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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #169129
Title: PATHOGENESIS OF SHIGA TOXIN-PRODUCING ESCHERICHIA COLI DISEASE

Author
item Nystrom, Evelyn

Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 9/9/2004
Publication Date: 11/14/2004
Citation: Nystrom, E.A. 2004. Pathogenesis of Shiga toxin-producing Escherichia coli disease [abstract]. Conference of Research Workers in Animal Diseases. p. 105.

Interpretive Summary:

Technical Abstract: Shiga toxin-producing Escherichia coli (STEC) are associated with a wide range of clinical manifestations, including asymptomatic carriage, nonhemorrhagic diarrhea, hemorrhagic colitis, edema disease in pigs, and the hemolytic-uremic syndrome (HUS) in humans. Cattle, which are often asymptomatic carriers of STEC, are important sources of STEC associated with disease in humans. Several animal models have been used to study the diverse manifestations of STEC infection. STEC inoculation studies in cattle and sheep have identified several bacterial and host determinants involved in STEC colonization in ruminants, and helped develop intervention strategies to reduce the input of STEC into the food chain. STEC inoculation studies and Shiga toxin (Stx) inoculation studies in calves, dogs, ferrets, mice, monkeys, piglets, rabbits, and rats have identified specific events that occur after oral exposure to STEC or parenteral inoculation with Stx, and demonstrated that Stx is responsible for the later events. None of the models replicates all aspects of STEC-induced HUS in humans, but the various models are useful for studying the study the specific events that do occur. The predicted events in the development of HUS include: colonization of the intestines by ingested STEC, release of Shiga toxins (Stx) by STEC in the intestines, direct Stx damage to intestinal epithelial cells (resulting in hemorrhagic colitis), translocation of Stx from the intestinal lumen into the circulation (systemic toxemia), transport of Stx to target tissues, binding of Stx to cells containing Stx receptors (endothelial cells, epithelial cells, and immunocytes), and Stx-induced cytotoxicity and immunomodulation (resulting in hemolytic anemia, thrombocytopenia, and renal failure). Comparative studies using different STEC strains in different STEC infection models will facilitate determination of the sequence of these events and the importance of each event in the pathogenesis of STEC-mediated disease.