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| {{CMG}}; {{AE}}{{QS}} | | {{CMG}}; {{AE}}{{QS}} |
| ==Overview== | | ==Overview== |
| | Infectious colitis occurs following invasion of [[Mucous membrane|colonic mucosa]] or attachment to the [[Mucous membrane|colonic mucosa]] by a [[Microorganism|micro-organism]] causing [[inflammation]]. [[Enteric|Enteric pathogens]] that cause [[colitis]] are usually transmitted through [[fecal-oral route]] especially in children. Infectious colitis may also occur following [[antibiotics]] use, especially [[Broad-spectrum antibiotic|broad spectrum antibiotics]]. Infectious colitis may also be acquired as a [[Sexually transmitted infections|sexually transmitted infection]] (STI) among individuals who practice unsafe anal sex especially among men who have sex with men (MSM). |
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| ==Pathophysiology== | | ==Pathophysiology== |
| ===Pathogenesis=== | | ===Pathogenesis=== |
| Infectious colitis occurs following invasion of colonic mucosa or attachment to the colonic mucosa by a micro-organism causing inflammation | | Infectious colitis occurs following invasion of [[Mucous membrane|colonic mucosa]] or attachment to the [[Mucous membrane|colonic mucosa]] by a [[Microorganism|micro-organism]] causing [[inflammation]] |
| ====Pathogenesis of Infectious colitis==== | | ====Pathogenesis of Infectious colitis==== |
| *Enteric organisms that cause colitis are usually transmitted through fecal-oral route especially in children. As few as 100 bacterial cells can be enough to cause an infection.<ref>{{cite book|last=Levinson|first=Warren E|title=Review of Medical Microbiology and Immunology|year=2006|publisher=McGraw-Hill Medical Publishing Division|isbn=978-0-07-146031-6|edition=9|url=http://books.google.ca/books?id=Q_80CUAd_ikC&printsec=frontcover#v=onepage&q&f=false|accessdate=February 27, 2012|page=30}}</ref> | | *[[Enteric|Enteric organisms]] that cause colitis are usually transmitted through [[fecal-oral route]] especially in children. As few as 100 [[Bacteria|bacterial cells]] can be enough to cause an [[infection]].<ref>{{cite book|last=Levinson|first=Warren E|title=Review of Medical Microbiology and Immunology|year=2006|publisher=McGraw-Hill Medical Publishing Division|isbn=978-0-07-146031-6|edition=9|url=http://books.google.ca/books?id=Q_80CUAd_ikC&printsec=frontcover#v=onepage&q&f=false|accessdate=February 27, 2012|page=30}}</ref> |
| *May also occur following antibiotic use, especially broad spectrum antibiotics. | | *May also occur following [[Antibiotic-associated colitis|antibiotic use]], especially broad spectrum antibiotics. |
| *Can also be acquired as a sexually transmitted infection (STI) among individuals who practice unsafe anal sex especially among men who have sex with men (MSM) | | *Can also be acquired as a [[sexually transmitted infection]] (STI) among individuals who practice unsafe anal sex especially among men who have sex with men (MSM) |
| :*In MSM the pathogens are transmitted directly through overt abrasions or microabrasions in the rectal mucosa or indirectly during oral-anal contact.<ref name="Rompalo">{{Rompalo AM. Chapter 9: Proctitis and Proctocolitis. In Klausner JD, Hook III EW. CURRENT Diagnosis & Treatment of Sexually Transmitted Diseases. McGraw Hill Professional; 2007 }} </ref> | | :*In MSM the pathogens are transmitted directly through overt or microabrasions in the rectal mucosa or indirectly during oral-anal contact.<ref name="Rompalo">{{Rompalo AM. Chapter 9: Proctitis and Proctocolitis. In Klausner JD, Hook III EW. CURRENT Diagnosis & Treatment of Sexually Transmitted Diseases. McGraw Hill Professional; 2007 }} </ref> |
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| '''Shigella specie'''
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| *A small inoculum of ''Shigella'' (10 to 200 organisms) can cause shigellosis.<ref name="pmid2656880">{{cite journal| author=DuPont HL, Levine MM, Hornick RB, Formal SB| title=Inoculum size in shigellosis and implications for expected mode of transmission. | journal=J Infect Dis | year= 1989 | volume= 159 | issue= 6 | pages= 1126-8 | pmid=2656880 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2656880 }} </ref>
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| *''Shigella'' is transmitted most commonly through the fecal-oral route from contaminated food (e.g. vegetables or meat) or water in places with poor sanitation.<ref name="pmid2656880">{{cite journal| author=DuPont HL, Levine MM, Hornick RB, Formal SB| title=Inoculum size in shigellosis and implications for expected mode of transmission. | journal=J Infect Dis | year= 1989 | volume= 159 | issue= 6 | pages= 1126-8 | pmid=2656880 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2656880 }} </ref><ref name="pmid18202440">{{cite journal| author=Schroeder GN, Hilbi H| title=Molecular pathogenesis of Shigella spp.: controlling host cell signaling, invasion, and death by type III secretion. | journal=Clin Microbiol Rev | year= 2008 | volume= 21 | issue= 1 | pages= 134-56 | pmid=18202440 | doi=10.1128/CMR.00032-07 | pmc=PMC2223840 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18202440 }} </ref>
