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<p><i>Klebsiella pneumoniae</i> (<i>K. pneumoniae</i>) is a leading cause of nosocomial infections and is increasingly linked to multidrug resistance and hypervirulence. Comprehensive genomic characterization is essential for understanding the emergence of multidrug resistant and hypervirulent <i>K. pneumoniae</i> strains. Therefore, this study comprehensively investigated the resistome, virulome, and plasmidome profile of 310 clinical <i>K. pneumoniae</i> genomes to elucidate genetic determinants of virulence and antimicrobial resistance (AMR). Multi-locus sequence typing identified 86 sequence types, with ST11 being the predominant lineage associated with KL64 and KL47 capsular types. Resistome analysis detected widespread β-lactam resistance genes, with most genomes carrying extended-spectrum β-lactamases (ESBLs). Carbapenemases namely KPC and NDM were detected in 31% and 15% of genomes respectively. The co-occurrence of multiple ESBLs (CTX-M, SHV, and TEM) within the same genome was observed in nearly half of the genomes (146/310), suggesting a strong genetic determinant of resistance to third-generation cephalosporins. ST23 genomes showed an increased abundance of siderophore-associated virulence genes, including aerobactin, yersiniabactin, and colibactin. Plasmidome profiling revealed that several resistance determinants were found on conjugative plasmids encoding β-lactamase and aminoglycoside resistance genes which underscores their potential for horizontal dissemination. The open pan-genome exhibited substantial diversity, with accessory genome enriched in mobilome-associated genes (14.6%) compared to core genome (0.1%). Overall, these results reveal the extensive genomic plasticity of <i>K. pneumoniae</i> and widespread distribution of resistance and virulence determinants, largely mediated by mobile genetic elements. These findings are pivotal for guiding future genomic surveillance and to support the development of targeted therapeutic approaches to combat AMR.</p>

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WGS-based in silico analysis of clinically-associated Klebsiella pneumoniae genomes: insights into antimicrobial resistance, virulence determinants, and plasmid dynamics

  • 期刊论文

  • 发表日期：

    2026年4月6日

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  • Santhiya Vijayakumar,
  • Sudha Ramaiah

摘要

Klebsiella pneumoniae (K. pneumoniae) is a leading cause of nosocomial infections and is increasingly linked to multidrug resistance and hypervirulence. Comprehensive genomic characterization is essential for understanding the emergence of multidrug resistant and hypervirulent K. pneumoniae strains. Therefore, this study comprehensively investigated the resistome, virulome, and plasmidome profile of 310 clinical K. pneumoniae genomes to elucidate genetic determinants of virulence and antimicrobial resistance (AMR). Multi-locus sequence typing identified 86 sequence types, with ST11 being the predominant lineage associated with KL64 and KL47 capsular types. Resistome analysis detected widespread β-lactam resistance genes, with most genomes carrying extended-spectrum β-lactamases (ESBLs). Carbapenemases namely KPC and NDM were detected in 31% and 15% of genomes respectively. The co-occurrence of multiple ESBLs (CTX-M, SHV, and TEM) within the same genome was observed in nearly half of the genomes (146/310), suggesting a strong genetic determinant of resistance to third-generation cephalosporins. ST23 genomes showed an increased abundance of siderophore-associated virulence genes, including aerobactin, yersiniabactin, and colibactin. Plasmidome profiling revealed that several resistance determinants were found on conjugative plasmids encoding β-lactamase and aminoglycoside resistance genes which underscores their potential for horizontal dissemination. The open pan-genome exhibited substantial diversity, with accessory genome enriched in mobilome-associated genes (14.6%) compared to core genome (0.1%). Overall, these results reveal the extensive genomic plasticity of K. pneumoniae and widespread distribution of resistance and virulence determinants, largely mediated by mobile genetic elements. These findings are pivotal for guiding future genomic surveillance and to support the development of targeted therapeutic approaches to combat AMR.