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. N. gonorrhoeae infectivity is facilitated by type IV pilus-mediated motility of the bacterium. In the presence of seminal fluid, the bacterial motility is characterized by high velocity, low directional persistence and enhanced microcolony formation.[1] Once pilus is attached, local inflammation results from release of neutrophilic cytokines leading to purulent or mucopurulent discharge. C. trachomatis infection is often associated with intense lymphocytic and neutrophilic inflammtory reaction in the affected areas and occasionally with follicular aggregation of lymphocyte. The chronic course of chlamydial cervicitis is associated with low content of cytokines IL-1alpha, IL-1beta, TNF-alpha and an elevated concentration of IL-8 in the pathogenesis.[2] Inflammation and ulceration of the ectocervix is evident in herpetic cervicitis.
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 motility of the bacterium. In the presence of seminal fluid, the bacterial motility is characterized by high velocity, low directional persistence and enhanced microcolony formation.[1] Once pilus is attached, local inflammation results from release of neutrophilic cytokines leading to purulent or mucopurulent discharge.
Nongonococcal cervicitis
C. trachomatis infection is often associated with intense lymphocytic and neutrophilic inflammtory reaction in the affected areas and occasionally with follicular aggregation of lymphocyte. The chronic course of chlamydial cervicitis is associated with low content of cytokines IL-1alpha, IL-1beta, TNF-alpha and an elevated concentration of IL-8 in the pathogenesis.[2] Inflammation and ulceration of the ectocervix is evident in herpetic cervicitis.
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.
- ↑ 2.0 2.1 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.