- • 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
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
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 ...