An In Situ Hybridization and Immunohistochemical Study of Cytauxzoonosis in Domestic Cats

Abstract

Cytauxzoonosis, caused by the protozoan parasite, Cytauxzoon felis, is a tick-borne disease of domestic cats causing high mortality. The reservoir is wild felids. In this study, 7 archived cases of the disease were examined through in situ hybridization for localization of the parasite and by immunohistochemistry for various cell markers to characterize infected cells. The riboprobe used was specific for the 16S-like rRNA subunit of Babesia microti, which shares 91% identity with the same gene for C. felis. In situ hybridization highlighted the presence of the organism in several tissues, most prominently lung and spleen, and, in general, there were 2 to 10 times more infected cells seen with in situ hybridization than with HE. Parasite-laden cells were usually found within vessels. These cells were often tightly packed and frequently formed parasitic thrombi. Immunohistochemistry with an antilysozyme antibody confirmed the macrophage origin of the infected cells. Using an antibody specific for calprotectin (Mac387), parasitized cells were markedly devoid of this protein, which may explain the lack of diapedesis and vascular crowding of parasitized cells, providing more circulating parasites for the tick vector. Immunohistochemical labeling for 2 proliferation markers, proliferating cell nuclear antigen (PCNA) and p53, indicated that parasitized cells have a heightened replicative ability, which is probably an additional parasite-driven modification to facilitate survival and transmission.