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  • Review Article
  • Published:

Molecular mechanisms of Escherichia coli pathogenicity

Nature Reviews Microbiology volume 8, pages 26–38 (2010)Cite this article

A Corrigendum to this article was published on 24 December 2012

This article has been updated

Key Points

  • Major advances have been made in our understanding of the molecular mechanisms that are used by pathogenic Escherichia coli to cause disease. In this Review, we focus on these advancements for six diarrhoeagenic and two extraintestinal pathovars.

  • Pathogenic E. coli are diverse in their gene sets. Many virulence factors are maintained on a virulence plasmid and were acquired through horizontal gene transfer. Others were integrated into the chromosome by bacteriophages or transposable elements. Although the gain of traits is important in the evolution of a pathogen, the loss of certain genes was necessary for enteroinvasive E. coli (including Shigella) to become fully pathogenic.

  • We are beginning to dissect the interactions between E. coli virulence factors and host cell components. Several effector proteins that are secreted by the type III secretion system of enteropathogenic, enterohaemorrhagic and enteroinvasive E. coli have been shown to hijack and manipulate host cell processes for the benefit of the bacterium.

  • Other pathovars, such as enterotoxigenic E. coli, elaborate toxins that cause disease, whereas the attachment of enteroaggregative and diffusely adherent E. coli stimulates cellular signalling events that stimulate inflammation.

  • The extraintestinal isolates have remarkable lifestyles. Uropathogenic E. coli can invade the underlying bladder cells and form quiescent reservoirs, which are possibly the source of recurrent infections. Neonatal meningitis E. coli has been shown to be highly resistant to host immune responses and can cross the blood–brain barrier to cause disease.

Abstract

Escherichia coli is a remarkable and diverse organism. This normally harmless commensal needs only to acquire a combination of mobile genetic elements to become a highly adapted pathogen capable of causing a range of diseases, from gastroenteritis to extraintestinal infections of the urinary tract, bloodstream and central nervous system. The worldwide burden of these diseases is staggering, with hundreds of millions of people affected annually. Eight E. coli pathovars have been well characterized, and each uses a large arsenal of virulence factors to subvert host cellular functions to potentiate its virulence. In this Review, we focus on the recent advances in our understanding of the different pathogenic mechanisms that are used by various E. coli pathovars and how they cause disease in humans.

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Figure 1: Sites of pathogenic Escherichia coli colonization.
Figure 2: Pathogenic mechanisms of enteropathogenic and enterohaemorrhagic Escherichia coli.
Figure 3: Pathogenic mechanisms of Shigella (enteroinvasive Escherichia coli).
Figure 4: Pathogenic mechanisms of enterotoxigenic, enteroagreggative and diffusely adherent Escherichia coli.
Figure 5: Pathogenic mechanisms of extraintestinal Escherichia coli.

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  • 24 December 2012

    On page 31 of this article, in the third paragraph of the section 'Enterotoxic Escherichia coli', the sentence “This leads to increased intracellular levels of cyclic GMP and activates the cystic fibrosis transmembrane conductance regulator (CFTR), resulting in impaired absorption of Na+ and H2O efflux into the lumen63.” should have read “This leads to increased intracellular levels of cyclic GMP, resulting in impaired Na+ absorption, as well as activation of the cystic fibrosis transmembrane conductance regulator (CFTR)63.” The authors apologize to the readers for any misunderstanding caused.

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Acknowledgements

We thank the members of the Finlay laboratory for discussion and critical reading of the manuscript. We also apologize to those authors whose works were not cited owing to space constraints. Work in B.B.F.'s laboratory is supported by grants from the Canadian Institutes of Health Research (CIHR), the Howard Hughes Medical Institute (HHMI), the Foundation for the National Institutes of Health, the Canadian Crohn's and Colitis Foundation and Genome Canada. M.A.C. is supported by a Canadian Association of Gastroenterology/CIHR/Ferring Pharmaceuticals fellowship.

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  1. Michael Smith Laboratories, The University of British Columbia, 301-2185 East Mall, Vancouver, V6T 1Z4, British Columbia, Canada

    Matthew A. Croxen & B. Brett Finlay

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DATABASES

Entrez Genome Project

EPEC

Escherichia coli

UPEC str. CFT073

FURTHER INFORMATION

B. Brett Finlay's homepage

Glossary

Prophage

The latent form of a temperate bacteriophage, in which its genome is integrated into the bacterial chromosome without disrupting the bacterial cell.

Core genome

The pool of genes that is shared by all strains of a bacterial species.

Pan-genome

All of the genes that are found in the genomes of a given species.

Enterocyte

An epithelial cell that is found in the small intestine and colon.

Filopodium

A thin, transient actin protrusion that extends out from the cell surface and is formed by the elongation of bundled actin filaments.

Opsonophagocytosis

Increased uptake of bacteria by host cells owing to antibody or complement binding to the bacteria.

Haemolytic uraemic syndrome

A disease that primarily affects infants and children and is characterized by the loss and destruction of red blood cells, sometimes leading to kidney failure.

SOS response

The bacterial response to DNA damage that is regulated by the LexA and recombinase A proteins and involves the expression of a network of >40 genes.

Macropinocytosis

A form of regulated, actin-dependent endocytosis that involves the formation of large endocytic vesicles after the closure of cell surface membrane ruffles.

Microfold cell

A specialized epithelial cell that delivers antigens by transepithelial vesicular transport from the gut lumen directly to intraepithelial lymphocytes and subepithelial lymphoid tissues.

Inflammasome

A large multiprotein complex that stimulates caspase-1-dependent release of proinflammatory cytokines.

Pleocytosis

The presence of a higher number of cells than normal in the cerebrospinal fluid.

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Croxen, M., Finlay, B. Molecular mechanisms of Escherichia coli pathogenicity. Nat Rev Microbiol 8, 26–38 (2010). https://doi.org/10.1038/nrmicro2265

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