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Background <p><i>Elizabethkingia anophelis</i> has emerged as a formidable pathogen responsible for severe, life-threatening infections in immunocompromised populations. However, the genetic underpinnings of its virulence and antimicrobial resistance remain poorly characterized. Leveraging our previously assembled collection of 197 <i>E. anophelis</i> isolates with complete genome sequences, we performed an exhaustive, large-scale comparative analysis across global datasets to systematically map resistance determinants and virulence factors. Additionally, we constructed an integrated coexpression network to elucidate genotype-phenotype correlations in antibiotic resistance patterns.</p> Results <p>The distribution of virulence-associated genes displays moderate phylogenetic specificity, exhibiting constrained variation within established primary clades. Importantly, virulence gene profiles demonstrate little discernible association with specimen source, sample category, or geographic origin. Although diverse antimicrobial resistance genotypes were detected, these exhibited negligible lineage specificity with minimal differentiation among core phylogenetic clusters. Coexpression network analysis suggests that <i>E. anophelis</i> resistance to cephalosporins, carbapenems, and aztreonam primarily arises from the constitutive expression of chromosomally encoded resistance determinants. In contrast, these chromosomally encoded resistance mechanisms appear to exert either negligible or clinically insignificant effects on susceptibility patterns for the remaining fourteen tested antimicrobial agents.</p> Conclusions <p>This study demonstrates that the multidrug resistance and pathogenic potential of <i>E. anophelis</i> are predominantly intrinsic traits, regulated by complex, multilayered biological mechanisms. Comprehensive elucidation of the bacterium’s virulence and resistance pathways necessitates the discovery of novel molecular targets followed by systematic, in-depth characterization.</p>

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Genomic perspectives on the global dissemination of Elizabethkingia anophelis: unveiling inherent multidrug resistance and virulence determinants

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月27日

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  • Shaohua Hu,
  • Xiaohua Meng,
  • Hao Xu,
  • Shujun Ni,
  • Yonghong Xiao,
  • Beiwen Zheng

摘要

Background

Elizabethkingia anophelis has emerged as a formidable pathogen responsible for severe, life-threatening infections in immunocompromised populations. However, the genetic underpinnings of its virulence and antimicrobial resistance remain poorly characterized. Leveraging our previously assembled collection of 197 E. anophelis isolates with complete genome sequences, we performed an exhaustive, large-scale comparative analysis across global datasets to systematically map resistance determinants and virulence factors. Additionally, we constructed an integrated coexpression network to elucidate genotype-phenotype correlations in antibiotic resistance patterns.

Results

The distribution of virulence-associated genes displays moderate phylogenetic specificity, exhibiting constrained variation within established primary clades. Importantly, virulence gene profiles demonstrate little discernible association with specimen source, sample category, or geographic origin. Although diverse antimicrobial resistance genotypes were detected, these exhibited negligible lineage specificity with minimal differentiation among core phylogenetic clusters. Coexpression network analysis suggests that E. anophelis resistance to cephalosporins, carbapenems, and aztreonam primarily arises from the constitutive expression of chromosomally encoded resistance determinants. In contrast, these chromosomally encoded resistance mechanisms appear to exert either negligible or clinically insignificant effects on susceptibility patterns for the remaining fourteen tested antimicrobial agents.

Conclusions

This study demonstrates that the multidrug resistance and pathogenic potential of E. anophelis are predominantly intrinsic traits, regulated by complex, multilayered biological mechanisms. Comprehensive elucidation of the bacterium’s virulence and resistance pathways necessitates the discovery of novel molecular targets followed by systematic, in-depth characterization.