Acute Cervicitis - UpToDate
Acute Cervicitis - UpToDate
Acute Cervicitis - UpToDate
www.uptodate.com ©2019 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Acute cervicitis
Authors: Anna Maya Powell, MD MSc, Paul Nyirjesy, MD
Section Editors: Robert L Barbieri, MD, Jeanne Marrazzo, MD, MPH, FACP, FIDSA
Deputy Editor: Kristen Eckler, MD, FACOG
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2019. | This topic last updated: Apr 01, 2019.
INTRODUCTION
Cervicitis refers to inflammation of the uterine cervix. The inflammation primarily affects the
columnar epithelial cells of the endocervical glands but can also affect the squamous epithelium
of the ectocervix. It may be due to an infectious or noninfectious etiology and may be acute or
chronic. Acute cervicitis is often due to infection (eg, chlamydia, gonorrhea), although a specific
infection cannot be determined in a large proportion of cases. Chronic cervicitis usually has a
noninfectious source.
This topic will review the background, evaluation, diagnosis, and management of acute cervicitis in
postpubertal and adult women. Related discussions of vaginitis (in adults and children) and
endometritis are presented separately.
Herpes simplex virus and Trichomonas vaginalis, which primarily affect the squamous epithelium
of the ectocervix, also account for a few cases. Tuberculosis involves the cervix in a small
proportion of women with tuberculous endometritis [4,5] (see "Endometritis unrelated to
pregnancy", section on 'Tuberculous endometritis'). Mycoplasma genitalium may be an important
pathogen as well; a meta-analysis reported that women with M. genitalium detected at the cervix
had a significantly increased risk of cervicitis [3,6-9]. Finally, bacterial vaginosis (BV) and
streptococci (group A) have also been implicated as causative agents of acute cervicitis [1,10,11].
BV is unlikely to be a cause of isolated cervicitis without concurrent vaginal findings.
There is no evidence that human papillomavirus infection induces cervical inflammation, but it can
cause other histologic changes (eg, cervical intraepithelial neoplasia). However, organisms
involved in cervicitis may act as potential cofactors (not direct cause) in development of cervical
neoplasia (eg, U. urealyticum) [24].
Less common noninfectious causes include radiation therapy and systemic inflammatory
diseases such as Behçet syndrome or lichen planus. In hypoestrogenic women, desquamative
inflammatory vaginitis can cause inflammation of the cervix along with a more diffuse vaginal
inflammation; in these cases, the purulent discharge comes from both the cervix and vagina. (See
"Desquamative inflammatory vaginitis".)
SIGNIFICANCE
Apart from the symptoms such as vaginal discharge or bleeding, cervicitis resulting from cervical
infection is clinically important because infection can ascend and cause endometritis or pelvic
inflammatory disease (PID). Sequelae of PID include chronic pelvic pain, infertility, and an
increased risk of ectopic pregnancy. The pathogens can be transmitted to sexual partners. In
addition, cervicitis appears to be associated with a significant increase in risk of HIV-1 acquisition
and shedding [29].
In pregnant women, it may cause pregnancy or neonatal complications, including low birth weight
and preterm birth, as a result of infection of the fetus, placenta, amniotic fluid, decidua, or
membrane (table 1) [12].
CLINICAL PRESENTATION
Women with cervicitis may have presenting symptoms or be asymptomatic, in which case the
diagnosis is made at the time of physical examination for other indications. In an observational
study that included 59 women presenting for routine cervical cancer screening, 24 percent had
signs of cervicitis on examination, but only 5 percent had symptoms (vaginal discharge) [30].
Urinary symptoms are generally due to concomitant urethritis, which occurs in approximately 15
percent of women with cervical chlamydia infection. Pain and fever are atypical in the absence of
upper tract infection (endometritis, pelvic inflammatory disease) or herpes simplex virus infection.
DIAGNOSTIC EVALUATION
History — Evaluation of patient risk factors is important and should include a detailed discussion
of sexual history (number of partners, condom use, type of sexual activity, new sex partner, sex
partner with concurrent sex partners, sex partner with a sexually transmitted infection [STI]),
vaginal hygiene (douching), and age (<25). Clinicians should be aware of STI prevalence in their
communities. One example, from the US Centers for Disease Control and Prevention, can be found
here. Factors associated with noninfectious cervicitis are listed above. (See 'Noninfectious causes'
above.)
