Emergence of drug-resistant Klebsiella pneumoniae phylogroups (K. quasipneumoniae and K. variicola) causing human infections

Abstract

This prospective, cross-sectional study was undertaken to identify the emerging K. pneumoniae phylogeny groups (KpI, KpII, KpIII) and characterize their drug resistance. Phylogeny groups of 150 clinical isolates of biochemically identified K. pneumoniae were detected by targeting their chromosomal class A, β-lactamase genes bla<inf>SHV</inf>, bla<inf>LEN</inf>, and bla<inf>OKP</inf>, respectively, and their flanking gene (deoR). Antimicrobial susceptibility testing was done by disk diffusion and broth microdilution methods and statistically analyzed. Carbapenemases (Classes A, B, and D) were detected by multiplex PCR. Colistin resistance mechanisms to detect alteration in PhoP/PhoQ, pmrAB two-component signaling pathways, and mgrB were done by PCR and sequencing. Of the total, KpI, K. pneumoniae were 93 (62%), KpII, K. quasipneumoniae were 36 (24%), and KpIII, K. variicola were 21 (14%). Carbapenem resistance was in 77 (51.3%); 52 (55.9%), 17 (47.2%), and 8 (38%) in KpI, KpII, and KpIII, respectively. Colistin resistance was in 16 (10.6%), 11 (68.75%) in KpI and 5 (31.25%) in KpIII. K. variicola was resistant to polymyxin B as compared with KpI (P = 0.0008). bla<inf>NDM</inf> (63, 81.8%) was the commonest. Co-harboring of multiple carbapenemase genes was significant in all the phylogroups (P < 0.001). The majority of the cases of K. variicola were males (P = 0.0139) and in the intensive care unit (P = 0.0091). Several non-synonymous mutations were observed in the colistin-resistant isolates in PhoP and PhoQ genes, with the phylogenetic tree revealing different evolutionary relationships among the isolates. There is considerable emergence of K. quasipneumoniae and K. variicola as prominent human pathogens along with drug resistance, which requires attention. © © 2025 Mishra et al.