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'''This page is about microbiologic aspects of the organism.  To view a list of ''E. coli'' organ-based infections, click [[Escherichia coli infection|here]].'''<br>
'''To view specific information about ''E. coli'' O157:H7 strain, click [[Escherichia coli O157:H7|here]].'''
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| binomial_authority = (Migula 1895)<br>Castellani and Chalmers 1919
| binomial_authority = (Migula 1895)<br>Castellani and Chalmers 1919
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{{Redirect|E. coli|the [[protozoa]]n [[parasite]]|Entamoeba coli}}
==Overview==
==Overview==
'''''Escherichia coli''''' ({{pronEng|ˌɛʃ<s>ɪ</s>ˈrɪkiə ˈkoʊlaɪ}}) ('''''E. coli'''''), is a [[bacterium]] that is commonly found in the lower [[gastrointestinal tract|intestine]] of warm-blooded animals. Most ''E. coli'' [[Strain (biology)|strain]]s are harmless, but some, such as [[serovar|serotype]] [[Escherichia coli O157:H7|O157:H7]], can cause serious [[Foodborne illness|food poisoning]] in humans, and are occasionally responsible for costly [[product recall]]s.<ref name="CDC">{{cite web | title=''Escherichia coli'' O157:H7 | work=CDC Division of Bacterial and Mycotic Diseases | url=http://www.cdc.gov/ncidod/dbmd/diseaseinfo/escherichiacoli_g.htm | accessdate=2007-01-25}}</ref><ref name="Vogt">{{cite journal |last=Vogt |first=R.L. |coauthors=L. Dippold |year=2005 |month=Mar-Apr |title=''Escherichia coli'' O157:H7 outbreak associated with consumption of ground beef, June-July 2002 |journal=Public Health Reports |volume=2 |issue= |pages=174-178 |id= |url= |accessdate= |quote= }} PMID 15842119.</ref>  The [[wikt:harmless|harmless]] [[Strain (biology)|strains]] are part of the [[Human flora|normal flora]] of the [[gut]], and can benefit their hosts by producing [[vitamin K|vitamin K<sub>2</sub>]], or by preventing the establishment of [[pathogen]]ic [[bacteria]] within the [[intestine]].<ref name="Bentley">Bentley, R, Meganathan, R., Biosynthesis of Vitamin K (menaquinone) in Bacteria, ''Bacteriological Reviews'', 1982, 46(3):241-280. Review. </ref><ref name="Hudault">Hudault, S.; J. Guignot and A.L. Servin (July 2001). "''Escherichia coli'' strains colonizing the gastrointestinal tract protect germfree mice against ''Salmonella typhimurium'' infection." ''Gut'' '''49''':47-55. PMID 11413110.</ref><ref name="Reid">Reid, G.; J. Howard and B.S. Gan (September 2001). "Can bacterial interference prevent infection?" ''Trends in Microbiology'' '''9'''(9):424-428. PMID 11553454.</ref>


'''''Escherichia coli''''' ({{pronEng|ˌɛʃ<s>ɪ</s>ˈrɪkiə ˈkoʊlaɪ}}) ('''''E. coli'''''), is a [[bacterium]] that is commonly found in the lower [[gastrointestinal tract|intestine]] of warm-blooded animals. Most ''E. coli'' [[Strain (biology)|strain]]s are harmless, but some, such as [[serovar|serotype]] [[Escherichia coli O157:H7|O157:H7]], can cause serious [[Foodborne illness|food poisoning]] in humans, and are occasionally responsible for costly [[product recall]]s.<ref name=CDC>{{cite web | title=''Escherichia coli'' O157:H7 | work=CDC Division of Bacterial and Mycotic Diseases | url=http://www.cdc.gov/ncidod/dbmd/diseaseinfo/escherichiacoli_g.htm | accessdate=2007-01-25}}</ref><ref name="Vogt">{{cite journal |last=Vogt |first=R.L. |coauthors=L. Dippold |year=2005 |month=Mar-Apr |title=''Escherichia coli'' O157:H7 outbreak associated with consumption of ground beef, June-July 2002 |journal=Public Health Reports |volume=2 |issue= |pages=174-178 |id= |url= |accessdate= |quote= }} PMID 15842119.</ref>  The [[wikt:harmless|harmless]] [[Strain (biology)|strains]] are part of the [[Human flora|normal flora]] of the [[gut]], and can benefit their hosts by producing [[vitamin K|vitamin K<sub>2</sub>]],<ref name="Bentley">Bentley, R, Meganathan, R., Biosynthesis of Vitamin K (menaquinone) in Bacteria, ''Bacteriological Reviews'', 1982, 46(3):241-280. Review. </ref> or by preventing the establishment of [[pathogen]]ic bacteria within the intestine.<ref name="Hudault">Hudault, S.; J. Guignot and A.L. Servin (July 2001). "''Escherichia coli'' strains colonizing the gastrointestinal tract protect germfree mice against ''Salmonella typhimurium'' infection." ''Gut'' '''49''':47-55. PMID 11413110.</ref><ref name="Reid">Reid, G.; J. Howard and B.S. Gan (September 2001). "Can bacterial interference prevent infection?" ''Trends in Microbiology'' '''9'''(9):424-428. PMID 11553454.</ref>
''E. coli'' is not always confined to the [[intestine]], and its ability to survive for brief periods outside the [[Human body|body]] makes it an ideal [[indicator organism]] to test environmental samples for [[Feces|fecal contamination]].<ref name="Feng_2002" /><ref>{{cite news |first=Andrea |last=Thompson |title=E. coli Thrives in Beach Sands  |url=http://www.livescience.com/health/070604_beach_ecoli.html |work= |publisher=Live Science |date=June 4, 2007 |accessdate=2007-12-03 }}</ref> The [[bacteria]] can also be grown easily and its [[genetics]] are comparatively simple and easily-manipulated, making it one of the best-studied [[Prokaryote|prokaryotic]] [[model organism]]s, and an important [[species]] in [[biotechnology]]. ''E. coli'' was discovered by a German [[Pediatrics|pediatrician]] and [[Microbiology|bacteriologist]] [[Theodor Escherich]] in 1885, and is now classified as part of the [[Enterobacteriaceae]] family of [[Proteobacteria|gamma-proteobacteria]].<ref name="Feng_2002">{{cite web | author = Feng P, Weagant S, Grant, M | title=Enumeration of ''Escherichia coli'' and the Coliform Bacteria | work=Bacteriological Analytical Manual (8th ed.) | publisher = FDA/Center for Food Safety & Applied Nutrition | date=  2002-09-01 | url=http://www.cfsan.fda.gov/~ebam/bam-4.html | accessdate=2007-01-25}}</ref><ref>{{cite web |url=http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Tree&id=561&lvl=3&lin=f&keep=1&srchmode=1&unlock |title=''Escherichia'' |accessdate=2007-11-30 |last= |first= |coauthors= |date= |work=Taxonomy Browser |publisher=NCBI}}</ref>
 
''E. coli'' are not always confined to the intestine, and their ability to survive for brief periods outside the body makes them an ideal [[indicator organism]] to test environmental samples for [[Feces|fecal contamination]].<ref name="Feng_2002"/><ref>{{cite news |first=Andrea |last=Thompson |title=E. coli Thrives in Beach Sands  |url=http://www.livescience.com/health/070604_beach_ecoli.html |work= |publisher=Live Science |date=June 4, 2007 |accessdate=2007-12-03 }}</ref> The bacteria can also be grown easily and its [[genetics]] are comparatively simple and easily-manipulated, making it one of the best-studied prokaryotic [[model organism]]s, and an important species in [[biotechnology]]. ''E. coli'' was discovered by German pediatrician and bacteriologist [[Theodor Escherich]] in 1885,<ref name="Feng_2002">{{cite web | author = Feng P, Weagant S, Grant, M | title=Enumeration of ''Escherichia coli'' and the Coliform Bacteria | work=Bacteriological Analytical Manual (8th ed.) | publisher = FDA/Center for Food Safety & Applied Nutrition | date=  2002-09-01 | url=http://www.cfsan.fda.gov/~ebam/bam-4.html | accessdate=2007-01-25}}</ref> and is now classified as part of the [[Enterobacteriaceae]] family of [[Proteobacteria|gamma-proteobacteria]].<ref>{{cite web |url=http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Tree&id=561&lvl=3&lin=f&keep=1&srchmode=1&unlock |title=''Escherichia'' |accessdate=2007-11-30 |last= |first= |coauthors= |date= |work=Taxonomy Browser |publisher=NCBI}}</ref>


==Strains==
==Strains==


A [[strain (biology)|strain]] of ''E. coli'' is a sub-group within the species that has unique characteristics that distinguish it from other ''E. coli'' strains.  These differences are often detectable only on the molecular level; however, they may result in changes to the physiology or lifecycle of the bacterium.  For example, a strain may gain [[pathogenicity|pathogenic capacity]], the ability to use a unique carbon source, the ability to inhabit a particular ecological niche or the ability to resist antimicrobial agents.  Different strains of ''E. coli'' are often host-specific, making it possible to determine the source of fecal contamination in environmental samples.  Depending on which ''E. coli'' strains are present in a water sample, for example, assumptions can be made about whether the contamination originated from a human, other mammal or bird source.  
A [[strain (biology)|strain]] of ''E. coli'' is a sub-group within the [[species]] that has unique characteristics distinguishing it from other ''E. coli'' [[Strain (biology)|strains]].  These differences are often detectable only on the molecular level; however, they may result in changes to the [[physiology]] or [[Biological life cycle|life cycle]] of the [[Bacteria|bacterium]].  For example, a [[Strain (biology)|strain]] may gain [[pathogenicity|pathogenic capacity]], the ability to use a unique [[carbon]] source, the ability to inhabit a particular ecological niche, or the ability to resist [[Antimicrobial|antimicrobial agents]].  Different [[Strain (biology)|strains]] of ''E. coli'' are often [[Host (biology)|host]]-specific, making it possible to determine the source of [[Feces|fecal]] contamination in environmental samples.  Depending on which ''E. coli'' [[Strain (biology)|strains]] are present in a water sample, for example, assumptions can be made about whether the contamination originated from a human, other mammal, or bird source.  


New strains of ''E. coli'' [[evolution|evolve]] through the natural biological process of [[mutation]], and some strains develop traits that can be harmful to a host animal. Although virulent strains typically cause no more than a bout of diarrhea in healthy adult humans, particularly virulent strains, such as [[Escherichia coli O157:H7|O157:H7]] or O111:B4, can cause serious illness or death in the elderly, the very young or the [[immunocompromised]].<ref name="Hudault">Viljanen, M.K.; T. Peltola, S.Y. Junnila, L. Olkkonen, H. Järvinen, M. Kuistila and P. Huovinen (October 6, 1990). "Outbreak of diarrhoea due to ''Escherichia coli'' O111:B4 in schoolchildren and adults: association of Vi antigen-like reactivity." ''Lancet'' '''336'''(8719):831-834. PMID 1976876.</ref>
New [[Strain (biology)|strains]] of ''E. coli'' [[evolution|evolve]] through the natural [[Biology|biological]] process of [[mutation]], and some [[Strain (biology)|strains]] develop traits that can be harmful to a [[Host (biology)|host]] animal. Although [[Virulence|virulent]] [[Strain (biology)|strains]] typically cause no more than a bout of [[diarrhea]] in healthy adult humans, particularly [[Virulence|virulent]] [[Strain (biology)|strains]], such as [[Escherichia coli O157:H7|O157:H7]] or O111:B4, can cause serious [[illness]] or death in the elderly, the very young, or the [[immunocompromised]].<ref name="Hudault">Viljanen, M.K.; T. Peltola, S.Y. Junnila, L. Olkkonen, H. Järvinen, M. Kuistila and P. Huovinen (October 6, 1990). "Outbreak of diarrhoea due to ''Escherichia coli'' O111:B4 in schoolchildren and adults: association of Vi antigen-like reactivity." ''Lancet'' '''336'''(8719):831-834. PMID 1976876.</ref>
[[Image:Life cycle of Escherichia coli.png|thumb|left|400px|Model of successive binary fission in ''E. coli'']]
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==Biology and biochemistry==
==Biology and Biochemistry==
''E. coli'' is [[Gram-negative]], [[Facultative anaerobic organism|facultative anaerobic]] and [[Endospore|non-sporulating]]. It can live on a wide variety of substrates. ''E. coli'' uses mixed-acid fermentation in anaerobic conditions, producing [[lactic acid|lactate]], [[succinate]], [[ethanol]], [[acetate]] and carbon dioxide. Since many pathways in mixed-acid fermentation produce hydrogen gas, these pathways require the levels of hydrogen to be low, as is the case when ''E. coli'' lives together with hydrogen-consuming organisms such as [[methanogen]]s or [[sulfate-reducing bacteria]].<ref>{{cite book | title=Brock Biology of microorganisms| author=Madigan MT, Martinko JM| date=2006| publisher=Pearson| isbn=0-13-196893-9| edition=11th ed.}}</ref>
[[Image:Life cycle of Escherichia coli.png|thumb|right|400px|Model of successive binary fission in ''E. coli'']]
''E. coli'' is [[Gram-negative]], [[Facultative anaerobic organism|facultative anaerobic]] and [[Endospore|non-sporulating]]. It can live on a wide variety of substrates. ''E. coli'' uses mixed-acid fermentation in anaerobic conditions, producing [[lactic acid|lactate]], [[succinate]], [[ethanol]], [[acetate]], and carbon dioxide. Since many pathways in mixed-acid fermentation produce hydrogen gas, these pathways require the levels of hydrogen to be low, as is the case when ''E. coli'' lives together with hydrogen-consuming organisms such as [[methanogen]]s or [[sulfate-reducing bacteria]].<ref>{{cite book | title=Brock Biology of microorganisms| author=Madigan MT, Martinko JM| date=2006| publisher=Pearson| isbn=0-13-196893-9| edition=11th ed.}}</ref>