● Vaginal bleeding – Women with cervicitis often present with intermenstrual or postcoital
vaginal bleeding. We ask about symptoms in relation to timing of vaginal sexual activity.
● Abdominal or pelvic pain – Cervicitis alone generally does not cause pelvic or abdominal
pain. However, women with associated endometritis or pelvic inflammatory disease (PID)
often complain of pain.
● Estrogen status – Women with genitourinary syndrome of menopause can present with
symptoms similar to that of cervicitis. (See "Clinical manifestations and diagnosis of
genitourinary syndrome of menopause (vulvovaginal atrophy)", section on 'Clinical
presentation'.)
Discussion of patient history that is suggestive of Candida vulvovaginitis, BV, and trichomoniasis is
presented elsewhere.
Hallmark findings — The classic findings at the time of speculum examination are (1) a
purulent/mucopurulent discharge on the ectocervix or exuding from the endocervical canal
(picture 1) or (2) bleeding upon touching the cervix with a cotton or Dacron swab (ie, friability).
However, these findings are not diagnostic of etiology [31].
The cervical appearance varies with the type of infecting organism and severity of infection. The
quantity of cervical organisms correlates with the degree of inflammation.
● Mucopurulent cervical discharge, cervical friability, and edema in the zone of ectopy are
characteristic of both gonococcal and chlamydial cervicitis (picture 2 and picture 1). The
presence of one or more of these signs is more predictive of gonorrhea or chlamydia infection
in younger compared with older women (1 in 3 women <25 years infected versus 1 in 6 to 11
women >25 years) [31].
● Diffuse vesicular lesions/ulceration suggest herpes simplex virus (HSV) infection (picture 4).
Erosive inflammation can occur as well. Primary HSV infection is often associated with
systemic symptoms as well. Subclinical HSV shedding is not typically associated with
cervicitis [32]. (See "Epidemiology, clinical manifestations, and diagnosis of genital herpes
simplex virus infection".)
The clinical features of cervicitis caused by M. genitalium are not well-defined; some studies
suggest that the majority of cervical infections with this possible pathogen do not elicit visible
signs of inflammation [8,33,34]. It is not generally possible to distinguish infectious from
noninfectious acute cervicitis by physical examination. (See 'Recurrent or persistent disease'
below.)
In any woman with suspected cervicitis, visual evaluation of the cervix should be followed by
bimanual examination of the pelvic organs to exclude PID. (See "Pelvic inflammatory disease:
Clinical manifestations and diagnosis", section on 'Diagnosis'.)
Alarm findings — Women meeting criteria for PID (cervical motion tenderness OR uterine
tenderness OR adnexal tenderness) in addition to cervicitis should be evaluated and treated
appropriately. Most women with PID have either mucopurulent cervical discharge or leukorrhea on
saline preparation of vaginal fluid [3].
● Vaginal pH and saline microscopy – As women with cervicitis may also have concurrent
vaginitis, we perform vaginal pH and saline microscopy. (See "Approach to women with
symptoms of vaginitis", section on 'Diagnostic studies'.)
● Testing for chlamydia and gonorrhea – We advise nucleic acid amplification testing (NAAT)
for N. gonorrhoeae and C. trachomatis. These assays can be performed on a swab of vaginal
fluid, an endocervical sample (cells are obtained by rotating a swab within the endocervical
canal while applying gentle lateral pressure), or, if a speculum examination is not possible, on
urine [3]. Application of NAAT to these samples has excellent performance relative to that for
direct endocervical sampling. (See "Clinical manifestations and diagnosis of Chlamydia
trachomatis infections", section on 'Nucleic acid amplification' and "Clinical manifestations
and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents", section on
'Nucleic acid amplification'.)
● Testing for BV and trichomoniasis – T. vaginalis may cause isolated cervicitis; BV typically
affects the vagina (table 2). Either infection may occur concurrently with cervicitis.
