Detecting gyrA and parC mutations fluoroquinolone-resistant Pseudomonas aeruginosa

BACKGROUND AND ABJECTIVEPseudomonas aeruginosa as important nosocomial pathogen commonly associated with aquatic environments. Various mechanisms are involved in the development of resistance to multidrug-resistant P. aeruginosa. The aim of this study was to investigate the association of P. aeruginosa resistance to fluoroquinolones family antibiotics and mutation in two gyrA and parC genes.MATERIALS AND METHODSA total of fifty-three clinical strains of P. aeruginosa analyzed in this study, were obtained from inpatients of Loghman Hospital of Tehran Province. Then Kirby-Bauer disk diffusion assay was used for antibiotic resistance. Fluoroquinolone-resistant was confirmed by determining ciprofloxacin and levofloxacin minimum inhibitory concentration using the E-test according to the manufacturer’s instructions. Detection of gyrA and parC mutations was done by PCR-restriction Fragment Length Polymorphism (RFLP).RESULTS AND DISCUSSIONAccording to antibiotic susceptibility testing out of ۵۳ isolates, ۴۹ were resistant to ciprofloxacin (۹۲.۴%), ۴۷ isolates to levofloxacin (۸۸.۶%), ۴۶ isolates to imipenem (۸۶.۶%), ۴۶ isolates to trimethoprim-sulfamethoxazole (۸۶.۶%), ۴۲ isolates to gentamicin (۷۱.۱%), ۳۷ isolates to piperacillin-tazobactam (۶۹.۸%), ۳۳ isolates to ampicillin-sulbactam (۶۲.۲%), ۳۲ isolates to ceftriaxone (۶۰.۳%). Also, Out of ۴۹ isolates resistant to fluoroquinolones, ۴۶ mutations were observed in gyrA gene and ۲۵ mutation samples were observed in parC gene.CONCLUSIONMoreover, Although parC mutation is always necessary with mutation in gyrA to obtain high resistance to quinolones, three clinical samples in this study had mutations in parC without gyrA, so suggested that parC may not only be a secondary target for fluoroquinolones but maybe just as important as gyrA to increasing resistance to quinolones in P. aeruginosa isolates. Therefore, other mechanisms for antibiotic resistance of P. aeruginosa such as efflux systems and antimicrobial inactivating enzymes can be considered to clarify the mechanisms associated with P. aeruginosa resistance

کلیدواژه ها:

Pseudomonas Aeruginosa ، Fluoroquinolone-Resistant ، Antibiotic Susceptibility