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The evolution of ocular toxoplasmosis in anti-interferon gamma treated mice
P Olle1, M H Bessieres, F Malecaze
1Department of Parasitology-Mycology, Paul Sabatier University, Rangueil Hospital, 1 Av. du Pr J. Poulhès, 31054 Toulouse cedex, France.
Purpose:
A clinico-histopathological cross correlation was made to study the mechanism of tissue damage in toxoplasmic retino-choroiditis during an experimental reactivation of chronic toxoplasmosis and to compare the influence of treatment by sulfadiazine on the retinal lesions.
Methods:
Chronically infected Swiss-Webster mice were treated, six weeks after infection, with an avirulent strain of Toxoplasma gondii (Beverley strain) with polyclonal rabbit antibody directed against murine interferon gamma.
Results:
Mice treated by anti-interferon gamma developed clinical lesions between day 5 and day 30 (lesions including single foci of retinochoroiditis, multifocal lesions or diffuse areas of retinal necrosis). These lesions did not arise from borders of pre-existing 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 parasites migrated from extra-ocular cysts via the vasculature. No cysts were seen at the beginning of the study; they were found at the scar phase and appeared in mice treated with sulfadiazine. The clinical lesions were not caused by cysts but by coagulated necrosis in the retinal tissue. Parasite migration may have played a trigger role.
Conclusions:
The retinal damage was constituted either as a result of a toxic effect of the organisms or as a hypertensive reaction to the toxoplasma organism. The results of this study showed that the treatment with anti interferon gamma was sufficient to reactivate chronic infection.
Insights
Experimental reactivation of chronic toxoplasmosis using anti-interferon gamma caused retinal lesions in mice. Parasite migration, not cysts, triggered tissue damage via toxic effects or hypertensive reactions.
Area of Science:
- Ophthalmology
- Infectious Diseases
- Immunology
Background:
- Toxoplasmic retino-choroiditis is a significant cause of vision loss.
- The reactivation mechanism of chronic toxoplasmosis is not fully understood.
- Interferon gamma plays a role in controlling Toxoplasma gondii infections.
Purpose of the Study:
- To investigate the mechanism of retinal tissue damage in toxoplasmic retino-choroiditis during experimental reactivation.
- To compare the influence of sulfadiazine treatment on retinal lesions.
- To determine if anti-interferon gamma treatment can reactivate chronic toxoplasmosis.
Main Methods:
- Chronically infected Swiss-Webster mice were treated with an avirulent strain of Toxoplasma gondii.
- Mice received polyclonal rabbit antibody against murine interferon gamma.
- Retinal lesions were assessed clinically and histopathologically.
Main Results:
- Anti-interferon gamma treatment led to clinical lesions, including retinochoroiditis and retinal necrosis.
- Parasitemia increased significantly in the eye and brain.
- Histological examination revealed parasite dissemination via retinal vessels, with lesions confined to the inner retina and ciliary body.
Conclusions:
- Retinal damage resulted from the toxic effect of organisms or a hypertensive reaction.
- Anti-interferon gamma treatment was sufficient to reactivate chronic Toxoplasma gondii infection.
- Parasite migration, rather than cysts, appears to trigger acute lesions.