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| *[[Foodborne]] or [[waterborne]] epidemics may occur.<ref name="pmid2656880">{{cite journal| author=DuPont HL, Levine MM, Hornick RB, Formal SB| title=Inoculum size in shigellosis and implications for expected mode of transmission. | journal=J Infect Dis | year= 1989 | volume= 159 | issue= 6 | pages= 1126-8 | pmid=2656880 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2656880 }} </ref>
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| *Shigella can also be transmitted by flies and sexual contact.<ref name="pmid18202440">{{cite journal| author=Schroeder GN, Hilbi H| title=Molecular pathogenesis of Shigella spp.: controlling host cell signaling, invasion, and death by type III secretion. | journal=Clin Microbiol Rev | year= 2008 | volume= 21 | issue= 1 | pages= 134-56 | pmid=18202440 | doi=10.1128/CMR.00032-07 | pmc=PMC2223840 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18202440 }} </ref>
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| *''[[Shigella]]'' is able to survive the acidic environment in the [[stomach]] through acid resistance systems.<ref name="pmid8418063">{{cite journal| author=Gorden J, Small PL| title=Acid resistance in enteric bacteria. | journal=Infect Immun | year= 1993 | volume= 61 | issue= 1 | pages= 364-7 | pmid=8418063 | doi= | pmc=PMC302732 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8418063 }} </ref>
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| *''Shigella'' also downregulates the expression of antibacterial proteins released by the host (human) [[intestinal mucosa]].<ref name="pmid11175848">{{cite journal| author=Islam D, Bandholtz L, Nilsson J, Wigzell H, Christensson B, Agerberth B et al.| title=Downregulation of bactericidal peptides in enteric infections: a novel immune escape mechanism with bacterial DNA as a potential regulator. | journal=Nat Med | year= 2001 | volume= 7 | issue= 2 | pages= 180-5 | pmid=11175848 | doi=10.1038/84627 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11175848 }} </ref>
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| *Following transmission, ''[[Shigella]]'' first invades the epithelial cells of the large intestine from the basolateral side by using [[M cell]]s as entry ports for transcytosis.<ref name="pmid2645214">{{cite journal| author=Wassef JS, Keren DF, Mailloux JL| title=Role of M cells in initial antigen uptake and in ulcer formation in the rabbit intestinal loop model of shigellosis. | journal=Infect Immun | year= 1989 | volume= 57 | issue= 3 | pages= 858-63 | pmid=2645214 | doi= | pmc=PMC313189 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2645214 }} </ref> M cells are specialized cells that sample the gut lumen for pathogenic antigens and delivers these antigens to mucosal [[lymphoid tissue]] to activate an adequate [[immune response]].<ref name="pmid15312131">{{cite journal| author=Man AL, Prieto-Garcia ME, Nicoletti C| title=Improving M cell mediated transport across mucosal barriers: do certain bacteria hold the keys? | journal=Immunology | year= 2004 | volume= 113 | issue= 1 | pages= 15-22 | pmid=15312131 | doi=10.1111/j.1365-2567.2004.01964.x | pmc=PMC1782554 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15312131 }} </ref>
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| *''[[Shigella]]'' then invades macrophages and induces cellular apoptosis, intestinal inflammation, generation of [[proinflammatory cytokine]]s (IL-1-beta and IL-18), and subsequent activation of the [[innate immune system]]. Subsequently ''shigella'' is released from the macrophages and continues the invasion of the intestinal epithelium from the basolateral side. The bacteria further spreads to adjacent epithelial cells and avoids extracellular exposure by using intercellular [[actin polymerization]] processes (rocket propulsion).<ref name="Mounier">{{cite journal | title=Shigella flexneri Enters Human Colonic Caco-2 Epithelial Cells through the Basolateral Pole | author=Mounier, Joëlle | journal=Infection and Immunity |date=January 1992 | volume=60 | issue=1 | pages=237–248 | pmc=257528 | first2=T | last3=Hellio | first3=R | last4=Lesourd | first4=M | last5=Sansonetti | first5=PJ | pmid=1729185| last2=Vasselon }} </ref><ref name="pmid8083373">{{cite journal| author=Zychlinsky A, Fitting C, Cavaillon JM, Sansonetti PJ| title=Interleukin 1 is released by murine macrophages during apoptosis induced by Shigella flexneri. | journal=J Clin Invest | year= 1994 | volume= 94 | issue= 3 | pages= 1328-32 | pmid=8083373 | doi=10.1172/JCI117452 | pmc=PMC295219 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8083373 }} </ref><ref name="pmid10843390">{{cite journal| author=Sansonetti PJ, Phalipon A, Arondel J, Thirumalai K, Banerjee S, Akira S et al.| title=Caspase-1 activation of IL-1beta and IL-18 are essential for Shigella flexneri-induced inflammation. | journal=Immunity | year= 2000 | volume= 12 | issue= 5 | pages= 581-90 | pmid=10843390 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10843390 }} </ref>
