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Updated: Jul 15, 2026

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
Published on: October 29, 2014
Parallel evolution of virulence in pathogenic Escherichia coli
S D Reid1, C J Herbelin, A C Bumbaugh
1Institute of Molecular Evolutionary Genetics, Pennsylvania State University, University Park 16802, USA.
The evolution of pathogenic Escherichia coli, including E. coli O157:H7, began millions of years ago. Natural selection favored the ordered acquisition of virulence genes, leading to increased pathogen threat.
Area of Science:
- Microbiology
- Evolutionary Biology
- Genetics
Background:
- The evolutionary pathways leading to new bacterial pathogens remain largely unknown.
- Understanding the emergence of pathogenic Escherichia coli (E. coli) is crucial for public health.
Purpose of the Study:
- To elucidate the evolutionary history and virulence gene acquisition in pathogenic E. coli strains.
- To reconstruct the phylogenetic relationships and timeline of E. coli pathogen evolution.
Main Methods:
- Sequencing of seven housekeeping genes to construct a phylogenetic tree.
- Compatibility analysis to assess the impact of recombination on phylogenetic signals.
- Estimation of divergence times using synonymous substitution rates for E. coli and Salmonella enterica.
Main Results:
- Phylogenetic analysis revealed that recombination has not entirely obscured ancestral chromosomal signals.
- The radiation of E. coli clones initiated approximately 9 million years ago.
- The highly virulent E. coli O157:H7 diverged from an E. coli K-12 ancestor around 4.5 million years ago.
- Older E. coli lineages independently acquired identical virulence factors, such as pathogenicity islands, haemolysins, and Shiga toxins.
Conclusions:
- Parallel evolution of virulence factors suggests strong selective pressures in pathogenic E. coli.
- Natural selection has driven an ordered acquisition of genes, progressively enhancing bacterial virulence.
- This study provides insights into the stepwise development of pathogenic mechanisms in E. coli.
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