Escherichia coli virulence factors
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1
University of Liège, Infectious Diseases, Bacteriology, Belgium
Escherichia coli was described in 1885 by a German pediatrician, Theodor Escherich, in the faeces of a child suffering diarrhoea. At the time, according to the Koch’s postulates, one bacterial species was either pathogen or not. Therefore E. coli soon became a problem because it was sometimes associated with diseases, sometimes isolated from healthy patients. In 1893, a Danish veterinarian postulated that E. coli species comprises different strains, some being pathogens, others not. Not only his assertion proved to be true but also E. coli is today subdivided into several pathogenic strains causing different intestinal, urinary tract or internal infections and pathologies, in animal species and in humans. The question soon changed to how to identify in vitro pathogenic strains of E. coli instead of assaying the strains in natural or experimental hosts.
The first answer came from the serotyping system developed by Kauffmann in the 1940s and 1950s, i.e. the identification of somatic (O antigen), capsular (K antigen) and/or flagellar (H antigen) surface antigens. Some serotypes can indeed be more frequently than others associated with specific clinical syndromes. Those pathogenic E. coli serotypes were therefore named by the clinical syndrome they can cause: diarrhoeagenic E. coli, uropathogenic E. coli, septicaemic E. coli, meningitis-associated E. coli, …; or sometimes according to the target host: avian pathogenic E. coli.
Fortunately from the late 1960s and during the 1970s, several specific properties that differentiate the pathogenic strains from each other and from non-pathogenic strains were unravelled. It therefore became possible to name the different classes of pathogenic E. coli on the basis of these properties instead of the clinical syndrome they can produce. Focusing on diarrhoeagenic E. coli, three classes were so defined in humans by the WHO in 1970: enterotoxigenic E. coli (ETEC) producing toxins active on enterocytes of humans and domestic animals, enteroinvasive, E. coli (EIEC) invading the enterocytes and pathogenic for humans and primates, and enteropathogenic E. coli belonging to specific serotypes, pathogenic for humans, but whose virulence properties were still unknown at the time.
Since more properties were progressively discovered in the 1980s and 1990s, more classes of diarrhoeagenic E. coli have been defined besides ETEC and EIEC and named on the basis of adherence and/or toxic properties: attaching-effacing E. coli (AEEC), diffusely-adherent E. coli (DAEC), enteroaggregative E. coli (EAEC), enterohaemorrhagic E. coli (EHEC), Shiga/Vero-toxigenic E. coli (VTEC), enteropathogenic E. coli sensu stricto (EPEC), necrotoxigenic E. coli (NTEC), diarrhea-associated haemolytic E. coli (DHEC), and still others. Some classes overlap (AEEC, EPEC, EHEC) and some names still remind us of the original clinical syndrome (EHEC) and are a source of discussion between MIEC (Microbiologists Interested in E. coli).
Since this congress topic is the interaction between E. coli and the mucosal immune system, the presentation will focus on the properties that directly interact with the epithelial cells, i.e. adherence and “toxicity”. The adherence to the epithelial cells is mediated by surface structures like the different types of fimbrial adhesins, by the afimbrial adhesins and/or by outer membrane proteins. The cell “toxicity” is mediated by so-called “exotoxins” though not all are actually excreted in the extracellular environment. The exotoxins (or toxins) are proteins that can either target the cell cytoplasmic membrane (enzymatic and pore-forming cytolysins), or the cell metabolism sensu lato (binary proteins with enzymatic activity directly interacting after internalization; oligopeptides indirectly interacting via the activation of a metabolic cascade after fixation on the cell cytoplasmic membrane), or the cell ultra-structure (type 3-secreted effectors perturbing the cell skeleton).
The purpose of this lecture is to present the different classes of adhesins and toxins produced by E. coli, to describe their excretion pathways, and to explain their molecular interactions with eukaryotic cells.
Keywords:
adhesins,
E. coli,
Epithelial Cells,
Toxicity,
Exotoxins
Conference:
ECMIS - E. coli and the Mucosal Immune System : Interaction, Modulation and Vaccination, Ghent, Belgium, 2 Jul - 5 Jul, 2011.
Presentation Type:
Oral Presentation
Topic:
Virulence factors and influence on innate and/or adaptive immunity
Citation:
Mainil
J
(2011). Escherichia coli virulence factors.
Front. Immunol.
Conference Abstract:
ECMIS - E. coli and the Mucosal Immune System : Interaction, Modulation and Vaccination.
doi: 10.3389/conf.fimmu.2011.01.00002
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Received:
22 Sep 2011;
Published Online:
26 Sep 2011.
*
Correspondence:
Prof. Jacques Mainil, University of Liège, Infectious Diseases, Bacteriology, Liege, Belgium, jg.mainil@ulg.ac.be