Investigation of Plasmid-Mediated Quinolone Resistance in Pseudomonas aeruginosa Strains Isolated from Cystic Fibrosis Patients


MIKROBIYOLOJI BULTENI, vol.45, no.4, pp.602-608, 2011 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 45 Issue: 4
  • Publication Date: 2011
  • Title of Journal : MIKROBIYOLOJI BULTENI
  • Page Numbers: pp.602-608


Pseudomonas aeruginosa which is widely found in the environment, may lead to serious nosocomial infections. Due to its intrinsic resistance to many antibacterial agents, treatment of P.aeruginosa infections usually present difficulty. Quinolones, especially ciprofloxacin, are crutial antibiotics for the treatment of P.aeruginosa infections. However resistance developing to quinolones may become an important problem. Resistance to quinolones is often a result of chromosomal mutations and by the effect of efflux pumps. Recently plasmid-mediated quinolone resistance have been reportedin the members of Enterobacteriaceae family. The gene responsible for this resistance is called qnr. In addition to qnr genes there is also another gene called aac(6')-lb-cr responsible for plasmid-mediated quinolone resistance and aminoglycoside resistance. Limited studies which to screen P.aeruginosa strains for the presence of qnr gene region, revealed no positivity. The aim of this study was to investigate the plasmid-mediated quinolone resistance in P.aeruginosa strains isolated from cystic fibrosis patients. A total of 110 P.aeruginosa strains isolated from respiratory tract specimens from the patients were included in the study. Ciprofloxacin susceptibilities of the isolates were detected by Kirby-Bauer disk diffusion method according to CLSI guidelines. The presence of qnrA, qnrB, qnrC, qnrS and aac(6')-lb-cr genes were searched by multiplex polymerase chain reaction (PCR) with the use of specific individual primer pairs. As positive control strains, Escherichia coli J53 pMG252 (qnrA(1) positive), E.coli J53 pMG252 (qnrS(1) positive), E.coli J53 pMG258 (qnrB(1) and aac(6')-lb-cr positive), Klebsiella pneumoniae ref.15 (qnrB positive), Enterobacter cloacae ref.287 (qnrS positive), E.coli ref.20 (qnrA positive) and E.coli DH10 conjugated with pHS11 plasmid (qnrC positive) were used. Of 110 P.aeruginosa clinical isolates, 13 were found resistant to ciprofloxacin, while 7 were intermediate. However multiplex PCR yielded no positivity in terms of qnrA, qnrB, qnrC, qnrS and aac(6')-lb-cr gene regions. In conclusion, although our results indicated that none of the tested P.aeruginosa strains harboured those genes, further multicenter studies with large numbers of isolates are needed to confirm these results.