Le infezioni in medicina · 2026
Genomic epidemiology of Carbapenem-Resistant Enterobacterales in southern Vietnam: dominance of Klebsiella pneumoniae ST16 and horizontal gene transfer.
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Truong Thien Phu, Tran Trong Tin, Le Phuong Mai, Nguyen Van Thanh, Ta Tuan Khanh, Tran Thi Tuyet, Tran Cong Tri, Le Pham My Da, Nguyen Quang Tin, Nguyen Thi Nam Phuong
Аннотация
BACKGROUND: Carbapenem-resistant Enterobacterales (CRE) pose a critical global threat. However, the genomic epidemiology, transmission dynamics (clonal vs. horizontal gene transfer), and mechanisms driving co-resistance in Southern Vietnam remain poorly understood. This study aimed to use Whole-Genome Sequencing (WGS) to characterize the molecular epidemiology, transmission mechanisms, and co-resistance patterns of CRE from a major referral center in Southern Vietnam.
METHODOLOGY: We performed a cross-sectional study using whole-genome sequencing on 189 CRE isolates (K. pneumoniae, E. coli, E. cloacae) from a major referral hospital in Southern Vietnam. We analyzed Carbapenemase-Producing Genes (CPGs), MLST, colistin resistance mutations, plasmid clusters, and co-carried AMR genes.
RESULTS: K. pneumoniae ST16 (n=67, 35.4%) was the most frequently identified clone, detected in 10/12 ward strata. We identified two distinct colistin resistance pathways linked to CPG lineage: bla KPC/bla OXA-48 family clones (ST147, ST5815, ST11) showed a universal prevalence of chromosomal pmrB mutations (n=55/55, 100%), whereas the bla NDM clone (ST16) exhibited a low frequency of these mutations (6.0%). Analysis of 10 plasmid clusters carrying CPGs revealed the frequent co-carriage of qnrS1 (quinolone resistance) and rmtB1 (amikacin resistance).
CONCLUSIONS: CRE dissemination in Southern Vietnam is driven by a dual-transmission scenario. We identified distinct CPG-linked colistin resistance pathways and significant co-carriage of qnrS1 with CPGs. This highlights the potential risk of co-selection through antibiotic pressure. These findings underscore the urgent need for surveillance strategies targeting high-risk clones like K. pneumoniae ST16.
METHODOLOGY: We performed a cross-sectional study using whole-genome sequencing on 189 CRE isolates (K. pneumoniae, E. coli, E. cloacae) from a major referral hospital in Southern Vietnam. We analyzed Carbapenemase-Producing Genes (CPGs), MLST, colistin resistance mutations, plasmid clusters, and co-carried AMR genes.
RESULTS: K. pneumoniae ST16 (n=67, 35.4%) was the most frequently identified clone, detected in 10/12 ward strata. We identified two distinct colistin resistance pathways linked to CPG lineage: bla KPC/bla OXA-48 family clones (ST147, ST5815, ST11) showed a universal prevalence of chromosomal pmrB mutations (n=55/55, 100%), whereas the bla NDM clone (ST16) exhibited a low frequency of these mutations (6.0%). Analysis of 10 plasmid clusters carrying CPGs revealed the frequent co-carriage of qnrS1 (quinolone resistance) and rmtB1 (amikacin resistance).
CONCLUSIONS: CRE dissemination in Southern Vietnam is driven by a dual-transmission scenario. We identified distinct CPG-linked colistin resistance pathways and significant co-carriage of qnrS1 with CPGs. This highlights the potential risk of co-selection through antibiotic pressure. These findings underscore the urgent need for surveillance strategies targeting high-risk clones like K. pneumoniae ST16.