Open AccessInvestigation of Ciprofloxacin Resistance and Its Mechanisms in Clinical Pseudomonas aeruginosa Isolates
Author(s) -
Nilüfer Uzunbayır Akel,
Yamaç Tekintaş,
Fethiye Ferda Yılmaz,
İsmail Öztürk,
Mustafa Ökeer,
Sabire Aydemir,
Fatma Feriha Çilli,
Mine Hoşgör Limoncu
Publication year - 2021
Publication title -
ankem dergisi/ankem dergisi
Language(s) - English
Resource type - Journals
eISSN - 2667-7652
pISSN - 1301-3114
DOI - 10.5222/ankem.2021.022
Subject(s) - ciprofloxacin , pseudomonas aeruginosa , efflux , microbiology and biotechnology , quinolone , biology , minimum inhibitory concentration , antibiotics , bacteria , genetics
Pseudomonas aeruginosa is one of the most important causes of hospital infections. Although different antibiotic groups are used for the treatment of P.aeruginosa infections, quinolone groups are distinguished by the advantages of oral administration. However, in recent years, resistance against members of this group has made treatment more difficult. The aim of this study was to investigate the epidemiological relationship and possible mechanisms of resistance in ciprofloxacin resistant P. aeruginosa isolates from Ege University Hospital. The identification of P.aeruginosa bacteria isolated from clinical samples in Ege University Medical Faculty Medical Microbiology Laboratory was determined by VITEK MS automated systems by VITEK compact, antimicrobial susceptibility. The epidemiological relationships of the ciprofloxacin resistant isolates were determined by Enterobacterial repetitive intergenic consensus-polymerase chain reaction (ERIC-PCR). The presence of qnrA, qnrB, qnrS, qepA genes, the quinolone resistance genes and nfxB, mexR, the regulatory genes of the efflux pump, was determined by PCR. The phenylalanine-arginine β-naphthylamide (PAβN) assay was used to determine the activation of the efflux pump. Twenty-two isolates (26.5 %) were found resistant to ciprofloxacin. According to the ERIC-PCR results, 11 unrelated clones were detected. Ciprofloxacin minimum inhibitory concentration (MIC) values were decreased 2-64 times in 10 isolates in the presence of PAIN. No ciprofloxacin MIC change was detected in one isolate. The presence of pump regulatory genes was determined in 10 of the 11 representative isolates, while only qnrB of the genes associated with quinolone resistance was detected in seven representative isolates. qnrA, qnrS, qepA genes were not detected in any isolate. Ciprofloxacin resistant P.aeruginosa isolates are isolated from our hospital. It is noteworthy that the isolates belonging to different genetic groups are in circulation in clinics. Basic resistance mechanisms are thought to be efflux pumps and qnrB genes.