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==Overview== | ==Overview== | ||
''E. coli'' normally colonizes the human | ''[[Escherichia coli|E. coli]]'' normally colonizes the [[human]] [[gastrointestinal tract]] shortly following [[birth]]. However, the colonizing ''[[Escherichia coli|E.coli]]'' [[Strain (biology)|strains]] are different from the [[Pathogen|pathogenic]] [[Strain (biology)|strains]]. [[Transmission (medicine)|Transmission]] of [[Pathogen|pathogenic]] ''[[Escherichia coli|E. coli]]'' [[Strain (biology)|strains]] is usually by the [[fecal-oral route]] via [[Infection|infected]] [[food]] products (e.g. undercooked [[beef]], [[Vegetable|vegetables]], [[Raw milk|unpasteurized milk]] products or [[juice]]), contaminated [[water]], [[Infection|infected]] cattle, or [[Human feces|human fecal material]] (e.g. [[Mouth|oral]]-[[Anus|anal]] contact). Only [[Enteroinvasive E. coli|enteroinvasive ''E. coli'' (EIEC)]] has true [[replication]] ability within the [[Host (biology)|host]] [[Cell (biology)|cell]], whereas all other types of ''[[Escherichia coli|E. coli]]'' [[Replication|replicate]] outside the [[Host (biology)|host]] [[Cell (biology)|cell]]. The [[small intestine]] is the primary site of action of [[Enterotoxigenic Escherichia coli|ETEC]] and [[Enteropathogenic E. coli|EPEC]], whereas the [[Colon (anatomy)|colon]] is the primary site of action of [[Enterohemorrhagic escherichica coli|EHEC]] and [[Enteroinvasive Escherichia coli|EIEC]]. [[Escherichia coli|EAEC]] may act on either [[Enterocyte|enterocytes]] or colonocytes. The [[pathogenesis]] by which each ''[[Escherichia coli|E. coli]]'' [[Strain (biology)|strain]] causes manifestations is unique. For example, [[Enterotoxigenic Escherichia coli|ETEC]], [[Enterohemorrhagic escherichica coli|EHEC]], and [[Escherichia coli|EAEC]] secrete [[Toxin|toxins]], [[Enteroinvasive Escherichia coli|EIEC]] invades the [[Host (biology)|host]] colonocytes and migrates within [[Cell (biology)|cells]], whereas [[Enteropathogenic E. coli|EPEC]] uses [[Enteropathogenic E. coli|EPEC]]-elongation factor (EAF) to cause "attachment and effacing". Finally, [[Escherichia coli|DAEC]] is a subtype of [[Enteropathogenic E. coli|EPEC]] that utilizes unique patterns of adherence. | ||
==Pathophysiology== | ==Pathophysiology== | ||
*''E. coli'' normally colonizes the human | *''[[Escherichia coli|E. coli]]'' normally colonizes the [[human]] [[gastrointestinal tract]] shortly following [[birth]] and is part of the normal [[Gastrointestinal tract|gastrointestinal]] [[flora]]. However, the colonizing ''[[Escherichia coli|E.coli]]'' [[Strain (biology)|strains]] are different from the [[Pathogen|pathogenic]] [[Strain (biology)|strains]] that cause [[Escherichia coli enteritis|''E. coli'' enteritis]]. | ||
*Pathogenic ''E. coli'' are characterized by the presence of either O antigen alone or combination of O and H antigens.<ref name=book>{{cite book | ==Transmission== | ||
:*O antigen corresponds to the lipopolysaccaride antigen | *[[Transmission (medicine)|Transmission]] of [[Pathogen|pathogenic]] ''[[Escherichia coli|E. coli]]'' [[Strain (biology)|strains]] is usually by the [[fecal-oral route]] via the following: | ||
:*H antigen corresponds to the flagellar antigen | :*Contaminated [[food]], especially under cooked ground [[beef]], [[Raw milk|unpasteurized (raw) milk]] and [[juice]], [[Cheese|soft cheeses]] made from [[raw milk]], and raw [[Fruit|fruits]] and [[Vegetable|vegetables]] (such as sprouts) | ||
*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=book>{{cite book | :*Contaminated [[water]], including drinking untreated [[water]] and swimming in contaminated [[water]] | ||
*Pathogenic ''E. coli'' strains contain adhesin that may form distinct fimbriae (pili) or fibrillae. | :*Animals (particularly cows, sheep, and goats) and their environment | ||
:*[[Feces]] of [[Infection|infected]] people (e.g. [[Mouth|oral]]-[[Anus|anal]] contact) | |||
