ANALYSIS OF THE HUMORAL RESPONSES OF TOXOPLASMA GONDII-INFECTED CATS USING IMMUNOFLUORESCENT ASSAYS WITH TACHYZOITE, BRADYZOITE, AND

We investigated levels of Toxoplasma gondii-specific antibodies present in sera, intestinal secretions, and fecal extracts obtained from cats following primary and challenge infections. Antibodies specific to T. gondii tachyzoites, bradyzoites, sporozoites, and enteroepithelial stages were detected by indirect immunofluorescence assay. Enteroepithelial stage-specific an- tibodies were detected in serum as early as 2 wk after infection, whereas antibodies from intestinal secretions did not appear until 3 wk following infection. The T. gondii-specific IgG and IgA antibodies were present in serum, but only specific IgA antibodies were detected in the intestinal secretions. Serum IgG bound to tachyzoites, bradyzoites, sporozoites, and enteroepithelial stages of T. gondii, whereas serum IgA bound strongly to enteroepithelial stages but only weakly to tachyzoites and bradyzoites. IgA from intestinal secretions bound to antigens on all enteroepithelial stages and the distal tips of sporozoites and bradyzoites but did not bind to tachyzoites. IgA present in fecal extracts also bound to enteroepithelial stages of T. gondii. Toxoplasma gondii infection in cats induces the production of antibodies that bind with all forms of the parasite, including the enteroepithelial stages. Comparison of the staining patterns of T. gondii stages for serum and intestinal secretion IgA indicated differences. Thus, the intestinal antibody immune response may be uniquely focused on the intestinal stages relative to the circulating antibodies, resulting in a compartmentalization of the humoral response. Cats play a critical role in the transmission of Toxoplasma gondii. They are the only known definitive host, in which the parasite undergoes sexual development resulting in the excre- tion of oocysts in the feces. Under environmentally favorable conditions, the oocysts sporulate and are infectious to a wide range of animals, including most mammals and birds (Dubey and Beattie, 1988). Infection in all host species results in the production of slowly growing bradyzoites residing in tissue cysts that are infectious when consumed. In humans, infection of the developing fetus can cause congenital abnormalities, still- birth, or abortion (Remington and Desmonts, 1983), and infec- tion of the immunocompromised host may cause encephalitis