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      Pathogenesis and Diagnosis of Shiga Toxin-Producing Escherichia coli Infections

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      Clinical Microbiology Reviews
      American Society for Microbiology

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          Abstract

          Since their initial recognition 20 years ago, Shiga toxin-producing Escherichia coli (STEC) strains have emerged as an important cause of serious human gastrointestinal disease, which may result in life-threatening complications such as hemolytic-uremic syndrome. Food-borne outbreaks of STEC disease appear to be increasing and, when mass-produced and mass-distributed foods are concerned, can involve large numbers of people. Development of therapeutic and preventative strategies to combat STEC disease requires a thorough understanding of the mechanisms by which STEC organisms colonize the human intestinal tract and cause local and systemic pathological changes. While our knowledge remains incomplete, recent studies have improved our understanding of these processes, particularly the complex interaction between Shiga toxins and host cells, which is central to the pathogenesis of STEC disease. In addition, several putative accessory virulence factors have been identified and partly characterized. The capacity to limit the scale and severity of STEC disease is also dependent upon rapid and sensitive diagnostic procedures for analysis of human samples and suspect vehicles. The increased application of advanced molecular technologies in clinical laboratories has significantly improved our capacity to diagnose STEC infection early in the course of disease and to detect low levels of environmental contamination. This, in turn, has created a potential window of opportunity for future therapeutic intervention.

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          Author and article information

          Journal
          Clinical Microbiology Reviews
          Clin. Microbiol. Rev.
          American Society for Microbiology
          0893-8512
          1098-6618
          July 01 1998
          July 01 1998
          July 01 1998
          July 01 1998
          : 11
          : 3
          : 450-479
          Article
          10.1128/CMR.11.3.450
          88891
          9665978
          51d06ae9-a241-43e3-b98e-8157eeef7642
          © 1998
          History

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