Carbapenem resistance in non-carbapenemase-producing Pseudomonas aeruginosa strains: the role importance of OprD and AmpC

Carbapenem-resistance is a great challenge for antimicrobial therapy in Pseudomonas aeruginosa multidrug-resistant infections, as it reduces therapeutic options. This study investigated carbapenem-resistance mechanisms six strains of non-carbapenemase-producing P. aeruginosa. Minimal inhibitory concentrations imipenem and meropenem were determined by epsilometric test broth microdilution. Mutations the oprD gene PCR, followed sequencing. Transcriptional levels oprD, ampC, efflux pumps genes analysed through RT-qPCR. Detection AmpC activity was assessed MIC reduction presence inhibitors: PAβN cloxacillin, respectively. Resistant showed moderate resistance evaluated carbapenems. Sequencing revealed similar mutation patterns same Sequence Type -ST. A premature stop codon detected only resistant ST2236. Indel mutations found ST2237 strains. Failure to detect transcripts RT-qPCR further confirms absence porin on ST2236 low transcriptional oprD. MexXY-OprM system overexpressed However, no detected. High ampC 50% non-induced All imipem-induced an increase expression (>102 - 103 X). It concluded that and/or loss OprD associated with overexpression probably main mechanism