Klebsiella pneumoniae is a major cause of both hospital- and community-acquired infections, and is listed by the World Health Organization (WHO) as a priority antimicrobial-resistant (AMR) pathogen requiring new control strategies. However, in recent years, with the increasing clinical application of carbapenems in the treatment of K. pneumoniae infections, the incidence of carbapenem-resistant Klebsiella pneumoniae (CRKP) has increased at an alarming rate. In addition, bloodstream infections (BSIs) due to CRKP cause significant morbidity and mortality worldwide [1,2].

The dissemination of CRKP is mostly clonal, and the population structure is geographically specific. Sequence type (ST) 258 has become the most prevalent CRKP clone in North America, Latin America, and Europe [3,4]. However, in Asia, especially China, ST11 is the predominant clone, accounting for up to 60% of CRKP. ST11 is a single locus (tonB) variant of ST258, and both types belong to clonal group 258 [5]. The production of K. pneumoniae carbapenemases (KPC) and New Delhi β-lactamases (NDM) are the most common carbapenem resistance mechanisms in CRKP strains. KPC-2-producing ST11-KPN strains are widespread in China [6].

Compared with classic KPN (cKP), hypervirulent KPN (hvKP) infections are more aggressive, including pyogenic liver abscess, endophthalmitis, and meningitis [7], [8], [9]. Enhanced or high virulence is associated with specific capsular serotypes [10], such as KL1 and KL2, and with accessory genes (such as yersiniabactin and aerobacterin) carried by mobile elements that encode additional siderophore systems [11], [12], [13]. Aerobactin is always encoded on virulence plasmids. And aerobactin is very important to the virulence of hvKP. High virulence is also associated with rmpADC, a gene associated with a hypermucus phenotype-related gene [14]. The emergence of the fusion strain CRhvKP with high virulence and carbapenem resistance has become an important clinical problem.

Considering the clinical importance of CRKP and the emergence of the fusion strain CRhvKP in China, a single center retrospective study involving risk factors and molecular epidemiology analysis of CRKP was considered to be imperative. Compared with previous studies, we not only evaluated the risk factors and molecular epidemiology of blood infections caused by CRKP, but also evaluated the sequence evolution to assess whether the CRKP strains involved in clinical infection were horizontally transmitted isolates. In addition, our study provided an in-depth understanding of the nosocomial infection control and clinical antimicrobial treatment of CRKP.