Optimal growth of ''E. coli'' occurs at 37°C, but some laboratory strains can multiply at temperatures of up to 49°C.<ref>{{cite journal |author=Fotadar U, Zaveloff P, Terracio L |title=Growth of Escherichia coli at elevated temperatures |journal=J. Basic Microbiol. |volume=45 |issue=5 |pages=403–4 |year=2005 |pmid=16187264}}</ref> Growth can be driven by aerobic or anaerobic respiration, using a large variety of [[redox|redox pairs]], including the oxidation of [[pyruvic acid]], [[formic acid]], [[hydrogen]] and [[amino acid]]s, and the reduction of substrates such as [[oxygen]], [[nitrate]], [[dimethyl sulfoxide]] and [[trimethylamine N-oxide]].<ref name=Ingledew>{{cite journal |author=Ingledew WJ, Poole RK |title=The respiratory chains of Escherichia coli |journal=Microbiol. Rev. |volume=48 |issue=3 |pages=222&ndash;71 |year=1984 |pmid=6387427}}</ref>
Optimal growth of ''E. coli'' occurs at 37°C, but some laboratory strains can multiply at temperatures of up to 49°C.<ref>{{cite journal |author=Fotadar U, Zaveloff P, Terracio L |title=Growth of Escherichia coli at elevated temperatures |journal=J. Basic Microbiol. |volume=45 |issue=5 |pages=403–4 |year=2005 |pmid=16187264}}</ref> Growth can be driven by aerobic or anaerobic respiration, using a large variety of [[redox|redox pairs]], including the oxidation of [[pyruvic acid]], [[formic acid]], [[hydrogen]] and [[amino acid]]s, and the reduction of substrates such as [[oxygen]], [[nitrate]], [[dimethyl sulfoxide]] and [[trimethylamine N-oxide]].<ref name="Ingledew">{{cite journal |author=Ingledew WJ, Poole RK |title=The respiratory chains of Escherichia coli |journal=Microbiol. Rev. |volume=48 |issue=3 |pages=222&ndash;71 |year=1984 |pmid=6387427}}</ref>


Strains that possess [[flagellum|flagella]] can swim and are [[motile]], but other strains lack flagellum. The flagella of ''E. coli'' have a [[peritrichous]] arrangement.<ref>Darnton NC, Turner L, Rojevsky S, Berg HC, On torque and tumbling in swimming Escherichia coli. J Bacteriol. 2007 Mar;189(5):1756-64. Epub 2006 Dec 22.</ref>
Strains that possess [[flagellum|flagella]] can swim and are [[motile]], but other strains lack flagellum. The flagella of ''E. coli'' have a [[peritrichous]] arrangement.<ref>Darnton NC, Turner L, Rojevsky S, Berg HC, On torque and tumbling in swimming Escherichia coli. J Bacteriol. 2007 Mar;189(5):1756-64. Epub 2006 Dec 22.</ref>
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==Normal Role==
==Normal Role==
''E. coli'' normally colonizes an infant's [[gastrointestinal tract]] within 40 hours of birth, arriving with food or water or with the individuals handling the child.   
''E. coli'' normally colonizes an infant's [[gastrointestinal tract]] within 40 hours of birth, arriving with food or water or from the individuals handling the child.   
In the bowel, it adheres to the [[mucus]] of the [[large intestine]]. It is the primary [[Facultative anaerobic organism|facultative organism]] of the human gastrointestinal tract.<ref name="Todar" />  As long as these bacteria do not acquire [[bacteriophage|genetic elements]] encoding for [[virulence factor]]s, they remain benign [[Commensalism|commensals]].<ref name=Evans />
In the bowel, it adheres to the [[mucus]] of the [[large intestine]]. It is the primary [[Facultative anaerobic organism|facultative organism]] of the human gastrointestinal tract.<ref name="Todar" />  As long as these bacteria do not acquire [[bacteriophage|genetic elements]] encoding for [[virulence factor]]s, they remain benign [[Commensalism|commensals]].<ref name="Evans" />


==Role in disease==
==Role in Disease==


Virulent strains of ''E. coli'' can cause [[gastroenteritis]], [[urinary tract infection]]s, and [[neonatal]] [[meningitis]].  In rarer cases, virulent strains are also responsible for [[peritonitis]], [[mastitis]], [[septicemia]] and Gram-negative [[pneumonia]].<ref name="Todar" />
Virulent strains of ''E. coli'' can cause [[gastroenteritis]], [[urinary tract infection]]s, and [[neonatal]] [[meningitis]].  In rarer cases, virulent strains are also responsible for [[peritonitis]], [[mastitis]], [[septicemia]] and Gram-negative [[pneumonia]].<ref name="Todar" />
Recently it is thought that E. coli and certain other foodborne illnesses can sometimes trigger serious health problems months or years after patients survived that initial bout.[http://www.thirdage.com/news/articles/ALT02/08/02/07/ALT02080207-02.html Food poisoning can be a long-term problem.]
Recently it is thought that E. coli and certain other foodborne illnesses can sometimes trigger serious health problems months or years after patients survived that initial bout. [http://www.thirdage.com/news/articles/ALT02/08/02/07/ALT02080207-02.html Food poisoning can be a long-term problem.]


===Virulence properties=== <!--Virulence properties of escherichia coli redirects here-->
===Virulence properties=== <!--Virulence properties of escherichia coli redirects here-->
Enteric ''E. coli'' (EC) are classified on the basis of serological characteristics and virulence properties.<ref name="Todar">{{cite web |url=http://www.textbookofbacteriology.net/e.coli.html |title=Pathogenic ''E. coli'' |accessdate=2007-11-30 |last=Todar |first=K. |coauthors= |date= |work=Online Textbook of Bacteriology |publisher=University of Wisconsin-Madison Department of Bacteriology}}</ref>  Virotypes include:
Enteric ''E. coli'' (EC) are classified on the basis of serological characteristics and virulence properties.<ref name="Todar">{{cite web |url=http://www.textbookofbacteriology.net/e.coli.html |title=Pathogenic ''E. coli'' |accessdate=2007-11-30 |last=Todar |first=K. |coauthors= |date= |work=Online Textbook of Bacteriology |publisher=University of Wisconsin-Madison Department of Bacteriology}}</ref>   
*[[Enterotoxigenic Escherichia coli|'''Enterotoxigenic ''E. coli''''']] (ETEC) – causative agent of diarrhea (without fever) in humans, pigs, sheep, goats, cattle, dogs, and horses.  ETEC uses [[fimbria (bacteriology)|fimbrial adhesins]] (projections from the bacterial cell surface) to bind [[enterocyte]] cells in the [[small intestine]].  ETEC can produce two [[protein|proteinaceous]] [[enterotoxins]]: the larger of the two proteins, '''LT enterotoxin''', is similar to [[cholera toxin]] in structure and function, while the smaller protein, '''ST enterotoxin''' causes [[Cyclic guanosine monophosphate|cGMP]] accumulation in the target cells and a subsequent secretion of fluid and electrolytes into the intestinal [[lumen (anatomy)|lumen]].  ETEC strains are non-invasive, and they do not leave the intestinal lumen.
 
*'''Enteropathogenic ''E. coli''''' (EPEC) – causative agent of diarrhea in humans, rabbits, dogs, cats and horses.  Like ETEC, EPEC also causes diarrhea, but the molecular mechanisms of colonization and etiology are different.  EPEC lack fimbriae, ST and LT toxins, but they utilize an [[adhesin]] known as [[intimin]] to bind host intestinal cells.  This virotype has an array of virulence factors that are similar to those found in ''[[Shigella]]'', and may posses a [[shiga toxin]].  Adherence to the intestinal mucosa causes a rearrangement of [[actin]] in the host cell, causing significant deformation.  EPEC cells are moderately-invasive (i.e. they enter host cells) and elicit an inflammatory response.  Changes in intestinal cell ultrastructure due to "attachment and effacement" is likely the prime cause of diarrhea in those afflicted with EPEC.
Virotypes include:
*'''Enteroinvasive ''E. coli''''' (EIEC) – found only in humans.  EIEC infection causes a syndrome that is identical to [[Shigellosis]], with profuse diarrhea and high fever.  EIEC are highly invasive, and they utilize adhesin proteins to bind to and enter intestinal cells.  They produce no toxins, but severely damage the intestinal wall through mechanical cell destruction.
*[[Enterotoxigenic Escherichia coli|'''Enterotoxigenic ''E. coli''''']] (ETEC) – It is the causative agent of diarrhea (without fever) in humans, pigs, sheep, goats, cattle, dogs, and horses.  ETEC uses [[fimbria (bacteriology)|fimbrial adhesins]] (projections from the bacterial cell surface) to bind [[enterocytes]] in the [[small intestine]].  ETEC can produce two [[protein|proteinaceous]] [[enterotoxins]]: the larger of the two proteins, '''LT enterotoxin''', is similar to [[cholera toxin]] in structure and function, while the smaller protein, '''ST enterotoxin''' causes [[Cyclic guanosine monophosphate|cGMP]] accumulation in the target cells and a subsequent secretion of fluid and electrolytes into the intestinal [[lumen (anatomy)|lumen]].  ETEC strains are non-invasive, and they do not leave the intestinal lumen.
*'''Enterohemorrhagic ''E. coli''''' (EHEC) – found in humans, cattle, and goats.  The sole member of this virotype is strain [[O157:H7]], which causes bloody diarrhea and no fever.  EHEC can cause [[hemolytic uremic syndrome]] and sudden kidney failure.  It uses bacterial fimbriae for attachment, is moderately-invasive and possesses a phage-encoded Shiga toxin that can elicit an intense inflammatory response.
*'''Enteropathogenic ''E. coli''''' (EPEC) – It is the causative agent of diarrhea in humans, rabbits, dogs, cats and horses.  Like ETEC, EPEC also causes diarrhea, but the molecular mechanism of colonization and etiology are different.  EPEC lack fimbriae, ST and LT toxins, but they utilize an [[adhesin]] known as [[intimin]] to bind host intestinal cells.  This virotype has an array of virulence factors that are similar to those found in ''[[Shigella]]'', and may posses a [[shiga toxin]].  Adherence to the intestinal mucosa causes a rearrangement of [[actin]] in the host cell, causing significant deformation.  EPEC cells are moderately-invasive (i.e. they enter host cells) and elicit an inflammatory response.  Changes in intestinal cell ultrastructure due to "attachment and effacement" is likely the prime cause of diarrhea in those afflicted with EPEC.
*'''Enteroaggregative ''E. coli''''' (EAggEC) – found only in humans.  So named because they have fimbriae which aggregate [[tissue culture]] cells, EAggEC bind to the intestinal mucosa to cause watery diarrhea without fever. EAggEC are non-invasive.  They produce a [[hemolysin]] and an ST enterotoxin similar to that of ETEC.
*'''Enteroinvasive ''E. coli''''' (EIEC) – It is found only in humans.  EIEC infection causes a syndrome that is identical to [[Shigellosis]], with profuse diarrhea and high fever.  EIEC are highly invasive, and they utilize adhesin proteins to bind to and enter intestinal cells.  They produce no toxins, but can cause severe damage to the intestinal wall through mechanical cell destruction.
*'''Enterohemorrhagic ''E. coli''''' (EHEC) – It is found in humans, cattle, and goats.  The sole member of this virotype is strain [[O157:H7]], which causes bloody diarrhea and no fever.  EHEC can cause [[hemolytic uremic syndrome]] and sudden kidney failure.  It uses bacterial fimbriae for attachment and is moderately invasive. It possesses a phage-encoded Shiga toxin that can elicit an intense inflammatory response.
*'''Enteroaggregative ''E. coli''''' (EAggEC) – It is found only in humans.  This strain is named "aggregative" because their fimbriae aggregate [[tissue culture]] cells. EAggEC binds to the intestinal mucosa while being non-invasive and causes watery diarrhea without fever. It produces a [[hemolysin]] and an ST enterotoxin similar to that of ETEC.


