Incidence and Risk Factors of Ocular Infection Caused by Staphylococcus aureus Bacteremia.

Staphylococcus aureusbacteremia (SAB) often leads to ocular infections, including endophthalmitis and chorioretinitis. However, the incidence, risk factors, and outcomes of ocular infections complicated by SAB are largely unknown. We retrospectively analyzed the incidence and risk factors of ocular involvement in a prospective cohort of patients with SAB at a tertiary-care hospital. Ophthalmologists reviewed the fundoscopic findings and classified the ocular infections as endophthalmitis or chorioretinitis. During the 5-year study period, 1,109 patients had SAB, and data for 612 (55%) who underwent ophthalmic examinations within 14 days after SAB onset were analyzed. Of those 612 patients, 56 (9% [95% confidence interval [CI], 7 to 12%]) had ocular involvement, including 15 (2.5%) with endophthalmitis and 41 (6.7%) with chorioretinitis. In a multivariate analysis, infective endocarditis (adjusted odds ratio [aOR], 5.74 [95% CI, 2.25 to 14.64]) and metastatic infection (aOR, 2.38 [95% CI, 1.29 to 4.39]) were independent risk factors for ocular involvement. Of the 47 patients with ocular involvement who could communicate, only 17 (36%) had visual disturbances. Two-thirds of the patients with endophthalmitis (10/15 patients) were treated with intravitreal antibiotics combined with parenteral antibiotics, whereas all of the patients with chorioretinitis were treated only with systemic antibiotics. No patients became blind. Among 42 patients for whom follow-up assessments were available, the ocular lesions improved in 29 (69%) but remained the same in the others. Ocular involvement was independently associated with death within 30 days after SAB onset. Ocular involvement is not uncommon among patients with SAB. Routine ophthalmic examinations should be considered for patients with infective endocarditis or metastatic infections caused by SAB.

Effects of sulfamethoxazole on murine ocular toxoplasmosis in interferon-gamma knockout mice.

PURPOSE: To evaluate the effects of sulfamethoxazole (SMX) on experimental ocular toxoplasmosis by quantitative competitive polymerase chain reaction (QC-PCR) assay. METHODS: Wild-type (WT) C57BL/6 and WT BALB/c mice and interferon-gamma knockout (GKO) mice were infected orally with Toxoplasma gondii of the Fukaya strain. Mice were classified into groups. The first group (G1) remained untreated, the second group (G2) had a short SMX treatment period, and the third group (G3) received treatment continuously. WT and GKO mice were divided into G1 and G3, and G1, G2, and G3, respectively. T. gondii burdens were evaluated by QC-PCR assay. The effect on stage distribution was analyzed by reverse transcription-PCR. RESULTS: SMX significantly decreased mortality among the infected WT C57BL/6 and GKO mice. In WT G1 mice, T. gondii DNA was detected in all organs and tissues, although in G3 mice it was detected only in the brain. In GKO C57BL/6 G1 mice, the protozoan proliferated much more actively than in the WT mice. In the GKO C57BL/6 G2 mice, the number of T. gondii was less than in G1 during the treatment, although the protozoan reappeared after cessation of treatment. In GKO C57BL/6 G3 mice, T. gondii DNA was detected in the brain, optic nerve, and retina, but not in the iris, choroid, sclera, and blood. In GKO BALB/c mice, the patterns of the kinetics of protozoan abundance in various organs were similar or were milder than those in GKO C57BL/6 mice. In SMX-treated GKO mice, the percentage of bradyzoites increased and that of tachyzoites decreased in the organs and tissues. CONCLUSIONS: SMX decreased the parasitic load in both WT and GKO mice. SMX decreased the tachyzoite load but did not completely eliminate bradyzoites in GKO mice. The present mouse model was used successfully to assess treatment effects in a quantitative fashion.