Antibiotic Resistance in Endophthalmitis Pathogens

Abstract

Resistance to antimicrobial agents used to treat human infections is a major public health threat that results from the broad use of antibiotics in medicine, veterinary care, and agriculture. Exposure to antibiotics promotes the selection of successful resistant bacterial lineages possessing molecular mechanisms that lead to variable levels of resistance. Increasing use of antibiotics for treatment and prophylaxis of eye infections has resulted in the emergence of resistant ocular organisms. The use of topical antibiotics for prophylaxis of postoperative endophthalmitis, especially fluoroquinolones, has paralleled the recent increase in the number of patients undergoing intraocular procedures. This has resulted in the upsurge of antibiotic-resistant organisms colonizing the ocular microbiota and also as significant causes of postoperative infections. Contemporary ocular staphylococci isolates, the leading causes of bacterial endophthalmitis, are becoming increasingly resistant to the most commonly used topical fluoroquinolone agents. Despite the widespread use of these agents for prophylaxis, current evidence does not support the efficacy of topical fluoroquinolones in preventing endophthalmitis, but does support an association with their use and the selection of spontaneous resistant mutants in the ocular surface microbiota. Studies of pharmacokinetics and pharmacodynamics have demonstrated that due to reduced penetration in association with increasing levels of resistance, none of the currently used topical fluoroquinolones are likely to be effective in eliminating staphylococci isolates in the anterior chamber. This highlights the need for prospective randomized studies to evaluate whether or not these topical antibiotics are really needed for preventing postoperative or post-injection endophthalmitis. The development of new strategies to increase regimens or delivery mechanisms that would optimize the intraocular concentration of antibiotics may help prevent the selection and spread of resistant mutants and improve clinical effectiveness.