Infectious colitis pathophysiology

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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)
  • The pathogens are transmitted directly through overt abrasions or microabrasions in the rectal mucosa or indirectly during oral-anal contact.[2]

Chlamydia trachomatis

  • Chlamydiae are obligate intracellular bacterial pathogens, which means they survive only in a host cell.[3][4]
    • Chlamydia trachomatis 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 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).[5]
    • 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.[6]
    • 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[7][8]

Shigella specie

  • A small inoculum of Shigella (10 to 200 organisms) can cause shigellosis.[9]
  • 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.[9][10]
  • Foodborne or waterborne epidemics may occur.[9]
  • Shigella can also be transmitted by flies and sexual contact.[10]
  • Shigella is able to survive the acidic environment in the stomach through acid resistance systems.[11]
  • Shigella also downregulates the expression of antibacterial proteins released by the host (human) intestinal mucosa.[12]
  • Following transmission, Shigella first invades the epithelial cells of the large intestine from the basolateral side by using M cells as entry ports for transcytosis.[13] 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.[14]
  • Shigella then invades macrophages and induces cellular apoptosis, intestinal inflammation, generation of proinflammatory cytokines (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).[15][16][17]
  • 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).[18][19]
  • 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.

[19][20] Ultimately, more PMNs are recruited and Shigella organisms are killed.

Salmonella specie

  • nontyphoidal Salmonella (NTS) serovars (serovar Typhimurium) induce a greater inflammatory interaction with human gut mucosa causing colitis compared to typhoidal serovars[21]
  • Human disease usually occurs after ingesting more than 50 000 bacteria.[21]
  • 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.[22]
  • 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.[23]
  • Disease among humans usually occurs after ingesting more than 50 000 bacteria.[21]
  • S. enterica serovars cause intestinal disease by attracting PMNs, specifically by inducing interleukin-8[23][21]
  • 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.[23][21]

Campylobacter

  • Regarding Campylobacter jejuni colitis the exact pathogenesis by which it causes colitis after transmission is not fully understood.
    • 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.[24]
    • C. jejuni is known to also secrete proteins that may contribute to the ability of the bacterium to invade the host epithelial cells.[24]

Entameoba histolytica

    • Following transmission of Entameoba histolytica, the trophozoites undergo excystation in the small intestine, after which it migrates to the large intestine using pseudopods.
    • In the large intestine, the trophozoites invades the intestinal mucosa into the bloodstream. Simultaneously, they form resistant cysts in the large intestines that are then excreted in human stools.[25]
    • E. histolytica trophozoites secrete proteases, which induce the release of mucin from goblet cells, resulting in glandular hyperplasia.[25]
    • E. histolytica is also said to contain glycosidases that cleave glycsolyated mucin molecules, resulting in mucin degradation.[26][27]

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.[28]
    • 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.[29][28]
    • 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.
    • Food protein-induced proctocolitis (FPIP) shows patchy or diffuse erythematous and friable mucosa. Characteristic circumscribed nodular hyperplasia with central pit-like erosions and ulcers may also be seen.[30][31]
    • 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.
    • Ulcerative colitis. On gross pathology, the inflammation is seen in the innermost part of the lamina propria.
    • Ischemic proctocolitis shows marked mucosal congestion with areas of necrosis and ulceration on gross patholgy.[32]
  • Pseudomembranous colitis. (WC) [33]

    Pseudomembranous colitis. (WC) [33]

  • Pseudomembranous colitis. [34]

    Pseudomembranous colitis. [34]

  • Ulcerative colitis.[35]

    Ulcerative colitis.[35]

Microscopic pathology

  • In pseudomembranous colitis microscopy shows[36]
    • 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 [37]

    Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis [37]

