Adhesion and its role in the virulence of enteropathogenic Escherichia coli

Abstract

Enteropathogenic Escherichia coli (EPEC) organisms are an important cause of diarrheal disease in young children. The virulence of EPEC is a multifactorial process and involves a number of distinct stages. Initial adherence to intestinal mucosa is mediated by fimbriae which bring about a distinct form of adhesion, localized adhesion. Intimate adhesion of the bacterium to the eukaryotic membrane occurs, resulting in the activation of signal transduction pathways. Microvilli are disrupted and effaced from the apical membrane which then cups around the organism to form pedestal structures, the attaching and effacing lesion. Diarrhea may be produced by alteration of the permeability of the apical membrane and also through a malabsorption mechanism. The pathways involved in the production of the attaching and effacing lesion are described. EPEC organisms were originally thought to belong to a number of distinct serogroups; it is now apparent that many isolates belonging to these serogroups are not pathogenic or belong to other pathogenic groups of E. coli. In addition, isolates falling outside of these serogroups are considered to be true EPEC. The definition of EPEC based on serotyping is inaccurate and should be replaced by methods that specifically detect the virulence properties of EPEC.

Serotyping and categorisation of Escherichia coli strains isolated between 1958 and 1992 from diarrhoeal diseases in Asia

“…( 10) NM (36) NM (2) NM (28) [31,32]. In his review of adhesion and virulence of EPEC, Law [37] described EPEC serogroups and serovars traditionally associated with infantile diarrhoea. Most of these serogroups and serovars were also predominant in our EPEC collection.…”

Enteroaggregative Escherichia coli

“…Strains of E. coli have been characterized by serotyping, by the clinical manifestations of the diseases they cause and the virulence mechanisms they express. The currently recognized groups include enterotoxigenic E. coli (ETEC), enteroinvasive E. coli, enteropathogenic E. coli (EPEC), Shiga-like toxin (or Verocytotoxin)-producing E. coli, and enterohaemorrhagic E. coli (EHEC) (Law 1994). Each affects different population groups and produces disease by distinct pathogenic mechanisms.…”

The Mucosal Immune System: Modulation by Microemulsion

“…However, the physiological functions of defensins remain incompletely understood. Paneth cells also produce cathelicidin, which contributes to the mucosal defence against epithelial-adherent bacterial pathogens, helps to set a threshold for productive infection, and is expressed constitutively by neutrophils, mast cells and differentiated epithelial cells in the colon and stomach but not the small intestine 32 .…”

“…This system consists of immuno-competent cells that infiltrate the mucosae, nodules that form lymphoid structures such as Peyer's plates and its equivalent in bronchial mucosae, and regional lymph nodes such as the mesenterics 32 .…”