===Gastrointestinal infection===  
===Gastrointestinal infection===  
[[Image:E coli at 10000x, original.jpg|thumb|left|250px|Low-temperature electron micrograph of a cluster of ''E. coli'' bacteria, magnified 10,000 times. Each individual bacterium is oblong shaped.]]
[[Image:E coli at 10000x, original.jpg|thumb|left|250px|Low-temperature electron micrograph of a cluster of ''E. coli'' bacteria, magnified 10,000 times. Each individual bacterium is oblong shaped.]]


Certain strains of ''E. coli'', such as [[Escherichia coli O157:H7|O157:H7]], [[Escherichia coli O121|O121]] and [[Escherichia coli O104:H21|O104:H21]], produce [[toxin]]s. [[Food poisoning]] caused by ''E. coli'' are usually associated with eating unwashed vegetables and meat contaminated post-slaughter. O157:H7 is further notorious for causing serious and even life-threatening complications like [[Hemolytic Uremic Syndrome]] (HUS). This particular strain is linked to the [[2006 United States E. coli outbreak]] of fresh spinach. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly or the immunocompromised, but is more often mild. ''E. coli'' can harbor both heat-stable and heat-labile enterotoxins. The latter, termed LT, contains one 'A' subunit and five 'B' subunits arranged into one holotoxin, and is highly similar in structure and function to [[Cholera]] toxins. The B subunits assist in adherence and entry of the toxin into host intestinal cells, while the A subunit is cleaved and prevents cells from absorbing water, causing [[diarrhea]]. LT is secreted by the Type 2 secretion pathway.<ref>{{cite journal |author=Tauschek M, Gorrell R, Robins-Browne RM, |title=Identification of a protein secretory pathway for the secretion of heat-labile enterotoxin by an enterotoxigenic strain of Escherichia coli | journal=PNAS | volume=99 |pages=7066-7071 | url=http://www.pnas.org/cgi/content/abstract/99/10/7066}} </ref>
Certain strains of ''E. coli'', such as [[Escherichia coli O157:H7|O157:H7]], [[Escherichia coli O121|O121]] and [[Escherichia coli O104:H21|O104:H21]], produce [[toxin]]s. [[Food poisoning]] caused by ''E. coli'' are usually associated with eating unwashed vegetables and meat contaminated post-slaughter. O157:H7 is further notorious for causing serious and even life-threatening complications such as [[Hemolytic Uremic Syndrome]] (HUS). This particular strain is linked to the [[2006 United States E. coli outbreak]] of fresh spinach and the most recent multistate outbreak linked to romaine lettuce from the Central Coastal growing regions in northern and central California. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly, or the immunocompromised, but is more often mild. ''E. coli'' can harbor both heat-stable and heat-labile enterotoxins. The latter, termed LT, contains one 'A' subunit and five 'B' subunits arranged into one holotoxin, and is highly similar in structure and function to [[Cholera]] toxins. The 'B' subunits assist in adherence and entry of the toxin into host intestinal cells, while the 'A' subunit is cleaved and prevents cells from absorbing water, causing [[diarrhea]]. LT is secreted by the Type 2 secretion pathway.<ref>{{cite journal |author=Tauschek M, Gorrell R, Robins-Browne RM, |title=Identification of a protein secretory pathway for the secretion of heat-labile enterotoxin by an enterotoxigenic strain of Escherichia coli | journal=PNAS | volume=99 |pages=7066-7071 | url=http://www.pnas.org/cgi/content/abstract/99/10/7066}} </ref>


If ''E. coli'' bacteria escape the intestinal tract through a perforation (for example from an [[ulcer]], a [[ruptured appendix]], or a [[surgical error]]) and enter the abdomen, they usually cause [[peritonitis]] that can be fatal without prompt treatment. However, ''E. coli'' are extremely sensitive to such [[antibiotics]] as [[streptomycin]] or [[gentamicin]], so treatment with antibiotics is usually effective. This could change since, as noted below, ''E. coli'' quickly acquires drug resistance.<ref name=SciDaily_2001>{{cite web | title=Gene Sequence Of Deadly E. Coli Reveals Surprisingly Dynamic Genome | publisher=Science Daily | url=http://www.sciencedaily.com/releases/2001/01/010125082330.htm | date=2001-01-25 | accessdate=2007-02-08}}</ref>
If ''E. coli'' escapes the intestinal tract through a perforation (for example from an [[ulcer]], a [[ruptured appendix]], or a [[surgical error]]) and enters the abdomen, it usually causes [[peritonitis]] that can be fatal without prompt treatment. ''E. coli'' is extremely sensitive to [[antibiotics]] such as [[streptomycin]] or [[gentamicin]] and treatment with these antibiotics is usually effective.''E. coli'' can also quickly acquire drug resistance which can be troublesome.<ref name="SciDaily_2001">{{cite web | title=Gene Sequence Of Deadly E. Coli Reveals Surprisingly Dynamic Genome | publisher=Science Daily | url=http://www.sciencedaily.com/releases/2001/01/010125082330.htm | date=2001-01-25 | accessdate=2007-02-08}}</ref>


Intestinal mucosa-associated ''E. coli'' are observed in increased numbers in the [[inflammatory bowel disease]]s, [[Crohn's disease]] and [[ulcerative colitis]].<ref name="Rolhion">{{cite journal |author=Rolhion N, Darfeuille-Michaud A |title=Adherent-invasive Escherichia coli in inflammatory bowel disease |journal=Inflamm. Bowel Dis. |volume=13 |issue=10 |pages=1277–83 |year=2007 |pmid=17476674 |doi=10.1002/ibd.20176}}</ref> Invasive strains of ''E. coli'' exist in high numbers in the inflamed tissue, and the number of bacteria in the inflamed regions correlates to the severity of the bowel inflammation.<ref name="Baumgart">{{cite journal |author=Baumgart M, Dogan B, Rishniw M, ''et al'' |title=Culture independent analysis of ileal mucosa reveals a selective increase in invasive Escherichia coli of novel phylogeny relative to depletion of Clostridiales in Crohn's disease involving the ileum |journal=ISME J |volume=1 |issue=5 |pages=403–18 |year=2007 |pmid=18043660 |doi=10.1038/ismej.2007.52}}</ref>
Intestinal mucosa-associated ''E. coli'' is observed in increased numbers in patients with inflammatory bowel disease such as [[Crohn's disease]] and [[ulcerative colitis]].<ref name="Rolhion">{{cite journal |author=Rolhion N, Darfeuille-Michaud A |title=Adherent-invasive Escherichia coli in inflammatory bowel disease |journal=Inflamm. Bowel Dis. |volume=13 |issue=10 |pages=1277–83 |year=2007 |pmid=17476674 |doi=10.1002/ibd.20176}}</ref> Invasive strains of ''E. coli'' exist in high numbers in the inflamed tissue, and the number of bacteria in the inflammatory foci correlates with the severity of the bowel inflammation.<ref name="Baumgart">{{cite journal |author=Baumgart M, Dogan B, Rishniw M, ''et al'' |title=Culture independent analysis of ileal mucosa reveals a selective increase in invasive Escherichia coli of novel phylogeny relative to depletion of Clostridiales in Crohn's disease involving the ileum |journal=ISME J |volume=1 |issue=5 |pages=403–18 |year=2007 |pmid=18043660 |doi=10.1038/ismej.2007.52}}</ref>