==Pathogenesis== | |||
*[[Pathogen|Pathogenic]] ''[[Escherichia coli|E. coli]]'' are characterized by the presence of either [[O antigen]] alone or combination of [[O antigen|O]] and [[H antigen|H antigens]].<ref name="book">{{cite book |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> | |||
:*[[O antigen]] corresponds to the [[Lipopolysaccharide|lipopolysaccaride]] [[antigen]] | |||
:*[[H antigen]] corresponds to the [[Flagellum|flagellar]] [[antigen]] | |||
*Only [[Enteroinvasive E. coli|enteroinvasive ''E. coli'' (EIEC)]] has true [[replication]] within the [[Host (biology)|host]] [[Cell (biology)|cell]], whereas all other types of ''[[Escherichia coli|E. coli]]'' [[Replication|replicate]] outside the [[Host (biology)|host]] [[Cell (biology)|cell]].<ref name="book">{{cite book |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> | |||
*[[Pathogen|Pathogenic]] ''[[Escherichia coli|E. coli]]'' [[Strain (biology)|strains]] contain [[adhesin]] that may form distinct [[Fimbriae|fimbriae (pili)]] or fibrillae. | |||
===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 [[Enterotoxigenic Escherichia coli|ETEC]] is the [[small intestine]]. | ||
*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> | *[[Enterotoxigenic Escherichia coli|ETEC]] adheres to [[Enterocyte|enterocytes]] then secretes 2 [[Enterotoxin|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).<ref name=book>{{cite book | *Both [[Enterotoxin|enterotoxins]] are responsible for the development of clinical manifestations (e.g. [[diarrhea]]).<ref name="book">{{cite book |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. | :*Heat-labile toxin is composed of one [[Enzyme|enzymatically]] active [[subunit]] and 5 surrounding inactive [[subunits]]. It induces [[diarrhea]] by binding to [[GM1]] [[Receptor (biochemistry)|receptor]], the same [[ganglioside]] [[Receptor (biochemistry)|receptor]] that the [[cholera toxin]] of ''[[Vibrio cholerae|V. cholerae]]'' 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> | :*Heat-stable toxin is composed of several [[Peptide|peptides]] that are not inactivated by [[heat]]. It binds to and activates [[guanylate cyclase]], resulting in [[diarrhea]] by increasing [[secretion]] of [[Fluid|fluids]] and [[Electrolyte|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 [[Enterohemorrhagic escherichica coli|EHEC]] is the [[Colon (anatomy)|colon]]. | ||
*EHEC attaches to the colonocyte and causes hemorrhagic colitis by inducing the elaboration of the Shiga toxin (Stx) and secretion of enterohemolysin. | *[[Enterohemorrhagic escherichica coli|EHEC]] attaches to the colonocyte and causes [[hemorrhagic]] [[colitis]] by inducing the elaboration of the [[Shiga toxin|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. | *The [[Shiga toxin|''Shiga'' toxin]] is systemically [[Absorption|absorbed]] and results in [[Inflammation|inflammatory reactions]] and [[systemic]] [[Complication (medicine)|complications]], including [[Hemolytic-uremic syndrome|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=book>{{cite book | *[[Enterohemorrhagic escherichica coli|EHEC]] are not considered highly invasive as [[Enteroinvasive Escherichia coli|EIEC]] or ''[[Shigella]]'' because the [[organism]] invades the [[Cell (biology)|cell]] but does not multiply within the [[Cell (biology)|cell]].<ref name="book">{{cite book |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 [[Enteroinvasive Escherichia coli|EIEC]] is the [[Colon (anatomy)|colon]]. | ||
*EIEC is invasive and multiplies within the host colonocytes. | *[[Enteroinvasive Escherichia coli|EIEC]] is invasive and multiplies within the [[Host (biology)|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=book>{{cite book | *[[Enteroinvasive Escherichia coli|EIEC]] contains nonfimbrial [[Adhesin|adhesins]]. It [[Lysis|lyses]] [[Phagosome|phagosomes]] and migrates through the [[Host (biology)|host]] [[Cell (biology)|cell]] and within [[Cell (biology)|cells]] (either lateral direct [[Cell (biology)|cell]]-to-[[Cell (biology)|cell]] spread or exit then re-enter) via the action of nucleating [[actin]] [[Microfilament|microfilaments]].<ref name="book">{{cite book |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 [[Enteroaggressive E. coli|EAEC]] is the [[small intestine]] and the [[Colon (anatomy)|colon]]. | ||
