Quinolone resistance of Pseudomonas aeruginosa isolated from hospital infections and MexAB-OprM efflux pumps

INTRODUCTION: Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen frequently associated with multidrug-resistant nosocomial infections. The MexAB-OprM efflux system, a member of the Resistance-Nodulation-Division (RND) family, contributes to intrinsic and acquired resistance by extruding structurally diverse antimicrobial agents, including quinolones, from the bacterial cell. AIM: This study aimed to evaluate the association between quinolone resistance phenotypes and the presence of the mexAB-oprM determinant in clinical P. aeruginosa isolates, and to assess the functional contribution of efflux activity using the inhibitor PAβN. METHODOLOGY: This cross-sectional descriptive study was performed on 55 samples of P. aeruginosa isolated from patients visiting the Martyr Zare hospital in the city of Sari, Iran. The genus and types of isolated strains were first characterized by biochemical tests. Antibiotic-resistance patterns of the strains were evaluated based on the disk diffusion method toward 13 common antibiotics and minimum inhibitory concentration (MIC) in the presence of the PAβN inhibitor of levofloxacin antibiotic-2 and ciprofloxacin. Finally, the presence of the mexAB-oprM operon was surveyed using the polymerase chain reaction (PCR) method. RESULTS: In this experiment, the highest bacterial resistance was observed toward nalidixic acid (100%), ofloxacin (80.2%), and levofloxacin (74.82%) antibiotics. The lowest resistance of antibiotics was seen toward piperacillin (39.4%), meropenem (44.3%), and imipenem (48.9%). In this study, a total of 55 clinical P. aeruginosa isolates were analyzed, of which 39 (70.90%) carried the mexB determinant. CONCLUSION: The findings demonstrate a strong association between the presence of the mexAB-oprM determinant and elevated quinolone resistance in clinical P. aeruginosa isolates. The significant reduction in MIC values following PAβN exposure supports the contribution of RND-type efflux mechanisms to resistance. However, given the intrinsic nature of MexAB-OprM and the broad inhibitory spectrum of PAβN, these results should be interpreted as correlative rather than causative. These data underscore efflux activity as a key resistance factor and highlight the need for expression-based profiling in future mechanistic studies.