====Epidemiology of gastrointestinal infection====
====Epidemiology of gastrointestinal infection====
Transmission of pathogenic ''E. coli'' often occurs via [[fecal-oral route|fecal-oral transmission]].<ref name="haccp">{{cite web |url=http://www.cfsan.fda.gov/~dms/hret2-a3.html |title=Retail Establishments; Annex 3 - Hazard Analysis |accessdate=2007-12-02 |last= |first= |coauthors= |date=April 2006 |work=Managing Food Safety: A Manual for the Voluntary Use of HACCP Principles for Operators of Food Service and Retail Establishments |publisher=U.S. Department of Health and Human Services Food and Drug Administration Center for Food Safety and Applied Nutrition}}</ref><ref name=Evans>{{cite web |url=http://www.gsbs.utmb.edu/microbook/ch025.htm |title=Escherichia Coli |accessdate=2007-12-02 |last=Evans Jr. |first=Doyle J. |coauthors=Dolores G. Evans |date= |work=Medical Microbiology, 4th edition |publisher=The University of Texas Medical Branch at Galveston}}</ref><ref>{{cite journal |last=Gehlbach |first=S.H. |coauthors=J.N. MacCormack, B.M. Drake, W.V. Thompson |year=1973 |month=April |title=Spread of disease by fecal-oral route in day nurseries |journal=Health Service Reports |volume=88 |issue=4 |pages=320-322 |id=PMID 4574421 |url= |quote= }}</ref> Common routes of transmission include: unhygienic food preparation,<ref name="haccp"/> farm contamination due to manure fertilization,<ref name="spinach">{{cite news |author=Sabin Russell |coauthors= |title=Spinach E. coli linked to cattle; Manure on pasture had same strain as bacteria in outbreak |url=http://www.sfgate.com/cgi-bin/article.cgi?file=/c/a/2006/10/13/MNG71LOT711.DTL |publisher=San Francisco Chronicle |id= |date=Friday, October 13, 2006 |accessdate=2007-12-02 }}</ref> irrigation of crops with contaminated greywater
Transmission of pathogenic ''E. coli'' often occurs via [[fecal-oral route|fecal-oral route]]. Common sources of contamination include: unhygienic food preparation, farm contamination due to manure fertilization, irrigation of crops with contaminated greywater or raw sewage, feral pigs on cropland, or direct consumption of sewage-contaminated water.<ref name="haccp">{{cite web |url=http://www.cfsan.fda.gov/~dms/hret2-a3.html |title=Retail Establishments; Annex 3 - Hazard Analysis |accessdate=2007-12-02 |last= |first= |coauthors= |date=April 2006 |work=Managing Food Safety: A Manual for the Voluntary Use of HACCP Principles for Operators of Food Service and Retail Establishments |publisher=U.S. Department of Health and Human Services Food and Drug Administration Center for Food Safety and Applied Nutrition}}</ref><ref name="Evans">{{cite web |url=http://www.gsbs.utmb.edu/microbook/ch025.htm |title=Escherichia Coli |accessdate=2007-12-02 |last=Evans Jr. |first=Doyle J. |coauthors=Dolores G. Evans |date= |work=Medical Microbiology, 4th edition |publisher=The University of Texas Medical Branch at Galveston}}</ref><ref>{{cite journal |last=Gehlbach |first=S.H. |coauthors=J.N. MacCormack, B.M. Drake, W.V. Thompson |year=1973 |month=April |title=Spread of disease by fecal-oral route in day nurseries |journal=Health Service Reports |volume=88 |issue=4 |pages=320-322 |id=PMID 4574421 |url= |quote= }}</ref><ref name="spinach">{{cite news |author=Sabin Russell |coauthors= |title=Spinach E. coli linked to cattle; Manure on pasture had same strain as bacteria in outbreak |url=http://www.sfgate.com/cgi-bin/article.cgi?file=/c/a/2006/10/13/MNG71LOT711.DTL |publisher=San Francisco Chronicle |id= |date=Friday, October 13, 2006 |accessdate=2007-12-02 }}</ref><ref>{{cite journal |last=Heaton |first=J.C. |coauthors=K. Jones |year=2007 |month=October 10 |title=Microbial contamination of fruit and vegetables and the behaviour of enteropathogens in the phyllosphere: a review |journal=Journal of Applied Microbiology |volume= |issue= |pages= |id=PMID 17927745 |doi=10.1111/j.1365-2672.2007.03587.x}} <!-- Epub ahead of print - please add volume and page numbers when they are available --></ref><ref name="DeGregori">{{cite web  
or raw sewage,<ref>{{cite journal |last=Heaton |first=J.C. |coauthors=K. Jones |year=2007 |month=October 10 |title=Microbial contamination of fruit and vegetables and the behaviour of enteropathogens in the phyllosphere: a review |journal=Journal of Applied Microbiology |volume= |issue= |pages= |id=PMID 17927745 |doi=10.1111/j.1365-2672.2007.03587.x}} <!-- Epub ahead of print - please add volume and page numbers when they are available --></ref>
feral pigs on cropland,<ref name="DeGregori">{{cite web  
   |author=Thomas R. DeGregori |year=2007-08-17|url= http://www.cgfi.org/cgficommentary/maddening-media-misinformation-on-biotech-and-industrial-agriculture-part-5-of-5  
   |author=Thomas R. DeGregori |year=2007-08-17|url= http://www.cgfi.org/cgficommentary/maddening-media-misinformation-on-biotech-and-industrial-agriculture-part-5-of-5  
   |title=CGFI: Maddening Media Misinformation on Biotech and Industrial Agriculture
   |title=CGFI: Maddening Media Misinformation on Biotech and Industrial Agriculture
  |accessdate=2007-12-08 |format= |work=}}</ref>
  |accessdate=2007-12-08 |format= |work=}}</ref><ref>{{cite journal |last=Chalmers |first=R.M. |coauthors=H. Aird, F.J. Bolton |year=2000 |month= |title=Waterborne ''Escherichia coli'' O157 |journal=Society for Applied Microbiology Symposium Series |volume= |issue=29 |pages=124S-132S |id=PMID 10880187}}</ref>
or direct consumption of sewage-contaminated water.<ref>{{cite journal |last=Chalmers |first=R.M. |coauthors=H. Aird, F.J. Bolton |year=2000 |month= |title=Waterborne ''Escherichia coli'' O157 |journal=Society for Applied Microbiology Symposium Series |volume= |issue=29 |pages=124S-132S |id=PMID 10880187}}</ref> Dairy and beef cattle are primary reservoirs of ''E. coli'' O157:H7,<ref name="bach"/> and they can carry it asymptomatically and shed it in their feces.<ref name="bach">{{cite journal |last=Bach |first=S.J. |coauthors=T.A. McAllister, D.M. Veira, V.P.J. Gannon, and R.A. Holley |year=2002 |month= |title=Transmission and control of ''Escherichia coli'' O157:H7 |journal=Canadian Journal of Animal Science |volume=82 |issue= |pages=475–490 |id= |url=http://pubs.nrc-cnrc.gc.ca/aic-journals/2002ab/cjas02/dec02/cjas02-021.html |accessdate= |quote= }}</ref> Food products associated with ''E. coli'' outbreaks include raw ground beef,<ref>{{cite book |last=Institute of Medicine of the National Academies |first= |authorlink= |coauthors= |editor= |others= |title=''Escherichia coli'' O157:H7 in Ground Beef: Review of a Draft Risk Assessment |url=http://www.nap.edu/catalog.php?record_id=10528 |edition= |series= |year=2002 |publisher=The National Academies Press |location=Washington, D.C. |isbn=0-309-08627-2 |pages= |chapter= |chapterurl= |quote= }}</ref> raw seed sprouts or spinach,<ref name="spinach"/> raw milk, unpasteurized juice, and foods contaminated by infected food workers via fecal-oral route.<ref name="haccp"/>
 
Dairy and beef cattle are the primary reservoirs of ''E. coli'' O157:H7. They can carry it while being asymptomatic and shed it in their feces. Food products associated with ''E. coli'' outbreaks include raw ground beef, raw seed sprouts or spinach, raw milk, unpasteurized juice, lettuce (as observed in the most recent [October-November 2018] multistate outbreak of Shiga toxin-producing Escherichia coli O157:H7 (E. coli O157:H7) infections linked to romaine lettuce from the Central Coastal growing regions in northern and central California), and foods contaminated by infected food workers via fecal-oral route.<ref name="haccp" /><ref name="spinach" /><ref name="bach">{{cite journal |last=Bach |first=S.J. |coauthors=T.A. McAllister, D.M. Veira, V.P.J. Gannon, and R.A. Holley |year=2002 |month= |title=Transmission and control of ''Escherichia coli'' O157:H7 |journal=Canadian Journal of Animal Science |volume=82 |issue= |pages=475–490 |id= |url=http://pubs.nrc-cnrc.gc.ca/aic-journals/2002ab/cjas02/dec02/cjas02-021.html |accessdate= |quote= }}</ref><ref>{{cite book |last=Institute of Medicine of the National Academies |first= |authorlink= |coauthors= |editor= |others= |title=''Escherichia coli'' O157:H7 in Ground Beef: Review of a Draft Risk Assessment |url=http://www.nap.edu/catalog.php?record_id=10528 |edition= |series= |year=2002 |publisher=The National Academies Press |location=Washington, D.C. |isbn=0-309-08627-2 |pages= |chapter= |chapterurl= |quote= }}</ref>


According to the [[U.S. Food and Drug Administration]], the fecal-oral cycle of transmission can be disrupted by cooking food properly, preventing cross-contamination, instituting barriers such as gloves for food workers, instituting health care policies so food industry employees seek treatment when they are ill, pasteurization of juice or dairy and proper hand washing requirements.<ref name="haccp"/>
According to the [[U.S. Food and Drug Administration]], the fecal-oral cycle of transmission can be disrupted by cooking food properly, preventing cross-contamination, instituting barriers such as gloves for food workers, pasteurization of juice or dairy, proper hand washing requirements, and instituting health care policies requiring food industry employees to seek medical care when they are ill.<ref name="haccp" />


Shiga toxin-producing ''E. coli'' (STEC), specifically serotype O157:H7, have also been transmitted by flies,<ref>{{cite journal |author=Szalanski A, Owens C, McKay T, Steelman C |title=Detection of ''Campylobacter'' and ''Escherichia coli'' O157:H7 from filth flies by polymerase chain reaction |journal=Med Vet Entomol |volume=18 |issue=3 |pages=241-6 |year=2004 |url=http://www.blackwell-synergy.com/links/doi/10.1111/j.0269-283X.2004.00502.x/abs/ | pmid = 15347391}}</ref><ref>{{cite journal |author=Sela S, Nestel D, Pinto R, Nemny-Lavy E, Bar-Joseph M |title=Mediterranean fruit fly as a potential vector of bacterial pathogens |journal=Appl Environ Microbiol |volume=71 |issue=7 |pages=4052-6 |year=2005 |pmid = 16000820}}</ref><ref>{{cite journal |author=Alam M, Zurek L |title=Association of ''Escherichia coli'' O157:H7 with houseflies on a cattle farm |journal=Appl Environ Microbiol |volume=70 |issue=12 |pages=7578-80 |year=2004 |id=PMID 15574966}}</ref> as well as direct contact with farm animals,<ref>{{cite journal |last=Rahn |first=K. |coauthors=S.A. Renwick, R.P. Johnson, J.B. Wilson, R.C. Clarke, D. Alves, S.A. McEwen, H. Lior, J. Spika |title=Follow-up study of verocytotoxigenic Escherichia coli infection in dairy farm families |journal=Journal of Infectious Disease |volume=177 |issue=4 |pages=1139-1140 |year=1998 |month=April |id=PMID 9535003}}</ref><ref>{{cite journal |last=Trevena |first=W.B. |coauthors=G.A Willshaw, T. Cheasty, G. Domingue, C. Wray |title=Transmission of Vero cytotoxin producing ''Escherichia coli'' O157 infection from farm animals to humans in Cornwall and west Devon |journal=Community Disease and Public Health |volume=2 |issue=4 |pages=263-268 |year=1999 |month=December |id=PMID 10598383}}</ref> [[petting zoo]] animals,<ref>{{cite journal |last=Heuvelink |first=A.E. |coauthors=C. van Heerwaarden, J.T. Zwartkruis-Nahuis, R. van Oosterom, K. Edink, Y.T. van Duynhoven and E. de Boer |title=''Escherichia coli'' O157 infection associated with a petting zoo |journal=Epidemiology and Infection |volume=129 |issue=2 |pages=295-302 |year=2002 |month=October |id=PMID 12403105}}</ref> and airborne particles found in animal-rearing environments.<ref>{{cite journal |last=Varma |first=J.K. |coauthors=K.D. Greene, M.E. Reller, S.M. DeLong, J. Trottier, S.F. Nowicki, M. DiOrio, E.M. Koch, T.L. Bannerman, S.T. York, M.A. Lambert-Fair, J.G. Wells, P.S. Mead |title=An outbreak of ''Escherichia coli'' O157 infection following exposure to a contaminated building |journal=JAMA |volume=290 |issue=20 |pages=2709-2712 |year=2003 |month=November 26 |id=PMID 14645313}}</ref>
Shiga toxin-producing ''E. coli'' (STEC), specifically serotype O157:H7, can also be transmitted by flies. Tranmission can also occur via direct contact with farm animals, [[petting zoo]] animals, and airborne particles found in animal-rearing environments.<ref>{{cite journal |last=Heuvelink |first=A.E. |coauthors=C. van Heerwaarden, J.T. Zwartkruis-Nahuis, R. van Oosterom, K. Edink, Y.T. van Duynhoven and E. de Boer |title=''Escherichia coli'' O157 infection associated with a petting zoo |journal=Epidemiology and Infection |volume=129 |issue=2 |pages=295-302 |year=2002 |month=October |id=PMID 12403105}}</ref><ref>{{cite journal |last=Rahn |first=K. |coauthors=S.A. Renwick, R.P. Johnson, J.B. Wilson, R.C. Clarke, D. Alves, S.A. McEwen, H. Lior, J. Spika |title=Follow-up study of verocytotoxigenic Escherichia coli infection in dairy farm families |journal=Journal of Infectious Disease |volume=177 |issue=4 |pages=1139-1140 |year=1998 |month=April |id=PMID 9535003}}</ref><ref>{{cite journal |last=Trevena |first=W.B. |coauthors=G.A Willshaw, T. Cheasty, G. Domingue, C. Wray |title=Transmission of Vero cytotoxin producing ''Escherichia coli'' O157 infection from farm animals to humans in Cornwall and west Devon |journal=Community Disease and Public Health |volume=2 |issue=4 |pages=263-268 |year=1999 |month=December |id=PMID 10598383}}</ref><ref>{{cite journal |author=Szalanski A, Owens C, McKay T, Steelman C |title=Detection of ''Campylobacter'' and ''Escherichia coli'' O157:H7 from filth flies by polymerase chain reaction |journal=Med Vet Entomol |volume=18 |issue=3 |pages=241-6 |year=2004 |url=http://www.blackwell-synergy.com/links/doi/10.1111/j.0269-283X.2004.00502.x/abs/ | pmid = 15347391}}</ref><ref>{{cite journal |author=Sela S, Nestel D, Pinto R, Nemny-Lavy E, Bar-Joseph M |title=Mediterranean fruit fly as a potential vector of bacterial pathogens |journal=Appl Environ Microbiol |volume=71 |issue=7 |pages=4052-6 |year=2005 |pmid = 16000820}}</ref><ref>{{cite journal |author=Alam M, Zurek L |title=Association of ''Escherichia coli'' O157:H7 with houseflies on a cattle farm |journal=Appl Environ Microbiol |volume=70 |issue=12 |pages=7578-80 |year=2004 |id=PMID 15574966}}</ref><ref>{{cite journal |last=Varma |first=J.K. |coauthors=K.D. Greene, M.E. Reller, S.M. DeLong, J. Trottier, S.F. Nowicki, M. DiOrio, E.M. Koch, T.L. Bannerman, S.T. York, M.A. Lambert-Fair, J.G. Wells, P.S. Mead |title=An outbreak of ''Escherichia coli'' O157 infection following exposure to a contaminated building |journal=JAMA |volume=290 |issue=20 |pages=2709-2712 |year=2003 |month=November 26 |id=PMID 14645313}}</ref>