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| *As ''Shigella'' infiltrates the epithelial cells, activation of nuclear factor kappa-B (NF-KB) by ''Shigella'' generates [[IL-8]], mediates the recruitment of polymorphonuclear neutrophils (PMN) to the site. The PMN damage the intestinal epithelial barrier and allow more ''Shigella'' organisms to easily invade the intestinal epithelium. The damage to the intestinal epithelial cells results in impaired adsorption of nutrients and fluids and leads to clinical manifestations of shigellosis (diarrhea).<ref name="pmid12791997">{{cite journal| author=Girardin SE, Boneca IG, Carneiro LA, Antignac A, Jéhanno M, Viala J et al.| title=Nod1 detects a unique muropeptide from gram-negative bacterial peptidoglycan. | journal=Science | year= 2003 | volume= 300 | issue= 5625 | pages= 1584-7 | pmid=12791997 | doi=10.1126/science.1084677 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12791997 }} </ref><ref name="pmid9176079">{{cite journal| author=Fasano A, Noriega FR, Liao FM, Wang W, Levine MM| title=Effect of shigella enterotoxin 1 (ShET1) on rabbit intestine in vitro and in vivo. | journal=Gut | year= 1997 | volume= 40 | issue= 4 | pages= 505-11 | pmid=9176079 | doi= | pmc=PMC1027126 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9176079 }} </ref>
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| *''Shigella'' produces toxins including enterotoxin 1 (ShET1), enterotoxin 2 (ShET2) and ''Shigella dysenteriae'' serotype 1 toxin, during the inflammatory process. These toxins and are thought to account, at least in part, for fluid secretion that results in shigellosis-associated and development of vascular lesions at the level of the colon, the kidneys, and the central nervous system.<ref name="pmid9176079">{{cite journal| author=Fasano A, Noriega FR, Liao FM, Wang W, Levine MM| title=Effect of shigella enterotoxin 1 (ShET1) on rabbit intestine in vitro and in vivo. | journal=Gut | year= 1997 | volume= 40 | issue= 4 | pages= 505-11 | pmid=9176079 | doi= | pmc=PMC1027126 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9176079 }} </ref><ref name="pmid14638419">{{cite journal| author=Cherla RP, Lee SY, Tesh VL| title=Shiga toxins and apoptosis. | journal=FEMS Microbiol Lett | year= 2003 | volume= 228 | issue= 2 | pages= 159-66 | pmid=14638419 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14638419 }} </ref>
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| *Ultimately, more PMNs are recruited and ''Shigella'' organisms are killed.
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| '''Escherichia coli'''
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| *Pathogenic ''E. coli'' are characterized by the presence of either O (lipopolysaccaride ) antigen alone or combination of O and H (flagellar) antigens.<ref name=book>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260 }} </ref>
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| *Only enteroinvasive ''E. coli'' (EIEC) has true replication within the host cell, whereas all other types of ''E. coli'' replicate outside the host cell. Pathogenic ''E. coli'' strains contain adhesin that may form distinct fimbriae (pili) or fibrilla. <ref name=book>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref>
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| *Transmission of pathogenic ''E. coli'' strains is usually by the fecal-oral route via contaminated food and water; direct contact with animals; or occasionally direct contact with feces of infected people including sexual contact from anal sex.<ref name=book>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref>
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| :*[[''Enterohemorrhagic E. coli'' (EHEC)]]
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| *The primary site of action of EHEC is the colon.
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| *EHEC attaches to the colonocyte and causes hemorrhagic colitis by inducing the elaboration of the Shiga toxin (Stx) and secretion of enterohemolysin.
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| *The ''Shiga'' toxin is systemically absorbed and results in inflammatory reactions and systemic complications, including hemolytic uremic syndrome.
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| *EHEC are not considered highly invasive as EIEC or ''Shigella'' because the organism invades the cell but does not multiply within the cell.<ref name=book>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260 }} </ref>
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| :*[[''Enteroinvasive E. coli'' (EIEC)]]
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| *The primary site of action of EIEC is the colon.
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| *EIEC is invasive and multiplies within the host colonocytes.
