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Infect Immun, August 1998, p. 3810-3817, Vol. 66, No. 8
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Molecular Evolution of a Pathogenicity Island from Enterohemorrhagic Escherichia coli O157:H7dagger

Nicole T. Perna,1 * George F. Mayhew,1 György Pósfai,2 Simon Elliott,3 Michael S. Donnenberg,4 James B. Kaper,3 and Frederick R. Blattner1

Laboratory of Genetics, University of Wisconsin-Madison, Madison Wisconsin 537061; Institute of Biochemistry, Biological Research Center, H-6701 Szeged, Hungary2; and Center for Vaccine Development3 and Division of Infectious Disease,4 University of Maryland School of Medicine, Baltimore, Maryland 21201

Received 29 December 1997/Returned for modification 6 March 1998/Accepted 27 May 1998

We report the complete 43,359-bp sequence of the locus of enterocyte effacement (LEE) from EDL933, an enterohemorrhagic Escherichia coli O157:H7 serovar originally isolated from contaminated hamburger implicated in an outbreak of hemorrhagic colitis. The locus was isolated from the EDL933 chromosome with a homologous-recombination-driven targeting vector. Recent completion of the LEE sequence from enteropathogenic E. coli (EPEC) E2348/69 afforded the opportunity for a comparative analysis of the entire pathogenicity island. We have identified a total of 54 open reading frames in the EDL933 LEE. Of these, 13 fall within a putative P4 family prophage designated 933L. The prophage is not present in E2348/69 but is found in a closely related EPEC O55:H7 serovar and other O157:H7 isolates. The remaining 41 genes are shared by the two complete LEEs, and we describe the nature and extent of variation among the two strains for each gene. The rate of divergence is heterogeneous along the locus. Most genes show greater than 95% identity between the two strains, but other genes vary more than expected for clonal divergence among E. coli strains. Several of these highly divergent genes encode proteins that are known to be involved in interactions with the host cell. This pattern suggests recombinational divergence coupled with natural selection and has implications for our understanding of the interaction of both pathogens with their host, for the emergence of O157:H7, and for the evolutionary history of pathogens in general.

* Corresponding author. Mailing address: Laboratory of Genetics, University of Wisconsin-Madison, 445 Henry Mall, Rm. B44, Madison, WI 53706. Phone: (608) 262-2534. Fax: (608) 263-7459. E-mail: nicole{at}genetics.wisc.edu.

dagger Laboratory of Genetics paper 3516.

Infect Immun, August 1998, p. 3810-3817, Vol. 66, No. 8
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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