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Infection and Immunity, December 2004, p. 7131-7139, Vol. 72, No. 12
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.12.7131-7139.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Diversity and Host Range of Shiga Toxin-Encoding Phage
Shantini D. Gamage,
Angela K. Patton,
James F. Hanson,
and
Alison A. Weiss*
Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, Cincinnati, Ohio
Received 18 May 2004/
Returned for modification 16 August 2004/
Accepted 31 August 2004
Shiga toxin 2 (Stx2) from the foodborne pathogen Escherichia coli O157:H7 is encoded on a temperate bacteriophage. Toxin-encoding phages from C600::933W and from six clinical E. coli O157:H7 isolates were characterized for PCR polymorphisms, phage morphology, toxin production, and lytic and lysogenic infection profiles on O157 and non-O157 serotype E. coli. The phages were found to be highly variable, and even phages isolated from strains with identical pulsed-field gel electrophoresis profiles differed. Examination of cross-plaquing and lysogeny profiles further substantiated that each phage is distinct; reciprocal patterns of susceptibility and resistance were not observed and it was not possible to define immunity groups. The interaction between Shiga toxin-encoding phage and intestinal E. coli was examined. Lytic infection was assessed by examining Shiga toxin production following overnight incubation with phage. While not common, lytic infection was observed, with a more-than-1,000-fold increase in Stx2 seen in one case, demonstrating that commensal E. coli cells can amplify Shiga toxin if they are susceptible to infection by the Shiga toxin-encoding phages. Antibiotic-resistant derivatives of the Stx2-encoding phages were used to examine lysogeny. Different phages were found to lysogenize different strains of intestinal E. coli. Lysogeny was found to occur more commonly than lytic infection. The presence of a diverse population of Shiga toxin-encoding phages may increase the pathogenic fitness of E. coli O157:H7.
* Corresponding author. Mailing address: Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267-0524. Phone: (513) 558-2820. Fax: (513) 558-8474. E-mail:
Alison.Weiss{at}uc.edu.
Editor: A. D. O'Brien
Present address: Armed Forces Institute of Pathology, Washington, DC 20306-6000.
Infection and Immunity, December 2004, p. 7131-7139, Vol. 72, No. 12
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.12.7131-7139.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
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