Purpose of review: The Shiga toxin-producing Escherichia coli strains, such as E. coli O157:H7, have emerged as major diarrheal pathogens both in the United States and elsewhere. These organisms are important because gastrointestinal infection (afebrile hemorrhagic colitis) can trigger microangiopathic hemolytic anemia and renal failure (hemolytic uremic syndrome). Understanding the pathophysiology of this illness is likely to lead to important new treatment interventions.
Recent findings: It is now recognized that children with hemorrhagic colitis routinely develop a spectrum of coagulation abnormalities and that only a fraction of children develop full blown hemolytic uremic syndrome. Individual variability in expression of inflammatory mediators is likely to be a key element in determining which children progress to the severe end of the spectrum of disease. The value of antibiotic therapy is unknown.
Summary: The pathophysiology of HUS remains incompletely understood. The lag between onset of diarrhea and onset of HUS represents an opportunity to intervene and prevent renal failure. However, there currently is no way to prevent such life threatening complications. The management should focus on diagnosis and close observation so that early intervention can prevent complications.