===Urinary tract infection===
===Urinary tract infection===
Uropathogenic ''E. coli'' ('''UPEC''') is responsible for approximately 90% of [[urinary tract infection]]s (UTI) seen in individuals with ordinary anatomy.<ref name="Todar"/>  In '''ascending infections''', fecal bacteria colonize the [[urethra]] and spread up the [[urinary tract]] to the [[bladder]]. Because women have a shorter urethra compared with men, they are 14-times more likely to suffer from an ascending UTI.<ref name="Todar"/>
Uropathogenic ''E. coli'' ('''UPEC''') is responsible for approximately 90% of [[urinary tract infection]]s (UTI) seen in individuals with ordinary anatomy. In '''ascending infections''', fecal bacteria colonize the [[urethra]] and spread up the [[urinary tract]] to the [[bladder]]. Women are 14-times more likely to suffer from an ascending UTI as compared to men because of the anatomical difference in the urethral length.<ref name="Todar" />


Uropathogenic ''E. coli'' utilize P fimbriae ([[pyelonephritis]]-associated [[pili]]) to  [[wikt:bind|bind]] urinary tract [[endothelial cell]]s and colonize the bladder.  These [[wikt:adhesin|adhesin]]s specifically bind D-galactose-D-galactose [[moiety|moieties]] on the P blood group [[antigen]] of [[erythrocytes]] and uroepithelial cells.<ref name="Todar"/>  Approximately 1% of the human population lacks this receptor, and its presence or absence dictates an individual's susceptibility to ''E. coli'' urinary tract infections.  Uropathogenic ''E. coli'' produce [[Hemolysis (microbiology)|alpha- and beta-hemolysins]], which cause [[lysis]] of urinary tract cells.
Uropathogenic ''E. coli'' utilize P fimbriae ([[pyelonephritis]]-associated [[pili]]) to  [[wikt:bind|bind]] urinary tract epithelium and colonize the bladder.  These [[wikt:adhesin|adhesin]]s specifically bind D-galactose-D-galactose [[moiety|moieties]] on the P blood group [[antigen]] of [[erythrocytes]] and uroepithelial cells. Approximately 1% of the human population lacks this receptor, and its presence or absence dictates an individual's susceptibility to urinary tract infections caused by ''E. coli''.  Uropathogenic ''E. coli'' produce [[Hemolysis (microbiology)|alpha- and beta-hemolysins]], which cause [[lysis]] of urinary tract cells.<ref name="Todar" />


UPEC can evade the body's innate immune defenses (e.g. the [[complement system]]) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs).<ref>{{cite journal |author=Justice S, Hunstad D, Seed P, Hultgren S |title=Filamentation by Escherichia coli subverts innate defenses during urinary tract infection |journal=Proc Natl Acad Sci U S A |volume=103 |issue=52 |pages=19884-9 |year=2006 |id=PMID 17172451}}</ref> They also have the ability to form K antigen, capsular polysaccharides that contribute to [[biofilm]] formation.  Biofilm-producing ''E. coli'' are recalcitrant to [[antibody|immune factors]] and [[antibiotic]] therapy and are often responsible for chronic urinary tract infections.<ref>{{cite journal |author=Ehrlich G, Hu F, Shen K, Stoodley P, Post J |title=Bacterial plurality as a general mechanism driving persistence in chronic infections |journal=Clin Orthop Relat Res |volume= |issue= |pages=20-4 |year=2005 |month=Aug |id=PMID 16056021 |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16056021}}</ref>  K antigen-producing ''E. coli'' infections are commonly found in the upper urinary tract.<ref name="Todar"/>
UPEC can evade the body's innate immune defenses (e.g. the [[complement system]]) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). It can also have the ability to form K antigen and capsular polysaccharides that contribute to [[biofilm]] formation.  Biofilm-producing ''E. coli'' is recalcitrant to [[antibody|immune factors]] and [[antibiotic]] therapy and can be responsible for chronic urinary tract infections. K antigen-producing ''E. coli'' commonly cause infection of the upper urinary tract.<ref name="Todar" /><ref>{{cite journal |author=Justice S, Hunstad D, Seed P, Hultgren S |title=Filamentation by Escherichia coli subverts innate defenses during urinary tract infection |journal=Proc Natl Acad Sci U S A |volume=103 |issue=52 |pages=19884-9 |year=2006 |id=PMID 17172451}}</ref><ref>{{cite journal |author=Ehrlich G, Hu F, Shen K, Stoodley P, Post J |title=Bacterial plurality as a general mechanism driving persistence in chronic infections |journal=Clin Orthop Relat Res |volume= |issue= |pages=20-4 |year=2005 |month=Aug |id=PMID 16056021 |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16056021}}</ref>  


'''Descending infections''', though relatively rare, occur when ''E. coli'' cells enter the upper urinary tract organs ([[kidney]]s, [[bladder]] or [[ureters]]) from the blood stream.
'''Descending infections''', though relatively rare, occur when ''E. coli'' enters the upper urinary tract ([[kidney]]s, [[bladder]] or [[ureters]]) from the blood stream.


==Diagnosis==
==Diagnosis==


'''Enteropathogenic ''E. coli'' (EPEC)''' and '''Enterotoxigenic ''E. coli'' (ETEC)''' - [[UTI]] or [[GIT]] infections in infants are caused by EPEC which presents as watery diarrhea, meaning that [[Polymorphonuclear_cells|PMN's]] will not be observed in the stool neither with [[methylene blue]] nor [[Gram stain]]. First off, G - ve, rods, with no particular arrangement are seen in [[Gram stain]]. Then, either [[MacConkey agar]] or EMB agar (or both) are inoculated with the stool. On MacConkey agar, deep red colonies are produced as the organism is [[lactose]] positive, and this utilization will cause the medium's [[pH]] to drop leading to darkening of the medium. Growth on Levine EMB agar would show black colonies with greenish-black metallic sheen. This is diagnosic of ''E. coli''. The organism is [[lysine]] positive, and grows on [[TSI slant]] with a (A/A/g+/H<sub>2</sub>S-) profile. Also, [[IMViC]] is ++-- for ''E. coli''; as it's [[indol]] positive (red ring) and [[methyl red]] positive (bright red), but VP  negative (no change-colorless) and [[citrate]] negative (no change-green color). [[Serology]] is done using the SSS-Coagglutination test.
'''Enteropathogenic ''E. coli'' (EPEC)''' and '''Enterotoxigenic ''E. coli'' (ETEC)''' - [[UTI]] or [[GIT]] infections in infants are caused by EPEC which present as watery diarrhea, meaning that [[Polymorphonuclear_cells|PMN's]] will not be observed in the stool neither with [[methylene blue]] nor [[Gram stain]]. Gram negative rods, with no particular arrangement, are seen on [[Gram stain]]. On MacConkey agar inoculated with stool, deep red colonies are produced as the organism is [[lactose]] positive, and this utilization will cause the medium's [[pH]] to drop leading to darkening of the medium. Growth on Levine EMB agar inoculated with stool will show black colonies with greenish-black metallic sheen. This is diagnosic of ''E. coli''. The organism is [[lysine]] positive, and grows on [[TSI slant]] with a (A/A/g+/H<sub>2</sub>S-) profile. [[IMViC]] is ++-- for ''E. coli'' as it is [[indol]] positive (red ring) and [[methyl red]] positive (bright red), but Voges–Proskauer (VP) negative (no change - colorless) and [[citrate]] negative (no change-green color). [[Serology]] is done using the SSS-Coagglutination test.


'''Enterohaemorrhagic ''E. coli'' O157:H7''' - isolated either from urine or, more commonly, stool. There exist three protocols for diagnosis:
'''Enterohaemorrhagic ''E. coli'' O157:H7''' - It is isolated either from urine or, more commonly, stool. There exist three protocols for diagnosis:


(a) Diagnosis is carried out as is the case with EPEC and ETEC.  
#Diagnosis is made in the manner similar to the diagnostic protocol of EPEC and ETEC. [[Sorbitol-MacConkey agar|Sorbitol-MacConkey agar]], a modified [[MacConkey agar]] which has [[sorbitol]] instead of [[lactose]], is used and the EHEC produce colorless colonie due to is inability to utilize sorbitol. [[TSI|TSI slant]] and IMViC are then performed. [[Serology]] detects O157:H7 [[antigens]].
#[[Gram stain]] demonstrating gram negative rods with no particular arrangement.
#Two bottles of verocells are used. One is inoculated with equal portions of stool extract and antitoxin, while the other containing only stool extract. If the first bottle shows neutralization (no [[cytopathic effect|cytopathic effects]]) while the second doesn't; the test is considered positive. This is based on the fact that the toxin produced by this strain is neutralized in the presence of its specific [[antibody]], meaning that it will not be able to exert its effects on cells.


(b) [[Gram stain]]:- G - ve, rods, with no particular arrangement.
==Antibiotic Therapy and Resistance==
[[Sorbitol-MacConkey agar|Sorbitol-MacConkey agar]] is a modified [[MacConkey agar]] which has [[sorbitol]] instead of [[lactose]]. EHEC would produce colorless colonies as it can't utilize sorbitol.
[[TSI|TSI slant]] and IMViC are then performed. [[Serology]] detects O157:H7 [[antigens]].


(c) Two bottles of verocells are used. One is inoculated with equal
portions of a stool extract and antitoxin, while the other has
only a stool extract. If the first bottle shows neutralization
(no [[cytopathic effect|cytopathic effects]]) while the second
doesn't, then the test is considered positive. Otherwise, it's
not. This is based on the fact that the toxin produced by this
strain is neutralized in the presence of its specific
[[antibody]], meaning that it won't be able to exert its effects
on cells.


==Antibiotic therapy and resistance==
Bacterial infections are usually treated with [[antibiotic]]s. However, the antibiotic sensitivities of different strains of ''E. coli'' vary widely. As a Gram-negative organism, ''E. coli'' is resistant to many antibiotics that are effective against [[Gram-positive]] organisms. Antibiotics which may be used to treat ''E. coli'' infection include [[amoxicillin]] as well as other semi-synthetic penicillins, many [[cephalosporin]]s, [[carbapenems]], [[aztreonam]], [[trimethoprim-sulfamethoxazole]], [[ciprofloxacin]], [[nitrofurantoin]], and [[aminoglycoside]]s.  
{{Main|Antibiotic resistance}}
Bacterial infections are usually treated with [[antibiotic]]s. However, the antibiotic sensitivities of different strains of ''E. coli'' vary widely. As Gram-negative organisms, ''E. coli'' are resistant to many antibiotics that are effective against [[Gram-positive]] organisms. Antibiotics which may be used to treat ''E. coli'' infection include [[amoxicillin]] as well as other semi-synthetic penicillins, many [[cephalosporin]]s, [[carbapenems]], [[aztreonam]], [[trimethoprim-sulfamethoxazole]], [[ciprofloxacin]], [[nitrofurantoin]] and the [[aminoglycoside]]s.  


