The bacterial genetic determinants of Escherichia coli capacity to cause bloodstream infections in humans

PLoS Genet. 2023 Aug 2;19(8):e1010842. doi: 10.1371/journal.pgen.1010842. eCollection 2023 Aug.

Abstract

Escherichia coli is both a highly prevalent commensal and a major opportunistic pathogen causing bloodstream infections (BSI). A systematic analysis characterizing the genomic determinants of extra-intestinal pathogenic vs. commensal isolates in human populations, which could inform mechanisms of pathogenesis, diagnostic, prevention and treatment is still lacking. We used a collection of 912 BSI and 370 commensal E. coli isolates collected in France over a 17-year period (2000-2017). We compared their pangenomes, genetic backgrounds (phylogroups, STs, O groups), presence of virulence-associated genes (VAGs) and antimicrobial resistance genes, finding significant differences in all comparisons between commensal and BSI isolates. A machine learning linear model trained on all the genetic variants derived from the pangenome and controlling for population structure reveals similar differences in VAGs, discovers new variants associated with pathogenicity (capacity to cause BSI), and accurately classifies BSI vs. commensal strains. Pathogenicity is a highly heritable trait, with up to 69% of the variance explained by bacterial genetic variants. Lastly, complementing our commensal collection with an older collection from 1980, we predict that pathogenicity continuously increased through 1980, 2000, to 2010. Together our findings imply that E. coli exhibit substantial genetic variation contributing to the transition between commensalism and pathogenicity and that this species evolved towards higher pathogenicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Escherichia coli
  • Escherichia coli Infections* / genetics
  • Escherichia coli Infections* / microbiology
  • Genes, Bacterial
  • Humans
  • Phylogeny
  • Sepsis* / genetics
  • Virulence / genetics

Grants and funding

ED was partially supported by the “Fondation pour la Recherche Médicale” (Equipe FRM 2016, grant number DEQ20161136698). GR was supported by a “Poste d’accueil” funded by the “Assistance Publique-Hôpitaux de Paris” (AP-HP) and the “Commissariat à l'énergie atomique et aux énergies alternatives” (CEA) personal grant for his PhD. MG and JB were supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany's Excellence Strategy - EXC 2155 - project number 390874280. JB was further supported by the Deutsche Forschungsgemeinschaft grant number GA 3191/1-1. F.B. was funded by the ERC StG 949208 EvoComBac. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.