Immunity to Feline Toxoplasmosis: Modification by Administration of Corticosteroids

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Abstract
Forty-nine cats were infected orally or parenterally with Toxoplasma gondii. The duration of oocyst shedding after primary infection was similar after single or multiple infection. After 2–32 weeks, cats were challenged orally with toxoplasma cysts, measuring immunity by the degree of suppression of oocyst shedding. None of the 15 cats previously infected with toxoplasma as adults excreted oocysts after challenge; however, eight of 17 first infected as weaned kittens and nine of 11 first infected as suckling kittens excreted oocysts. The stage of toxoplasma inoculated, route of inoculation, and the height of antibody titers did not appear to correlate either with immunity or the lack thereof; however, after challenge, cats excreted fewer toxoplasma oocysts, and for shorter periods, than during primary infection. Of cats infected with T. gondii, Isospora felis and I. rivolta and later challenged with all three coccidia simultaneously, more cats reexcreted I. felis and I. rivolta oocysts than T. gondii oocysts. Effects of hypercorticism on immunity were studied in 29 cats. Oocysts were re-shed by 11 of 21 toxoplasma-infected cats injected with 10–80 mg/kg body weight/week of methyl prednisolone acetate, and by five of eight cats fed prednisone, 10–80 mg/kg body weight/day. Most of the cats died; active toxoplasmic lesions were found in 24 of 29 cats, with pneumonia in 15, hepatitis in 14, pancreatic necrosis in nine, myocarditis in seven, intestinal myositis in eight, and small foci of encephalitis in 11 cats.

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