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Background <p><i>Pseudomonas aeruginosa</i> remains a major cause of burn wound infections and exhibits a remarkable ability to develop resistance to carbapenems, primarily through multidrug efflux systems belonging to the Resistance–Nodulation–Division (RND) family. This study investigated the contribution of the MexAB-OprM and MexXY-OprM efflux pumps to carbapenem resistance in <i>P. aeruginosa</i> isolates from burn wounds and evaluated the effect of an efflux pump inhibitor on antibiotic susceptibility.</p> Methods <p>A total of 100 <i>P. aeruginosa</i> isolates were collected from burn patients. Antimicrobial susceptibility to imipenem and meropenem was determined by minimum inhibitory concentration (MIC) assays according to CLSI guidelines. The presence of <i>mexAB-oprM</i> and <i>mexXY-oprM</i> genes was confirmed via PCR. The functional role of efflux activity was assessed using carbonyl cyanide 3-chlorophenylhydrazone (CCCP), a proton-motive force inhibitor, and MIC reductions ≥ 4-fold were interpreted as efflux-mediated resistance.</p> Results <p>Resistance to imipenem and meropenem was observed in 44% and 27% of isolates, respectively. Among imipenem-resistant isolates, <i>mexXY-oprM</i> was detected in 50% and <i>mexAB-oprM</i> in 18%, while 23% co-presented both systems. In contrast, <i>mexAB-oprM</i> predominated in meropenem-resistant strains (48%), followed <i>by mexXY-oprM</i> (22%). Upon CCCP addition, MICs decreased by ≥ 4-fold in 84% of imipenem-resistant and 52% of meropenem-resistant isolates, suggesting the involvement of efflux pumps (<i>P</i> &lt; 0.05).</p> Conclusion <p>A high prevalence of carbapenem resistance and efflux pump-associated genes was observed among <i>P. aeruginosa</i> isolates from burn wound infections. Significant reductions in carbapenem MICs following CCCP exposure suggest that efflux-mediated mechanisms may contribute to the resistance phenotype in a substantial proportion of isolates. These findings indicate a potential role for efflux activity in carbapenem resistance and warrant further investigation of its clinical and mechanistic significance.</p>

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Role of MexAB-OprM and MexXY-OprM efflux pumps in carbapenem-resistant Pseudomonas aeruginosa from burn wounds

  • 期刊论文

  • 发表日期：

    2026年7月10日

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  • Shahin Khalilipanah,
  • Hadi Sedigh Ebrahim-Saraie,
  • Iraj Nikokar,
  • Hamed Naziri,
  • Meysam Hasannejad-Bibalan

摘要

Background

Pseudomonas aeruginosa remains a major cause of burn wound infections and exhibits a remarkable ability to develop resistance to carbapenems, primarily through multidrug efflux systems belonging to the Resistance–Nodulation–Division (RND) family. This study investigated the contribution of the MexAB-OprM and MexXY-OprM efflux pumps to carbapenem resistance in P. aeruginosa isolates from burn wounds and evaluated the effect of an efflux pump inhibitor on antibiotic susceptibility.

Methods

A total of 100 P. aeruginosa isolates were collected from burn patients. Antimicrobial susceptibility to imipenem and meropenem was determined by minimum inhibitory concentration (MIC) assays according to CLSI guidelines. The presence of mexAB-oprM and mexXY-oprM genes was confirmed via PCR. The functional role of efflux activity was assessed using carbonyl cyanide 3-chlorophenylhydrazone (CCCP), a proton-motive force inhibitor, and MIC reductions ≥ 4-fold were interpreted as efflux-mediated resistance.

Results

Resistance to imipenem and meropenem was observed in 44% and 27% of isolates, respectively. Among imipenem-resistant isolates, mexXY-oprM was detected in 50% and mexAB-oprM in 18%, while 23% co-presented both systems. In contrast, mexAB-oprM predominated in meropenem-resistant strains (48%), followed by mexXY-oprM (22%). Upon CCCP addition, MICs decreased by ≥ 4-fold in 84% of imipenem-resistant and 52% of meropenem-resistant isolates, suggesting the involvement of efflux pumps (P < 0.05).

Conclusion

A high prevalence of carbapenem resistance and efflux pump-associated genes was observed among P. aeruginosa isolates from burn wound infections. Significant reductions in carbapenem MICs following CCCP exposure suggest that efflux-mediated mechanisms may contribute to the resistance phenotype in a substantial proportion of isolates. These findings indicate a potential role for efflux activity in carbapenem resistance and warrant further investigation of its clinical and mechanistic significance.