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| *EIEC contains nonfimbrial adhesins. It lyses phagosomes and migrates through the host cell and within cells (either lateral direct cell-to-cell spread or exit then re-enter) via the action of nucleating actin microfilaments.<ref name=book>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260 }} </ref>
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| :*[[''Enteroaggregative E. coli'' (EAEC)]]
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| *The primary site of action of EAEC is the small intestine and the colon.
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| *EAEC is characteristically aggressive and adheres to enterocytes and colonocytes in a thick biofilm.
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| *EAEC elaborates cytotoxins, such as hemolysin, and enterotoxins, such as ShET1, Pic, EAST1, Pet toxins.<ref name=book>{{cite book |last=Evans |first= DJ |last=Evans |first=DG|date=1996 |title= Escherichia Coli in Diarrheal Disease. In: Baron S, editor. Medical Microbiology, 4th Ed. |publisher=Galveston (TX): University of Texas Medical}}</ref><ref name="pmid15040260">{{cite journal| author=Kaper JB, Nataro JP, Mobley HL| title=Pathogenic Escherichia coli. | journal=Nat Rev Microbiol | year= 2004 | volume= 2 | issue= 2 | pages= 123-40 | pmid=15040260 | doi=10.1038/nrmicro818 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15040260 }} </ref>
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| '''Salmonella specie'''
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| *[[Salmonella|Nontyphoidal ''Salmonella'']] (NTS) serovars (serovar Typhimurium) induce a greater inflammatory interaction within the human gut mucosa and causing colitis when compared to typhoidal serovars<ref name="pmid17146467">{{cite journal| author=Coburn B, Grassl GA, Finlay BB| title=Salmonella, the host and disease: a brief review. | journal=Immunol Cell Biol | year= 2007 | volume= 85 | issue= 2 | pages= 112-8 | pmid=17146467 | doi=10.1038/sj.icb.7100007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17146467 }} </ref>
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| *Salmonellosis in humans is usually contracted through the consumption of contaminated food of animal origin. Other foods, including green vegetables contaminated by manure and water have also been implicated in its transmission. Person-to-person transmission through the fecal-oral route can also occur. Human cases also occur where individuals have contact with infected animals, including pets.<ref name=WHO>{{cite web | title = Salmonella(non-typhoidal) | url = http://www.who.int/mediacentre/factsheets/fs139/en/ }}</ref>
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| *Human disease usually occurs after ingesting more than 50 000 bacteria.<ref name="pmid17146467">{{cite journal| author=Coburn B, Grassl GA, Finlay BB| title=Salmonella, the host and disease: a brief review. | journal=Immunol Cell Biol | year= 2007 | volume= 85 | issue= 2 | pages= 112-8 | pmid=17146467 | doi=10.1038/sj.icb.7100007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17146467 }} </ref>
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| *[[Non-typhoidal Salmonella]] ([[NTS]]) usually cause self-limiting [[diarrhea]]. Typhoidal serovars do not usually cause acute diarrhea or induce a large neutrophil recruitment into the intestinal lumen.<ref name="pmid23055923">{{cite journal| author=de Jong HK, Parry CM, van der Poll T, Wiersinga WJ| title=Host-pathogen interaction in invasive Salmonellosis. | journal=PLoS Pathog | year= 2012 | volume= 8 | issue= 10 | pages= e1002933 | pmid=23055923 | doi=10.1371/journal.ppat.1002933 | pmc=PMC3464234 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23055923 }} </ref>
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| *S. enterica serovars cause intestinal disease by attracting PMNs, specifically by inducing interleukin-8<ref name="pmid23055923">{{cite journal| author=de Jong HK, Parry CM, van der Poll T, Wiersinga WJ| title=Host-pathogen interaction in invasive Salmonellosis. | journal=PLoS Pathog | year= 2012 | volume= 8 | issue= 10 | pages= e1002933 | pmid=23055923 | doi=10.1371/journal.ppat.1002933 | pmc=PMC3464234 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23055923 }} </ref><ref name="pmid17146467">{{cite journal| author=Coburn B, Grassl GA, Finlay BB| title=Salmonella, the host and disease: a brief review. | journal=Immunol Cell Biol | year= 2007 | volume= 85 | issue= 2 | pages= 112-8 | pmid=17146467 | doi=10.1038/sj.icb.7100007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17146467 }} </ref>
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| :*This recruitment occurs within the first few hours of infection serovar ''Typhimurium''. Massive migration of neutrophils and exudate secretion into the intestinal lumen typically occurs approximately 8-10 hours after infection.<ref name="pmid23055923">{{cite journal| author=de Jong HK, Parry CM, van der Poll T, Wiersinga WJ| title=Host-pathogen interaction in invasive Salmonellosis. | journal=PLoS Pathog | year= 2012 | volume= 8 | issue= 10 | pages= e1002933 | pmid=23055923 | doi=10.1371/journal.ppat.1002933 | pmc=PMC3464234 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23055923 }} </ref><ref name="pmid17146467">{{cite journal| author=Coburn B, Grassl GA, Finlay BB| title=Salmonella, the host and disease: a brief review. | journal=Immunol Cell Biol | year= 2007 | volume= 85 | issue= 2 | pages= 112-8 | pmid=17146467 | doi=10.1038/sj.icb.7100007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17146467 }} </ref>
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| '''Campylobacter'''
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| *Regarding ''[[Campylobacter jejuni]]'' colitis the exact pathogenesis by which it causes colitis after transmission is not fully understood.
