The article investigates the evolutionary pathways underlying the dichotomy between pathogenic and non-pathogenic *Escherichia coli*. Pathogenic *E. coli* causes over 160 million cases of dysentery and one million deaths annually, while non-pathogenic *E. coli* is part of the normal intestinal flora of healthy mammals and birds. The study used multilocus sequence typing to analyze a global collection of isolates, finding that specific pathogen types have arisen independently and repeatedly in several lineages, while other lineages contain few pathogens. Rates of evolution have accelerated in pathogenic lineages, leading to highly virulent organisms with frequent genomic changes due to increased homologous recombination. This suggests a link between bacterial sex and virulence. The evolution of virulence is observed in genes distributed throughout the genome, indicating that it is a long-term pattern resulting from episodic selection for strains that can evade the host immune response. The study also highlights the widespread presence of recombination within *E. coli*, which blurs phylogenetic signals and reduces the degree of differentiation between groups. The population structure of *E. coli* is characterized by a star-like phylogeny, suggesting a major historical bottleneck or selective sweep. The most virulent strains, such as Shigella and EIEC, have undergone the greatest degree of homologous recombination between ancestral sources. The authors propose a model where virulence drives higher mutation and recombination rates, leading to more frequent HGT events and the evolution of epidemic strains.The article investigates the evolutionary pathways underlying the dichotomy between pathogenic and non-pathogenic *Escherichia coli*. Pathogenic *E. coli* causes over 160 million cases of dysentery and one million deaths annually, while non-pathogenic *E. coli* is part of the normal intestinal flora of healthy mammals and birds. The study used multilocus sequence typing to analyze a global collection of isolates, finding that specific pathogen types have arisen independently and repeatedly in several lineages, while other lineages contain few pathogens. Rates of evolution have accelerated in pathogenic lineages, leading to highly virulent organisms with frequent genomic changes due to increased homologous recombination. This suggests a link between bacterial sex and virulence. The evolution of virulence is observed in genes distributed throughout the genome, indicating that it is a long-term pattern resulting from episodic selection for strains that can evade the host immune response. The study also highlights the widespread presence of recombination within *E. coli*, which blurs phylogenetic signals and reduces the degree of differentiation between groups. The population structure of *E. coli* is characterized by a star-like phylogeny, suggesting a major historical bottleneck or selective sweep. The most virulent strains, such as Shigella and EIEC, have undergone the greatest degree of homologous recombination between ancestral sources. The authors propose a model where virulence drives higher mutation and recombination rates, leading to more frequent HGT events and the evolution of epidemic strains.