Genetic plasticity of Escherichia coli causing bloodstream infections in India: A focus on phylogroups A to F.

BACKGROUND

Escherichia coli is a major pathogen in bloodstream infections (BSIs), with increasing concern over antimicrobial resistance (AMR) and the evolving pathogenic potential of phylogroups traditionally considered commensal. This study investigates the genetic characteristics of E. coli isolates causing BSIs in India, with a focus on phylogroups A to F.

METHODS

204 E. coli bloodstream isolates received at a tertiary hospital in India were whole genome sequenced. Phylogroups, sequence types (STs), antimicrobial resistance genes (ARGs), virulence factors (VFs), and plasmid replicon types were determined. Bioinformatics analyses include MLST, ResFinder, VirulenceFinder, PlasmidFinder, and ClermonTyping for phylogroup assignment.

RESULTS

Phylogroup B2 (35 %) was the most prevalent, followed by phylogroup A (32 %) and D (19 %). ST131 (B2) emerged as the dominant clone (22 %). Phylogroup A isolates, previously considered commensal and primarily associated with high AMR, now demonstrated notable acquisition of virulence factors such as fimH and iutA, indicating an emerging role as significant BSI pathogens. These isolates also showed high clonal diversity (e.g., ST167, ST410, ST617). Key resistance genes included blaCTX-M (53 %) and blaTEM (25 %), frequently associated with IncF plasmids. Multi-replicon plasmid profiles, particularly IncF variants, were significantly associated with co-carriage of both AMR and VF genes, contributing to enhanced pathogenicity.

CONCLUSION

This study highlights the emerging role of phylogroup A E. coli, traditionally commensal and AMR-rich as a leading cause of BSIs in India following the acquisition of virulence factors. In parallel, B2 clones like ST131 continue to drive infections through their established virulence and resistance repertoire. Such multi-replicon IncF plasmids driving AMR-VF co-selection, calls for focused surveillance and intervention in E. coli BSIs.