Open Access
CC BY-NC-ND 4.0 · J Lab Physicians 2022; 14(03): 271-277
DOI: 10.1055/s-0042-1742636
Original Article

Plasmid-Mediated Fluoroquinolone Resistance in Pseudomonas aeruginosa and Acinetobacter baumannii

Autoren

  • Geetha P. Venkataramana

    1   Department of Microbiology, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, Tamil Nadu, India
  • Aishwarya K.V. Lalitha

    1   Department of Microbiology, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, Tamil Nadu, India
  • Shanthi Mariappan

    1   Department of Microbiology, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, Tamil Nadu, India
  • Uma Sekar

    1   Department of Microbiology, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, Tamil Nadu, India

Funding This study is funded by Department of Science & Technology (DST) under Women Scientists Scheme (WOS-A).

Abstract

IntroductionPseudomonas aeruginosa and Acinetobacter baumannii are important pathogens in health care–associated infections. Fluoroquinolone resistance has emerged in these pathogens. In this study, we aimed to determine the occurrence of plasmid-mediated quinolone resistance (PMQR) determinants (qnrA, qnrB, qnrS, aac(6′)-Ib-cr, oqxAB, and qepA) by polymerase chain reaction (PCR) and the transmissibility of plasmid-borne resistance determinants in clinical isolates of P. aeruginosa and A. baumannii.

Materials and Methods The study included P. aeruginosa (85) and A. baumannii (45) which were nonduplicate, clinically significant, and ciprofloxacin resistant. Antibiotic susceptibility testing was done by disk diffusion method for other antimicrobial agents, namely amikacin, ceftazidime, piperacillin/tazobactam, ofloxacin, levofloxacin, and imipenem. Minimum inhibitory concentration of ciprofloxacin was determined. Efflux pump activity was evaluated using carbonyl-cyanide m-chlorophenylhydrazone (CCCP). The presence of PMQR genes was screened by PCR amplification. Transferability of PMQR genes was determined by conjugation experiment, and plasmid-based replicon typing was performed.

Results Resistance to other classes of antimicrobial agents was as follows: ceftazidime (86.9%), piperacillin/tazobactam (73.8%), imipenem (69.2%), and amikacin (63.8%). The minimal inhibitory concentration (MIC)50 and MIC90 for ciprofloxacin were 64 and greater than or equal to 256 µg/mL, respectively. There was a reduction in MIC for 37 (28.4%) isolates with CCCP. In P. aeruginosa, 12 (14.1%) isolates harbored qnrB, 12 (14.1%) qnrS, 9 (10.5%) both qnrB and qnrS, 66 (77.6%) aac(6′)-Ib-cr, and 3 (3.5%) oqxAB gene. In A. baumannii, qnrB was detected in 2 (4.4%), 1 (2.2%) harbored both the qnrA and qnrS, 1 isolate harbored qnrB and qnrS, 21 (46.6%) aac(6′)-Ib-cr, and 1 (2.2%) isolate harbored oqxAB gene. Notably, qepA gene was not detected in any of the study isolates. Conjugation experiments revealed that 12 (9.2%) were transferable. Of the transconjugants, seven (58.3%) belonged to IncFII type plasmid replicon, followed by four (33.3%) IncA/C and one (8.3%) IncFIC type.

Conclusion The plasmid-mediated resistance aac(6′)-Ib-cr gene is primarily responsible for mediating fluoroquinolone resistance in clinical isolates of P. aeruginosa and A. baumannii. The predominant plasmid type is IncFII.



Publikationsverlauf

Artikel online veröffentlicht:
09. Februar 2022

© 2022. The Indian Association of Laboratory Physicians. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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