INTRODUCTION
The emergence and persistence of pks-positive Klebsiella pneumoniae (pks⁺ KPN) have garnered significant attention due to their potent genotoxicity and elevated virulence potential. These strains harbor the pks genomic island responsible for the biosynthesis of colibactin, a genotoxin linked to DNA damage and colorectal cancer. Despite their clinical significance, comprehensive data on their epidemiology and evolution remain sparse. This study focuses on elucidating the molecular epidemiology and evolutionary patterns of pks⁺ KPN strains using extensive clinical isolate data and global genomic resources. By integrating multilocus sequence typing (MLST), virulence profiling, pan-genomics, and KEGG functional enrichment, the investigation aims to unveil the genetic architecture and biological functions that may drive the dominance and spread of these strains. The findings contribute critical insights into the development of precision-targeted surveillance and infection control strategies.
MOLECULAR EPIDEMIOLOGY OF pks⁺ KPN
An in-depth molecular epidemiological survey of 873 K. pneumoniae isolates revealed that 105 (12.03%) were pks⁺, predominantly obtained from infectious disease and surgical departments. Notably, these strains were more common in non-carbapenem-resistant isolates, suggesting a distinct evolutionary trajectory and clinical profile compared to drug-resistant variants. The disproportionately higher prevalence in non-CRKP isolates (25.45% vs. 1.04%, p < 0.001) indicates a trade-off between virulence and resistance, aligning with previous hypotheses that high-virulence KPN often lack carbapenem resistance. This epidemiological trend underpins the importance of routine pks island screening, particularly in departments managing younger and more vulnerable patient populations.
CLONAL STRUCTURE AND VIRULENCE TRAITS
pks⁺ K. pneumoniae isolates exhibited a remarkably conserved clonal structure, with ST23-KL1 representing 66.7% of the strains, contrasting with the genetic diversity seen in pks⁻ populations. Virulence gene profiling revealed significantly elevated rates of peg344, iucA, rmpA, rmpA2, and iroB in pks⁺ strains, corroborating their hypervirulent phenotype. Moreover, infections caused by these strains occurred in relatively younger patients, reinforcing the hypothesis that virulence traits may compensate for antibiotic susceptibility. These findings highlight the necessity of clonal and virulence gene surveillance in routine diagnostic protocols to better predict pathogenic potential.
GLOBAL DISTRIBUTION AND PHYLOGENETIC INSIGHTS
The analysis of 706 global pks⁺ KPN genomes demonstrated the predominance of ST23 (45.18%), ST11 (15.72%), and ST258 (15.16%) across diverse geographic regions. The phylogenetic construction revealed five distinct evolutionary clades, reflecting varied evolutionary pressures and transmission routes. The predominance of ST23 across both local and international datasets further supports its adaptation and survival advantage. The clustering of strains into defined phylogenetic clades offers a framework for understanding the evolutionary dynamics and helps trace epidemiological links across institutions and regions.
GENOMIC EVOLUTION AND FUNCTIONAL ENRICHMENT
Comparative core-genome analysis between dominant pks⁺ strains uncovered 245 lineage-specific genes, with 96 genes conserved among key clonal groups. KEGG pathway analysis indicated significant enrichment in galactose metabolism—a potentially crucial adaptation mechanism enhancing environmental survival, host colonization, and possibly metabolic crosstalk with the host microbiota. The genomic convergence around this metabolic pathway suggests evolutionary selection favoring specific metabolic capabilities in successful clones like ST23. These data highlight the importance of metabolic profiling in the context of virulence and fitness.
IMPLICATIONS FOR INFECTION CONTROL AND FUTURE RESEARCH
This study provides foundational evidence supporting the integration of genomic surveillance into hospital infection control programs. The delineation of pks⁺ KPN's clonal dissemination, virulence attributes, and metabolic enrichment opens avenues for targeted therapeutic and preventive measures. Strategies should prioritize early detection of hypervirulent clones and exploration of metabolic inhibitors as adjunct therapies. Future research should expand functional analyses of lineage-specific genes and their roles in host-pathogen interactions. Additionally, evaluating pks island expression and colibactin production in clinical contexts may yield deeper insights into their pathogenic role.
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HASHTAGS
#KlebsiellaPneumoniae, #pksIsland, #HypervirulentKlebsiella, #ST23, #GenomicSurveillance, #MLST, #KEGGAnalysis, #GalactoseMetabolism, #VirulenceGenes, #AntibioticResistance, #CarbapenemSensitive, #ClinicalMicrobiology, #MolecularEpidemiology, #Colibactin, #PathogenEvolution, #BacterialGenomics, #HospitalInfections, #PublicHealthGenomics, #InfectionControl, #Pencis,
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