Microscopy (wet prep), the amine (whiff) test, and vaginal pH are useful for identifying BV. The
sensitivity of microscopy to detect T. vaginalis is relatively low (approximately 50 percent);
therefore, symptomatic women with cervicitis and negative microscopy for trichomonads
should undergo further testing, preferably NAAT. NAAT offers a more sensitive means of
detection than the other options and can be performed on the same screening specimen used
for chlamydia and gonorrhea testing. (See "Trichomoniasis", section on 'Preferred tests' and
"Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Diagnosis'.)
● Testing for M. genitalium – NAATs are the only clinically useful method of detecting M.
genitalium on urogenital specimens but are not widely available nor standardized. A US Food
and Drug Administration (FDA)-cleared transcription-mediated amplification (TMA) test has
been approved in the United States [35]. As this test has just been approved, its use in
evaluation of women with cervicitis is not yet known. (See "Mycoplasma genitalium infection
in men and women", section on 'Diagnostic tests'.)
Routinely testing for infections other than T. vaginalis, gonorrhea, chlamydia, and BV is not useful
unless a specific organism, such as HSV, is suspected. There is generally no role for other
bacterial cultures (eg, general vaginal culture) or polymerase chain reaction, which can be very
costly and often detects vaginal bacteria that are unrelated to the cervical process. (See
"Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus infection".)
DIAGNOSIS
The diagnosis of acute cervicitis is clinical and based upon the presence of purulent or
mucopurulent cervical exudate or sustained endocervical bleeding (friability) easily induced by
gently touching the area with a swab [2,3].
DIFFERENTIAL DIAGNOSIS
Women with signs or symptoms of cervicitis are evaluated for other processes that can present
with cervicitis as one component. Differential diagnosis includes sexually transmitted infections
(gonorrhea, chlamydia, trichomoniasis, herpes simplex virus 1 or 2 infection, human
papillomavirus, M. genitalium) and vaginitis (bacterial vaginosis, desquamative inflammatory
vaginitis [18]).
Women whose testing for infection is negative are evaluated for contact dermatitis, allergy, and
dermatoses such as lichen planus. The approach to evaluation is the same for cervical
presentations of these entities as vaginal/vulvar presentations. (See "Approach to women with
symptoms of vaginitis", section on 'Women without a diagnosis after initial evaluation' and "Vulvar
lichen planus", section on 'Erosive lichen planus'.)
Postmenopausal women may have cervicitis as a result of their hypoestrogenic status but
typically have findings of atrophic vaginitis as well. Isolated cervicitis related to hypoestrogenism
alone (ie, no infection) is unusual. (See "Clinical manifestations and diagnosis of genitourinary
syndrome of menopause (vulvovaginal atrophy)".)
Women with desquamative inflammatory vaginitis typically have a high vaginal pH, negative amine
text, and saline wet mount microscopy shows an increased number of parabasal and
inflammatory cells, with a leukocyte to epithelial cell ratio greater than 1:1 (picture 5) [36,37]. (See
"Desquamative inflammatory vaginitis".)
TREATMENT
The goals of treatment are relief of symptoms and prevention of infection of the upper genital
tract.
Empiric therapy — We suggest that women with cervicitis receive empiric antibiotic therapy at the
time of initial evaluation, without waiting for results of laboratory tests, especially if follow-up is
uncertain or if a relatively insensitive diagnostic test is used in place of nucleic acid amplification
testing (NAAT).
● High sexually transmitted infection (STI) risk – For women with cervicitis, we provide empiric
treatment that covers both gonorrhea and chlamydia. The minimum empiric regimen should
include coverage of chlamydia, especially for women ≤25 years old, as the prevalence of this
infection is highest in this age group. Other risk factors for chlamydia are history of a previous
chlamydial infection in the prior several months, new or more than one sexual partner, and
inconsistent use of condoms. (See 'Targeted treatment of specific infections' below.)
We follow the Centers for Disease Control and Prevention's (CDC) Sexually Transmitted
Diseases Treatment Guidelines and add therapy for gonorrhea as well if either the individual
patient's risk is high or if the local prevalence is high [3]. The threshold prevalence that defines
"high" is not clear, but most experts agree that >5 percent is reasonable, given the
consequences of untreated infection and the ease with which treatment can be accomplished
(ie, single-dose therapy) [2,3]. The patient should be instructed to return for follow-up in 14
days if no symptomatic improvement or as needed pending STI evaluation. (See 'Targeted
treatment of specific infections' below.)
