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==Pathophysiology==
==Pathophysiology==
*''E. coli'' normally colonizes the human GI tract shortly following birth. However, the colonizing ''E.coli'' strains are different from the pathogenic strains.
*''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 combintion of O and H antigens.
*Pathogenic ''E. coli'' are characterized by the presence of either O antigen alone or combination of O and H antigens.<ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
:*O antigen corresponds to the lipopolysaccaride antigen
:*O antigen corresponds to the lipopolysaccaride antigen
:*H antigen corresponds to the flagellar antigen
:*H antigen corresponds to the flagellar antigen
===Extracellular vs. Intracellular Replication===
*Only enteroinvasive ''E. coli'' (EIEC) has true replication within the host cell, whereas all other types of ''E. coli'' replicate outside the host cell.<ref name=>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref>
*Only enteroinvasive ''E. coli'' (EIEC) has true replication within the host cell
*All other types of ''E. coli'' replicate outside the host cell.
===Adhesion and Colonization===
*Pathogenic ''E. coli'' strains contain adhesin that may form distinct fimbriae (pili) or fibrillae.
*Pathogenic ''E. coli'' strains contain adhesin that may form distinct fimbriae (pili) or fibrillae.
*A
===Enterotoxic E. coli (ETEC)===
===Enterotoxic E. coli (ETEC)===
*The primary site of action of ETEC is the small intestine.
*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).
*ETEC adheres to enterocytes then secretes 2 enterotoxins: heat-labile toxin (LT) and heat-stable toxin (ST).<ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
*Both enterotoxins are responsible for the development of clinical manifestations (e.g. diarrhea).
*Both enterotoxins are responsible for the development of clinical manifestations (e.g. diarrhea).<ref name=>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref>
:*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.<ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
:*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.<ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
===Enterohemorrhagic E. coli (EHEC)===
===Enterohemorrhagic E. coli (EHEC)===
*The primary site of action of EHEC is the colon.
*The primary site of action of EHEC is the colon.
*EHEC attaches to the colonocyte and induces the elaboration of the Shiga toxin (Stx).
*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 systemic complications
*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.<ref name=>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
===Enteroinvasive E. coli (EIEC)===
===Enteroinvasive E. coli (EIEC)===
*The primary site of action of EIEC is the colon.
*The primary site of action of EIEC is the colon.
*EIEC 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.
*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.<ref name=>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
===Enteroaggregative E. coli (EAEC)===
===Enteroaggregative E. coli (EAEC)===
*The primary site of action of EAEC is the small intestine and the colon.
*The primary site of action of EAEC is the small intestine and the colon.
*EAEC adheres to enterocytes and colonocytes in a thick biofilm.
*EAEC is characteristically aggressive and adheres to enterocytes and colonocytes in a thick biofilm.
*EAEC elaborates cytotoxins and enterotoxins, such as ShET1, Pic, EAST1, Pet toxins.
*EAEC elaborates cytotoxins, such as hemolysin, and enterotoxins, such as ShET1, Pic, EAST1, Pet toxins.<ref name=>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
===Enteropathogenic E. coli (EPEC)===
===Enteropathogenic E. coli (EPEC)===
*The primary site of acction of EPEC is the small intestine.
*The primary site of acction of EPEC is the small intestine.
*EPEC adheres to enterocytes and destroy the normal architecture of the human microvilli, resulting in cytoskeletal deformities.
*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".<ref name=>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
*Similar to EHEC, it is not considered highly invasive.<ref name=>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
===Diffusely Adherent E. coli (DAEC)===
*DAEC is a subtype of EPEC, which contain unique patterns of adherence.<ref name=>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260  }} </ref>
==References==
==References==
{{reflist|2}}
{{reflist|2}}


[[Category:Infectious disease]]
[[Category:Infectious disease]]

Revision as of 02:30, 21 December 2015

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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.[2]
  • 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).[1]
  • Both enterotoxins are responsible for the development of clinical manifestations (e.g. diarrhea).[3]
  • 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.[4][1]

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.[5][1]

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.[6][1]

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".[7][1]
  • Similar to EHEC, it is not considered highly invasive.[8][1]

Diffusely Adherent E. coli (DAEC)

  • DAEC is a subtype of EPEC, which contain unique patterns of adherence.[9][1]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9 Kaper JB, Nataro JP, Mobley HL (2004). "Pathogenic Escherichia coli". Nat Rev Microbiol. 2 (2): 123–40. doi:10.1038/nrmicro818. PMID 15040260.
  2. ↑ Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
  3. ↑ Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
  4. ↑ Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
  5. ↑ Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
  6. ↑ Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
  7. ↑ Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
  8. ↑ Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
  9. ↑ Evans, DG (1996). Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. Galveston (TX): University of Texas Medical.
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