Urethritis pathophysiology: Difference between revisions
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==Microscopy== | ==Microscopy== | ||
On microscopic histopathological analysis, invaded epithelial cells, vacuoles that contain multiple organisms and [[PMN]]s | On microscopic histopathological analysis, characteristic findings include invaded [[epithelial cells]], [[vacuoles]] that contain multiple organisms, and [[PMN]]s.<ref name="pmid8627027">{{cite journal |vauthors=Apicella MA, Ketterer M, Lee FK, Zhou D, Rice PA, Blake MS |title=The pathogenesis of gonococcal urethritis in men: confocal and immunoelectron microscopic analysis of urethral exudates from men infected with Neisseria gonorrhoeae |journal=J. Infect. Dis. |volume=173 |issue=3 |pages=636–46 |year=1996 |pmid=8627027 |doi= |url=}}</ref> | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
Urethritis is an inflammation of the genital tract that is mostly due to infectious causes. Its pathogenesis depends on the causative pathogen.
Pathophysiology
Urethritis is divided into gonorrheal and non-gonorrheal cases. Its pathophysiology depends on the etiology.
Gonorrhea
- N. gonorrhoeae is usually transmitted via the genital tract to the human host.
- Following attachment to host cell, which is mediated by pili, gonococci become engulfed in a process known as parasite-directed endocytosis. This organism will survive inside the vacuoles and replicate.[1]
- Gonococcal virulence factors include:[2][3][4]:
- Pilli
- The ability to attach to urethral epithelial cells
- Production of extracellular proteases that cleave IgA
Non-Gonorrheal
- Among non-gonorrheal causes, Chlamydia trachomatis is most common.
- The infectious process begins with cell surface attachment and phagocytosis by the host cell. The pathogen survives inside the cell by debilitating the cellular lysosomes and replicating as elementary bodies (the infective form of pathogen).[5][6]
Microscopy
On microscopic histopathological analysis, characteristic findings include invaded epithelial cells, vacuoles that contain multiple organisms, and PMNs.[7]
References
- ↑ Scheuerpflug I, Rudel T, Ryll R, Pandit J, Meyer TF (1999). "Roles of PilC and PilE proteins in pilus-mediated adherence of Neisseria gonorrhoeae and Neisseria meningitidis to human erythrocytes and endothelial and epithelial cells". Infect. Immun. 67 (2): 834–43. PMC 96394. PMID 9916098.
- ↑ Sparling PF (1966). "Genetic transformation of Neisseria gonorrhoeae to streptomycin resistance". J Bacteriol. 92 (5): 1364–71. PMC 276432. PMID 4958881.
- ↑ Swanson J (1973). "Studies on gonococcus infection. IV. Pili: their role in attachment of gonococci to tissue culture cells". J Exp Med. 137 (3): 571–89. PMC 2139381. PMID 4631989.
- ↑ Wolfgang M, Lauer P, Park HS, Brossay L, Hébert J, Koomey M (1998). "PilT mutations lead to simultaneous defects in competence for natural transformation and twitching motility in piliated Neisseria gonorrhoeae". Mol Microbiol. 29 (1): 321–30. PMID 9701824.
- ↑ 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.
- ↑ Baron, Samuel. Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston, 1996. Print.
- ↑ Apicella MA, Ketterer M, Lee FK, Zhou D, Rice PA, Blake MS (1996). "The pathogenesis of gonococcal urethritis in men: confocal and immunoelectron microscopic analysis of urethral exudates from men infected with Neisseria gonorrhoeae". J. Infect. Dis. 173 (3): 636–46. PMID 8627027.