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Tiago E. Arantes, Claudio Silveira, Gary N. Holland, Cristina Muccioli, Fei Yu, Jeffrey L. Jones, Raquel Goldhardt, Kevan G. Lewis, Rubens Belfort, Jr.; Ocular Involvement Following Postnatally Acquired Toxoplasma gondii Infection in Southern Brazil. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4312.
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© ARVO (1962-2015); The Authors (2016-present)
To determine incidence of, and risk factors for, ocular involvement following postnatally acquired Toxoplasma gondii infection in a highly endemic region of Brazil.
Records for 297 consecutive patients with serologic evidence of recently acquired T. gondii infection (positive anti-T. gondii IgM antibody test) from Erechim, Rio Grande do Sul, Brazil (1974-2002) were analyzed. We sought relationships between demographic, medical, and ophthalmic data. Incidence of ocular involvement was calculated in terms of person-years (PY) of follow-up. Risk factors for ocular involvement were analyzed using log rank test and Fisher exact test.
At initial examination, 101 patients (34.0%) had necrotizing retinochoroiditis (47.5% in the macula); 30 others (10.1%) had intraocular inflammation only (anterior chamber cells and flare, vitreous inflammatory reactions, retinal vasculitis, or retinal infiltrates without retinal necrosis). Follow-up examinations were performed on 249 patients (median duration of follow-up, 12.6 mos. [range 0.6-261.9 mos.]). The incidence of necrotizing retinochoroiditis during follow-up was higher for those with intraocular inflammation at baseline (3 patients; incidence, 6.7/100 PY) than for those without previous ocular involvement (13 patients; incidence, 4.7/100 PY), but we could not confirm that the difference was statistically significant (p=0.55). The incidence of recurrences among patients with necrotizing retinochoroiditis at baseline was 7.0/100 PY. Male patients were more likely to have ocular disease at baseline, but the difference did not reach statistical significance (p=0.076). Patients >40 years of age had larger lesions (>1 disc area, p=0.044) and were more likely to develop retinochoroiditis during the first year after infection (p=0.002).
Intraocular inflammatory reactions without retinal necrosis can be an initial manifestation of T. gondii infection, and necrotizing retinochoroiditis can occur months or years after infection. Older age is a risk factor for earlier and more severe disease.
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