Full text loading...
Chapter 23 : How Noninvasive Pathogens Induce Disease: Lessons from Enteropathogenic and Enterohemorrhagic Escherichia Coli
How Noninvasive Pathogens Induce Disease: Lessons from Enteropathogenic and Enterohemorrhagic Escherichia Coli, Page 1 of 2< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555817848/9781555812614_Chap23-1.gif /docserver/preview/fulltext/10.1128/9781555817848/9781555812614_Chap23-2.gif
A novel focus of the work has been on defining the molecular and cellular mechanisms underlying the interactions between bacterial pathogens and host cells. During infection, enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) induce a characteristic ‘‘attaching and effacing’’ (A/E) histopathology on gut enterocytes. Since studies investigating the function of EPEC’s virulence factors are the most advanced, this chapter deals with EPEC as the prototype for the family of A/E-inducing pathogens. EPEC infection is estimated to cause the deaths of several hundred thousand children per year owing to dehydration and other complications. First widely recognized as the causative agent of hamburger disease, EHEC is a zoonotic pathogen that appears to be asymptomatically carried by various ruminants. Mutants lacking the bundle-forming pilus (BFP) plasmid still attach to host cells, but do not form microcolonies and produce fewer A/E lesions than wild-type EPEC. Immunofluorescence studies have shown that in addition to membrane-bound Tir, the tips of EPEC pedestals contain predominantly filamentous (F)-actin, as well as talin, α- actinin, ezrin, and several other cytoskeletal proteins. Diarrhea is undoubtedly the most prominent and widespread symptom associated with both EPEC and EHEC infection. Approaches using molecular biology, genetics, and cell biology have provided many new insights into how EPEC and related pathogens interact with and exploit host cells during the course of infection and how this ultimately leads to disease.