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7 - LuxS-dependent regulation of Escherichia coli virulence

Published online by Cambridge University Press:  08 August 2009

Marcie B. Clarke
Affiliation:
University of Texas Southwestern Medical Center Dallas, TX USA
Vanessa Sperandio
Affiliation:
University of Texas Southwestern Medical Center Dallas, TX USA
Donald R. Demuth
Affiliation:
University of Louisville, Kentucky
Richard Lamont
Affiliation:
University of Florida
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Summary

INTRODUCTION

Escherichia coli is the most abundant facultative anaerobe found in the human intestinal microbial flora. This organism resides in the mucus layer of the mammalian colon, and typically colonizes the gastrointestinal tract of humans a few hours after birth. However, there are several clones of E. coli that have acquired virulence traits that allow them to cause a broad spectrum of disease. These virulence traits are usually encoded within mobile genetic elements, such as plasmids and pathogenicity islands, that have evolved to be stable within these clones. Three general clinical syndromes result from the infection with these pathotypes: diarrheal disease, urinary tract infections, and meningitis/sepsis. Among the intestinal pathogens there are six well-described categories: enterohemorrhagic E. coli (EHEC), enteropathogenic E. coli (EPEC), enterotoxigenic E. coli (ETEC), enteroaggregative E. coli (EAEC), enteroinvasive E. coli (EIEC), and diffusely adherent E. coli (DAEC) (59). This chapter will focus primarily on EHEC and EPEC, given that quorum sensing has been mostly described within these pathotypes.

ENTEROHEMORRHAGIC E. COLI (EHEC)

Enterohemorrhagic E. coli (EHEC) O157:H7 is responsible for major outbreaks of bloody diarrhea and hemolytic uremic syndrome (HUS) throughout the world. EHEC causes an estimated 73,000 illnesses, 2,000 hospitalizations, and 60 deaths in the United States alone each year. EHEC has a very low infectious dose (as few as 50 cfu); this is one of the major contributing factors to EHEC outbreaks.

Type
Chapter
Information
Bacterial Cell-to-Cell Communication
Role in Virulence and Pathogenesis
, pp. 151 - 174
Publisher: Cambridge University Press
Print publication year: 2006

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