[[Antibiotic resistance]] is a growing problem. Some of this is due to overuse of antibiotics in humans, but some of it is probably due to the use of antibiotics as growth promoters in food of animals.<ref name=Johnson_2006>{{cite journal |author=Johnson J, Kuskowski M, Menard M, Gajewski A, Xercavins M, Garau J |title=Similarity between human and chicken Escherichia coli isolates in relation to ciprofloxacin resistance status |journal=J Infect Dis |volume=194 |issue=1 |pages=71-8 |year=2006 |url=http://www.journals.uchicago.edu/JID/journal/issues/v194n1/35787/35787.html | id=PMID 16741884}}</ref> A study published in the journal [[Science (journal)|''Science'']] in August 2007 found that the rate of adaptative [[mutation]]s in ''E. coli'' is "on the order of 10<sup>–5</sup> per [[genome]] per generation, which is 1,000 times as high as previous estimates," a finding which may have significance for the study and management of bacterial antibiotic resistance.<ref>{{cite web
[[Antibiotic resistance]] is a growing problem. A part of it is due to the overuse of antibiotics in humans, but the use of antibiotics as growth promoters in the food of animals is also a contributing factor. A study published in the journal [[Science (journal)|''Science'']] in August 2007 found that the rate of adaptative [[mutation]]s in ''E. coli'' is on the order of 10<sup>–5</sup> per [[genome]] per generation, which is 1,000 times as high as previous estimates. This finding is very significant for the study and management of bacterial antibiotic resistance.<ref name="Johnson_2006">{{cite journal |author=Johnson J, Kuskowski M, Menard M, Gajewski A, Xercavins M, Garau J |title=Similarity between human and chicken Escherichia coli isolates in relation to ciprofloxacin resistance status |journal=J Infect Dis |volume=194 |issue=1 |pages=71-8 |year=2006 |url=http://www.journals.uchicago.edu/JID/journal/issues/v194n1/35787/35787.html | id=PMID 16741884}}</ref><ref>{{cite web
|url=http://www.sciencemag.org/cgi/content/abstract/317/5839/813?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=isabel+gordo&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT|title= Adaptive Mutations in Bacteria: High Rate and Small Effects|publisher=Science Magazine|date=[[10 August]] [[2007]]|accessdaymonth=[[10 September]]|accessyear=[[2007]]}}</ref>   
|url=http://www.sciencemag.org/cgi/content/abstract/317/5839/813?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=isabel+gordo&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT|title= Adaptive Mutations in Bacteria: High Rate and Small Effects|publisher=Science Magazine|date=[[10 August]] [[2007]]|accessdaymonth=[[10 September]]|accessyear=[[2007]]}}</ref>   


Antibiotic-resistant ''E. coli'' may also pass on the genes responsible for antibiotic resistance to other species of bacteria, such as ''[[Staphylococcus aureus]]''. ''E. coli'' often carry multidrug resistant plasmids and under stress readily transfer those plasmids to other species. Indeed, ''E. coli'' is a frequent member of [[biofilm]]s, where many species of bacteria exist in close proximity to each other. This mixing of species allows ''E. coli'' strains that are piliated to accept and transfer [[plasmid]]s from and to other bacteria. Thus ''E. coli'' and the other [[enterobacteria]] are important reservoirs of transferable antibiotic resistance.<ref>{{cite journal |author=Salyers AA, Gupta A, Wang Y |title=Human intestinal bacteria as reservoirs for antibiotic resistance genes |journal=Trends Microbiol. |volume=12 |issue=9 |pages=412–6 |year=2004 |pmid=15337162}}</ref>
Antibiotic-resistant ''E. coli'' may also pass on the genes responsible for antibiotic resistance to other species of bacteria, such as ''[[Staphylococcus aureus]]''. ''E. coli'' often carry multidrug resistant plasmids and when under stress, it can readily transfer those plasmids to other species. ''E. coli'' is a frequent member of [[biofilm]]s, where many species of bacteria exist in close proximity to each other. This mixing of species allows ''E. coli'' strains that are piliated to accept and transfer [[plasmid]]s from and to other bacteria. Thus, ''E. coli'' and the other [[enterobacteria]] are important reservoirs of transferable antibiotic resistance.<ref>{{cite journal |author=Salyers AA, Gupta A, Wang Y |title=Human intestinal bacteria as reservoirs for antibiotic resistance genes |journal=Trends Microbiol. |volume=12 |issue=9 |pages=412–6 |year=2004 |pmid=15337162}}</ref>


===Beta-lactamase strains===
===Beta-lactamase strains===
Resistance to [[beta-lactam antibiotic]]s has become a particular problem in recent decades, as strains of bacteria that produce extended-spectrum [[beta-lactamase]]s have become more common.<ref>{{cite journal |author=Paterson DL, Bonomo RA |title=Extended-spectrum beta-lactamases: a clinical update |journal=Clin. Microbiol. Rev. |volume=18 |issue=4 |pages=657–86 |year=2005 |pmid=16223952 |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16223952}}</ref> These beta-lactamase enzymes make many, if not all, of the [[penicillin]]s and [[cephalosporin]]s ineffective as therapy.  Extended-spectrum beta-lactamase–producing ''E. coli'' are highly resistant to an array of antibiotics and infections by these strains is difficult to treat. In many instances, only two oral antibiotics and a very limited group of intravenous antibiotics remain effective.
Resistance to [[beta-lactam antibiotic]]s has become a particular problem in the recent decades, as strains of bacteria that produce extended-spectrum [[beta-lactamase]]s have become more common. The beta-lactamase makes many, if not all, of the [[penicillin]]s and [[cephalosporin]]s ineffective as therapeutic measures. Extended-spectrum beta-lactamase–producing ''E. coli'' are highly resistant to an array of antibiotics and infections caused by these strains are difficult to treat. In many instances, only two oral antibiotics and a very limited group of intravenous antibiotics remain effective.<ref>{{cite journal |author=Paterson DL, Bonomo RA |title=Extended-spectrum beta-lactamases: a clinical update |journal=Clin. Microbiol. Rev. |volume=18 |issue=4 |pages=657–86 |year=2005 |pmid=16223952 |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16223952}}</ref>  


Increased concern about the prevalence of this form of "[[Antibiotic resistance|superbug]]" in the United Kingdom has led to calls for further monitoring and a UK-wide strategy to deal with infections and the deaths.<ref>{{cite web |title= HPA Press Statement: Infections caused by ESBL-producing E. coli |url= http://www.hpa.org.uk/hpa/news/articles/press_releases/2007/070924_esbl.htm}}</ref> Susceptibility testing should guide treatment in all infections in which the organism can be isolated for culture.
Increased concern about the prevalence of this form of "[[Antibiotic resistance|superbug]]" in the United Kingdom has led to calls for further monitoring and a UK-wide strategy to deal with infections and the deaths. Susceptibility testing should guide treatment in all infections in which the organism can be isolated for culture.<ref>{{cite web |title= HPA Press Statement: Infections caused by ESBL-producing E. coli |url= http://www.hpa.org.uk/hpa/news/articles/press_releases/2007/070924_esbl.htm}}</ref>


==Phage therapy==
==Phage therapy==
[[Phage therapy]]&mdash;viruses that specifically target pathogenic bacteria&mdash;has been developed over the last 80 years, primarily in the former Soviet Union, where it was used to prevent diarrhea caused by ''E. coli''.<ref>{{cite web|url=http://www.iitd.pan.wroc.pl/phages/phages.html|title=Therapeutic use of bacteriophages in bacterial infections|publisher=Polish Academy of Sciences}}</ref> Presently, phage therapy for humans is available only at the Phage Therapy Center in the Republic of Georgia and in Poland.<ref>{{cite web|url=http://www.phagetherapycenter.com/pii/PatientServlet?command=static_conditions&language=0|title=Medical conditions treated with phage therapy|publisher=Phage Therapy Center}}</ref> However, on January 2 2007, the United States FDA gave Omnilytics approval to apply its ''E. coli'' O157:H7 killing phage in a mist, spray or wash on live animals that will be slaughtered for human consumption.<ref>{{cite web|url=http://home.businesswire.com/portal/site/google/index.jsp?ndmViewId=news_view&newsId=20070102005459&newsLang=en|title= OmniLytics Announces USDA/FSIS Approval for Bacteriophage Treatment of ''E. coli'' O157:H7 on Livestock|publisher=OmniLytics}}</ref>
[[Phage therapy]] involves the use of viruses that specifically target pathogenic bacteria. It has been developed over the last 80 years, primarily in the former Soviet Union, where it was used to prevent diarrhea caused by ''E. coli''. Presently, phage therapy for humans is available only at the Phage Therapy Center in the Republic of Georgia and Poland. However, on January 2 2007, the United States Food and Drug Administration (FDA) gave Omnilytics (a biotech company focused on developing solutions for infectious disease and pest control) the approval to apply its ''E. coli'' O157:H7 killing phage in a mist, spray, or wash on live cattle bred for harvest.<ref>{{cite web|url=http://www.phagetherapycenter.com/pii/PatientServlet?command=static_conditions&language=0|title=Medical conditions treated with phage therapy|publisher=Phage Therapy Center}}</ref><ref>{{cite web|url=http://www.iitd.pan.wroc.pl/phages/phages.html|title=Therapeutic use of bacteriophages in bacterial infections|publisher=Polish Academy of Sciences}}</ref> <ref>{{cite web|url=http://home.businesswire.com/portal/site/google/index.jsp?ndmViewId=news_view&newsId=20070102005459&newsLang=en|title= OmniLytics Announces USDA/FSIS Approval for Bacteriophage Treatment of ''E. coli'' O157:H7 on Livestock|publisher=OmniLytics}}</ref>


==Vaccination==
==Vaccination==
Researchers have actively been working to develop safe, effective [[vaccine]]s to lower the worldwide incidence of ''E. coli'' infection.<ref name=Girard_2006>{{cite journal |author=Girard M, Steele D, Chaignat C, Kieny M |title=A review of vaccine research and development: human enteric infections |journal=Vaccine |volume=24 |issue=15 |pages=2732-50 |year=2006 |id=PMID 16483695}}</ref> In March of 2006, a vaccine eliciting an immune response against the ''E. coli'' O157:H7 O-specific polysaccharide conjugated to [[recombinant]] exotoxin A of ''[[Pseudomonas aeruginosa]]'' (O157-rEPA) was reported to be safe in children two to five years old. Previous work had already indicated that it safe for adults.<ref name=Ahmed_2006>{{cite journal |author=Ahmed A, Li J, Shiloach Y, Robbins J, Szu S |title=Safety and immunogenicity of ''Escherichia coli'' O157 O-specific polysaccharide conjugate vaccine in 2-5-year-old children |journal=J Infect Dis |volume=193 |issue=4 |pages=515-21 |year=2006 |id=PMID 16425130}}</ref> A [[Phase III trials#Phase III|phase III clinical trial]] to verify the large-scale [[efficacy]] of the treatment is planned.<ref name=Ahmed_2006 />
Researchers have actively been working to develop safe, effective [[vaccine]]s to lower the worldwide incidence of ''E. coli'' infection.  In March, 2006, a vaccine, eliciting an immune response against the ''E. coli'' O157:H7 O-specific polysaccharide conjugated to [[recombinant]] exotoxin A of ''[[Pseudomonas aeruginosa]]'' (O157-rEPA), was reported to be safe in children two to five years old. Previous work had already indicated its safety in adults. A [[Phase III trials#Phase III|phase III clinical trial]] to verify the large-scale [[efficacy]] of the treatment is planned.<ref name="Girard_2006">{{cite journal |author=Girard M, Steele D, Chaignat C, Kieny M |title=A review of vaccine research and development: human enteric infections |journal=Vaccine |volume=24 |issue=15 |pages=2732-50 |year=2006 |id=PMID 16483695}}</ref><ref name="Ahmed_2006">{{cite journal |author=Ahmed A, Li J, Shiloach Y, Robbins J, Szu S |title=Safety and immunogenicity of ''Escherichia coli'' O157 O-specific polysaccharide conjugate vaccine in 2-5-year-old children |journal=J Infect Dis |volume=193 |issue=4 |pages=515-21 |year=2006 |id=PMID 16425130}}</ref>


In January 2007 the Canadian bio-pharmaceutical company Bioniche announced it has developed a cattle vaccine which reduces the number of O157:H7 shed in manure by a factor of 1000, to about 1000 pathogenic bacteria per gram of manure.<ref name=Pearson_2007>{{cite journal |author=Pearson H |title=The dark side of E. coli |journal=Nature |volume=445 |issue=7123 |pages=8-9 |year=2007 |id=PMID 17203031}}</ref><ref name=CanadaAM_2007>{{cite web | title=New cattle vaccine controls ''E. coli'' infections | work=Canada AM | url=http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20070111/ecoli_vaccine_cattle_070111/20070111?hub=CanadaAM | date=2007-01-11 | accessdate=2007-02-08}}</ref><ref name=BionichePR_2007>{{cite press release | title = Canadian Research Collaboration Produces World's First Food Safety Vaccine: Against ''E. coli'' O157:H7 | publisher = Bioniche Life Sciences Inc. | date = [[2007-01-10]] | url = http://www.cnxmarketlink.com/en/releases/archive/January2007/10/c4698.html | accessdate = 2007-02-08}}</ref>
In January 2007 the Canadian bio-pharmaceutical company Bioniche announced the development of a cattle vaccine which reduces the number of ''E. coli'' O157:H7 shed in manure to about 1000 pathogenic bacteria per gram of manure.<ref name="Pearson_2007">{{cite journal |author=Pearson H |title=The dark side of E. coli |journal=Nature |volume=445 |issue=7123 |pages=8-9 |year=2007 |id=PMID 17203031}}</ref><ref name="CanadaAM_2007">{{cite web | title=New cattle vaccine controls ''E. coli'' infections | work=Canada AM | url=http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20070111/ecoli_vaccine_cattle_070111/20070111?hub=CanadaAM | date=2007-01-11 | accessdate=2007-02-08}}</ref><ref name="BionichePR_2007">{{cite press release | title = Canadian Research Collaboration Produces World's First Food Safety Vaccine: Against ''E. coli'' O157:H7 | publisher = Bioniche Life Sciences Inc. | date = [[2007-01-10]] | url = http://www.cnxmarketlink.com/en/releases/archive/January2007/10/c4698.html | accessdate = 2007-02-08}}</ref>


==Role in biotechnology==
==Role in Biotechnology==
[[Image:E coli metabolic network.png|thumb|right|Metabolic map of aerobic energy production in ''E. coli''.]]
[[Image:E coli metabolic network.png|thumb|right|Metabolic map of aerobic energy production in ''E. coli''.]]


