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

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. 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. 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). 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.