The present study aimed to characterise carbapenem-nonsusceptible P. aeruginosa recovered over one year at a tertiary care hospital in Ho Chi Minh City, focusing on the frequency and molecular profile of carbapenemase production
Abstract Background Pseudomonas aeruginosa is a leading cause of healthcare-associated infection, and carbapenem-resistant P. aeruginosa is classified as a high-priority pathogen. Genomic data on carbapenem-resistant P. aeruginosa in Vietnam, particularly on recently recognized AFM-family carbapenemases, remain scarce and have largely been generated in northern Vietnam. The present study aimed to characterize the carbapenemase content, resistance determinants, antimicrobial susceptibility and phylogenetic structure of CRPA at a tertiary hospital in Ho Chi Minh City, and to determine the distribution of carbapenemase genes across international high-risk lineages. Methods  Among all positive samples for Pseudomonas aeruginosa isolated from clinical specimens over a 1-year period, 177 carbapenem-non-susceptible isolates were screened for carbapenemase production by the modified carbapenem inactivation method (mCIM); susceptibility was determined using BD Phoenix M50 system. A subset of 21 isolates underwent short-read whole-genome sequencing, multilocus sequence typing, and core-genome SNP phylogenetic analysis. Results Overall, 116/177 isolates (65.5%) were mCIM-positive, and non-susceptibility was high across all agents; ceftazidime-avibactam and aztreonam retained the greatest activity, yet only 26.0% and 23.2% remained susceptible. Among 21 sequenced isolates, 19 (90.5%) carried at least one acquired carbapenemase gene, most commonly blaIMP-26 and blaAFM-5, with two carbapenemases co-occurring in seven. blaAFM-5 was recovered predominantly on two high-risk lineages in distinct pairings: with blaIMP-26 in ST235 and blaIMP-15 in ST357. ST235 predominated and formed tight clusters (0-5 SNPs). Conclusions Carbapenem-non-susceptible Pseudomonas aeruginosa in this setting was dominated by metallo-ß-lactamases and concentrated within high-risk clones, with blaAFM-5 emerging on distinct lineage backgrounds, more consistent with lineage-associated acquisition than with spread of a single clone.
Abstract Background Pseudomonas aeruginosa is a leading cause of healthcare-associated infection, and carbapenem-resistant P. aeruginosa is classified as a high-priority pathogen. Genomic data on carbapenem-resistant P. aeruginosa in Vietnam, particularly on recently recognized AFM-family carbapenemases, remain scarce and have largely been generated in northern Vietnam. The present study aimed to characterize the carbapenemase content, resistance determinants, antimicrobial susceptibility and phylogenetic structure of CRPA at a tertiary hospital in Ho Chi Minh City, and to determine the distribution of carbapenemase genes across international high-risk lineages. Methods  Among all positive samples for Pseudomonas aeruginosa isolated from clinical specimens over a 1-year period, 177 carbapenem-non-susceptible isolates were screened for carbapenemase production by the modified carbapenem inactivation method (mCIM); susceptibility was determined using BD Phoenix M50 system. A subset of 21 isolates underwent short-read whole-genome sequencing, multilocus sequence typing, and core-genome SNP phylogenetic analysis. Results Overall, 116/177 isolates (65.5%) were mCIM-positive, and non-susceptibility was high across all agents; ceftazidime-avibactam and aztreonam retained the greatest activity, yet only 26.0% and 23.2% remained susceptible. Among 21 sequenced isolates, 19 (90.5%) carried at least one acquired carbapenemase gene, most commonly blaIMP-26 and blaAFM-5, with two carbapenemases co-occurring in seven. blaAFM-5 was recovered predominantly on two high-risk lineages in distinct pairings: with blaIMP-26 in ST235 and blaIMP-15 in ST357. ST235 predominated and formed tight clusters (0-5 SNPs). Conclusions Carbapenem-non-susceptible Pseudomonas aeruginosa in this setting was dominated by metallo-ß-lactamases and concentrated within high-risk clones, with blaAFM-5 emerging on distinct lineage backgrounds, more consistent with lineage-associated acquisition than with spread of a single clone.