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| **However, it is hypothesized that requirement for C. jejuni virulence include (1) motility, (2) drug resistance, (3) host cell adherence, (4) host cell invasion, (5) alteration of the host cell signaling pathways, (6) induction of host cell death, (7) evasion of the host immune system defenses, and (9) acquisition of iron which serves as a micronutrient for growth and works as a catalyst for hydroxyl radical formation.<ref name="pmid4522793">{{cite journal| author=Capra JD, Kehoe JM| title=Variable region sequences of five human immunoglobulin heavy chains of the VH3 subgroup: definitive identification of four heavy chain hypervariable regions. | journal=Proc Natl Acad Sci U S A | year= 1974 | volume= 71 | issue= 3 | pages= 845-8 | pmid=4522793 | doi= | pmc=388111 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4522793 }} </ref>
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| **''C. jejuni'' also secretes proteins that may contribute to the ability of the bacterium to invade the host epithelial cells.<ref name="pmid4522793">{{cite journal| author=Capra JD, Kehoe JM| title=Variable region sequences of five human immunoglobulin heavy chains of the VH3 subgroup: definitive identification of four heavy chain hypervariable regions. | journal=Proc Natl Acad Sci U S A | year= 1974 | volume= 71 | issue= 3 | pages= 845-8 | pmid=4522793 | doi= | pmc=388111 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4522793 }} </ref>
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| '''Entameoba histolytica'''
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| *''Entameoba histolytica'' cyst is usually transmitted by the fecal-oral route through contaminated drinking water or food. ''E. histolytica'' cyst may also be transmitted through direct contact with infected individuals via anorectal route.<ref name="pmid10756002">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002 }} </ref>
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| *Following transmission of ''[[Entameoba histolytica]]'' cyst, it undergo excystation in the small intestine to become a trophozoite, after which it migrates to the large intestine using pseudopods.<ref name="pmid10756002">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002 }} </ref>
| |
| **In the large intestine, the trophozoites invades the intestinal mucosa. Simultaneously, they form resistant cysts in the large intestines that are then excreted in human stools.<ref name="pmid10756002">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002 }} </ref>
| |
| **''E. histolytica'' contains glycosidases that cleave glycosylated mucin molecules, resulting in mucin degradation.<ref name="pmid2456386">{{cite journal| author=Müller FW, Franz A, Werries E| title=Secretory hydrolases of Entamoeba histolytica. | journal=J Protozool | year= 1988 | volume= 35 | issue= 2 | pages= 291-5 | pmid=2456386 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2456386 }} </ref><ref name="pmid9561780">{{cite journal| author=Spice WM, Ackers JP| title=The effects of Entamoeba histolytica lysates on human colonic mucins. | journal=J Eukaryot Microbiol | year= 1998 | volume= 45 | issue= 2 | pages= 24S-27S | pmid=9561780 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9561780 }} </ref>
| |
| **Following degradation of the mucin layer, ''E. histolytica'' adheres to the enterocyte plasma membrane and uses lectins, amebapores, and proteases to cause damage by a characteristic "hit and run" phenomenon.<ref name="pmid10756002">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002 }} </ref>
| |
| **The trophozoites creates interglandular lesions and degrades the extracellular matrix. It is then propelled forward by locomotion.<ref name="pmid10756002">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002 }} </ref><ref name="pmid2897372">{{cite journal| author=Talamás-Rohana P, Meza I| title=Interaction between pathogenic amebas and fibronectin: substrate degradation and changes in cytoskeleton organization. | journal=J Cell Biol | year= 1988 | volume= 106 | issue= 5 | pages= 1787-94 | pmid=2897372 | doi= | pmc=PMC2115038 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2897372 }} </ref><ref name="pmid7957761">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Entamoeba histolytica: mechanism of surface receptor capping. | journal=Exp Parasitol | year= 1994 | volume= 79 | issue= 3 | pages= 424-35 | pmid=7957761 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7957761 }} </ref>
