Escherichia coli enteritis pathophysiology
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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.
Overview
E. coli normally colonizes the human GI 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 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: 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.
Pathophysiology
- E. coli normally colonizes the human GI tract shortly following birth and is part of the normal gastrointestinal flora. However, the colonizing E.coli strains are different from the pathogenic strains that cause E. coli enteritis.
Transmission
- Transmission of pathogenic E. coli strains is usually by the fecal-oral route via the following:
- Contaminated food, especially undercooked ground beef, unpasteurized (raw) milk and juice, soft cheeses made from raw milk, and raw fruits and vegetables (such as sprouts)
- Contaminated water, including drinking untreated water and swimming in contaminated water
- Animals and their environment: particularly cows, sheep, and goats
- Feces of infected people (e.g. oral-anal contact)
Pathogenesis
- Pathogenic E. coli are characterized by the presence of either O antigen alone or combination of O and H antigens.[1][2]
- 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.[1]
- Pathogenic E. coli strains contain adhesin that may form distinct fimbriae (pili) or fibrillae.
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).[2]
- Both enterotoxins are responsible for the development of clinical manifestations (e.g. diarrhea).[1]
- 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.[2]
- 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.[2]
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) and secretion of enterohemolysin.
- 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.[1][2]
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.[1][2]
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.[1][2]
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".[1][2]
- Similar to EHEC, it is not considered highly invasive.[1][2]
Diffusely Adherent E. coli (DAEC)
References
- ↑ 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.
- ↑ 2.0 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.