*EAEC is characteristically aggressive and adheres to enterocytes and colonocytes in a thick biofilm. | *[[Enteroaggressive E. coli|EAEC]] is characteristically aggressive and adheres to [[Enterocyte|enterocytes]] and colonocytes in a thick [[biofilm]]. | ||
*EAEC elaborates cytotoxins, such as hemolysin, and enterotoxins, such as ShET1, Pic, EAST1, Pet toxins.<ref name=book>{{cite book | *[[Enteroaggressive E. coli|EAEC]] elaborates [[Cytotoxin|cytotoxins]], such as [[hemolysin]], and [[Enterotoxin|enterotoxins]], such as ShET1, Pic, EAST1, Pet [[Toxin|toxins]].<ref name="book">{{cite book |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 | *The primary site of action of [[Enteropathogenic E. coli|EPEC]] is the [[small intestine]]. | ||
*EPEC contains EPEC-adherence factor (EAF), a plasma encoded protein. | *[[Enteropathogenic E. coli|EPEC]] contains [[Enteropathogenic E. coli|EPEC]]-adherence factor (EAF), a [[Blood plasma|plasma]] [[Code|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=book>{{cite book | *Using EAF, [[Enteropathogenic E. coli|EPEC]] adheres to [[Enterocyte|enterocytes]] and destroy the normal architecture of the [[human]] [[Microvillus|microvilli]], resulting in [[Cytoskeleton|cytoskeletal]] deformities. The process is referred to as "attachment and effacing".<ref name="book">{{cite book |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=book>{{cite book | *Similar to [[Enterohemorrhagic escherichica coli|EHEC]], it is not considered highly invasive.<ref name="book">{{cite book |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)=== | ===Diffusely Adherent E. coli (DAEC)=== | ||
*DAEC is a subtype of EPEC, which | *[[Escherichia coli|DAEC]] is a subtype of [[Enteropathogenic E. coli|EPEC]], which contains unique patterns of adherence.<ref name="book">{{cite book |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: | [[Category:Disease]] | ||
[[Category:Gastroenterology]] | |||
[[Category:Foodborne illnesses]] | |||
[[Category:Emergency medicine]] | |||
[[Category:Bacterial diseases]] | |||
Latest revision as of 01:29, 17 December 2018
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Escherichia coli enteritis Microchapters |
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Differentiating Escherichia coli enteritis from other Diseases |
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Diagnosis |
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Escherichia coli enteritis pathophysiology On the Web |
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American Roentgen Ray Society Images of Escherichia coli enteritis pathophysiology |
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Risk calculators and risk factors for Escherichia coli enteritis pathophysiology |
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 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.
Pathophysiology
- E. coli normally colonizes the human gastrointestinal 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 under cooked 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 (particularly cows, sheep, and goats) and their environment
- 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]
- 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. cholerae 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 action 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.
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 Kaper JB, Nataro JP, Mobley HL (2004). "Pathogenic Escherichia coli". Nat Rev Microbiol. 2 (2): 123–40. doi:10.1038/nrmicro818. PMID 15040260.