| |
| **The host immune cells are activated as the trophozoites invade resulting in upregulation of IL-8 and TNF-alpha secretion.<ref name="pmid7657801">{{cite journal| author=Eckmann L, Reed SL, Smith JR, Kagnoff MF| title=Entamoeba histolytica trophozoites induce an inflammatory cytokine response by cultured human cells through the paracrine action of cytolytically released interleukin-1 alpha. | journal=J Clin Invest | year= 1995 | volume= 96 | issue= 3 | pages= 1269-79 | pmid=7657801 | doi=10.1172/JCI118161 | pmc=PMC185748 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7657801 }} </ref><ref name="pmid9136832">{{cite journal| author=Yu Y, Chadee K| title=Entamoeba histolytica stimulates interleukin 8 from human colonic epithelial cells without parasite-enterocyte contact. | journal=Gastroenterology | year= 1997 | volume= 112 | issue= 5 | pages= 1536-47 | pmid=9136832 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9136832 }} </ref>
| |
| **Neutrophils migrate to the site of invasion and contribute to the inflammatory damage induced by ''E. histolytica'', but are generally incapable of destroying the organism. The mechanism by which ''E. histolytica'' evades neutrophils is unknown.<ref name="pmid7657801">{{cite journal| author=Eckmann L, Reed SL, Smith JR, Kagnoff MF| title=Entamoeba histolytica trophozoites induce an inflammatory cytokine response by cultured human cells through the paracrine action of cytolytically released interleukin-1 alpha. | journal=J Clin Invest | year= 1995 | volume= 96 | issue= 3 | pages= 1269-79 | pmid=7657801 | doi=10.1172/JCI118161 | pmc=PMC185748 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7657801 }} </ref><ref name="pmid9136832">{{cite journal| author=Yu Y, Chadee K| title=Entamoeba histolytica stimulates interleukin 8 from human colonic epithelial cells without parasite-enterocyte contact. | journal=Gastroenterology | year= 1997 | volume= 112 | issue= 5 | pages= 1536-47 | pmid=9136832 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9136832 }} </ref><ref name="pmid10756002">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002 }} </ref>
| |
| **In addition to neutrophils, macrophages and eosinophils are also activated.<ref name="pmid10756002">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002 }} </ref>
| |
| | |
| '''Chlamydia trachomatis'''
| |
| *Chlamydiae'' are [[obligate]] intracellular bacterial pathogens, which means they survive only in a host cell.<ref>Beatty, Wandy L., Richard P. Morrison, and Gerald I. Byrne. "Persistent chlamydiae: from cell culture to a paradigm for chlamydial pathogenesis." Microbiological reviews 58.4 (1994): 686-699.</ref><ref>Baron, Samuel. Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston, 1996. Print.</ref>
| |
| **''[[Chlamydia trachomatis]]'' [[Serovar|serovars]] L1, L2, or L3 causes Lymphogranuloma venereum (LGV) which manifests as proctocolitis when transmitted through the anal route
| |
| **Inoculation and replication of ''[[Chlamydia trachomatis]]'' [[Serovar|serovars]] L1, L2, or L3 depends on alternation between two forms of the bacterium: the infectious elementary body (EB) and noninfectious, replicating reticulate body (RB).<ref name="pmid11159992">{{cite journal| author=Taraktchoglou M, Pacey AA, Turnbull JE, Eley A| title=Infectivity of Chlamydia trachomatis serovar LGV but not E is dependent on host cell heparan sulfate. | journal=Infect Immun | year= 2001 | volume= 69 | issue= 2 | pages= 968-76 | pmid=11159992 | doi=10.1128/IAI.69.2.968-976.2001 | pmc=PMC97976 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11159992 }} </ref>
| |
| **The EB form is responsible for inoculation with ''C. trachomatis''.
| |
| **The ''C. trachomatis'' EB enters the body during sexual intercourse or by crossing [[epithelial cells]] of [[mucous membranes]].<ref name="pmid12081191">{{cite journal| author=Mabey D, Peeling RW| title=Lymphogranuloma venereum. | journal=Sex Transm Infect | year= 2002 | volume= 78 | issue= 2 | pages= 90-2 | pmid=12081191 | doi= | pmc=PMC1744436 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12081191 }} </ref>
| |
| **Once inside the host cell, EBs immediately start differentiating into reticulate bodies (RBs) that undergo replication.
