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. Gonococcal cervicitis results after the exposure of the cervix to N. gonorrhea in seminal fluid during sexual intercourse. N. gonorrhea 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 the pili are attached, local inflammation results from the release of neutrophilic cytokines, leading to purulent or mucopurulent discharge. C. trachomatis infection is often associated with intense lymphocytic and neutrophilic inflammtory reactions in the affected areas, and is occasionally associated with follicular aggregation of lymphocytes.[2][3] The chronic course of chlamydial cervicitis is associated with low content of cytokines, mainly IL-1α, IL-1β, and TNFα, and an elevated concentration of IL-8 in the pathogenesis.[4]
Pathophysiology
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. gonorrhea in seminal fluid during sexual intercourse. N. gonorrhea 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 the pili are attached, local inflammation results from the release of neutrophilic cytokines, leading to purulent or mucopurulent discharge.
C. trachomatis infection is often associated with intense lymphocytic and neutrophilic inflammtory reactions in the affected areas, and is occasionally associated with follicular aggregation of lymphocytes.[2][3] The chronic course of chlamydial cervicitis is associated with low content of cytokines, mainly IL-1α, IL-1β, and TNFα, and an elevated concentration of IL-8 in the pathogenesis.[4]
Inflammation and ulceration of the ectocervix is evident in herpetic cervicitis.
Gonococcal cervicitis
Gonococcal cervicitis results after the exposure of the cervix to N. gonorrhea in seminal fluid during sexual intercourse. N. gonorrhea 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 the pili are attached, local inflammation results from the release of neutrophilic cytokines, leading to purulent or mucopurulent discharge.
Nongonococcal cervicitis
C. trachomatis infection is often associated with intense lymphocytic and neutrophilic inflammtory reactions in the affected areas, and is occasionally associated with follicular aggregation of lymphocytes.[2][3] The chronic course of chlamydial cervicitis is associated with low content of cytokines, mainly IL-1α, IL-1β, and TNFα, and an elevated concentration of IL-8 in the pathogenesis.[4]
Inflammation and ulceration of the ectocervix is evident in herpetic cervicitis.
References
- ↑ 1.0 1.1 1.2 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 2.2 Paavonen J, Vesterinen E, Meyer B, Saksela E (1982). "Colposcopic and histologic findings in cervical chlamydial infection". Obstet Gynecol. 59 (6): 712–5. PMID 7078909.
- ↑ 3.0 3.1 3.2 Dunlop EM, Garner A, Darougar S, Treharne JD, Woodland RM (1989). "Colposcopy, biopsy, and cytology results in women with chlamydial cervicitis". Genitourin Med. 65 (1): 22–31. PMC 1196182. PMID 2921049.
- ↑ 4.0 4.1 4.2 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.