasm, so-called lipid pneumonia.