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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 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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| The pathogenesis of infectious colitis will depend on the causative organism as follows: | | The [[pathogenesis]], [[Gross examination|gross]] and [[Microscopy|microscopic pathology]] of infectious colitis will depend on the causative organism as follows: |
| *[[Shigellosis#Pathophysiology|''Shigella spp.'']] | | *[[Shigellosis pathophysiology|''Shigella spp.'']] |
| *[[Campylobacteriosis#Pathophysiology|''Campylobacter jejuni'']] | | *[[Campylobacteriosis pathophysiology|''Campylobacter jejuni'']] |
| *[[Clostridium difficile#Pathophysiology|''Clostridium difficile'']] | | *[[Clostridium difficile infection pathophysiology|''Clostridium difficile'']] |
| *[[Escherichia coli enteritis#Pathophysiology|''Escherichia coli'']] | | *[[Escherichia coli enteritis pathophysiology|''Escherichia coli'']] |
| *[[Salmonellosis#Pathophysiology|Nontyphoidal ''Salmonella'']] | | *[[Salmonellosis pathophysiology|Nontyphoidal ''Salmonella'']] |
| *[[Amoebiasis#Pathophysiology|''Entameoba histolytica'']] | | *[[Amoebiasis pathophysiology|''Entameoba histolytica'']] |
| *[[Lymphogranuloma venereum#Pathophysiology|''Chlamydia trachomatis'']] | | *[[Lymphogranuloma venereum pathophysiology|''Chlamydia trachomatis'']] |
| *[[Cytomegalovirus infection#Pathophysiology|''Cytomegalovirus'']] | | *[[Cytomegalovirus infection pathophysiology|''Cytomegalovirus'']] |
| *[[Yersinia enterocolitica infection#Pathophysiology|''Yersinia enterocolitica'']] | | *[[Yersinia enterocolitica infection pathophysiology|''Yersinia enterocolitica'']] |
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| '''Chlamydia trachomatis'''
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| *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>
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| **''[[Chlamydia trachomatis]]'' [[Serovar|serovars]] L1, L2, or L3 causes Lymphogranuloma venereum (LGV) which manifests as proctocolitis when transmitted through the anal route
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| **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>
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| **The EB form is responsible for inoculation with ''C. trachomatis''.
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| **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>
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| **Once inside the host cell, EBs immediately start differentiating into reticulate bodies (RBs) that undergo replication.
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| **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'''
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| *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>
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| *Infection with CMV requires close, intimate contact with a person excreting the virus in their [[saliva]], [[urine]], [[blood]], [[tears]], and [[semen]].
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| *CMV can be [[Sexually transmitted disease|sexually transmitted]].
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| *Primary infection is usually asymptomatic in immunocompetent individuals.
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| *Latency state develops after the primary infection in immunocompetent individuals with CMV infection persisting in the host tissues by evading the immune system.
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| *Reactivation of the infection occurs in persons with latent CMV when the host's immune system becomes compromised.
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| *CMV usually colonizes inflamed tissues than healthy tissues.
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| *Cytokines such as TNF-α and IFN-γ, are released following local inflammation in the bowel wall.
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| *CMV gets to the mucosa of the colon through the macrophages.
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| *The cytokines reactivate latent CMV infection and promote the migration of CMV-infected macrophages to inflamed colon. This further causes damage to the tissue.
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| '''Pseudomembranous colitis'''
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| **Under normal condition, there is usually a balance in the normal intestinal commensals.
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| **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.
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| **''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>
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| **''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>
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| **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.
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| ===Gross pathology===
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| *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.
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| **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>
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| 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>
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| 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>
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| </gallery>
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| ===Microscopic pathology===
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| *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>
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| **Heaped necrotic tissue
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| **Polymorphonuclear neutrophils in the lamina propria, breeching the epithelium like a "volcanic eruption".
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| **With or without capillary thrombi
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| *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).
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| **Crypt architecture is destroyed.
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| **Abscesses may also be seen in the crypts.
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| <gallery>
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| 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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