THE EVOLUTION OF OCULAR TOXOPLASMOSIS IN ANTIINTERFERON GAMMA-TREATEDMICE

Purpose. A clinico-histopathological cross correlation was made to stu dy the mechanism of tissue damage in toxoplasmic retinochoroiditis dur ing an experimental reactivation of chronic toxoplasmosis and to compa re the influence of treatment by sulfaddiazine on the retinal lesions. Methods. Chronically infected Swiss-Webster mice were treated, six we eks after infection, with an avirulent strain of Toxoplasma gondii (Be verley strain) with polyclonal rabbit antibody directed against murine interferon gamma. Results. Mice treated by anti-interferon gamma deve loped clinical lesions between day 15 and day 30 (lesions including si ngle foci of retinochoroiditis, multifocal lesions or diffuse areas of retinal necrosis). These lesions did not arise from borders of pre-ex isting scars. The retina was photographed with an operating microscope fitted with a 90 diopter lens. Biological study showed a significant rise of parasitic loads in the eye and brain. Histological examination is in favour of free organism dissemination via retinal vessels; the lesions are restricted to the inner retina and ciliary body, the paras ites migrated from extra-ocular cysts via the vasculature. No cysts we re seen at the beginning of the study; they were found at the scar pha se and appeared in mice treated with sulfadiazine. The clinical lesion s were not caused by cysts but by coagulated necrosis in the retinal t issue. Parasite migration may have played a trigger role. Conclusions. The retinal damage was constituted either as a result of a toxic effe ct of the organisms or as a hypersensitive reaction to the toxoplasma organism. The results of this study showed that the treatment with ant i interferon gamma was sufficient to reactivate chronic infection.