Mutations within the Quinolone Resistance Determining Region in Fluoroquinolone-Resistant Staphylococcus epidermidis Recovered from Different Ocular Isolates

Abstract

Staphylococcus epidermidis (S. epidermidis) is a common pathogen in ocular infection. Mutations contribute to drug resistance. We intended to identify mutations in genes within the quinolone resistance determining region (QRDR) of fluoroquinolone-resistant S. epidermidis ocular isolates and to study their phenotypic and genotypic correlation. A total of 50 phenotypically fluoroquinolones-resistant S. epidermidis isolates were studied. Fluoroquinolones susceptibility was evaluated by Kirby-Bauer disk diffusion method. Polymerase chain reaction (PCR) was optimized and applied followed by DNA sequencing to detect mutations in gyrA, gyrB, parC and parE in the QRDR region among the fluoroquinolone-resistant S. epidermidis isolates recovered from ocular specimens. The majority of the samples (74%) were from conjunctival swabs (n = 37). gyrA, gyrB, parC, and parE genes were detected in 47 samples (94%). gyrA gene (n = 47) was the most common, followed by parE (n = 35), gyrB (n = 30) and parC (n = 28). In 25 isolates, all four mutated genes were present. In 25(50%) S. epidermidis isolates mutations were observed in all four genes of QRDR region of S. epidermidis genome. This is the first study in a tertiary eye care hospital in India to characterise ocular S. epidermidis for fluoroquinolone resistance which showed mutations were predominant in gyrA gene in the QRDR region compared to 3 other genes.

Antimicrobial Resistance Profiling of Coagulase-Negative Staphylococci in a Referral Center in South Italy: A Surveillance Study

“…Ligozzi et al demonstrated that norA-like genes played an important role in the resistance of CoNS to fluoroquinolones [46]. Resistance mechanisms to quinolones include mutations of DNA gyrase and topoisomerase IV [47]. Rifampicin is one of the antibiotics of choice for the treatment of joint and bone infections, due to its ability to penetrate staphylococcal biofilm.…”