IS 26 -mediated chromosomal integration of virulence plasmid fragments in ST2237 carbapenem-resistant Klebsiella pneumoniae

Hypervirulent carbapenem-resistant Klebsiella pneumoniae (hv-CRKP) poses a severe threat to public health due to its broad resistance spectrum, strong pathogenicity and high clinical mortality rates.1,2 The emergence of hv-CRKP is typically attributed to the acquisition of exogenous virulence plasmids by carbapenem-resistant K. pneumoniae (CRKP). However, these plasmids are often unstable within the host due to associated fitness costs.3 Previous studies have shown that fragments of virulence plasmids can integrate into the chromosome of ST11 K. pneumoniae via insertion sequence-mediated recombination, potentially enabling stable inheritance and enhancing clinical virulence.4 To investigate whether this phenomenon also occurs in other sequence types, we conducted a year-long surveillance study at a hospital in Henan Province, China. Our investigation identified fragments of the p17-15-vir-like virulence plasmid integrated into the chromosomes of ST2237 CRKP isolates, and we systematically characterized the underlying mechanisms driving their formation. During this period, we identified two blaKPC-positive ST2237 CRKP isolates (serotype: K19) harbouring fragments of virulence plasmid p17-15-vir-like integrated into their chromosomes (CP082005 and CP082029). Clinical data revealed that these two CRKP isolates, positive for rmpA2, iuc and blaKPC, were obtained from blood samples of patients (a 39-year-old male and a 60-year-old female) admitted to the medical intensive care units. Notably, although ST2237 CRKP has been previously identified, to our knowledge, this is the first report of virulence genes such as rmpA2 and iuc being detected in ST2237 CRKP. Whether the virulence potential of ST2237 CRKP will increase over time with further strain evolution warrants close monitoring and ongoing vigilance.