Enteropathogenic and enterohaemorrhagic Escherichia coli : more subversive elements

Abstract

SummaryEnteropathogenic (EPEC) and enterohaemorrhagic Escherichia coli (EHEC) constitute a significant risk to human health worldwide. Both pathogens colonize the intestinal mucosa and, by subverting intestinal epithelial cell function, produce a characteristic histopathological feature known as the 'attaching and effacing' (A/E) lesion. Although EPEC was the first E. coli to be associated with human disease in the 1940s and 1950s, it was not until the late 1980s and early 1990s that the mechanisms and bacterial gene products used to induce this complex brush border membrane lesion and diarrhoeal disease started to be unravelled. During the past few months, there has been a burst of new data that have revolutionized some basic concepts of the molecular basis of bacterial pathogenesis in general and EPEC pathogenesis in particular. Major breakthroughs and developments in the genetic basis of A/E lesion formation, signal transduction, protein translocation, host cell receptors and intestinal colonization are highlighted in this review.

Pathogenesis and evolution of virulence in enteropathogenic and enterohemorrhagic Escherichia coli

“…This ability, known as attaching and effacing activity, has been observed in vitro and in duodenal and rectal biopsies from infants with EPEC infection (11,13). A 35-kb genetic element known as the locus of enterocyte effacement (LEE) is necessary for this effect and, when cloned from EPEC strain E2348/69 into a nonpathogenic E. coli strain, is sufficient to confer attaching and effacing activity (18). The LEE is considered to be a pathogenicity island because it contains virulence loci, it is not found in nonpathogenic E. coli strains, it is inserted into the genome of E. coli at specific sites (tRNA genes), and finally because its distinctive G+C content (38%) indicates its origin in another species.…”

“…The LEE is considered to be a pathogenicity island because it contains virulence loci, it is not found in nonpathogenic E. coli strains, it is inserted into the genome of E. coli at specific sites (tRNA genes), and finally because its distinctive G+C content (38%) indicates its origin in another species. The LEE is inserted near different tRNA loci in different EPEC strains (18). The LEE from strain E2348/69 carries 41 genes, which encode a type III secretion system and various proteins secreted via this system, including an adhesin and its cognate receptor, a regulator, and several proteins of unknown function.…”

Identification of the intimin-binding domain of Tir of enteropathogenic Escherichia coli

“…The structure thus formed is known as an attaching and effacing (A /E) lesion, which is also formed by other related pathogens. A model for the mechanism of EPEC infection has recently been reviewed in detail elsewhere (Frankel et al, 1998;Kaper, 1998;Goosney et al, 1999).…”

A putative lytic transglycosylase tightly regulated and critical for the EHEC type three secretion

“…This pathogenic characteristic has been attributed to that the bacteria attach to the epithelial cells and employ a type III secretion system (TTSS) to deliver effector proteins into the infected cells to result in rearrangement of cellular actin and formation of pedestal structures [1,2]. TTSS has been found in many Gram negative bacteria and is composed of a basal part, which transverses the inner membrane, periplasmic region and the outer membrane, and a filament part, which directly connects bacteria to the infected cells.…”

“…In EHEC, EspA is the major component that polymerizes into the filamentous structure enclosing a channel of 25-Å diameter for translocating effector proteins EspF, EspG, EspH, Map and the intimin receptor (Tir) into the target cells [2]. Along with EspA, EspB and EspD are also assembled into the filamentous needle but at tips, which insert onto the cell membrane to facilitate the effectors' translocation.…”