Abstract
Carbapenemase-producing Pseudomonas aeruginosa (CRPA) poses a significant challenge to the effectiveness of antimicrobial therapy in patients, further complicated by the emergence of colistin resistance (CLR). This study aimed to provide molecular epidemiological insights into clinical P. aeruginosa strains that produce carbapenemases and exhibit CLR. A total of fifty clinical isolates of CRPA were collected from Milad Hospital in Tehran, Iran. Antimicrobial susceptibility testing and colistin broth disk elution were performed to determine the resistance patterns. PCR assays were conducted to investigate the prevalence of resistance-associated genes, including bla(KPC), bla(IMP), bla(VIM), bla(OXA-48), bla(NDM), and mcr-1 to -10. Molecular typing using pulsed-field gel electrophoresis (PFGE) was employed to determine the relationship between strains and assess their spread. The study showed that 94% of the tested strains were resistant to imipenem, and 92% were resistant to meropenem. CLR (MIC ≥ 4 µg/L) was observed in 14 isolates (28%) using the broth disk elution method, 84% isolates were identified as XDR. The most prevalent carbapenemase identified was the IMP enzyme, present in 24 strains (48%), followed by the VIM, NDM, KPC, and OXA-48 detected in 12 (24%), 5 (10%) and 2 (4%) isolates, respectively. Additionally, the mcr-1 gene was detected in 8% of the isolates, and a co-occurrence of the mcr-1 and mcr-3 genes was observed in 2% of the isolates. No other mcr genes were detected in the studied isolates. All isolates were grouped under eight clusters (A-H). The major one was related to the A cluster with 19 isolates. This study reports, for the first time, the co-occurrence of the mcr-1 and mcr-3 genes. To mitigate the spread of resistant P. aeruginosa and prevent the further evolution of mcr genes, it is crucial to enhance surveillance efforts, strictly adhere to infection prevention protocols, and practice antibiotic stewardship. These measures are essential for controlling the transmission of drug-resistant P. aeruginosa strains and preserving the effectiveness of available treatment options.