Parallel evolution of virulence in pathogenic Escherichia coli

Sean D. Reid, Corinne J. Herbelin, Alyssa C. Bumbaugh, Robert K. Selander and Thomas S. Whittam ()
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Sean D. Reid: Institute of Molecular Evolutionary Genetics, Pennsylvania State University
Corinne J. Herbelin: Institute of Molecular Evolutionary Genetics, Pennsylvania State University
Alyssa C. Bumbaugh: Institute of Molecular Evolutionary Genetics, Pennsylvania State University
Robert K. Selander: Institute of Molecular Evolutionary Genetics, Pennsylvania State University
Thomas S. Whittam: Institute of Molecular Evolutionary Genetics, Pennsylvania State University

Nature, 2000, vol. 406, issue 6791, 64-67

Abstract: Abstract The mechanisms underlying the evolution and emergence of new bacterial pathogens are not well understood. To elucidate the evolution of pathogenic Escherichia coli strains, here we sequenced seven housekeeping genes to build a phylogenetic tree and trace the history of the acquisition of virulence genes. Compatibility analysis indicates that more than 70% of the informative sites agree with a single phylogeny, suggesting that recombination has not completely obscured the remnants of ancestral chromosomes1,2,3. On the basis of the rate of synonymous substitution for E. coli and Salmonella enterica (4.7 × 10-9 per site per year3), the radiation of clones began about 9 million years ago and the highly virulent pathogen responsible for epidemics of food poisoning, E. coli O157:H7, separated from a common ancestor of E. coli K-12 as long as 4.5 million years ago. Phylogenetic analysis reveals that old lineages of E. coli have acquired the same virulence factors in parallel, including a pathogenicity island involved in intestinal adhesion, a plasmid-borne haemolysin, and phage-encoded Shiga toxins. Such parallel evolution indicates that natural selection has favoured an ordered acquisition of genes and the progressive build-up of molecular mechanisms that increase virulence.

Date: 2000
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DOI: 10.1038/35017546

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