Gatifloxacin, Moxifloxacin, and alofloxacin Resistance due to Mutations in the gyrA and parC Genes of Staphylococcus epidermidis Strains Isolated from Patients with ndophthalmitis, Corneal Ulcers and Conjunctivitis

Abstract

Aims: Staphylococcus epidermidis is considered a commensalbacterium; however, it is frequently isolated from ocular infectionsshowing a multidrug resistance. Ciprofloxacin-resistantstrains have been isolated from ocular infections;however, resistance to quinolone, such as gatifloxacin andmoxifloxacin, is not often studied, consequently the resistancemechanism is unknown. Our aim was to address thequinolone resistance and to explore the resistance mechanismin S. epidermidis strains isolated from ocular infections.Methods: S. epidermidis strains were isolated from patientswith conjunctivitis (n = 23), endophthalmitis (n = 14) and cornealulcers (n = 7). Minimum inhibition concentrations weredetermined by broth and agar dilution methods for moxifloxacin,gatifloxacin, balofloxacin, rufloxacin and pazufloxacin.Mutations were identified by sequencing the gyrA andparC genes, and their expression was determined by reverse transcriptase polymerase chain reaction. Results: We foundthat 13.6% (6/44) of the strains were quinolone resistant. Inendophthalmitis, 21.4% were gatifloxacin, moxifloxacin andbalofloxacin resistant. In corneal ulcers, 14.2, 14.2 and 28.5%were gatifloxacin, moxifloxacin and balofloxacin resistant,respectively, and in conjunctivitis only 4.3% were gatifloxacinresistant. The 6 strains with quinolone resistance showedmutations at Ser84Phe for the gyrA gene, and Ser80Phe forthe parC gene. Gatifloxacin did not change the expressionlevels of gyrA and parC genes. Conclusion: S. epidermidisstrains isolated from three ocular pathologies were gatifloxacinand moxifloxacin resistant due to mutations on the gyrAand parC genes.