| |
| **The process of endocytosis and accumulation of RBs within host epithelial cells causes host cell destruction ([[necrosis]]) which leads to the formation of a [[papule]] at the site of inoculation which may ulcerate, depending on the extent of infection and number or EBs transmitted. After necrosis, EBs and RBs travel via [[lymphatics]] to regional [[lymph nodes]], primarily to [[inguinal lymph nodes]].Systemic infection occurs when this process repeats as ''C. trachomatis'' is phagocytized by and continues to replicate in [[monocytes]], causing [[lymphadenopathy]] and eventually the formation of inguinal [[buboes]]<ref name="pmidPMID 2030670">{{cite journal| author=Moulder JW| title=Interaction of chlamydiae and host cells in vitro. | journal=Microbiol Rev | year= 1991 | volume= 55 | issue= 1 | pages= 143-90 | pmid=PMID 2030670 | doi= | pmc=372804 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2030670 }} </ref><ref name="pmid25870512">{{cite journal| author=Ceovic R, Gulin SJ| title=Lymphogranuloma venereum: diagnostic and treatment challenges. | journal=Infect Drug Resist | year= 2015 | volume= 8 | issue= | pages= 39-47 | pmid=25870512 | doi=10.2147/IDR.S57540 | pmc=PMC4381887 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25870512 }} </ref>
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|
| |
|
| '''Cytomegalovirus'''
| | The [[pathogenesis]], [[Gross examination|gross]] and [[Microscopy|microscopic pathology]] of infectious colitis will depend on the causative organism as follows: |
| *Transmission of cytomegalovirus (CMV) occurs from person to person.[[Seroprevalence]] is age-dependent: 58.9% of individuals aged 6 years and over are infected with CMV while 90.8% of individuals aged 80 years and over are positive for CMV.<ref>{{cite journal | author=Staras SAS, Dollard SC, Radford KW, ''et al.'' | title=Seroprevalence of cytomegalovirus infection in the United States, 1988–1994 | year=2006 | journal=Clin Infect Dis | volume=43 | pages=1143–51 | pmid = 17029132}}</ref><ref name="pmid25097085">{{cite journal| author=Goodman AL, Murray CD, Watkins J, Griffiths PD, Webster DP| title=CMV in the gut: a critical review of CMV detection in the immunocompetent host with colitis. | journal=Eur J Clin Microbiol Infect Dis | year= 2015 | volume= 34 | issue= 1 | pages= 13-8 | pmid=25097085 | doi=10.1007/s10096-014-2212-x | pmc=4281362 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25097085 }} </ref><ref name="pmid18371229">{{cite journal| author=Rafailidis PI, Mourtzoukou EG, Varbobitis IC, Falagas ME| title=Severe cytomegalovirus infection in apparently immunocompetent patients: a systematic review. | journal=Virol J | year= 2008 | volume= 5 | issue= | pages= 47 | pmid=18371229 | doi=10.1186/1743-422X-5-47 | pmc=2289809 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18371229 }} </ref><ref name="pmid27460032">{{cite journal| author=Khan TV, Toms C| title=Cytomegalovirus Colitis and Subsequent New Diagnosis of Inflammatory Bowel Disease in an Immunocompetent Host: A Case Study and Literature Review. | journal=Am J Case Rep | year= 2016 | volume= 17 | issue= | pages= 538-43 | pmid=27460032 | doi= | pmc=4968430 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27460032 }} </ref><ref name="pmid18194509">{{cite journal| author=Einbinder Y, Wolf DG, Pappo O, Migdal A, Tsvang E, Ackerman Z| title=The clinical spectrum of cytomegalovirus colitis in adults. | journal=Aliment Pharmacol Ther | year= 2008 | volume= 27 | issue= 7 | pages= 578-87 | pmid=18194509 | doi=10.1111/j.1365-2036.2008.03595.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18194509 }} </ref>
| | *[[Shigellosis pathophysiology|''Shigella spp.'']] |
| *Infection with CMV requires close, intimate contact with a person excreting the virus in their [[saliva]], [[urine]], [[blood]], [[tears]], and [[semen]].
| | *[[Campylobacteriosis pathophysiology|''Campylobacter jejuni'']] |
| *CMV can be [[Sexually transmitted disease|sexually transmitted]].
| | *[[Clostridium difficile infection pathophysiology|''Clostridium difficile'']] |
| *Primary infection is usually asymptomatic in immunocompetent individuals.
| | *[[Escherichia coli enteritis pathophysiology|''Escherichia coli'']] |
| *Latency state develops after the primary infection in immunocompetent individuals with CMV infection persisting in the host tissues by evading the immune system.
| | *[[Salmonellosis pathophysiology|Nontyphoidal ''Salmonella'']] |
| *Reactivation of the infection occurs in persons with latent CMV when the host's immune system becomes compromised.
| | *[[Amoebiasis pathophysiology|''Entameoba histolytica'']] |
| *CMV usually colonizes inflamed tissues than healthy tissues.
| | *[[Lymphogranuloma venereum pathophysiology|''Chlamydia trachomatis'']] |
| *Cytokines such as TNF-α and IFN-γ, are released following local inflammation in the bowel wall.
| | *[[Cytomegalovirus infection pathophysiology|''Cytomegalovirus'']] |
| *CMV gets to the mucosa of the colon through the macrophages. | | *[[Yersinia enterocolitica infection pathophysiology|''Yersinia enterocolitica'']] |
| *The cytokines reactivate latent CMV infection and promote the migration of CMV-infected macrophages to inflamed colon. This further causes damage to the tissue.