● Low STI risk – Even for women who are not at apparently high risk for STIs, empiric antibiotic
therapy for both chlamydia and gonorrhea is reasonable if patient follow-up of test results is a
concern or the local prevalence of gonorrhea or chlamydia infection is high [3]. We take this
approach and generally treat low risk women for both infections as well.
In general, patients and their sexual partners should abstain from sexual intercourse until
treatment has been completed (seven days after a single-dose regimen or after completion of a
seven-day regimen) [3]. Treatment, follow-up, and management of sexual partners depend upon
the results of the diagnostic tests. (See 'Treatment of unique populations' below and 'Follow-up'
below.)
Targeted treatment of specific infections — Laboratory and microscopy findings guide targeted
therapy.
● Gonorrhea, chlamydia, and mycoplasma – For women in whom empiric therapy of chlamydia,
gonorrhea, or both is deferred, the results of sensitive tests for C. trachomatis and N.
gonorrhoeae (eg, NAATs) should guide treatment subsequent to the initial evaluation.
• Gonorrhea – We follow the CDC guidelines for treatment with ceftriaxone 250 mg
intramuscularly with azithromycin 1 g orally (regardless of the results of chlamydia
testing), both in a single dose [3]. Fluoroquinolones and doxycycline are not appropriate
alternatives because of increasing resistance to these drugs, nor is therapy with oral
azithromycin alone [3,38]. (See "Treatment of uncomplicated Neisseria gonorrhoeae
infections", section on 'Rationale for dual therapy'.)
● Bacterial vaginosis – Oral or topical medication may be used (table 3). Treatment of sexual
partners is not required. The presentation, diagnosis, and management of patients with BV is
discussed in detail in related content.
● Herpes simplex virus – Treatment options for herpes simplex virus infection include [3] (see
"Treatment of genital herpes simplex virus infection"):
• Acyclovir – 400 mg orally three times per day or 200 mg orally five times per day for 7 to
10 days
• Famciclovir – 250 mg orally three times daily for 7 to 10 days
• Valacyclovir – 1000 mg orally twice daily for 7 to 10 days
Noninfectious acute cervicitis should be considered in women with persistent cervicitis despite
antibiotic therapy. Management of women with persistent disease after this therapy is discussed
below. (See 'Recurrent or persistent disease' below.)
● Physical examination findings consistent with cervicitis – For asymptomatic women with
physical examination findings consistent with cervicitis, we assess the patient's risk of STI
exposure/acquisition. For women with significant risk factors, we offer treatment for
chlamydia. If the patient lives in a high prevalence area for gonorrhea, we offer concurrent
treatment for gonorrhea. Clinical judgment should be used, but for patients at low risk for STI
(by risk factors or residence in a community with low STI prevalence), waiting for STI test
results prior to making treatment decisions is also reasonable. (See 'Empiric therapy' above.)
Inflammation on cervical cytology is also not an indication for treatment. The presence of a
few lymphocytes on cytologic smears is normal and should not be misdiagnosed as
inflammation.
● Pregnant women – No data suggest different treatment is warranted for pregnant women,
although doxycycline should be avoided [3].
● Women living with HIV – No data suggest different treatment for this patient population [3].
However, cervicitis is thought to increase HIV-1 shedding from the cervix in the presence of
cervicitis; treatment reduces shedding. Women with HIV were observed to have a high
prevalence of M. genitalium (7.4 percent), which was associated with increased cytokines in
cervicovaginal fluid [44]. In this population, treatment that covers for M. genitalium may be
important in decreasing the risk of HIV transmission to an HIV-negative sexual partner. (See
'Targeted treatment of specific infections' above.)
