Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2012 Jul 12:2:90.
doi: 10.3389/fcimb.2012.00090. eCollection 2012.

Enterohemorrhagic E. coli (EHEC) pathogenesis

Y Nguyen  1 , Vanessa Sperandio
Affiliations
Review

Enterohemorrhagic E. coli (EHEC) pathogenesis

Y Nguyen et al. Front Cell Infect Microbiol. .

Abstract

Enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 is a human pathogen responsible for outbreaks of bloody diarrhea and hemolytic uremic syndrome (HUS) worldwide. Conventional antimicrobials trigger an SOS response in EHEC that promotes the release of the potent Shiga toxin that is responsible for much of the morbidity and mortality associated with EHEC infection. Cattle are a natural reservoir of EHEC, and approximately 75% of EHEC outbreaks are linked to the consumption of contaminated bovine-derived products. This review will discuss how EHEC causes disease in humans but is asymptomatic in adult ruminants. It will also analyze factors utilized by EHEC as it travels through the bovine gastrointestinal (GI) tract that allow for its survival through the acidic environment of the distal stomachs, and for its ultimate colonization in the recto-anal junction (RAJ). Understanding the factors crucial for EHEC survival and colonization in cattle will aid in the development of alternative strategies to prevent EHEC shedding into the environment and consequent human infection.

Keywords: EHEC; LEE; acid resistance; cattle; colonization.

PubMed Disclaimer

Figures

Figure 1
Figure 1
The model of acid resistance system 2 and 3 (A) and the schematic diagram of the formation of attaching and effacing (A/E) lesions (B). EHEC injects effector proteins such as Tir and EspFu into the host cytoplasm through the T3SS (1). Tir localizes to the host membrane and binds to intimin to intimately attach the bacteria to the cell. Tir and EspFu recruit host factors (2) to subvert host cytoskeleton and actin polymerization (3).
Figure 2
Figure 2
Proposed EHEC SdiA-AHL signaling in cattle.
See this image and copyright information in PMC

References

    1. Ahmer B. M., van Reeuwijk J., Timmers C. D., Valentine P. J., Heffron F. (1998). Salmonella typhimurium encodes an SdiA homolog, a putative quorum sensor of the LuxR family, that regulates genes on the virulence plasmid. J. Bacteriol. 180, 1185–1193 - PMC - PubMed
    1. Armstrong G. L., Hollingsworth J., Morris J. G., Jr. (1996). Emerging foodborne pathogens: Escherichia coli O157, H7 as a model of entry of a new pathogen into the food supply of the developed world. Epidemiol. Rev. 18, 29–51 - PubMed
    1. Brown C. A., Harmon B. G., Zhao T., Doyle M. P. (1997). Experimental Escherichia coli O157, H7 carriage in calves. Appl. Environ. Microbiol. 63, 27–32 - PMC - PubMed
    1. Callaway T. R., Carr M. A., Edrington T. S., Anderson R. C., Nisbet D. J. (2009). Diet, Escherichia coli O157, H7, and cattle: a review after 10 years. Curr. Issues Mol. Biol. 11, 67–79 - PubMed
    1. Campellone K. G., Robbins D., Leong J. M. (2004). EspFU is a translocated EHEC effector that interacts with Tir and N-WASP and promotes Nck-independent actin assembly. Dev. Cell 7, 217–228 10.1016/j.devcel.2004.07.004 - DOI - PubMed

MeSH terms