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Background <p>The global dissemination of multidrug-resistant (MDR) <i>Escherichia coli</i> (<i>E. coli</i>) clones, particularly the pandemic ST131 and the emerging ST1193, poses a serious public health threat. While ST131 is well-studied, the factors enabling ST1193’s rapid dissemination across both urinary and bloodstream infection niches remain unclear.</p> Methods <p>We compared 48 urinary (UPEC) and bloodstream (BPEC) <i>E. coli</i> isolates of ST1193 (<i>n</i> = 24) and ST131 (<i>n</i> = 24) from Shanghai, using integrated phenotypic-genotypic analysis, including antimicrobial susceptibility, whole-genome sequencing (WGS), hemolysin assays, <i>Galleria mellonella</i> larval infection model.</p> Results <p>Both lineages exhibited high rates of multidrug resistance with strongly genotype-phenotype concordance. Key contrasts emerged: ST1193-BPEC showed significantly higher resistance to trimethoprim/sulfamethoxazole than ST131-BPEC (<i>p</i> &lt; 0.05), while ST131 overall demonstrated greater resistance to cefotaxime/cefazolin and a higher ESBL prevalence (ST131 83.33% vs. ST1193 50.00%, <i>p</i> &lt; 0.05). All ST1193 isolates were resistant to fluoroquinolones but remained susceptible to carbapenems and ceftazidime-avibactam. Genomic analysis revealed striking conservation in ST1193, with near-uniform presence of <i>fimH</i>64 (23/24), K1 capsule (100%), and O75:H5 serotype (91.7%), along with unique virulence genes (<i>vat</i>, <i>neuABCD</i>, <i>hcp2</i>, <i>kpsT</i>, <i>espL1</i>). In contrast, ST131 displayed heterogeneity in <i>fimH</i> alleles (predominantly <i>fimH</i>30), K5 capsule (95.8%), and serotypes (O25:H4/O16:H5). Hemolysin production was exclusive to ST131 isolates (5/24). Virulence assays revealed divergent patterns: ST131-UPEC isolates showed significantly higher lethality in <i>G. mellonella</i> than ST131-BPEC (<i>p</i> = 0.024), whereas ST1193 virulence remained consistent across niches (UPEC vs. BPEC: <i>p</i> = 0.843).</p> Conclusions <p>Our study confirms that ST1193 and ST131 are high-risk MDR clones employing distinct strategies—genomic conservation in ST1193 versus heterogeneity in ST131. Both exhibit substantial virulence and resistance, with <i>fimH</i>64 and <i>fimH</i>30 representing stable, lineage-specific markers. These conserved FimH variants present promising targets for future anti-adhesion therapeutics. Further mechanistic and multi-center studies are warranted to validate these findings.</p>

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Comparative genomic and phenotypic analysis of Escherichia coli ST1193 and ST131 from urinary and bloodstream infections: insights into resistance, virulence, and divergent strategies

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月24日

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  • Qian Zeng,
  • Su Wang,
  • Shuzhen Xiao,
  • Huifang Liu,
  • Feifei Gu,
  • Lizhong Han,
  • Xiaofei Jiang

摘要

Background

The global dissemination of multidrug-resistant (MDR) Escherichia coli (E. coli) clones, particularly the pandemic ST131 and the emerging ST1193, poses a serious public health threat. While ST131 is well-studied, the factors enabling ST1193’s rapid dissemination across both urinary and bloodstream infection niches remain unclear.

Methods

We compared 48 urinary (UPEC) and bloodstream (BPEC) E. coli isolates of ST1193 (n = 24) and ST131 (n = 24) from Shanghai, using integrated phenotypic-genotypic analysis, including antimicrobial susceptibility, whole-genome sequencing (WGS), hemolysin assays, Galleria mellonella larval infection model.

Results

Both lineages exhibited high rates of multidrug resistance with strongly genotype-phenotype concordance. Key contrasts emerged: ST1193-BPEC showed significantly higher resistance to trimethoprim/sulfamethoxazole than ST131-BPEC (p < 0.05), while ST131 overall demonstrated greater resistance to cefotaxime/cefazolin and a higher ESBL prevalence (ST131 83.33% vs. ST1193 50.00%, p < 0.05). All ST1193 isolates were resistant to fluoroquinolones but remained susceptible to carbapenems and ceftazidime-avibactam. Genomic analysis revealed striking conservation in ST1193, with near-uniform presence of fimH64 (23/24), K1 capsule (100%), and O75:H5 serotype (91.7%), along with unique virulence genes (vat, neuABCD, hcp2, kpsT, espL1). In contrast, ST131 displayed heterogeneity in fimH alleles (predominantly fimH30), K5 capsule (95.8%), and serotypes (O25:H4/O16:H5). Hemolysin production was exclusive to ST131 isolates (5/24). Virulence assays revealed divergent patterns: ST131-UPEC isolates showed significantly higher lethality in G. mellonella than ST131-BPEC (p = 0.024), whereas ST1193 virulence remained consistent across niches (UPEC vs. BPEC: p = 0.843).

Conclusions

Our study confirms that ST1193 and ST131 are high-risk MDR clones employing distinct strategies—genomic conservation in ST1193 versus heterogeneity in ST131. Both exhibit substantial virulence and resistance, with fimH64 and fimH30 representing stable, lineage-specific markers. These conserved FimH variants present promising targets for future anti-adhesion therapeutics. Further mechanistic and multi-center studies are warranted to validate these findings.