Escherichia coli enteritis pathophysiology
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Differentiating Escherichia coli enteritis from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D., Yazan Daaboul, M.D.
Overview
Pathophysiology
- E. coli normally colonizes the human GI tract shortly following birth. However, the colonizing E.coli strains are different from the pathogenic strains.
- Pathogenic E. coli are characterized by the presence of either O antigen alone or combination of O and H antigens.[1]
- O antigen corresponds to the lipopolysaccaride antigen
- H antigen corresponds to the flagellar antigen
- Only enteroinvasive E. coli (EIEC) has true replication within the host cell, whereas all other types of E. coli replicate outside the host cell.Invalid
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Enterotoxic E. coli (ETEC)
- The primary site of action of ETEC is the small intestine.
- ETEC adheres to enterocytes then secretes 2 enterotoxins: heat-labile toxin (LT) and heat-stable toxin (ST).[1]
- Both enterotoxins are responsible for the development of clinical manifestations (e.g. diarrhea).Invalid
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- Heat-labile toxin is composed of one enzymatically active subunit and 5 surrounding inactive subunits. It induces diarrhea by binding to GM1 receptor, the same ganglioside receptor that the cholera toxin of V. cholera binds to.[1]
- Heat-stable toxin is composed of several peptides that are not inactivated by heat. It binds to and activates guanylate cyclase, resulting in diarrhea by increasing secretion of fluids and electrolytes.[1]
Enterohemorrhagic E. coli (EHEC)
- The primary site of action of EHEC is the colon.
- EHEC attaches to the colonocyte and causes hemorrhagic colitis by inducing the elaboration of the Shiga toxin (Stx).
- The Shiga toxin is systemically absorbed and results in inflammatory reactions and systemic complications, including hemolytic uremic syndrome.
- EHEC are not considered highly invasive as EIEC or Shigella because the organism invades the cell but does not multiply within the cell.Invalid
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Enteroinvasive E. coli (EIEC)
- The primary site of action of EIEC is the colon.
- EIEC is invasive and multiplies within the host colonocytes.
- EIEC contains nonfimbrial adhesins. It lyses phagosomes and migrates through the host cell and within cells (either lateral direct cell-to-cell spread or exit then re-enter) via the action of nucleating actin microfilaments.Invalid
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Enteroaggregative E. coli (EAEC)
- The primary site of action of EAEC is the small intestine and the colon.
- EAEC is characteristically aggressive and adheres to enterocytes and colonocytes in a thick biofilm.
- EAEC elaborates cytotoxins, such as hemolysin, and enterotoxins, such as ShET1, Pic, EAST1, Pet toxins.Invalid
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Enteropathogenic E. coli (EPEC)
- The primary site of acction of EPEC is the small intestine.
- EPEC contains EPEC-adherence factor (EAF), a plasma encoded protein.
- Using EAF, EPEC adheres to enterocytes and destroy the normal architecture of the human microvilli, resulting in cytoskeletal deformities. The process is referred to as "attachment and effacing".Invalid
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Diffusely Adherent E. coli (DAEC)
- DAEC is a subtype of EPEC, which contain unique patterns of adherence.Invalid
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