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Journal of Bacteriology, April 2002, p. 1873-1879, Vol. 184, No. 7
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.7.1873-1879.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Strains of Escherichia coli O157:H7 Differ Primarily by Insertions or Deletions, Not Single-Nucleotide Polymorphisms

Indira T. Kudva,1 Peter S. Evans,2,{dagger} Nicole T. Perna,3 Timothy J. Barrett,4 Frederick M. Ausubel,5,6 Frederick R. Blattner,2 and Stephen B. Calderwood1,7*

Division of Infectious Diseases,1 Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114,5 Department of Microbiology and Molecular Genetics,2 Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115,6 Laboratory of Genetics,7 Department of Animal Health and Biomedical Sciences, University of Wisconsin—Madison, Madison, Wisconsin 53706,3 Foodborne and Diarrheal Diseases Branch, Centers for Disease Control, Atlanta, Georgia 303334

Received 17 September 2001/ Accepted 31 December 2001

Escherichia coli O157:H7 (O157) strains demonstrate varied pulsed-field gel electrophoresis patterns following XbaI digestion, which enable epidemiological surveillance of this important human pathogen. The genetic events underlying PFGE differences between strains, however, are not defined. We investigated the mechanisms for strain variation in O157 by recovering and examining nucleotide sequences flanking each of the XbaI restriction enzyme sites in the genome. Our analysis demonstrated that differences between O157 strains were due to discrete insertions or deletions that contained the XbaI sites polymorphic between strains rather than single-nucleotide polymorphisms in the XbaI sites themselves. These insertions and deletions were found to be uniquely localized within the regions of the genome that are specific to O157 compared to E. coli K-12 (O islands), suggesting that strain-to-strain variation occurs in these O islands. These results may be utilized to devise novel strain-typing tools for this pathogen.

* Corresponding author. Mailing address: Division of Infectious Diseases, Massachusetts General Hospital, Boston, MA 02114. Phone: (617) 726-3811. Fax: (617) 726-7416. E-mail: scalderwood{at}partners.org.

{dagger} Present address: Institute of Human Virology, Baltimore, MD 21201.

Journal of Bacteriology, April 2002, p. 1873-1879, Vol. 184, No. 7
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.7.1873-1879.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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