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Extensive genomic diversity and selective conservation of virulence-determinants in enterohemorrhagic Escherichia coli strains of O157 and non-O157 serotypes

Yoshitoshi Ogura12, Tadasuke Ooka2, Asadulghani2, Jun Terajima3, Jean-Philippe Nougayrède4, Ken Kurokawa5, Kousuke Tashiro6, Toru Tobe7, Keisuke Nakayama2, Satoru Kuhara6, Eric Oswald4, Haruo Watanabe3 and Tetsuya Hayashi12*

Author Affiliations

1 Division of Bioenvironmental Science, Frontier Science Research Center, University of Miyazaki,5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan

2 Division of Microbiology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki,5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan

3 Department of Bacteriology, National Institute for Infectious Diseases, 1-23-1 Toyama, Shinjuku, Tokyo, 162-8640, Japan

4 UMR1225, INRA-ENVT, 23 chemin des Capelles, 31076 Toulouse, France

5 Laboratory of Comparative Genomics, Graduate School of Information Science, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara, 630-0192, Japan

6 Laboratory of Molecular Gene Technics, Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakosaki, Fukuoka, 812-8581, Japan

7 Division of Applied Bacteriology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan

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Genome Biology 2007, 8:R138  doi:10.1186/gb-2007-8-7-r138

Published: 10 July 2007



Enterohemorrhagic Escherichia coli (EHEC) O157 causes severe food-borne illness in humans. The chromosome of O157 consists of 4.1 Mb backbone sequences shared by benign E. coli K-12, and 1.4 Mb O157-specific sequences encoding many virulence determinants, such as Shiga toxin genes (stx genes) and the locus of enterocyte effacement (LEE). Non-O157 EHECs belonging to distinct clonal lineages from O157 also cause similar illness in humans. According to the 'parallel' evolution model, they have independently acquired the major virulence determinants, the stx genes and LEE. However, the genomic differences between O157 and non-O157 EHECs have not yet been systematically analyzed.


Using microarray and whole genome PCR scanning analyses, we performed a whole genome comparison of 20 EHEC strains of O26, O111, and O103 serotypes with O157. In non-O157 EHEC strains, although genome sizes were similar with or rather larger than O157 and the backbone regions were well conserved, O157-specific regions were very poorly conserved. Around only 20% of the O157-specific genes were fully conserved in each non-O157 serotype. However, the non-O157 EHECs contained a significant number of virulence genes that are found on prophages and plasmids in O157, and also multiple prophages similar to, but significantly divergent from, those in O157.


Although O157 and non-O157 EHECs have independently acquired a huge amount of serotype- or strain-specific genes by lateral gene transfer, they share an unexpectedly large number of virulence genes. Independent infections of similar but distinct bacteriophages carrying these virulence determinants are deeply involved in the evolution of O157 and non-O157 EHECs.