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Curr Opin Gastroenterol. 2008 Jan;24(1):38-47.

Pathogenesis and treatment of Shiga toxin-producing Escherichia coli infections.

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Division of Gastroenterology/Hepatology, Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131-0001, USA.



Shiga toxin-producing Escherichia coli cause hemorrhagic colitis and hemolytic uremic syndrome. We will summarize the literature on incidence and outcomes of these infections, and then review the pathogenesis to explain the current recommendations against antibiotic use and to suggest alternative therapies.


Shiga toxin-producing E. coli continue to be prevalent in the industrialized world because of dissemination in food products contaminated by ruminant feces. Declines in ground beef-related outbreaks have been matched by increased cases related to green vegetables. Fifteen percent of patients infected with E. coli O157:H7 progress to hemolytic uremic syndrome, but this figure may reach 50% if antibiotics are used. Mechanisms for bacteriophage induction causing Shiga toxin production, and for Shiga toxin dissemination to endothelium in gut, kidney and brain, may explain the negative effects of antibiotics and lead to rational therapies. Shiga toxin binders were not effective in clinical trials, but more avid binding agents may be. Current treatment recommendations are to maintain hydration to prevent thrombotic complications. Human vaccines are unlikely to be utilized. Cattle vaccines may prove the most significant approach to this disease.


Improved understanding of Shiga toxin-producing Escherichia coli pathophysiology and progression to hemolytic uremic syndrome provides the basis for prevention, prophylactic and treatment strategies.

[Indexed for MEDLINE]

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