Journal of infection and public health · 2026
Novel polymyxin-resistant Klebsiella pneumoniae with ten resistance determinants and associated mutations drive localized outbreaks.
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Yuan Kaixuan, Zhang Jiao, Qin Yurong, Yang Xinyue, Zhang Ni, Ling Yong, Liu Xinyi, Zhou Jingfang, Yu Yixi, Ge Shuyue, Liu Weijiang, Liao Yiwen, Chen Huimin, Wang Weisha, Chen Xiaoli, Liu XiaoXiao, Liu Suling, Zhao Yunhu
Аннотация
OBJECTIVE: To characterize the genomic features, resistance mechanisms and potential transmission chains of polymyxin-resistant Klebsiella pneumoniae (PR-KP).
METHODS: PR-KP isolates were retrospectively recovered from clinical specimens. Whole-genome sequencing (WGS) was performed, and transmission single-nucleotide polymorphism (SNP) profiling and core-genome phylogenetic analysis were used to reconstruct putative transmission chains.
RESULTS: From June to October in 2023, among the 21 non-duplicate PR-KP isolates obtained from hospitalized patients (including ICU, with 96 beds), 85.71% (18/21) were derived from ICU patients, and 61.90% (13/21) were cultured from sputum samples. The KPC-2 phenotype was predominant, accounting for 85.71% (18/21) of the isolates, and was associated with near-pan-drug resistance. Core-genome alignment identified three clusters: cluster 1 (P7), cluster 2 (P15 and P18), and cluster 3 (comprising 18 highly homologous isolates). Multilocus sequence typing (MLST) further characterized these clusters, with cluster 3 identified as ST11. This genetic homology strongly indicates clonal transmission, suggesting horizontal spread and a localized hospital outbreak. Ten distinct genes associated with polymyxin resistance were identified, with mechanisms involving alterations in cell wall charge, proteins conferring antimicrobial resistance, and antimicrobial efflux pumps. Notably, acquired resistance in PR-KP was putatively acquired, including horizontally transferable genes such as MCR-3, basS-1, basS-2, basR, arnA-1, arnA-2, PmrE, PmrF, PmrC, and vanRF, which contributed to severe resistance phenotypes and significantly limited therapeutic options. Additionally, multiple non-synonymous mutations within these resistance genes resulted in 21 amino acid substitutions (e.g., Gly70Arg in basS-1). These mutations likely enhance the complexity of resistance development and dissemination.
CONCLUSION: Genomic epidemiology confirmed an outbreak of ST11 PR-KP carrying multiple acquired resistance determinants. Horizontal gene acquisition and target-gene mutations drive high-level polymyxin resistance, underscoring the need for enhanced surveillance and infection-control interventions.
METHODS: PR-KP isolates were retrospectively recovered from clinical specimens. Whole-genome sequencing (WGS) was performed, and transmission single-nucleotide polymorphism (SNP) profiling and core-genome phylogenetic analysis were used to reconstruct putative transmission chains.
RESULTS: From June to October in 2023, among the 21 non-duplicate PR-KP isolates obtained from hospitalized patients (including ICU, with 96 beds), 85.71% (18/21) were derived from ICU patients, and 61.90% (13/21) were cultured from sputum samples. The KPC-2 phenotype was predominant, accounting for 85.71% (18/21) of the isolates, and was associated with near-pan-drug resistance. Core-genome alignment identified three clusters: cluster 1 (P7), cluster 2 (P15 and P18), and cluster 3 (comprising 18 highly homologous isolates). Multilocus sequence typing (MLST) further characterized these clusters, with cluster 3 identified as ST11. This genetic homology strongly indicates clonal transmission, suggesting horizontal spread and a localized hospital outbreak. Ten distinct genes associated with polymyxin resistance were identified, with mechanisms involving alterations in cell wall charge, proteins conferring antimicrobial resistance, and antimicrobial efflux pumps. Notably, acquired resistance in PR-KP was putatively acquired, including horizontally transferable genes such as MCR-3, basS-1, basS-2, basR, arnA-1, arnA-2, PmrE, PmrF, PmrC, and vanRF, which contributed to severe resistance phenotypes and significantly limited therapeutic options. Additionally, multiple non-synonymous mutations within these resistance genes resulted in 21 amino acid substitutions (e.g., Gly70Arg in basS-1). These mutations likely enhance the complexity of resistance development and dissemination.
CONCLUSION: Genomic epidemiology confirmed an outbreak of ST11 PR-KP carrying multiple acquired resistance determinants. Horizontal gene acquisition and target-gene mutations drive high-level polymyxin resistance, underscoring the need for enhanced surveillance and infection-control interventions.
Предметные рубрики MeSH
Klebsiella pneumoniaeHumansKlebsiella InfectionsDisease OutbreaksAnti-Bacterial AgentsPolymyxinsWhole Genome SequencingMultilocus Sequence TypingPhylogenyRetrospective StudiesMicrobial Sensitivity TestsMutationDrug Resistance, BacterialPolymorphism, Single NucleotideDrug Resistance, Multiple, BacterialGenome, Bacterial