Because of its long history of laboratory culture and ease of manipulation, ''E. coli'' also plays an important role in modern biological engineering and industrial microbiology.<ref name="lee1996">{{cite journal |author=Lee SY |title=High cell-density culture of Escherichia coli |journal=Trends Biotechnol. |volume=14 |issue=3 |pages=98–105 |year=1996 |pmid=8867291 |doi=10.1016/0167-7799(96)80930-9}}</ref> The work of [[Stanley Norman Cohen]] and [[Herbert Boyer]] in ''E. coli'', using [[plasmid]]s and [[restriction enzyme]]s to create [[recombinant DNA]], became a foundation of biotechnology.<ref name="birth">[http://www.nature.com/nature/journal/v421/n6921/full/nj6921-456a.html "Special Report: The birth of biotechnology"], ''Nature'' 421, 456-457 (23 January 2003)</ref>
Because of its long history of laboratory culture and ease of manipulation, ''E. coli'' also plays an important role in modern biological engineering and industrial microbiology. The work of [[Stanley Norman Cohen]] and [[Herbert Boyer]] on ''E. coli'', using [[plasmid]]s and [[restriction enzyme]]s to create [[recombinant DNA]], has become a foundation.<ref name="lee1996">{{cite journal |author=Lee SY |title=High cell-density culture of Escherichia coli |journal=Trends Biotechnol. |volume=14 |issue=3 |pages=98–105 |year=1996 |pmid=8867291 |doi=10.1016/0167-7799(96)80930-9}}</ref> <ref name="birth">[http://www.nature.com/nature/journal/v421/n6921/full/nj6921-456a.html "Special Report: The birth of biotechnology"], ''Nature'' 421, 456-457 (23 January 2003)</ref>


Considered a very versatile host for the production of [[heterologous]] [[protein]]s,<ref name="Cornelis"/> researchers can introduce genes into the microbes using plasmids, allowing for the mass production of proteins in [[industrial fermentation]] processes. Genetic systems have also been developed which allow the production of [[recombinant proteins]] using ''E. coli''. One of the first useful applications of [[recombinant DNA]] technology was the manipulation of ''E. coli'' to produce human [[insulin]].<ref>{{cite web |url=http://www.littletree.com.au/dna.htm |title=Recombinant DNA Technology in the Synthesis of Human Insulin |accessdate=2007-11-30 |last=Tof |first=Ilanit |coauthors= |date=1994 |work= |publisher=Little Tree Pty. Ltd.}}</ref> Modified ''E. coli'' have been used in [[vaccine]] development, [[bioremediation]], and production of immobilised [[enzyme]]s.<ref name="Cornelis">{{cite journal |author=Cornelis P |title=Expressing genes in different Escherichia coli compartments |journal=Curr. Opin. Biotechnol. |volume=11 |issue=5 |pages=450–4 |year=2000 |pmid=11024362 |doi=10.1016/S0958-1669(00)00131-2}}</ref> ''E. coli'' cannot, however, be used to produce some of the more large, complex proteins which contain multiple [[disulfide bond]]s and, in particular, unpaired [[thiol]]s, or proteins that also require [[post-translational modification]] for activity.<ref name="lee1996"/>
''E. coli'' is considered a very versatile host for the production of [[heterologous]] [[protein]]s. Researchers can introduce genes into the microbes using plasmids, allowing for the mass production of proteins used in the [[industrial fermentation]] processes. Genetic systems have also been developed which allow the production of [[recombinant proteins]] using ''E. coli''. One of the first useful applications of [[recombinant DNA]] technology was the manipulation of ''E. coli'' to produce human [[insulin]]. Modified ''E. coli'' have been used in [[vaccine]] development, [[bioremediation]], and production of immobilised [[enzyme]]s. ''E. coli'' cannot, however, be used to produce some of the more large, complex proteins which contain multiple [[disulfide bond]]s and, in particular, unpaired [[thiol]]s, or proteins that also require [[post-translational modification]] for activity.<ref name="lee1996" /><ref name="Cornelis">{{cite journal |author=Cornelis P |title=Expressing genes in different Escherichia coli compartments |journal=Curr. Opin. Biotechnol. |volume=11 |issue=5 |pages=450–4 |year=2000 |pmid=11024362 |doi=10.1016/S0958-1669(00)00131-2}}</ref><ref>{{cite web |url=http://www.littletree.com.au/dna.htm |title=Recombinant DNA Technology in the Synthesis of Human Insulin |accessdate=2007-11-30 |last=Tof |first=Ilanit |coauthors= |date=1994 |work= |publisher=Little Tree Pty. Ltd.}}</ref>


==Model organism==
==Model organism==
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Latest revision as of 20:20, 14 December 2018

This page is about microbiologic aspects of the organism. To view a list of E. coli organ-based infections, click here.
To view specific information about E. coli O157:H7 strain, click here.

Escherichia coli

Scientific classification
Domain: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Escherichia
Species: E. coli
Binomial name
Escherichia coli
(Migula 1895)
Castellani and Chalmers 1919

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Escherichia coli (Template:PronEng) (E. coli), is a bacterium that is commonly found in the lower intestine of warm-blooded animals. Most E. coli strains are harmless, but some, such as serotype O157:H7, can cause serious food poisoning in humans, and are occasionally responsible for costly product recalls.[1][2] The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2, or by preventing the establishment of pathogenic bacteria within the intestine.[3][4][5]

E. coli is not always confined to the intestine, and its ability to survive for brief periods outside the body makes it an ideal indicator organism to test environmental samples for fecal contamination.[6][7] The bacteria can also be grown easily and its genetics are comparatively simple and easily-manipulated, making it one of the best-studied prokaryotic model organisms, and an important species in biotechnology. E. coli was discovered by a German pediatrician and bacteriologist Theodor Escherich in 1885, and is now classified as part of the Enterobacteriaceae family of gamma-proteobacteria.[6][8]

Strains

A strain of E. coli is a sub-group within the species that has unique characteristics distinguishing it from other E. coli strains. These differences are often detectable only on the molecular level; however, they may result in changes to the physiology or life cycle of the bacterium. For example, a strain may gain pathogenic capacity, the ability to use a unique carbon source, the ability to inhabit a particular ecological niche, or the ability to resist antimicrobial agents. Different strains of E. coli are often host-specific, making it possible to determine the source of fecal contamination in environmental samples. Depending on which E. coli strains are present in a water sample, for example, assumptions can be made about whether the contamination originated from a human, other mammal, or bird source.

New strains of E. coli evolve through the natural biological process of mutation, and some strains develop traits that can be harmful to a host animal. Although virulent strains typically cause no more than a bout of diarrhea in healthy adult humans, particularly virulent strains, such as O157:H7 or O111:B4, can cause serious illness or death in the elderly, the very young, or the immunocompromised.[4]

Biology and Biochemistry

Model of successive binary fission in E. coli

E. coli is Gram-negative, facultative anaerobic and non-sporulating. It can live on a wide variety of substrates. E. coli uses mixed-acid fermentation in anaerobic conditions, producing lactate, succinate, ethanol, acetate, and carbon dioxide. Since many pathways in mixed-acid fermentation produce hydrogen gas, these pathways require the levels of hydrogen to be low, as is the case when E. coli lives together with hydrogen-consuming organisms such as methanogens or sulfate-reducing bacteria.[9]

Optimal growth of E. coli occurs at 37°C, but some laboratory strains can multiply at temperatures of up to 49°C.[10] Growth can be driven by aerobic or anaerobic respiration, using a large variety of redox pairs, including the oxidation of pyruvic acid, formic acid, hydrogen and amino acids, and the reduction of substrates such as oxygen, nitrate, dimethyl sulfoxide and trimethylamine N-oxide.[11]

Strains that possess flagella can swim and are motile, but other strains lack flagellum. The flagella of E. coli have a peritrichous arrangement.[12]

E. coli and related bacteria possess the ability to transfer DNA via bacterial conjugation, transduction or transformation, which allows genetic material to spread horizontally through an existing population. It is believed that this process led to the spread of shiga toxin from Shigella to E. coli O157:H7.

Normal Role

E. coli normally colonizes an infant's gastrointestinal tract within 40 hours of birth, arriving with food or water or from the individuals handling the child. In the bowel, it adheres to the mucus of the large intestine. It is the primary facultative organism of the human gastrointestinal tract.[13] As long as these bacteria do not acquire genetic elements encoding for virulence factors, they remain benign commensals.[14]

Role in Disease

Virulent strains of E. coli can cause gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for peritonitis, mastitis, septicemia and Gram-negative pneumonia.[13] Recently it is thought that E. coli and certain other foodborne illnesses can sometimes trigger serious health problems months or years after patients survived that initial bout. Food poisoning can be a long-term problem.

Virulence properties

Enteric E. coli (EC) are classified on the basis of serological characteristics and virulence properties.[13]

Virotypes include:

  • Enterotoxigenic E. coli (ETEC) – It is the causative agent of diarrhea (without fever) in humans, pigs, sheep, goats, cattle, dogs, and horses. ETEC uses fimbrial adhesins (projections from the bacterial cell surface) to bind enterocytes in the small intestine. ETEC can produce two proteinaceous enterotoxins: the larger of the two proteins, LT enterotoxin, is similar to cholera toxin in structure and function, while the smaller protein, ST enterotoxin causes cGMP accumulation in the target cells and a subsequent secretion of fluid and electrolytes into the intestinal lumen. ETEC strains are non-invasive, and they do not leave the intestinal lumen.
  • Enteropathogenic E. coli (EPEC) – It is the causative agent of diarrhea in humans, rabbits, dogs, cats and horses. Like ETEC, EPEC also causes diarrhea, but the molecular mechanism of colonization and etiology are different. EPEC lack fimbriae, ST and LT toxins, but they utilize an adhesin known as intimin to bind host intestinal cells. This virotype has an array of virulence factors that are similar to those found in Shigella, and may posses a shiga toxin. Adherence to the intestinal mucosa causes a rearrangement of actin in the host cell, causing significant deformation. EPEC cells are moderately-invasive (i.e. they enter host cells) and elicit an inflammatory response. Changes in intestinal cell ultrastructure due to "attachment and effacement" is likely the prime cause of diarrhea in those afflicted with EPEC.
  • Enteroinvasive E. coli (EIEC) – It is found only in humans. EIEC infection causes a syndrome that is identical to Shigellosis, with profuse diarrhea and high fever. EIEC are highly invasive, and they utilize adhesin proteins to bind to and enter intestinal cells. They produce no toxins, but can cause severe damage to the intestinal wall through mechanical cell destruction.
  • Enterohemorrhagic E. coli (EHEC) – It is found in humans, cattle, and goats. The sole member of this virotype is strain O157:H7, which causes bloody diarrhea and no fever. EHEC can cause hemolytic uremic syndrome and sudden kidney failure. It uses bacterial fimbriae for attachment and is moderately invasive. It possesses a phage-encoded Shiga toxin that can elicit an intense inflammatory response.
  • Enteroaggregative E. coli (EAggEC) – It is found only in humans. This strain is named "aggregative" because their fimbriae aggregate tissue culture cells. EAggEC binds to the intestinal mucosa while being non-invasive and causes watery diarrhea without fever. It produces a hemolysin and an ST enterotoxin similar to that of ETEC.

