Enteropathogenic and enterohaemorrhagic Escherichia coli : more subversive elements

  title={Enteropathogenic and enterohaemorrhagic Escherichia coli : more subversive elements},
  author={Gad Frankel and Alan D. Phillips and Ilan Rosenshine and Gordon Dougan and James B. Kaper and Stuart Knutton},
  journal={Molecular Microbiology},
Enteropathogenic (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… 

Enteropathogenic Escherichia coli (EPEC)-- a crafty subversive little bug.

The onset and severity of A}E-induced diarrhoea is considered too rapid to result solely from the loss of absorptive microvilli, indicating that host secretory mechanism(s) may be activated.

Enteropathogenic and enterohemorrhagic Escherichia coli infections: emerging themes in pathogenesis and prevention.

Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E coli (EHEC) are important causes of infectious diarrhea, particularly among pediatric populations. While EPEC is a significant health

Enteropathogenic and enterohaemorrhagic Escherichia coli: even more subversive elements

The findings have highlighted the multifunctional nature of the effectors and their ability to participate in redundant, synergistic or antagonistic relationships, acting in a co‐ordinated spatial and temporal manner on different host organelles and cellular pathways during infection.

Enterohaemorrhagic Escherichia coli: emerging issues on virulence and modes of transmission.

Enterohaemorrhagic Escherichia coli (EHEC) constitute a subset of serotypes (E. coli O157 and some other serogroups) of Shiga toxin (Stx)-producing E. coli (STEC) firmly associated with severe human

Distribution of espI among clinical enterohaemorrhagic and enteropathogenic Escherichia coli isolates.

EspI was detected in 86 % and 53 % of LEE+ EHEC and EPEC strains, respectively, and the espI gene was more commonly found in patients suffering from a more severe disease.

Enterohaemorrhagic E. coli in veterinary medicine.

Pathogenesis and evolution of virulence in enteropathogenic and enterohemorrhagic Escherichia coli.

Some of the known virulence factors that contribute to the heterogeneity of E. coli strains are explored, and what is known regarding the origin and distribution of these factors is reviewed.

Current progress in enteropathogenic and enterohemorrhagic Escherichia coli vaccines

This review discusses the pathogenesis of enterohemorrhagic and enteropathogenic E. coli, the host immune response and the current application of this knowledge towards efficacious vaccine strategies and indicates the feasibility of such strategies.



A genetic locus of enterocyte effacement conserved among diverse enterobacterial pathogens.

It is reported that in EPEC a 35-kbp locus containing several regions implicated in formation of these lesions is found, which hybridize to E. coli O157:H7 and other pathogens of three genera that cause similar lesions but do not hybridized to avirulent members of the same species.

The complete sequence of the locus of enterocyte effacement (LEE) from enteropathogenic Escherichia coli E2348/69

The entire LEE of EPEC strain E2348/69 is sequenced and the final LEE sequence entry contains corrections to some of these previously reported genes and predicted proteins and changes the name of several previously described genes comprising the type III secretion system ofEPEC.

Role of Intimin and Bundle-Forming Pili in Enteropathogenic Escherichia coli Adhesion to Pediatric Intestinal Tissue In Vitro

In human intestinal organ culture, BFP do not appear to be involved in the initial stages of EPEC nonintimate adhesion but are implicated in the formation of complex, three-dimensional colonies via bacterium-bacterium interactions.

Rapid modulation of electrolyte transport in Caco-2 cell monolayers by enteropathogenic Escherichia coli (EPEC) infection

The study directly shows that, after initial adhesion, EPEC induce major alterations in host cell electrolyte transport, including stimulation of chloride secretion, for which signal transduction to host cells is a prerequisite.

An inducible bundle-forming pilus of enteropathogenic Escherichia coli.

Enteropathogenic Escherichia coli (EPEC), a cause of childhood diarrhea, grow on the surface of the small intestine and on cultured epithelial cells as colonies of adherent bacteria. When propagated

A cloned pathogenicity island from enteropathogenic Escherichia coli confers the attaching and effacing phenotype on E. coli K‐12

Cloned a 35.4 kb ‘pathogenicity island’ from the prototype AE bacterium, enteropathogenic Escherichia coli, containing all previously described AE genes, demonstrating that the defining feature of this class of pathogens can be acquired by an avirulent bacterium in a single genetic step.

Down regulation of intimin expression during attaching and effacing enteropathogenic Escherichia coli adhesion

Results indicate that surface expression of intimin is regulated by environmental factors during bacterial growth and following A/E lesion formation and that virulence plasmid-encoded genes participate in these regulation processes.

The role of the eaeA gene in diarrhea and neurological complications in a gnotobiotic piglet model of enterohemorrhagic Escherichia coli infection

In gnotobiotic piglets the pathogenicities of wild-type O157:H7 strain 86-24 and its eaeA mutant UMD619 are compared with those of the two plasmid-complemented strains expressing IntiminO157 (EHEC) and IntimInO127 (EPEC).

Protein translocation into host epithelial cells by infecting enteropathogenic Escherichia coli

It is demonstrated that contact of EPEC with HeLa cells is associated with the induction of production and secretion of EspB, which indicates that EspB is both translocated and required for protein translocation by EPEC.