Therapy for ocular toxoplasmosis.

PURPOSE: To review current evidence for the treatment of ocular toxoplasmosis (OT). DESIGN: Narrative review and expert recommendations. METHODS: Meta-analysis and selected original articles from the medical literature were reviewed critically. Expert recommendations were analyzed. RESULTS: Numerous observational studies suggest a benefit of short-term antimicrobial therapy for toxoplasmic retinochoroiditis in immunocompetent patients, although its efficacy has not been proven in randomized clinical trials. A randomized clinical trial revealed that intermittent trimethoprim/sulfamethoxazole treatment could decrease the rate of recurrence in high-risk patients. Intravitreal injection of clindamycin and dexamethasone was an acceptable alternative to the classic treatment for OT in a randomized clinical trial. CONCLUSIONS: Opinions about therapy differ and controversy remains about its type, efficacy, and length. Intravitreal therapy may be promising for OT. A recent description of the presence of parasitemia in patients with active and inactive ocular toxoplasmosis raises new questions that need to be explored.

Intraocular inflammation associated with ocular toxoplasmosis: relationships at initial examination.

PURPOSE: To describe characteristics of intraocular inflammation in eyes with active ocular toxoplasmosis and to identify relationships between signs of inflammation, complications (including elevated intraocular pressure [IOP]), other disease features, and host characteristics. DESIGN: Multicenter, retrospective, cross-sectional study. METHODS: We reviewed the medical records of 210 patients with toxoplasmic retinochoroiditis at seven international sites (North America, South America, and Europe) for information from the first examination at each site during which patients had active retinal lesions. Signs of inflammation included anterior chamber (AC) cells and flare and vitreous humor cells and haze. Retinal lesion characteristics included size (< or =1 disc area [DA] or >1 DA) and presence or absence of macular involvement. RESULTS: AC cells and flare were related to vitreous inflammatory reactions (P < or = .041). One or more signs of increased inflammation were related to the following factors: older patient age, larger retinal lesions, and extramacular location. In 30% of involved eyes, there was evidence of elevated IOP (despite use of glaucoma medications by some patients); other complications were uncommon. IOP of more than 21 mm Hg was associated with both increased AC cells and elevated flare (both P < or = .001) and with macular involvement (P = .009). Inflammation seemed to be more severe among patients in Brazil than among those at other sites. CONCLUSIONS: There is substantial variation between patients in the severity of intraocular inflammation associated with ocular toxoplasmosis, attributable to multiple host- and disease-related factors. Results suggest that disease characteristics also vary in different areas of the world. Elevated IOP at initial examination reflects the severity of inflammation.

Ocular sequelae of congenital toxoplasmosis in Brazil compared with Europe.

BACKGROUND: Toxoplasmic retinochoroiditis appears to be more severe in Brazil, where it is a leading cause of blindness, than in Europe, but direct comparisons are lacking. Evidence is accumulating that more virulent genotypes of Toxoplasma gondii predominate in South America. METHODS: We compared prospective cohorts of children with congenital toxoplasmosis identified by universal neonatal screening in Brazil and neonatal or prenatal screening in Europe between 1992 and 2003, using the same protocol in both continents. RESULTS: Three hundred and eleven (311) children had congenital toxoplasmosis: 30 in Brazil and 281 in Europe, where 71 were identified by neonatal screening. Median follow up was 4.1 years in Europe and 3.7 years in Brazil. Relatively more children had retinochoroiditis during the first year in Brazil than in Europe (15/30; 50% versus 29/281; 10%) and the risk of lesions by 4 years of age was much higher: the hazard ratio for Brazil versus Europe was 5.36 (95%CI: 3.17, 9.08). Children in Brazil had larger lesions, which were more likely to be multiple and to affect the posterior pole (p<0.0001). In Brazil, visual impairment (<6/12 Snellen) was predicted for most affected eyes (87%, 27/31), but not in Europe (29%; 20/69, p<0.0001). The size of newly detected lesions decreased with age (p = 0.0007). CONCLUSIONS: T. gondii causes more severe ocular disease in congenitally infected children in Brazil compared with Europe. The marked differences in the frequency, size and multiplicity of retinochoroidal lesions may be due to infection with more virulent genotypes of the parasite that predominate in Brazil but are rarely found in Europe.