Gastrointestinal infection

Low-temperature electron micrograph of a cluster of E. coli bacteria, magnified 10,000 times. Each individual bacterium is oblong shaped.

Certain strains of E. coli, such as O157:H7, O121 and O104:H21, produce toxins. Food poisoning caused by E. coli are usually associated with eating unwashed vegetables and meat contaminated post-slaughter. O157:H7 is further notorious for causing serious and even life-threatening complications such as Hemolytic Uremic Syndrome (HUS). This particular strain is linked to the 2006 United States E. coli outbreak of fresh spinach and the most recent multistate outbreak linked to romaine lettuce from the Central Coastal growing regions in northern and central California. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly, or the immunocompromised, but is more often mild. E. coli can harbor both heat-stable and heat-labile enterotoxins. The latter, termed LT, contains one 'A' subunit and five 'B' subunits arranged into one holotoxin, and is highly similar in structure and function to Cholera toxins. The 'B' subunits assist in adherence and entry of the toxin into host intestinal cells, while the 'A' subunit is cleaved and prevents cells from absorbing water, causing diarrhea. LT is secreted by the Type 2 secretion pathway.[15]

If E. coli escapes the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or a surgical error) and enters the abdomen, it usually causes peritonitis that can be fatal without prompt treatment. E. coli is extremely sensitive to antibiotics such as streptomycin or gentamicin and treatment with these antibiotics is usually effective.E. coli can also quickly acquire drug resistance which can be troublesome.[16]

Intestinal mucosa-associated E. coli is observed in increased numbers in patients with inflammatory bowel disease such as Crohn's disease and ulcerative colitis.[17] Invasive strains of E. coli exist in high numbers in the inflamed tissue, and the number of bacteria in the inflammatory foci correlates with the severity of the bowel inflammation.[18]

Epidemiology of gastrointestinal infection

Transmission of pathogenic E. coli often occurs via fecal-oral route. Common sources of contamination include: unhygienic food preparation, farm contamination due to manure fertilization, irrigation of crops with contaminated greywater or raw sewage, feral pigs on cropland, or direct consumption of sewage-contaminated water.[19][14][20][21][22][23][24]

Dairy and beef cattle are the primary reservoirs of E. coli O157:H7. They can carry it while being asymptomatic and shed it in their feces. Food products associated with E. coli outbreaks include raw ground beef, raw seed sprouts or spinach, raw milk, unpasteurized juice, lettuce (as observed in the most recent [October-November 2018] multistate outbreak of Shiga toxin-producing Escherichia coli O157:H7 (E. coli O157:H7) infections linked to romaine lettuce from the Central Coastal growing regions in northern and central California), and foods contaminated by infected food workers via fecal-oral route.[19][21][25][26]

According to the U.S. Food and Drug Administration, the fecal-oral cycle of transmission can be disrupted by cooking food properly, preventing cross-contamination, instituting barriers such as gloves for food workers, pasteurization of juice or dairy, proper hand washing requirements, and instituting health care policies requiring food industry employees to seek medical care when they are ill.[19]

Shiga toxin-producing E. coli (STEC), specifically serotype O157:H7, can also be transmitted by flies. Tranmission can also occur via direct contact with farm animals, petting zoo animals, and airborne particles found in animal-rearing environments.[27][28][29][30][31][32][33]

Urinary tract infection

Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. In ascending infections, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder. Women are 14-times more likely to suffer from an ascending UTI as compared to men because of the anatomical difference in the urethral length.[13]

Uropathogenic E. coli utilize P fimbriae (pyelonephritis-associated pili) to bind urinary tract epithelium and colonize the bladder. These adhesins specifically bind D-galactose-D-galactose moieties on the P blood group antigen of erythrocytes and uroepithelial cells. Approximately 1% of the human population lacks this receptor, and its presence or absence dictates an individual's susceptibility to urinary tract infections caused by E. coli. Uropathogenic E. coli produce alpha- and beta-hemolysins, which cause lysis of urinary tract cells.[13]

UPEC can evade the body's innate immune defenses (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). It can also have the ability to form K antigen and capsular polysaccharides that contribute to biofilm formation. Biofilm-producing E. coli is recalcitrant to immune factors and antibiotic therapy and can be responsible for chronic urinary tract infections. K antigen-producing E. coli commonly cause infection of the upper urinary tract.[13][34][35]

Descending infections, though relatively rare, occur when E. coli enters the upper urinary tract (kidneys, bladder or ureters) from the blood stream.

Diagnosis

Enteropathogenic E. coli (EPEC) and Enterotoxigenic E. coli (ETEC) - UTI or GIT infections in infants are caused by EPEC which present as watery diarrhea, meaning that PMN's will not be observed in the stool neither with methylene blue nor Gram stain. Gram negative rods, with no particular arrangement, are seen on Gram stain. On MacConkey agar inoculated with stool, deep red colonies are produced as the organism is lactose positive, and this utilization will cause the medium's pH to drop leading to darkening of the medium. Growth on Levine EMB agar inoculated with stool will show black colonies with greenish-black metallic sheen. This is diagnosic of E. coli. The organism is lysine positive, and grows on TSI slant with a (A/A/g+/H2S-) profile. IMViC is ++-- for E. coli as it is indol positive (red ring) and methyl red positive (bright red), but Voges–Proskauer (VP) negative (no change - colorless) and citrate negative (no change-green color). Serology is done using the SSS-Coagglutination test.

Enterohaemorrhagic E. coli O157:H7 - It is isolated either from urine or, more commonly, stool. There exist three protocols for diagnosis:

  1. Diagnosis is made in the manner similar to the diagnostic protocol of EPEC and ETEC. Sorbitol-MacConkey agar, a modified MacConkey agar which has sorbitol instead of lactose, is used and the EHEC produce colorless colonie due to is inability to utilize sorbitol. TSI slant and IMViC are then performed. Serology detects O157:H7 antigens.
  2. Gram stain demonstrating gram negative rods with no particular arrangement.
  3. Two bottles of verocells are used. One is inoculated with equal portions of stool extract and antitoxin, while the other containing only stool extract. If the first bottle shows neutralization (no cytopathic effects) while the second doesn't; the test is considered positive. This is based on the fact that the toxin produced by this strain is neutralized in the presence of its specific antibody, meaning that it will not be able to exert its effects on cells.

Antibiotic Therapy and Resistance

Bacterial infections are usually treated with antibiotics. However, the antibiotic sensitivities of different strains of E. coli vary widely. As a Gram-negative organism, E. coli is resistant to many antibiotics that are effective against Gram-positive organisms. Antibiotics which may be used to treat E. coli infection include amoxicillin as well as other semi-synthetic penicillins, many cephalosporins, carbapenems, aztreonam, trimethoprim-sulfamethoxazole, ciprofloxacin, nitrofurantoin, and aminoglycosides.

Antibiotic resistance is a growing problem. A part of it is due to the overuse of antibiotics in humans, but the use of antibiotics as growth promoters in the food of animals is also a contributing factor. A study published in the journal Science in August 2007 found that the rate of adaptative mutations in E. coli is on the order of 10–5 per genome per generation, which is 1,000 times as high as previous estimates. This finding is very significant for the study and management of bacterial antibiotic resistance.[36][37]

Antibiotic-resistant E. coli may also pass on the genes responsible for antibiotic resistance to other species of bacteria, such as Staphylococcus aureus. E. coli often carry multidrug resistant plasmids and when under stress, it can readily transfer those plasmids to other species. E. coli is a frequent member of biofilms, where many species of bacteria exist in close proximity to each other. This mixing of species allows E. coli strains that are piliated to accept and transfer plasmids from and to other bacteria. Thus, E. coli and the other enterobacteria are important reservoirs of transferable antibiotic resistance.[38]

Beta-lactamase strains

Resistance to beta-lactam antibiotics has become a particular problem in the recent decades, as strains of bacteria that produce extended-spectrum beta-lactamases have become more common. The beta-lactamase makes many, if not all, of the penicillins and cephalosporins ineffective as therapeutic measures. Extended-spectrum beta-lactamase–producing E. coli are highly resistant to an array of antibiotics and infections caused by these strains are difficult to treat. In many instances, only two oral antibiotics and a very limited group of intravenous antibiotics remain effective.[39]

Increased concern about the prevalence of this form of "superbug" in the United Kingdom has led to calls for further monitoring and a UK-wide strategy to deal with infections and the deaths. Susceptibility testing should guide treatment in all infections in which the organism can be isolated for culture.[40]

Phage therapy

Phage therapy involves the use of viruses that specifically target pathogenic bacteria. It has been developed over the last 80 years, primarily in the former Soviet Union, where it was used to prevent diarrhea caused by E. coli. Presently, phage therapy for humans is available only at the Phage Therapy Center in the Republic of Georgia and Poland. However, on January 2 2007, the United States Food and Drug Administration (FDA) gave Omnilytics (a biotech company focused on developing solutions for infectious disease and pest control) the approval to apply its E. coli O157:H7 killing phage in a mist, spray, or wash on live cattle bred for harvest.[41][42] [43]

Vaccination

Researchers have actively been working to develop safe, effective vaccines to lower the worldwide incidence of E. coli infection. In March, 2006, a vaccine, eliciting an immune response against the E. coli O157:H7 O-specific polysaccharide conjugated to recombinant exotoxin A of Pseudomonas aeruginosa (O157-rEPA), was reported to be safe in children two to five years old. Previous work had already indicated its safety in adults. A phase III clinical trial to verify the large-scale efficacy of the treatment is planned.[44][45]

In January 2007 the Canadian bio-pharmaceutical company Bioniche announced the development of a cattle vaccine which reduces the number of E. coli O157:H7 shed in manure to about 1000 pathogenic bacteria per gram of manure.[46][47][48]

Role in Biotechnology

File:E coli metabolic network.png

Because of its long history of laboratory culture and ease of manipulation, E. coli also plays an important role in modern biological engineering and industrial microbiology. The work of Stanley Norman Cohen and Herbert Boyer on E. coli, using plasmids and restriction enzymes to create recombinant DNA, has become a foundation.[49] [50]

E. coli is considered a very versatile host for the production of heterologous proteins. Researchers can introduce genes into the microbes using plasmids, allowing for the mass production of proteins used in the industrial fermentation processes. Genetic systems have also been developed which allow the production of recombinant proteins using E. coli. One of the first useful applications of recombinant DNA technology was the manipulation of E. coli to produce human insulin. Modified E. coli have been used in vaccine development, bioremediation, and production of immobilised enzymes. E. coli cannot, however, be used to produce some of the more large, complex proteins which contain multiple disulfide bonds and, in particular, unpaired thiols, or proteins that also require post-translational modification for activity.[49][51][52]

Model organism

E. coli is frequently used as a model organism in microbiology studies. Cultivated strains (e.g. E. coli K12) are well-adapted to the laboratory environment, and, unlike wild type strains, have lost their ability to thrive in the intestine. Many lab strains lose their ability to form biofilms.[53][54] These features protect wild type strains from antibodies and other chemical attacks, but require a large expenditure of energy and material resources.

In 1946, Joshua Lederberg and Edward Tatum first described the phenomenon known as bacterial conjugation using E. coli as a model bacterium,[55] and it remains the primary model to study conjugation. E. coli was an integral part of the first experiments to understand phage genetics,[56] and early researchers, such as Seymour Benzer, used E. coli and phage T4 to understand the topography of gene structure.[57] Prior to Benzer's research, it was not known whether the gene was a linear structure, or if it had a branching pattern.

See also

References

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