● Women with a foreign body/substance – For women with cervicitis that appears to be
associated with a foreign body/substance, removal or avoidance of the foreign
body/substance will often lead to resolution of inflammation. Therefore, chemical douches,
vaginal contraceptives and deodorants, and pessaries should be discontinued and the patient
reevaluated for therapeutic response. For women with mild to moderate symptoms and no
purulent discharge, we remove the foreign body/substance and assess for symptom
resolution before we treat with an antimicrobial drug such as topical metronidazole or
clindamycin. For women with severe purulent vaginitis associated with a foreign body, we
remove the foreign body and treat with antibiotic treatment (oral amoxicillin or topical
metronidazole or clindamycin), although there are no data to guide the choice of drug therapy.
● Women with an intrauterine device (IUD) – Women with an IUD who also develop symptoms
or signs of cervicitis can generally be treated for the cervicitis with the IUD in place. If a
patient has chronic cervicitis and other causes have been excluded, it may be reasonable to
remove the IUD to assess for symptom resolution. In one trial of 132 women with copper IUDs
and cervicitis, the cervicitis resolved in 131 women after treatment with daily oral estriol 0.25
mg for three months [45,46]. However, oral estriol is not universally available, and empiric
estrogen treatment is not advised in the absence of established indications. Women with an
IUD and PID are treated as per PID guidelines [3]. (See "Intrauterine contraception:
Management of side effects and complications", section on 'Infection and/or pelvic
inflammatory disease'.)
FOLLOW-UP
Symptoms of cervicitis typically respond within a week or two of treatment; no other follow-up is
typically indicated for the cervicitis symptoms. All patients being evaluated for chlamydia,
gonorrhea, or trichomoniasis should be offered counseling and testing for HIV and syphilis [3].
(See "Screening for sexually transmitted infections".)
Test of cure (performed at one month post-treatment) for chlamydia and gonorrhea is not required
unless symptoms persist or the woman is pregnant [3]. However, repeat testing three to six
months after a diagnosis of either of these sexually transmitted infections is recommended, given
high rates of recurrent infection documented in many populations.
● Our approach – Women who present with recurrent symptoms are reevaluated for possible re-
exposure or treatment failure [3]. We repeat the diagnostic work-up and ensure that (1)
nucleic acid amplification testing is negative for detection of C. trachomatis and N.
gonorrhoeae, and (2) sexual partners have been appropriately treated, and (3) the patient has
not been re-exposed to potential pathogens (ie, new sexual partner). Diagnostic testing is
performed for trichomoniasis and bacterial vaginosis (BV). Exposure to potential intravaginal
irritants (lubricants, spermicides, douching) is reassessed. If possible, sexual partners should
be examined and tested for chlamydia and gonorrhea, particularly if they were not treated
presumptively at the time of the woman's initial treatment for cervicitis. (See 'Treatment of
unique populations' above.)
● Treatment of anaerobic organisms – For women with persistent cervicitis, some experts also
advise additional coverage aimed at vaginal anaerobes (especially if BV is present); one
option is metronidazole 500 mg orally twice daily for seven days. There are no data
supporting one proven BV treatment over another. If cervicitis resolves, no further treatment is
required. (See "Bacterial vaginosis: Treatment", section on 'Symptomatic'.)
CHRONIC CERVICITIS
The term "chronic" in this context generally refers to women in whom the usual infectious causes
of acute cervicitis described above have been treated or excluded, yet abnormal physical signs
persist for at least three months. A minority of women have persistent mucopurulent endocervical
discharge. Chronic cervicitis usually has a noninfectious source [50]. In women with chronic
cervicitis, the cervical mucosa is hyperemic and may be ulcerated. Obstruction of the mucous
glands may result in formation of nabothian cysts. (See "Benign cervical lesions and congenital
anomalies of the cervix", section on 'Nabothian cysts'.)
Women with chronic cervicitis who fail to respond to antibiotics are a therapeutic challenge; there
is no standardized approach for these patients [50]. Some may respond to two doses of depot
medroxyprogesterone or cauterization of the bleeding points with silver nitrate, which can be
applied repeatedly every two weeks until the cervicitis resolves or they have failed to show a
response. As a last resort, electrocautery, laser, or shallow loop excision can successfully reduce
persistent mucopurulent discharge unresponsive to other measures and for which an etiology has
not been determined [41]. It is imperative that malignancy be excluded by biopsy before any
ablative treatment is undertaken.