References

  1. ↑ 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.
  2. ↑ 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
  3. ↑ 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.
  4. ↑ Baron, Samuel. Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston, 1996. Print.
  5. ↑ Taraktchoglou M, Pacey AA, Turnbull JE, Eley A (2001). "Infectivity of Chlamydia trachomatis serovar LGV but not E is dependent on host cell heparan sulfate". Infect Immun. 69 (2): 968–76. doi:10.1128/IAI.69.2.968-976.2001. PMC 97976. PMID 11159992.
  6. ↑ Mabey D, Peeling RW (2002). "Lymphogranuloma venereum". Sex Transm Infect. 78 (2): 90–2. PMC 1744436. PMID 12081191.
  7. ↑ Moulder JW (1991). "Interaction of chlamydiae and host cells in vitro". Microbiol Rev. 55 (1): 143–90. PMC 372804. PMID 2030670 PMID 2030670 Check |pmid= value (help).
  8. ↑ Ceovic R, Gulin SJ (2015). "Lymphogranuloma venereum: diagnostic and treatment challenges". Infect Drug Resist. 8: 39–47. doi:10.2147/IDR.S57540. PMC 4381887. PMID 25870512.
  9. ↑ 9.0 9.1 9.2 DuPont HL, Levine MM, Hornick RB, Formal SB (1989). "Inoculum size in shigellosis and implications for expected mode of transmission". J Infect Dis. 159 (6): 1126–8. PMID 2656880.
  10. ↑ 10.0 10.1 Schroeder GN, Hilbi H (2008). "Molecular pathogenesis of Shigella spp.: controlling host cell signaling, invasion, and death by type III secretion". Clin Microbiol Rev. 21 (1): 134–56. doi:10.1128/CMR.00032-07. PMC 2223840. PMID 18202440.
  11. ↑ Gorden J, Small PL (1993). "Acid resistance in enteric bacteria". Infect Immun. 61 (1): 364–7. PMC 302732. PMID 8418063.
  12. ↑ Islam D, Bandholtz L, Nilsson J, Wigzell H, Christensson B, Agerberth B; et al. (2001). "Downregulation of bactericidal peptides in enteric infections: a novel immune escape mechanism with bacterial DNA as a potential regulator". Nat Med. 7 (2): 180–5. doi:10.1038/84627. PMID 11175848.
  13. ↑ Wassef JS, Keren DF, Mailloux JL (1989). "Role of M cells in initial antigen uptake and in ulcer formation in the rabbit intestinal loop model of shigellosis". Infect Immun. 57 (3): 858–63. PMC 313189. PMID 2645214.
  14. ↑ Man AL, Prieto-Garcia ME, Nicoletti C (2004). "Improving M cell mediated transport across mucosal barriers: do certain bacteria hold the keys?". Immunology. 113 (1): 15–22. doi:10.1111/j.1365-2567.2004.01964.x. PMC 1782554. PMID 15312131.
  15. ↑ Mounier, Joëlle; Vasselon, T; Hellio, R; Lesourd, M; Sansonetti, PJ (January 1992). "Shigella flexneri Enters Human Colonic Caco-2 Epithelial Cells through the Basolateral Pole". Infection and Immunity. 60 (1): 237–248. PMC 257528. PMID 1729185.
  16. ↑ Zychlinsky A, Fitting C, Cavaillon JM, Sansonetti PJ (1994). "Interleukin 1 is released by murine macrophages during apoptosis induced by Shigella flexneri". J Clin Invest. 94 (3): 1328–32. doi:10.1172/JCI117452. PMC 295219. PMID 8083373.
  17. ↑ Sansonetti PJ, Phalipon A, Arondel J, Thirumalai K, Banerjee S, Akira S; et al. (2000). "Caspase-1 activation of IL-1beta and IL-18 are essential for Shigella flexneri-induced inflammation". Immunity. 12 (5): 581–90. PMID 10843390.
