Pathogenesis of Feline Infectious Peritonitis: Nature and Development of Viremia

Abstract

SUMMARY Kittens that were seropositive or seronegative to feline infectious peritonitis virus ( fipv ) and were experimentally infected with fipv by aerosol exposure developed a persistent cell-associated viremia. When test kittens were inoculated with whole blood, intact or disrupted buffy coat ( bc ) cells, or cell-free supernatants of disrupted bc cells from these infected kittens, the test kittens developed feline infectious peritonitis ( fip ). When test kittens were inoculated with plasma or wbc -free erythrocyte suspensions from the infected kittens, they did not develop fip . Viremia could not be detected in healthy fipv -seropositive kittens before aerosol challenge exposure. Viremia was first detected on postchallenge-exposure day ( pcd ) 2 in seropositive kittens and on pcd 6 in seronegative kittens. The onset of viremia correlated with the appearance of fever, pulmonary vascular lesions, and fipv antigen in lung macrophages of infected kittens. The fipv -infected wbc were detected by immunofluorescence microscopy in the lumen, intima and wall of pulmonary veins and in perivascular foci in lungs of viremic kittens. Marked pulmonary necrosis and severe clinical disease occurred by pcd 7 in seropositive kittens and on or after pcd 16 in seronegative kittens. Significant ( P < 0.05) reductions in numbers of circulating platelets and lymphocytes developed earlier in seropositive kittens than in seronegative kittens. Survival times in seropositive kittens were significantly ( P < 0.001) decreased compared with survival times in seronegative kittens. Immunofluorescent or electron microscopic examination of blood smears and bc cells from viremic kittens failed in most instances to demonstrate intracellular virus or viral antigen. Specific antiviral immunofluorescence was, however, readily observed in bc cells from viremic kittens when the cells were maintained in vitro for ≥ 24 hours. Seemingly, an immune-mediated mechanism is involved in the pathogenesis of fip . The fipv -seropositive kittens developed viremia, antiviral immunofluorescence, and lesions earlier and died more rapidly after virus challenge exposure than did fipv -seronegative kittens. In both groups, a fatal disease characterized by progressive vasculitis and necrosis developed during a period of persistent viremia and elevated or increasing serum antibody titers.