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Overview and Historical Perspectives

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  • Authors: James B. Kaper1, Alison D. O'Brien2
  • Editors: Vanessa Sperandio3, Carolyn J. Hovde4
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21122; 2: Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814; 3: University of Texas Southwestern Medical Center, Dallas, TX; 4: University of Idaho, Moscow, ID
  • Source: microbiolspec November 2014 vol. 2 no. 6 doi:10.1128/microbiolspec.EHEC-0028-2014
  • Received 25 March 2014 Accepted 26 March 2014 Published 21 November 2014
  • James B. Kaper, jkaper@umaryland.edu
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  • Abstract:

    In this overview, we describe the history of Shiga toxin (Stx)-producing (STEC) in two phases. In phase one, between 1977 and 2011, we learned that could produce Shiga toxin and cause both hemorrhagic colitis and the hemolytic-uremic syndrome in humans and that the prototype STEC— O157:H7—adheres to and effaces intestinal epithelial cells by a mechanism similar to that of enteropathogenic . We also recognized that the genes for Stx are typically encoded on a lysogenic phage; that STEC O157:H7 harbors a large pathogenicity island that encodes the elements needed for the characteristic attaching and effacing lesion; and that the most severe cases of human disease are linked to production of Stx type 2a, not Stx type 1a. Phase two began with a large food-borne outbreak of hemorrhagic colitis and hemolytic-uremic syndrome in Germany in 2011. That outbreak was caused by a novel strain consisting of enteroaggregative O104:H4 transduced by a Stx2a-converting phage. From this outbreak we learned that any strain that can adhere tightly to the human bowel (either by a biofilm-like mechanism as in O104:H4 or by an attaching and effacing mechanism as in O157:H7) can cause severe diarrheal and systemic illness when it acquires the capacity to produce Stx2a. This overview provides the basis for the review of current information regarding these fascinating and complex pathogens.

  • Citation: Kaper J, O'Brien A. 2014. Overview and Historical Perspectives. Microbiol Spectrum 2(6):EHEC-0028-2014. doi:10.1128/microbiolspec.EHEC-0028-2014.

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Abstract:

In this overview, we describe the history of Shiga toxin (Stx)-producing (STEC) in two phases. In phase one, between 1977 and 2011, we learned that could produce Shiga toxin and cause both hemorrhagic colitis and the hemolytic-uremic syndrome in humans and that the prototype STEC— O157:H7—adheres to and effaces intestinal epithelial cells by a mechanism similar to that of enteropathogenic . We also recognized that the genes for Stx are typically encoded on a lysogenic phage; that STEC O157:H7 harbors a large pathogenicity island that encodes the elements needed for the characteristic attaching and effacing lesion; and that the most severe cases of human disease are linked to production of Stx type 2a, not Stx type 1a. Phase two began with a large food-borne outbreak of hemorrhagic colitis and hemolytic-uremic syndrome in Germany in 2011. That outbreak was caused by a novel strain consisting of enteroaggregative O104:H4 transduced by a Stx2a-converting phage. From this outbreak we learned that any strain that can adhere tightly to the human bowel (either by a biofilm-like mechanism as in O104:H4 or by an attaching and effacing mechanism as in O157:H7) can cause severe diarrheal and systemic illness when it acquires the capacity to produce Stx2a. This overview provides the basis for the review of current information regarding these fascinating and complex pathogens.

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