Twenty-three cats with spontaneous
feline infectious peritonitis (FIP) were examined by light microscopy including immunohistology and histochemistry in order to determine the cellular composition and the expression of
viral antigen in lesions in FIP. Furthermore, the presence of plasma-cells producing coronavirus-specific
antibodies was evaluated in situ. Macrophages and neutrophils were demonstrated by an antibody against
calprotectin (leukocyte
protein L1, myeloid/histiocyte
antigen), neutrophils were recognized due to their
chloroacetate esterase activity, and B- and T-lymphocytes were identified by
antibodies against the
CD3 antigen and the CD45R
antigen, respectively. Expression of
viral antigen was immunohistologically demonstrated by a
monoclonal antibody (mAb) against coronavirus while coronavirus-specific
antibodies in situ were identified by the application of feline coronavirus prior to the coronavirus antibody. Lesions were classified as diffuse alterations at serosal surfaces,
granulomas with areas of
necrosis,
granulomas without extended
necrosis, focal and perivascular lymphoplasmocytic infiltrates, and granulomatous-necrotizing
vasculitis. Diffuse alterations on serosal surfaces were represented either by activated mesothelial cells with single coronavirus
antigen-bearing macrophages or by layers of precipitated exudate containing single to numerous
granulomas with areas of
necrosis. In liver and spleen, the exudate was often underlaid by a small band of subcapsular B-cells with an occasional plasma-cell producing coronavirus-specific
antibodies. In other locations, a variably broad band of B-cells and plasma-cells, often infiltrating between underlying muscle fibers, separated the exudate from the unaltered tissue. Some of these plasma-cells were positive for coronavirus-specific
antibodies. In
granulomas with areas of
necrosis, the central
necrosis was surrounded by macrophages usually expressing considerable amounts of
viral antigen. Few B-cells and plasma-cells were found in the periphery. In
granulomas without extended
necrosis, the number of macrophages were lower. Only few macrophages expressing low amounts of
viral antigen were present. B-cells and plasma-cells formed a broad rim. Few plasma-cells stained positive for coronavirus-specific
antibodies. In both types of
granulomas, few neutrophils were found between macrophages. Few T-cells were seen scattered throughout the lesions. Focal and perivascular lymphoplasmocytic infiltrates were mainlyseen in omentum and leptomeninx. B-cells were the predominant cells; some plasma-cells were positive for coronavirus-specific
antibodies.
Viral antigen was not readily detected in these alterations. Granulomatous-necrotizing
vasculitis was occasionally found in kidneys and leptomeninx. It was dominated by macrophages which often stained strongly positive for coronavirus
antigen. Different types of alteration were often seen in the same animal and even the same tissue. There was no obvious correlation between the cat's age, gross pathological changes, and the histological types of alteration. Single plasma-cells positive for coronavirus-specific
antibodies were found around blood vessels distant from inflammatory alterations, within the lung parenchyma, as infiltrating cells in the mucosa of the small intestine, and in spleen and mesenteric lymph node. Results show that alterations in FIP are heterogeneous concerning cellular composition and expression of
viral antigen. The dominance of B-cells in part of the lesions together with the presence of plasma-cells positive for coronavirus-specific
antibodies indicate that these cells may play a role in the maintenance of inflammatory processes in FIP.