Infectious colitis pathophysiology: Difference between revisions
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]
Overview
Pathophysiology
Pathogenesis
Infectious colitis occurs following invasion of colonic mucosa or attachment to the colonic mucosa by a micro-organism causing inflammation
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.[1]
- May also occur following 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)
- In MSM the pathogens are transmitted directly through overt or microabrasions in the rectal mucosa or indirectly during oral-anal contact.[2]
The pathogenesis of infectious colitis will depend on the causative organism as follows:
- Shigella spp.
- Campylobacter jejuni
- Clostridium difficile
- Escherichia coli
- Nontyphoidal Salmonella
- Entameoba histolytica
- Chlamydia trachomatis
- Cytomegalovirus
- Yersinia enterocolitica
Cytomegalovirus
- 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.[3][4][5][6][7]
- Infection with CMV requires close, intimate contact with a person excreting the virus in their saliva, urine, blood, tears, and semen.
- CMV can be sexually transmitted.
- Primary infection is usually asymptomatic in immunocompetent individuals.
- Latency state develops after the primary infection in immunocompetent individuals with CMV infection persisting in the host tissues by evading the immune system.
- Reactivation of the infection occurs in persons with latent CMV when the host's immune system becomes compromised.
- CMV usually colonizes inflamed tissues than healthy tissues.
- Cytokines such as TNF-α and IFN-γ, are released following local inflammation in the bowel wall.
- CMV gets to the mucosa of the colon through the macrophages.
- 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, cephalosporins, 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.[8]
- 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.[9][8]
- 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.
![Pseudomembranous colitis. (WC) [10]](/index.php/File:Pseudomembranous_colitis.JPG)
![Pseudomembranous colitis. [11]](/index.php/File:800px-Pseudomembranous_Colitis,_Colectomy_(Gross)_(7410584264).jpg)
Microscopic pathology
- In pseudomembranous colitis microscopy shows[12]
- 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.
-
![Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis [13]](/images/0/09/1440px-Colonic_pseudomembranes_low_mag.jpg)
Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis [13]
![Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis [13]](/index.php/File:1440px-Colonic_pseudomembranes_low_mag.jpg)
References
- ↑ Levinson, Warren E (2006). Review of Medical Microbiology and Immunology (9 ed.). McGraw-Hill Medical Publishing Division. p. 30. ISBN 978-0-07-146031-6. Retrieved February 27, 2012.
- ↑ Template:Rompalo AM. Chapter 9: Proctitis and Proctocolitis. In Klausner JD, Hook III EW. CURRENT Diagnosis & Treatment of Sexually Transmitted Diseases. McGraw Hill Professional; 2007
- ↑ Staras SAS, Dollard SC, Radford KW; et al. (2006). "Seroprevalence of cytomegalovirus infection in the United States, 1988–1994". Clin Infect Dis. 43: 1143&ndash, 51. PMID 17029132.
- ↑ Goodman AL, Murray CD, Watkins J, Griffiths PD, Webster DP (2015). "CMV in the gut: a critical review of CMV detection in the immunocompetent host with colitis". Eur J Clin Microbiol Infect Dis. 34 (1): 13–8. doi:10.1007/s10096-014-2212-x. PMC 4281362. PMID 25097085.
- ↑ Rafailidis PI, Mourtzoukou EG, Varbobitis IC, Falagas ME (2008). "Severe cytomegalovirus infection in apparently immunocompetent patients: a systematic review". Virol J. 5: 47. doi:10.1186/1743-422X-5-47. PMC 2289809. PMID 18371229.
- ↑ Khan TV, Toms C (2016). "Cytomegalovirus Colitis and Subsequent New Diagnosis of Inflammatory Bowel Disease in an Immunocompetent Host: A Case Study and Literature Review". Am J Case Rep. 17: 538–43. PMC 4968430. PMID 27460032.
- ↑ Einbinder Y, Wolf DG, Pappo O, Migdal A, Tsvang E, Ackerman Z (2008). "The clinical spectrum of cytomegalovirus colitis in adults". Aliment Pharmacol Ther. 27 (7): 578–87. doi:10.1111/j.1365-2036.2008.03595.x. PMID 18194509.
- ↑ 8.0 8.1 Surawicz CM, McFarland LV (1999). "Pseudomembranous colitis: causes and cures". Digestion. 60 (2): 91–100. doi:7633 Check
|doi=value (help). PMID 10095149. - ↑ Sarah A. Kuehne, Stephen T. Cartman, John T. Heap, Michelle L. Kelly, Alan Cockayne & Nigel P. Minton (2010). "The role of toxin A and toxin B inClostridium difficile infection". Nature. 467 (7316): 711–3. doi:10.1038/nature09397. PMID 20844489.
- ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/Pseudomembranous_colitis Accessed on August 31, 2016
- ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org Accessed on September 1, 2016
- ↑ 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}}
- ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/File:Colonic_pseudomembranes_low_mag.jpg Accessed on September 1, 2016
