Infectious colitis pathophysiology: Difference between revisions
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===Gross pathology=== | ===Gross pathology=== | ||
Gross pathology findings of infectious colitis will depend on the causative organism as follows: | Gross pathology findings of infectious colitis will depend on the causative organism as follows: | ||
*[[Shigellosis#Gross pathology|''Shigella spp.'']] | *[[Shigellosis pathophysiology#Gross pathology|''Shigella spp.'']] | ||
*[[Campylobacteriosis#Gross pathology|''Campylobacter jejuni'']] | *[[Campylobacteriosis pathophysiology#Gross pathology|''Campylobacter jejuni'']] | ||
*[[Clostridium difficile infection#Gross pathology|''Clostridium difficile'']] | *[[Clostridium difficile infection pathophysiology#Gross pathology|''Clostridium difficile'']] | ||
*[[Escherichia coli enteritis#Gross pathology|''Escherichia coli'']] | *[[Escherichia coli enteritis pathophysiology#Gross pathology|''Escherichia coli'']] | ||
*[[Salmonellosis#Gross pathology|Nontyphoidal ''Salmonella'']] | *[[Salmonellosis pathophysiology#Gross pathology|Nontyphoidal ''Salmonella'']] | ||
*[[Amoebiasis#Gross pathology|''Entameoba histolytica'']] | *[[Amoebiasis pathophysiology#Gross pathology|''Entameoba histolytica'']] | ||
*[[Lymphogranuloma venereum#Gross pathology|''Chlamydia trachomatis'']] | *[[Lymphogranuloma venereum pathophysiology#Gross pathology|''Chlamydia trachomatis'']] | ||
*[[Cytomegalovirus infection#Gross pathology|''Cytomegalovirus'']] | *[[Cytomegalovirus infection pathophysiology#Gross pathology|''Cytomegalovirus'']] | ||
*[[Yersinia enterocolitica infection#Gross pathology|''Yersinia enterocolitica'']] | *[[Yersinia enterocolitica infection pathophysiology#Gross pathology|''Yersinia enterocolitica'']] | ||
Revision as of 19:50, 17 October 2016
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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
Gross pathology
Gross pathology findings 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
- 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.
Microscopic pathology
- In pseudomembranous colitis microscopy shows[5]
- 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 [6]
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
- ↑ 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