The mechanisms of resistance, epidemiological characteristics, and molecular evolution of carbapenem-resistant hypervirulent Klebsiella pneumoniae

Abstract Introduction Carbapenem-resistant hypervirulent Klebsiella pneumoniae (CR-hvKP) is a highly pathogenic, drug-resistant, and transmissible “superbug” that causes infections in hospitals and communities. Because of the lack of effective antimicrobial treatment options, morbidity and mortality from CR-hvKP infections have increased dramatically, and outbreaks and the rapid spread of CR-hvKP in hospitals have become a major global public health challenge. Methods The mechanisms of molecular evolution in CR-hvKP include the acquisition of a hypervirulent plasmid encoding a virulence gene by carbapenemase-producing K pneumoniae, the horizontal transfer of plasmids carrying carbapenem resistance genes to hvKP, and the acquisition of fusion plasmids carrying both carbapenem resistance genes and hypervirulent genes by classic K pneumoniae. In addition, hvKP can develop a resistance phenotype under antibiotic pressure. Results CR-hvKP arises through plasmid-mediated convergence of resistance genes and virulence factors. Its multidrug resistance and lethal pathogenicity fuel hospital outbreaks, requiring urgent action to block plasmid transmission and strengthen surveillance to contain the spread of this evolving superbug. Discussion In this article, we have summarized the carbapenemase resistance mechanism, evolution mechanism, virulence factors, and epidemiology of CR-hvKP. Our aim was to elucidate the molecular evolutionary mechanism of CR-hvKP and provide a reference for curbing the spread of CR-hvKP.