Pathogenic diversity of Klebsiella pneumoniae strains with different serotypes and sequence types from human liver...

Klebsiella pneumoniae (K. pneumoniae) strains exhibit diverse virulence phenotypes influenced by serotype (K-type) and sequence type (ST). However, the interplay between bacterial molecular/biological characteristics and specific pathogenicity remains poorly understood.

We characterized 11 clinical K. pneumoniae isolates from liver abscess patients with varying serotypes (K1, K2, K5, K20, K57, K80), STs (including novel variants), and virulent factors. Phenotypic assays included the determination of growth curves, assessment of biofilm formation, and observation via electron microscopy. The Vitek 2 automated system was used to evaluate the minimum inhibitory concentration (MIC) of 11 clinical Klebsiella pneumoniae strains against common antibiotics. Mouse infection models were used to assess survival rates, analyze organ pathology, and detect hematological changes; these experimental data were complemented by clinical patient data.

Eleven clinically isolated Klebsiella pneumoniae strains displayed serotype/genotype-associated virulence and short bacilli morphology under TEM, with seven being hypermucoviscosity-positive. Growth and biofilm phenotypes varied: K2-ST65 (S2-029) had superior proliferation, K2-ST86 (S2-048) the weakest growth; K1-ST23 (S1-001) formed the strongest biofilm, while K57-ST218 (S57-077) the weakest. Phylogenetic analysis based on core SNPs derived from whole-genome sequencing of 11 K. pneumoniae strains revealed that S5-105 and S5-036 formed a distinct independent clade, significantly separated from the remaining strains. Notably, S5-105 and S5-036 exhibited significantly higher levels of differentiation compared to the other strains. Antibiotic susceptibility testing showed 9/11 of strains were fully sensitive, with overall low resistance. All strains were 100% susceptible to carbapenems, cephalosporins, aminoglycosides, and aztreonam. Only S5-105 was ciprofloxacin-resistant/levofloxacin-intermediate among quinolones; two strains had sulbactam-related non-susceptibility (S5-036: intermediate; S57-066: piperacillin-intermediate + sulbactam-resistant). Notably, two novel ST-type strains exhibited unique pathogenicity: K1-novel ST (S1-009) caused rapid systemic infection, 50% 72 h survival, severe liver abscess, and neutrophilic inflammation; K80-novel ST selectively induced pulmonary abscesses without hepatic involvement, an atypical tropism. K2 strain virulence correlated with ST: hypervirulent K2-ST65 led to 50% survival, while K2-ST86 resulted in 100% survival. Other serotypes showed distinct pathogenicity: K20 caused liver damage, K57 was nearly non-pathogenic, and slow-growing K5 induced mild tissue injury.

Specific serotype-STs combination potentiates lethality under certain circumstances (e.g., K2-ST65), but its impact is complicated. Novel STs correlate with acute lethality (K1) or atypical tropism (K80 lung-specific virulence). These findings highlight strain-specific virulence mechanisms, which are critical for the risk stratification of K. pneumoniae infection.