Virulence of enteropathogenic Escherichia coli, a global pathogen
Virulence of enteropathogenic Escherichia coli, a global pathogen
Enteropathogenic Escherichia coli (EPEC) remains an important cause of diarrheal disease worldwide. Research into EPEC is intense and provides a good virulence model of other E. coli infections as well as other pathogenic bacteria. Although the virulence mechanisms are now better understood, they are extremely complex and much remains to be learnt. The pathogenesis of EPEC depends on the formation of an ultrastructural lesion in which the bacteria make intimate contact with the host apical enterocyte membrane. The formation of this lesion is a consequence of the ability of EPEC to adhere in a localized manner to the host cell, aided by bundle-forming pili. Tyrosine phosphorylation and signal transduction events occur within the host cell at the lesion site, leading to a disruption of the host cell mechanisms and, consequently, to diarrhea. These result from the action of highly regulated EPEC secreted proteins which are released via a type III secretion system, many genes of which are located within a pathogenicity island known as the locus of enterocyte effacement. Over the last few years, dramatic increases in our knowledge of EPEC virulence have taken place. This review therefore aims to provide a broad overview of and update to the virulence aspects of EPEC.
Bacterial Adhesion, Enterocytes/pathology, Escherichia coli/genetics, Fimbriae, Bacterial/physiology, Phosphorylation, Plasmids, Proteins/metabolism, Signal Transduction, Virulence
365-378
Clarke, S C
f7d7f7a2-4b1f-4b36-883a-0f967e73fb17
Haigh, R D
108c217e-fcf0-4550-9505-26e04ae63611
Freestone, P P E
207e08a2-e851-44c1-a12a-0d5a1490ea90
Williams, P H
f7e83b44-8a65-4ce9-b672-80b016dfc169
1 July 2003
Clarke, S C
f7d7f7a2-4b1f-4b36-883a-0f967e73fb17
Haigh, R D
108c217e-fcf0-4550-9505-26e04ae63611
Freestone, P P E
207e08a2-e851-44c1-a12a-0d5a1490ea90
Williams, P H
f7e83b44-8a65-4ce9-b672-80b016dfc169
Clarke, S C, Haigh, R D, Freestone, P P E and Williams, P H
(2003)
Virulence of enteropathogenic Escherichia coli, a global pathogen.
Clinical Microbiology Reviews, 16 (3), .
(doi:10.1128/CMR.16.3.365-378.2003).
Abstract
Enteropathogenic Escherichia coli (EPEC) remains an important cause of diarrheal disease worldwide. Research into EPEC is intense and provides a good virulence model of other E. coli infections as well as other pathogenic bacteria. Although the virulence mechanisms are now better understood, they are extremely complex and much remains to be learnt. The pathogenesis of EPEC depends on the formation of an ultrastructural lesion in which the bacteria make intimate contact with the host apical enterocyte membrane. The formation of this lesion is a consequence of the ability of EPEC to adhere in a localized manner to the host cell, aided by bundle-forming pili. Tyrosine phosphorylation and signal transduction events occur within the host cell at the lesion site, leading to a disruption of the host cell mechanisms and, consequently, to diarrhea. These result from the action of highly regulated EPEC secreted proteins which are released via a type III secretion system, many genes of which are located within a pathogenicity island known as the locus of enterocyte effacement. Over the last few years, dramatic increases in our knowledge of EPEC virulence have taken place. This review therefore aims to provide a broad overview of and update to the virulence aspects of EPEC.
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Published date: 1 July 2003
Additional Information:
Copyright © 2003 American Society for Microbiology
Keywords:
Bacterial Adhesion, Enterocytes/pathology, Escherichia coli/genetics, Fimbriae, Bacterial/physiology, Phosphorylation, Plasmids, Proteins/metabolism, Signal Transduction, Virulence
Identifiers
Local EPrints ID: 455399
URI: http://eprints.soton.ac.uk/id/eprint/455399
ISSN: 0893-8512
PURE UUID: b94f3248-e32f-4bbc-8cf8-8ea7a1f401ce
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Date deposited: 21 Mar 2022 17:34
Last modified: 17 Mar 2024 03:07
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Author:
R D Haigh
Author:
P P E Freestone
Author:
P H Williams
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