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  • • Inflammatory condition of the cervix defined by the presence of mucopurulent endocervical discharge, easily induced endocervical friability, or edematous cervical ectopy.
  • • Most often a result of chlamydia, gonorrhea, trichomoniasis, or genital herpes infection.
  • • Associated with an increased risk of upper genital tract infection, adverse pregnancy outcomes, and HIV acquisition.

Cervicitis is typically the consequence of infection with sexually acquired pathogens, most commonly Chlamydia trachomatis or Neisseria gonorrhoeae and, occasionally, Trichomonas vaginalis or herpes simplex virus (HSV). The diagnosis is made when either mucopurulent discharge or easily induced bleeding (friability) is present at the endocervical os; more subtle signs include edema of the cervical ectropion (edematous ectopy). Recent data suggest that disruption of normal vaginal flora, most often manifesting as bacterial vaginosis, may also promote cervicitis. Although C trachomatis is probably the most common cause of cervicitis, and N gonorrhoeae is also implicated, the majority of women (80–90%) infected with these pathogens have no signs of cervicitis.

The cervix consists of an underlying connective tissue matrix overlaid by two types of distinct epithelium, each of which is vulnerable to infection by distinct pathogens. The endocervical canal and ectropion (cervical ectopy), if present, are lined by columnar epithelial cells. These cells, which line what is commonly called the endocervix, provide vulnerable targets for infections with C trachomatis and N gonorrhoeae. The ectocervix, in contrast, is lined by squamous epithelium that is contiguous with the vaginal mucosa. For this reason, the ectocervix is susceptible to T vaginalis, an agent more commonly associated with vaginitis.

Estrogen, produced endogenously or administered exogenously, promotes the formation and maintenance of cervical ectopy, which is present in adolescents, pregnant women, and women who take estrogen-containing contraceptives. Estrogen is also needed to maintain adequate thickness of the squamous cervicovaginal epithelium (≥20 cell layers). This promotes sustenance of a healthy population of hydrogen peroxide-producing Lactobacillus species, which maintain normal (acidic) vaginal pH. The quality of endocervical mucous is also affected by these hormones. Relatively high levels of estrogen during the follicular phase leading up to ovulation thin the endocervical mucous; this can result in elaboration of so-called physiologic discharge. In the luteal phase of the cycle, progesterone increases the viscosity and reduces the volume of endocervical mucous.

Recently, some investigators have proposed a direct role for these hormones in modulating the balance of cell-mediated (Th1) and humoral (Th2) immune responses, with estrogen predominance promoting Th2 and progesterone augmenting Th1 responses. Because endocervical mucous possesses intrinsic antimicrobial activity by virtue of lactic acid, low pH, and antimicrobial peptides, these hormonal changes are potentially important in mediating susceptibility to and natural history of cervical infection. For example, it is not at all clear why only a subset of women develops inflammatory signs of cervicitis when infected by chlamydia, gonorrhea, or trichomoniasis.

Acquisition of the sexually transmitted diseases (STDs) that cause cervicitis—in particular, chlamydia, gonorrhea, trichomoniasis, and genital ...

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