ABSTRACT
Carbapenem-resistant Klebsiella pneumoniae (CRKP) is highly prevalent and poses a great health challenge due to the lack of effective treatments. Klebsiella pneumoniae carbapenemase-2 (KPC-2), encoded by blaKPC-2 gene, is one of the major contributors to carbapenem resistance in CRKP. In China and other Asian regions, Tn1721 and plasmid IncFⅡ are the main vectors for blaKPC-2 transfer between Kpn ST11 strains, which lack clustered regularly interspaced short palindromic repeats (CRISPR) and restriction-modification (R-M) systems. The structure of transposons has a significant impact on the transposition frequency of blaKPC-2, which may be related to the different transposition patterns of transposons. The prevalence advantage of blaKPC-2 in Kpn ST11 strains is highly associated with the immune deficiency in Kpn ST11. By acquiring a re-engineered CRISPR-Cas3 system via conjugation, the high-risk IncFⅡ plasmid can be successfully cleaved and ST11 CRKP can regain antibiotic sensitivity, which provides a promising approach for clinical treatment and prevention of CRKP.