Treatment of enterohemorrhagic Escherichia coli (EHEC) infection and hemolytic uremic syndrome (HUS)

Paul N Goldwater,Karl A Bettelheim

doi:10.1186/1741-7015-10-12

Abstract

Verotoxigenic Escherichia coli (VTEC) are a specialized group of E. coli that can cause severe colonic disease and renal failure. Their pathogenicity derives from virulence factors that enable the bacteria to colonize the colon and deliver extremely powerful toxins known as verotoxins (VT) or Shiga toxins (Stx) to the systemic circulation. The recent devastating E. coli O104:H4 epidemic in Europe has shown how helpless medical professionals are in terms of offering effective therapies. By examining the sources and distribution of these bacteria, and how they cause disease, we will be in a better position to prevent and treat the inevitable future cases of sporadic disease and victims of common source outbreaks. Due to the complexity of pathogenesis, it is likely a multitargeted approach is warranted. Developments in terms of these treatments are discussed.See related article: http://www.biomedcentral.com/1741-7015/10/11

Highlights

The association of verotoxigenic Escherichia coli (VTEC) with human disease goes back over 30 years [1,2,3]
The potential for VTEC spread is further compounded by globalization of food, which presents a great opportunity for VTEC to spread quickly to large sections of the population
No attention appears to have been given to the generally observed fact that there is a widespread diversity of E. coli serotypes in the human intestine at any one time [8] and this has been found in animals, especially cattle [9]

Summary

Introduction

The association of verotoxigenic Escherichia coli (VTEC) with human disease goes back over 30 years [1,2,3]. Pathogenesis of post-diarrheal hemolytic uremic syndrome VTEC/STEC/enterohemorrhagic E. coli (EHEC) belong to clones of zoonotic E. coli of different O serogroups These serogroups have evolved and acquired specific virulence factors that enable the bacteria to colonize and infect the human colon, usually without invasion of the blood stream [13]. Delayed administration of the peptide significantly reduced thrombocytopenia, but had no effect on anemia This cell-permeable agent shows promise in counteracting Stx lethality in a baboon model; outcomes of human trials are awaited. Inhibition of terminal complement complex formation Based on evidence that Shiga toxin activates complement and binds factor H and evidence for an active role of complement via the alternative pathway in diarrheaassociated hemolytic uremic syndrome [51,52], a few anecdotal reports of successful treatment of severe Stxassociated HUS with the monoclonal antibody eculizumab have been published [53]. Competing interests The authors declare that they have no competing interests

17. Denamur E

Findings

29. McLeod BC