title: Gatifloxacin, moxifloxacin, and balofloxacin resistance due to mutations in the gyrA and parC genes of Staphylococcus epidermidis strains isolated from patients with endophthalmitis, corneal ulcers and conjunctivitis.
abstract: OBJECTIVE
  Staphylococcus epidermidis is considered a commensal bacterium; however, it is frequently isolated from ocular infections showing a multidrug resistance. Ciprofloxacin-resistant strains have been isolated from ocular infections; however, resistance to quinolone, such as gatifloxacin and moxifloxacin, is not often studied, consequently the resistance mechanism is unknown. Our aim was to address the quinolone resistance and to explore the resistance mechanism in S. epidermidis strains isolated from ocular infections.
  
  
  METHODS
  S. epidermidis strains were isolated from patients with conjunctivitis (n = 23), endophthalmitis (n = 14) and corneal ulcers (n = 7). Minimum inhibition concentrations were determined by broth and agar dilution methods for moxifloxacin, gatifloxacin, balofloxacin, rufloxacin and pazufloxacin. Mutations were identified by sequencing the gyrA and parC genes, and their expression was determined by reverse transcriptase polymerase chain reaction.
  
  
  RESULTS
  We found that 13.6% (6/44) of the strains were quinolone resistant. In endophthalmitis, 21.4% were gatifloxacin, moxifloxacin and balofloxacin 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 gatifloxacin resistant. The 6 strains with quinolone resistance showed mutations at Ser84Phe for the gyrA gene, and Ser80Phe for the parC gene. Gatifloxacin did not change the expression levels of gyrA and parC genes.
  
  
  CONCLUSIONS
  S. epidermidis strains isolated from three ocular pathologies were gatifloxacin and moxifloxacin resistant due to mutations on the gyrA and parC genes.
authors.affiliation: Area Académica de Nutrición, Instituto de Ciencias de la Salud, Universidad Autónoma del Estado de Hidalgo, Pachuca, México.
authors.forename: Gabriel
authors.initials: G
authors.lastname: Betanzos-Cabrera
authors.forename: Marco A
authors.initials: MA
authors.lastname: Juárez-Verdayes
authors.forename: Gabriel
authors.initials: G
authors.lastname: González-González
authors.forename: Mario E
authors.initials: ME
authors.lastname: Cancino-Díaz
authors.forename: Juan C
authors.initials: JC
authors.lastname: Cancino-Díaz
mesh_terms: D000890:Anti-Infective Agents / Q000494:pharmacology*; D001372:Aza Compounds / Q000494:pharmacology; D003231:Conjunctivitis / Q000382:microbiology; D003320:Corneal Ulcer / Q000382:microbiology; D027081:DNA Gyrase / Q000235:genetics*; D027101:DNA Topoisomerase IV / Q000235:genetics*; D004269:DNA, Bacterial / Q000032:analysis; D024901:Drug Resistance, Multiple, Bacterial / Q000187:drug effects / Q000235:genetics*; D009877:Endophthalmitis / Q000382:microbiology; D015818:Eye Infections, Bacterial / Q000382:microbiology*; D024841:Fluoroquinolones / Q000494:pharmacology; D000077734:Gatifloxacin; D006801:Humans; D008826:Microbial Sensitivity Tests; D000077266:Moxifloxacin; D009154:Mutation; D011804:Quinolines / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013212:Staphylococcus epidermidis / Q000235:genetics* / Q000302:isolation & purification
chemical_list: D000890:Anti-Infective Agents; D001372:Aza Compounds; D004269:DNA, Bacterial; D024841:Fluoroquinolones; D011804:Quinolines; D027101:DNA Topoisomerase IV; D027081:DNA Gyrase; D000077734:Gatifloxacin; C077155:balofloxacin; D000077266:Moxifloxacin