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Toxoplasmosis is the most common cause of posterior uveitis in immunocompetent subjects: 30% of the world population may be affected, with wide variability. However, despite high seroprevalence, the incidence of ocular toxoplasmosis (OT) is limited to about 2% of infected patients; thus, about one million patients in France may be estimated to have active or cicatricial OT. Microbiological tools available to the clinician have considerably advanced over the last two decades, allowing the diagnosis of toxoplasmosis to be confirmed in the vast majority of suspected cases. Regardless of the route of infection (congenital or acquired), laboratory confirmation of OT plays a major role in the patient's management, particularly in atypical cases., (Copyright © 2012 Elsevier Masson SAS. All rights reserved.)

We report a case of re-activation of Toxoplasma gondii as a cause of atypical retinal necrosis in an immunocompetent individual. The rapid development of necrotising confluent retinochoroiditis and vitreous inflammation necessitated urgent aqueous humor PCR analysis, which was positive for T gondii. The patient was treated with two intravitreal injections of clindamycin, along with oral sulphadiazine, pyrimethamine, folinic acid and prednisolone. He developed central retinal arterial occlusion, as a complication of toxoplasmic retinochoroiditis, and immediate anterior chamber paracentesis was performed with visual recovery. The injection of intravitreal clindamycin with concomitant oral therapy was associated with control of toxoplasmic retinochoroiditis and resolution of vitreous inflammation.

The SAG1 Toxoplasma gondii surface protein stimulates acute ileitis. To determine whether SAG1 is also important in the eye, wild-type or SAG1 knockout parasites were injected intravitreally into mice. No differences in retinal damage or parasite growth were observed, indicating that unlike the case for the intestine, factors besides SAG1 are important for retinal damage.

A serological study was carried out by ELIFA (Enzyme Linked Immuno-Filtration Assay) for 50 children with congenital toxoplasmosis diagnosed by several parasitological and serological methods showing that the fetus had been infected by the parasite and had developed it's own specific immune response. At birth, anti-Toxoplasma gondii IgE antibodies were detected in the sera of 66% of the 18 children who had retinochoroiditis and in 32% of the 32 children without this complication. During the 4 months before or at the time of diagnosis of retinochoroiditis, specific IgE antibodies were detected in 70% of the 20 cases (2 children with 2 successive lesions); but during the 4 months following the discovery of ocular lesions, anti-Toxoplasma IgE antibodies were only detected in 30% of the 20 cases. Among all the 50 children, the prolonged detection of specific IgM + IgE association (for at least 4 months) was followed in 46% of cases by the appearance of chorioretinitis (predictive value).

The rabbit serves as the only existing experimental model for ocular toxoplasmosis. This model has many deficiencies. Our technique for the production of acute toxoplasmic retinitis in monkeys is described herein. This primate model should be more representative than the rabbit model of human ocular toxoplasmosis.