THE EFFECT OF GLUCOCORTICOID ADMINISTRATION ON OOCYST SHEDDING, SEROLOGY, AND CELL-MEDIATED IMMUNE-RESPONSES OF CATS WITH RECENT OR CHRONIC TOXOPLASMOSIS

Glucocorticoid administration at very high dosages has been shown previously to induce reshedding of oocysts in cats with toxoplasmosis. In this study, methylprednisolone acetate (MPA) was administered at a dose of 5 mg/kg body weight intramuscularly weekly to cats with either recent or chronic toxoplasmosis and at a dose of 20 mg/kg body weight intramuscularly weekly to cats with chronic toxoplasmosis while monitoring oocyst shedding, lymphoblast transformation in response to concanavalin A, and changes in serum Toxoplasma gondii -specific immunoglobulin G, immunoglobulin M, and antigens. Toxoplasma gondii oocyst shedding did not develop in any cat. Clinical dosages of glucocorticoids suppressed lymphoblast transformation in recently infected cats but not those with chronic infection. Recurrence of positive immunoglobulin M titers developed in 50% of the cats. Based on the results of this study, it appears that 5 mg/kg body weight MPA administered weekly for four weeks will not induce repeat oocyst shedding in cats recently or chronically infected with T. gondii strain ME49; thus clinical dosages of glucocorticoids likely do not increase the zoonotic potential of individual cats with subclinical toxoplasmosis. Recent T. gondii infection is potentially immunosuppressive in adult cats. This immunosuppression may potentiate MPA effects on cell-mediated immunity. Glucocorticoid administration can alter T. gondii-specific antibody responses.