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Previous Volume 335:635-638 August 29, 1996 Number 9 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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In the United States, the hemolytic–uremic syndrome of childhood typically follows gastrointestinal infection with Escherichia coli O157:H7.^1,2,3 It is presumed that the absorption from the gastrointestinal tract of Shiga toxins 1, 2, or both (formerly called Shiga-like toxins⁴) produced by E. coli O157:H7 causes microangiopathic hemolytic anemia as a result of endothelial-cell injury.⁵ Shiga-toxin–producing E. coli belonging to serotypes other than O157:H7 can also cause the hemolytic–uremic syndrome.^5,6 However, even though such organisms have been implicated as causes of sporadic cases⁷ or outbreaks⁸ of gastroenteritis, they are not believed to be important causes of the hemolytic–uremic syndrome in this . . . [Full Text of this Article]

Case Report

Characteristics of the Infecting Strain

Discussion

Source Information

From the Children's Hospital and Medical Center, Seattle (P.I.T., L.S.F., H.H.K., J.C.V., C.R.C.); the Departments of Pediatrics (P.I.T., L.S.F.), Microbiology (P.I.T.), Medicine (A.E.S.), and Laboratory Medicine (C.R.C.), University of Washington School of Medicine, Seattle; and the Department of Veterinary Sciences and the Institute of Molecular Evolutionary Genetics, Pennsylvania State University, University Park (R.A.W.).

Address reprint requests to Dr. Tarr at the Division of Gastroenterology, Mail Stop CH-24, Children's Hospital and Medical Center, 4800 Sand Point Way NE, Seattle, WA 98105.

References

Related Letters:

Escherichia coli and the Hemolytic–Uremic Syndrome
Acheson D. W.K., Wolf L. E., Park C. H., Rossboth D. W., Tarr P. I., Stapleton A. E., Wilson R. A., Rondeau E., Peraldi M.-N.
Extract | Full Text  
N Engl J Med 1997; 336:515-516, Feb 13, 1997. Correspondence

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