Cervicitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]
Overview
The pathophysiology of Cervicitis depends on the etiological agent and the physiological state of the patient. Under the influence of estrogen, the normal vaginal epithelium cornifies making it somewhat resistant to infectious agents. The endocervix is lined by columnar epithelium which is susceptible to infectious agents leading to cervicitis. Gonococcal cervicitis results after the exposure of the cervix to N. gonorrhoeae in seminal fluid during sexual intercourse.[1] N. gonorrhoeae Infectivity is facilitated by type IV pilus-mediated twitching motility of the bacterium. Motility in the presence of seminal plasma is characterized by high velocity, low directional persistence and enhanced microcolony formation.[1] Once pilus is attached, local inflammation results leading to purulent or mucopurulent discharge. Chlamydia trachomatis cervicitis is often associated with intense lymphocytic and leukocytic inflammtory reaction in the epithelial and subepithelial areas and occasionally with follicular aggregation of lymphocytes. Herpes simplex virus 2 cervicitis leads to inflammation and ulceration of the ectocervix.
Gonococcal cervicitis
Gonococcal cervicitis results after the exposure of the cervix to N. gonorrhoeae in seminal fluid during sexual intercourse. N. gonorrhoeae Infectivity is facilitated by type IV pilus-mediated twitching motility of the bacterium. Motility in the presence of seminal plasma is characterized by high velocity, low directional persistence and enhanced microcolony formation. Once pilus is attached, local inflammation results leading to purulent or mucopurulent discharge.
Nongonococcal cervicitis
C. trachomatis infection is often associated with intense lymphocytic and leukocytic inflammtory reaction in the epithelial and subepithelial areas and occasionally with follicular aggregation of lymphocyte. Also, in the chronic course of chlamydial cervicitis a low content of cytokines IL-1alpha, IL-1beta, TNF-alpha and an elevated concentration of IL-8 have been identified in the pathogenesis.[2] Herpes simplex virus 2 cervicitis leads to inflammation and ulceration of the ectocervix.
References
- ↑ 1.0 1.1 Anderson MT, Dewenter L, Maier B, Seifert HS (2014). "Seminal plasma initiates a Neisseria gonorrhoeae transmission state". MBio. 5 (2): e01004–13. doi:10.1128/mBio.01004-13. PMC 3958800. PMID 24595372.
- ↑ Dolgushin II, Kurnosenko IV, Dolgushina VF, Ugaĭ IIu, Abramovskikh OS, Gol'tsfarb VM (2004). "[Clinical and immunological aspects of cervicitis of chlamydial etiology]". Zh Mikrobiol Epidemiol Immunobiol (3): 48–52. PMID 15346950.