Title

Enteropathogenic and Enterohemorrhagic Escherichia Coli Virulence Gene Regulation

Publication Date

9-1-2007

Document Type

Article

Abstract

Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) cause significant morbidity and mortality worldwide (18, 60, 63). Though these E. coli pathotypes are genetically related, many features of their epidemiology, their pathogenesis, and the niches they occupy within the human host are unique. EPEC causes profuse watery diarrhea, primarily in children under the age of 2 years, and mostly affects individuals residing in developing countries. In contrast, adults and children infected by EHEC bacteria can suffer from either bloody or nonbloody diarrhea, and in a small percentage of cases a life-threatening complication known as hemolytic uremic syndrome (HUS) occurs. Many patients with HUS experience long-term renal damage, and they often require dialysis or kidney transplantation. EHEC produces Shiga toxins (Stx), which can cause damage to renal endothelial cells, resulting in HUS, while EPEC bacteria do not possess stx (72). EHEC disease appears in primarily industrialized nations yet causes fewer disease outbreaks in developing countries. This observation has been anecdotally attributed to immunological cross-protection from the related EPEC bacteria prevalent in the less developed regions of the world. There are two additional important differences that distinguish these two E. coli pathotypes. Approximately 108 to 1010 EPEC bacteria are necessary to cause infection in adult human volunteers (6, 27), while the infectious dose for EHEC is far less, estimated to be less than 100 CFU (49). Intriguingly, EPEC infects the small intestine; EHEC infects the large bowel, inflicting bloody diarrhea resulting from damage to the colon. Variants of the outer membrane protein intimin, expressed by both pathotypes, have been implicated as contributors to tissue tropism (103), but whether intimin is the initial adhesin and, secondly, whether other factors contribute to the ability of EPEC to recognize the small bowel and of EHEC to colonize the large bowel are not clearly understood.

Publication Title

Infection and Immunity

Volume

75

Issue

9

First Page

4199

Last Page

4210

DOI

10.1128/IAI.01927-06

Version

publisher's pdf (with 6 month embargo)

This document is currently not available here.

Find in your library

Share

COinS