| |
| | |
| '''Pseudomembranous colitis''' | |
| **Under normal condition, there is usually a balance in the normal intestinal commensals.
| |
| **Following broad spectrum systemic antibiotics use, especially penicillin-based antibiotic such as [[amoxicillin]], [[cephalosporin]]s, [[fluoroquinolones]] and macrolides this balance is affected with killing susceptible bacteria and allowing for proliferation of the remaining non-susceptible bacteria. | |
| **''Clostridium difficile'', an obligate [[anaerobic]] gram positive spore forming bacillus tends to proliferate under such conditions and is the usual cause (almost 99 percent of cases) pseudomembranous colitis.<ref name="pmid10095149">{{cite journal| author=Surawicz CM, McFarland LV| title=Pseudomembranous colitis: causes and cures. | journal=Digestion | year= 1999 | volume= 60 | issue= 2 | pages= 91-100 | pmid=10095149 | doi=7633 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10095149 }} </ref>
| |
| **''Clostridium difficile'', produces toxin A (enterotoxin), toxin B (cytotoxin), and binary toxin. These toxins are required for it to colonize the gut, intestinal cell disruption, attract inflammatory cells and cause disease.<ref>{{cite journal | title=The role of toxin A and toxin B in''Clostridium difficile'' infection | author= Sarah A. Kuehne, Stephen T. Cartman, John T. Heap, Michelle L. Kelly, Alan Cockayne & Nigel P. Minton | journal=[[Nature (journal)|Nature]] | year=2010 |doi=10.1038/nature09397 | pmid=20844489 | volume=467 | issue=7316 | pages=711–3}}</ref><ref name="pmid10095149">{{cite journal| author=Surawicz CM, McFarland LV| title=Pseudomembranous colitis: causes and cures. | journal=Digestion | year= 1999 | volume= 60 | issue= 2 | pages= 91-100 | pmid=10095149 | doi=7633 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10095149 }} </ref> | |
| **Other reported causes of pseudomembranous colitis include infections such as ''[[Staphylococcus aureus]]'', ''[[Yersinia specie]]'', ''[[Salmonella specie]]'', ''[[Shigella specie]]'', NSAIDs such as indomethacin, chemotherapeutic drugs like - cisplatin and inflammatory bowel disease. | |
| | |
| ===Gross pathology===
| |
| *Gross pathological findings are often limited to the rectosigmoid region and show evidence of acute or chronic inflammation with or without necrosis, ulcers and hemorrhage. In addition, specific changes based on the cause may be seen.
| |
| **Pseudomembranous colitis. The gross pathologic finding is presence of diffuse, small, 2 to 10mm, raised yellowish (or whitish) lesions. Mucosa in between lesions may appear normal. Lesions may merge giving rise to a characteristic "pseudomembrane" layer over the mucosa.
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| | |
| <gallery>
| |
| Image:Pseudomembranous_colitis.JPG | Pseudomembranous colitis. (WC) <ref name=Pseudomembranous-Proctocolitis> Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/Pseudomembranous_colitis Accessed on August 31, 2016 </ref>
| |
| Image:800px-Pseudomembranous Colitis, Colectomy (Gross) (7410584264).jpg| Pseudomembranous colitis. <ref name=pseudomembranous-colitis> Libre Pathology. Pseudomembranous colitis. https://librepathology.org Accessed on September 1, 2016 </ref>
| |
| </gallery>
| |
| | |
| ===Microscopic pathology===
| |
| *In pseudomembranous colitis microscopy shows<ref name =HistologyPC>Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 837-8. ISBN 0-7216-0187-1}} </ref>
| |
| **Heaped necrotic tissue
| |
| **Polymorphonuclear neutrophils in the lamina propria, breeching the epithelium like a "volcanic eruption".
| |
| **With or without capillary thrombi
| |
| *On microscopy, the characteristic finding in ulcerative colitis is presence of lymphocytes and plasma cells in the deeper aspect of the lamina propria (basal lymphoplasmacytosis).
| |
| **Crypt architecture is destroyed.
| |
| **Abscesses may also be seen in the crypts.
| |
| | |
| <gallery>
| |
| Image:1440px-Colonic pseudomembranes low mag.jpg| Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis <ref name=pc> Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/File:Colonic_pseudomembranes_low_mag.jpg Accessed on September 1, 2016 </ref>
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| </gallery>
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| ==References== | | ==References== |
| {{Reflist|2}} | | {{Reflist|2}} |
| | {{WS}}{{WH}} |
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| | [[Category:Emergency mdicine]] |
| | [[Category:Disease]] |
| | [[Category:Up-To-Date]] |
| [[Category:Infectious disease]] | | [[Category:Infectious disease]] |
| [[Category:Gastroenterology]] | | [[Category:Gastroenterology]] |
| [[Category:Primary care]] | | [[Category:Surgery]] |
| {{WS}}{{WH}}
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