Update on the treatment of ocular toxoplasmosis

140 I In nt te er rn na at ti io on na al l J Jo ou ur rn na al l o of f M Me ed di ic ca al l S Sc ci ie en nc ce es s Ocular toxoplasmosis is the most frequent cause of posterior uveitis. [1] The parasite has an intracel-lular cycle. During the primary infection, the subject is usually asymptomatic and can present flu-like symptoms. A dissemination of the parasites occurs and the tissular cysts will persist during the all life of the host. An ocular reactivation of the disease can occur when the cysts are present within the retina (Figure 1). The patients present a photophobia and floaters are seen. The slit-lamp examination reveals the presence of a granulomatous inflammation, a mild to moderate anterior chamber inflammation. Fundo-scopy reveals the presence of a yellow focus of reti-nochoroiditis. Recent epidemiological data have shown that most cases of ocular toxoplasmosis result from reactivation of ocular toxoplasmosis and not from primary infection. Disease evolution depends on many factors: the immune response of the host, the virulence of the parasite and environmental factors and ocular toxoplasmosis can heals spontaneously after two to three months even in the absence of therapy. A review of ophthalmic literature shows that no standard therapy could be proven by large multicen-tric clinical trials. [2] A survey of the opinion of oph-thalmic specialists in uveitis was performed recently by Gary Holland. [3] The reasons that were commonly accepted to introduce a therapy were the following: a) the presence of a lesion within the vascular arcades of the posterior pole (zone 1) b) the presence of a lesion in the proximity of the optic nerve or the macula c) or a severe inflammatory reaction within the eyes. The zone 1 area was defined as a lesion that was in a sight-threatning area and corresponding to an area extending 3000 μm (2 disk diameters) from the fovea (approximately that area enclosed by the major temporal vascular arcades or 1500 μm from the margins of the optic disk. The prospective study performed by Perkins in 1956 could not demonstrate the efficacy of daraprim in the therapy of ocular toxoplasmosis. But the outcome was measured 4 weeks after initiation of therapy. Dihydrofolate reductase inhibitors (DHFR) have shown their efficacy in vivo in the treatment of toxoplamosis. To increase the efficacy of therapy a combination …