After you ingest E. coli bacteria, they travel through the digestive system and arrive in the intestines, specifically the colon, and attach to epithelial cells. The attachment ability of E. coli O157:H7 is crucial to understanding the infection.
The genes that encode the proteins necessary for attachment are found at a specific place in the bacterial genome, a pathogenicity island called the locus for enterocyte effacement (LEE). Initial adherence to epithelial cells is made by bundle-forming pili, small appendages found in many types of bacterial cells that are used for motility and attachment. After initial contact, proteins produced from genes on the LEE locus are secreted into epithelial cells of the host. These E. coli-secreted proteins (this is indeed their name–scientists are very creative) affect signaling of the host cell and may aid other proteins in translocation from the bacteria to the host cell (1).
At this point, the E. coli bacterium is only superficially attached to the host cell. To complete the attachment process, intimin (an attachment protein found on the bacterial cell surface) must bind. But host cells do not normally produce a receptor for this protein. So attaching and effacing (AE) E. coli, such as E. coli O157:H7, also produce a receptor to intimin that is translocated to the host cell along with the E. coli-secreted proteins. This receptor is known as the translocated intimin receptor (Tir). Now Tir originally from the E. coli bacterium but now in the host cell can bind intimin, solidly attaching the E. coli bacterium and host cell (2). Further support to the E. coli is provided by actin pedestals (3). Actin is a made up of microfilaments and is one of the components that provides for muscle contraction, so it is extremely strong (3).
Now that the E. coli is bound tightly to the host cell and is able to secret various toxin agents or induces apoptosis (programmed cell death, essentially the cell commits suicide). Several virulence factors are found on a plasmid that is found in all E. coli O157:H7 strains. Plasmids are small circular strands of DNA, independent of the host cell DNA that can be transmitted between similar cells and thus share genetic information. Plasmids are one of the main factors associated with antibiotic resistance because they allow resistant bacteria to share their mechanism of resistance with other bacteria. The plasmid in E. coli O157:H7 strains, pO157 (another creative name), encodes cytotoxins such as enterohemolysin (lyses red blood cells) and a toxin similar to cytotoxin B of Clostridium difficile (a common cause of diarrhea) [4].
This damage to intestinal epithelial cells is called an attaching and effacing lesion, AE lesion. The AE lesion allows further penetration of Shiga toxin into the intestine where it leads to hemorrhagic colitis.
For more information:
Sources
1. Hueck CJ. Type III protein secretion systems in bacterial pathogens of animals and plants. Microbiology and Molecular Biology Review, 62 (1998) 379.
2. Goosney DL, Knoechel DG, Finlay BB. Enteropathogenic E. coli, Salmonella and Shigella: masters of host cell cytoskeletal exploitation. Emerging Infectious Diseases, 5:2 (1999). Online at http://www.cdc.gov/ncidod/eid/vol5no2/goosney.htm#09.
3 Rosenshine I, Rusckowski S, Stein M, Reinscheid DJ, Mills SD, Finlay BB. A pathogenic bacterium triggers epithelial signals to form a functional bacterial receptor that mediates actin pseudopod formation. The EMBO Journal, 15 (1996) 2613-24.
4 Tarr PI, Neill MA. Esherichia coli O157:H7. Gastroenterology Clinics of North America, 30:3 (2001) 735-751.
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Keywords: Ecoli Infection
