Propionibacterium acnes in capsular bag distension syndrome.

We report a case of capsular bag distension syndrome that developed 6 years after uneventful phacoemulsification with implantation of a foldable, single-piece acrylic intraocular lens (IOL) (AcrySof MA60BM). Slitlamp microscopy revealed a deep anterior chamber with no flare or cells. The posterior capsular bag was distended by a homogeneous milky substance between the back of the IOL and the capsular bag. Using a pars plana approach, a 23-gauge bimanual capsulotomy and anterior vitrectomy were performed. Microbiological analysis revealed Propionibacterium acnes in the material inside the capsular bag. The postoperative period was uneventful. Four weeks after surgery, visual acuity was restored and there were no signs of intraocular inflammation. The origin of late capsular bag distension is not fully understood; it may involve an infectious component with propionibacteria. A surgical approach and removal of the potentially infectious material can be considered as an alternative to neodymium:YAG capsulotomy.

Intracameral moxifloxacin: in vitro safety on human ocular cells.

PURPOSE: The fourth-generation fluoroquinolone, moxifloxacin, covers most gram-positive and gram-negative isolates causing endophthalmitis. It is safe and effective for systemic and topical use, but only limited data are available on prophylactic intracameral administration to prevent endophthalmitis. This study uses a cell culture model to investigate the safety of moxifloxacin for intracameral application. METHODS: Endothelial toxicity of moxifloxacin was evaluated in cultured human corneas. Possible toxic effects of moxifloxacin (10-750 microg/mL) in corneal endothelial cells (CEC), primary human trabecular meshwork cells (TMC), and primary human retinal pigment epithelial (RPE) cells were evaluated after 24 hours and under conditions of oxidative and inflammatory stress by treatment with tumor necrosis factor alpha, lipopolysaccharides, or interleukin-6. Toxicity was evaluated by tetrazolium dye reduction assay, and cell viability was quantified by a microscopic live-dead assay. RESULTS: No corneal endothelial toxicity could be detected after 30 days of treatment with 500 microg/mL moxifloxacin. Concentrations up to 150 microg/mL had no influence on CEC, TMC, or RPE cell proliferation or on cell viability when administered for 24 hours. After preincubation with tumor necrosis factor alpha, lipopolysaccharides, or interleukin-6 for 24 hours and subsequent treatment with moxifloxacin at concentrations from 10 to 150 microg/mL for 24 hours, no significant decrease in proliferation or viability was observed. Hydrogen peroxide exposure did not increase cellular toxicity. CONCLUSIONS: This study showed no significant toxicity for moxifloxacin on CEC, TMC, RPE cells, or human corneal endothelium for concentrations up to 150 microg/mL. The minimum inhibitory concentration of moxifloxacin to inhibit 90% of pathogens commonly encountered in endophthalmitis is known to be in the range of 0.25-2.5 microg/mL. Therefore, prophylactic intracameral use of moxifloxacin at concentrations up to 150 microg/mL may be safely used to prevent endophthalmitis after intraocular surgery.