Escherichia coli enteritis pathophysiology

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Escherichia coli enteritis Microchapters


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.


E. coli normally colonizes the human gastrointestinal tract shortly following birth. However, the colonizing E.coli strains are different from the pathogenic strains. Transmission of pathogenic E. coli strains is usually by the fecal-oral route via infected food products (e.g. undercooked beef, vegetables, unpasteurized milk products or juice), contaminated water, infected cattle, or human fecal material (e.g. oral-anal contact). Only enteroinvasive E. coli (EIEC) has true replication ability within the host cell, whereas all other types of E. coli replicate outside the host cell. The small intestine is the primary site of action of ETEC and EPEC, whereas the colon is the primary site of action of EHEC and EIEC. EAEC may act on either enterocytes or colonocytes. The pathogenesis by which each E. coli strain causes manifestations is unique. For example, ETEC, EHEC, and EAEC secrete toxins, EIEC invades the host colonocytes and migrates within cells, whereas EPEC uses EPEC-elongation factor (EAF) to cause "attachment and effacing". Finally, DAEC is a subtype of EPEC that utilizes unique patterns of adherence.




Enterotoxic E. coli (ETEC)

Enterohemorrhagic E. coli (EHEC)

Enteroinvasive E. coli (EIEC)

Enteroaggregative E. coli (EAEC)

Enteropathogenic E. coli (EPEC)

Diffusely Adherent E. coli (DAEC)

  • DAEC is a subtype of EPEC, which contains unique patterns of adherence.[1][2]


  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Kaper JB, Nataro JP, Mobley HL (2004). "Pathogenic Escherichia coli". Nat Rev Microbiol. 2 (2): 123–40. doi:10.1038/nrmicro818. PMID 15040260.