  18. ↑ Girardin SE, Boneca IG, Carneiro LA, Antignac A, Jéhanno M, Viala J; et al. (2003). "Nod1 detects a unique muropeptide from gram-negative bacterial peptidoglycan". Science. 300 (5625): 1584–7. doi:10.1126/science.1084677. PMID 12791997.
  19. ↑ 19.0 19.1 Fasano A, Noriega FR, Liao FM, Wang W, Levine MM (1997). "Effect of shigella enterotoxin 1 (ShET1) on rabbit intestine in vitro and in vivo". Gut. 40 (4): 505–11. PMC 1027126. PMID 9176079.
  20. ↑ Cherla RP, Lee SY, Tesh VL (2003). "Shiga toxins and apoptosis". FEMS Microbiol Lett. 228 (2): 159–66. PMID 14638419.
  21. ↑ 21.0 21.1 21.2 21.3 21.4 Coburn B, Grassl GA, Finlay BB (2007). "Salmonella, the host and disease: a brief review". Immunol Cell Biol. 85 (2): 112–8. doi:10.1038/sj.icb.7100007. PMID 17146467.
  22. ↑ "Salmonella(non-typhoidal)".
  23. ↑ 23.0 23.1 23.2 de Jong HK, Parry CM, van der Poll T, Wiersinga WJ (2012). "Host-pathogen interaction in invasive Salmonellosis". PLoS Pathog. 8 (10): e1002933. doi:10.1371/journal.ppat.1002933. PMC 3464234. PMID 23055923.
  24. ↑ 24.0 24.1 Capra JD, Kehoe JM (1974). "Variable region sequences of five human immunoglobulin heavy chains of the VH3 subgroup: definitive identification of four heavy chain hypervariable regions". Proc Natl Acad Sci U S A. 71 (3): 845–8. PMC 388111. PMID 4522793.
  25. ↑ 25.0 25.1 Espinosa-Cantellano M, Martínez-Palomo A (2000). "Pathogenesis of intestinal amebiasis: from molecules to disease". Clin Microbiol Rev. 13 (2): 318–31. PMC 100155. PMID 10756002.
  26. ↑ Müller FW, Franz A, Werries E (1988). "Secretory hydrolases of Entamoeba histolytica". J Protozool. 35 (2): 291–5. PMID 2456386.
  27. ↑ Spice WM, Ackers JP (1998). "The effects of Entamoeba histolytica lysates on human colonic mucins". J Eukaryot Microbiol. 45 (2): 24S–27S. PMID 9561780.
  28. ↑ 28.0 28.1 Surawicz CM, McFarland LV (1999). "Pseudomembranous colitis: causes and cures". Digestion. 60 (2): 91–100. doi:7633 Check |doi= value (help). PMID 10095149.
  29. ↑ 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.
  30. ↑ Hwang JB, Hong J (2013). "Food protein-induced proctocolitis: Is this allergic disorder a reality or a phantom in neonates?". Korean J Pediatr. 56 (12): 514–8. doi:10.3345/kjp.2013.56.12.514. PMC 3885785. PMID 24416045.
  31. ↑ Hwang JB, Park MH, Kang YN, Kim SP, Suh SI, Kam S (2007). "Advanced criteria for clinicopathological diagnosis of food protein-induced proctocolitis". J Korean Med Sci. 22 (2): 213–7. doi:10.3346/jkms.2007.22.2.213. PMC 2693584. PMID 17449926.
  32. ↑ Abhishek K, Kaushik S, Kazemi MM, El-Dika S (2008). "An unusual case of hematochezia: acute ischemic proctosigmoiditis". J Gen Intern Med. 23 (9): 1525–7. doi:10.1007/s11606-008-0673-2. PMC 2518031. PMID 18521689.
  33. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/Pseudomembranous_colitis Accessed on August 31, 2016
  34. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org Accessed on September 1, 2016
  35. ↑ Ulcerative colitis. Wikidoc. http://www.wikidoc.org/index.php/File:UC_granularity.png#filehistory Accessed on August 31, 2016
  36. ↑ 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}}
  37. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/File:Colonic_pseudomembranes_low_mag.jpg Accessed on September 1, 2016

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