Evaluation of Carbapenem Resistance Mechanisms and Molecular Typing of Pseudomonas aeruginosa Isolates in the Northwest of Iran

Background: The aim of this study was to determine carbapenem-resistance mechanisms, molecular epidemiological relationship, clinical impact, and patient outcome of carbapenem-resistant P. aeruginosa (CRPA) infections. Methods: A total of 42 non-duplicated CRPA were recovered from Urmia, Iran. Antimicrobial susceptibility tests were carried out using phenotypic methods. The carbapenem resistance mechanisms such as carbapenemase genes, Efflux pump hyper expression, AmpC overproduction, and OprD gene down-regulation were determined by phenotypic and molecular methods. Results: Eighteen metallo- β-lactamases (MBLs) - producer isolates were found to be sensitive to amikacin. Among the CRPA, 52.3 %, 26.1%, 26.1%, and 59.5% were identified as carbapenemase, efflux pump hyperexpression, AmpC overproduction, and reduced expression OprD gene respectively. Random Amplified Polymorphic DNA analysis yielded 26 distinct profiles. Most MBLs positive isolates were recovered from patients hospitalized in urology and internal wards with urinary tract infections. Most of the strains showed down-regulation of porin. The clonal distribution of the strains was related to carbapenem-resistance mechanisms (most of MBLs producer belong to the same clones) and the same hospital wards where the isolates were collected. Conclusion: The study demonstrates that the main risk factor of MBLs related infections was hospitalization in non-intensive wards. Amikacin was considered as a very efficient antibiotic to treatment of MBL producing CRPA isolates. Our results showed that OprD down-regulation and IMP-type MBL are the main carbapenem resistance mechanisms in CRPA isolates from northwest of Iran.

کلیدواژه ها:

carbapenem resistance ، epidemiological relationship ، Metallo-β-lactamase ، Pseudomonas aeruginosa