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Pathogenesis of Colitis in Germ-Free Mice Infected With EHEC O157:H7.

K A Eaton1, C Fontaine1, D I Friedman1

  • 11 University of Michigan Medical School, Ann Arbor, MI, USA.

Veterinary Pathology
|February 9, 2017
PubMed
Summary

Enterohemorrhagic Escherichia coli (EHEC) causes colitis and kidney disease. Shiga toxin 2 (Stx2) is essential for systemic disease, including kidney failure, but not for initial colitis.

Keywords:
Escherichia colianimal modelsbacterial infectionsgastrointestinal diseasesgerm-freemicepathogenicityvirulence factors

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Area of Science:

  • Microbiology
  • Pathogenesis
  • Gastroenterology

Background:

  • Enterohemorrhagic Escherichia coli (EHEC) causes hemorrhagic colitis and potentially fatal hemolytic uremic syndrome.
  • Shiga toxins (Stx) expression, often phage-mediated, is linked to both enteric and renal disease.
  • Previous studies showed EHEC toxin gene expression is enhanced in vivo.

Purpose of the Study:

  • To quantify necrotizing colitis and disease progression in EHEC infection.
  • To determine the roles of Stx2, phage genes, and type 3 secretion system (T3SS) in disease.
  • To elucidate the mechanisms of EHEC pathogenesis in a germ-free mouse model.

Main Methods:

  • Germ-free mice were inoculated with EHEC strains, including mutants.
  • Colitis severity, systemic disease, renal failure, and splenic necrosis were assessed.
  • The contribution of Stx2, T3SS, and prophage genes to colonization and disease was evaluated.

Main Results:

  • EHEC infection caused acute colitis followed by systemic disease.
  • Renal failure and splenic necrosis were strictly dependent on Stx2 expression.
  • Colitis was only partially dependent on Stx2, while T3SS and prophage excision were not essential for systemic disease.

Conclusions:

  • EHEC pathogenesis involves early colitis followed by systemic complications, mirroring human disease.
  • Stx2 is critical for systemic EHEC disease, including renal failure, but not for the initial enteric inflammation.
  • Understanding these distinct roles of virulence factors aids in developing targeted therapeutic strategies.