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
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 occationally with follicular aggregation of lymphocyte. Herpes simplex virus 2 cervicitis leads to inflammation and ulceration of the ectocervix.