Genomic analysis reveals VirB11 mutations drive virulence polymorphism in carbapenem-resistant Klebsiella pneumoniae, highlighting how antibacterial pressures shape pathogen evolution.
Carbapenem-resistant Klebsiella pneumoniae (CRKP) has become a major public health issue worldwide due to its high case fatality rate and transmissible nature. The plasmid containing drug-resistant and virulence genes obtained by CRKP can evolve into carbapenem-resistant hypervirulent Klebsiella pneumoniae (CR-hvKP), thus forming a new generation of superbacteria. However, systematic documentation of the mechanism of plasmid evolution that carries both drug resistance and virulence genes remains lacking. Fifty-four strains of CR-hvKP were collected here. The clinical data and bioinformatics were analyzed to explore the genomics and virulence plasmid evolution mechanism from the same source in the strains PFGE1-ST11-K64, PFGE2-ST11-K64, PFGE-ST11-K2, and PFGE-ST11-K47. The four groups from the same source exhibited virulent polymorphism, and mutations in the VirB11 gene may account for virulence variations across the strains of the same source. IMPORTANCE This study emphasizes that in the process of clinical anti-infective treatment, attention should be paid not only to the strain itself but also to the external environment of the strain, especially the targeted therapeutic dose and course of host antibacterial drugs, which provides the possibility of diversity for the evolution of bacterial virulence and is conducive to the spread and survival of the CR-hvKP strain.
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Fang et al. (2025) studied this question.
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