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Sexually transmitted
infections" and "Society guideline links: Bacterial vaginosis" and "Society guideline links:
Gynecologic infectious diseases (non-sexually transmitted)".)
SUMMARY AND RECOMMENDATIONS
● Cervicitis is an inflammatory disorder that primarily affects the endocervical glands. Sexually
transmitted infections are the most common cause; irritation from foreign bodies, irritants, or
allergens is another etiology. (See 'Epidemiology and etiology' above.)
● Neisseria gonorrhoeae and Chlamydia trachomatis are the two most common causes of acute
cervicitis. It is uncertain how much Mycoplasma genitalium contributes to cervicitis, but this
organism is likely responsible for a substantial minority of cases. (See 'Infection' above.)
● The presenting symptoms are purulent or mucopurulent discharge and/or easily induced
bleeding (friability) from the endocervix. Associated symptoms include abnormal vaginal
discharge, dysuria/urinary frequency, and intermenstrual or postcoital bleeding. (See 'Clinical
presentation' above.)
● Diagnostic evaluation includes a history, physical examination, and testing for potential
causative organisms (ie, chlamydia, gonorrhea, Trichomonas vaginalis, and bacterial
vaginosis). (See 'Diagnostic evaluation' above.)
● The clinical diagnosis of cervicitis is based upon the presence of mucopurulent cervical
discharge or friability. (See 'Diagnosis' above.)
● For women with physical examination findings of cervicitis, we suggest empiric therapy rather
than waiting for targeted test results. (Grade 2C). This should include coverage for chlamydia
and/or gonorrhea, depending on the patient's risk factors. For women in whom empiric
therapy is deferred for laboratory testing, test results guide treatment. (See 'Empiric therapy'
above and 'Targeted treatment of specific infections' above.)
● Treatment, follow-up, and management of sexual partners depend upon the causative
organism. Treatment of sexual partners is indicated for women with chlamydia, gonorrhea, or
trichomonas infections. (See 'Treatment of unique populations' above.)
● Women who present with recurrent symptoms are reevaluated for possible re-exposure or
treatment failure. We treat all women with persistent cervicitis for presumed M. genitalium
with single-dose azithromycin (1 g orally), if they have not already been treated with this agent,
or doxycycline (100 mg twice daily for seven days). (See 'Recurrent or persistent disease'
above.)
● Chronic cervicitis refers to women in whom the usual infectious causes of acute cervicitis
have been treated or excluded, yet abnormal physical signs persist for at least three months.
A minority of women have persistent mucopurulent endocervical discharge. Chronic cervicitis
usually has a noninfectious source. (See 'Chronic cervicitis' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate would like to acknowledge Dr. Jeanne Marrazzo who contributed to
an earlier version of this topic review.
REFERENCES
1. Manhart LE, Critchlow CW, Holmes KK, et al. Mucopurulent cervicitis and Mycoplasma
genitalium. J Infect Dis 2003; 187:650.
2. Marrazzo JM, Martin DH. Management of women with cervicitis. Clin Infect Dis 2007; 44
Suppl 3:S102.
3. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted
diseases treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.
5. Singh S, Gupta V, Modi S, et al. Tuberculosis of uterine cervix: a report of two cases with
variable clinical presentation. Trop Doct 2010; 40:125.
6. Rodrigues MM, Fernandes PÁ, Haddad JP, et al. Frequency of Chlamydia trachomatis,
Neisseria gonorrhoeae, Mycoplasma genitalium, Mycoplasma hominis and Ureaplasma
species in cervical samples. J Obstet Gynaecol 2011; 31:237.
10. Paraskevaides EC, Wilson MC. Fatal disseminated intravascular coagulation secondary to
streptococcal cervicitis. Eur J Obstet Gynecol Reprod Biol 1988; 29:39.
11. Marrazzo JM, Wiesenfeld HC, Murray PJ, et al. Risk factors for cervicitis among women with
bacterial vaginosis. J Infect Dis 2006; 193:617.
12. Nugent RP, Hillier SL. Mucopurulent cervicitis as a predictor of chlamydial infection and
adverse pregnancy outcome. The Investigators of the Johns Hopkins Study of Cervicitis and
Adverse Pregnancy Outcome. Sex Transm Dis 1992; 19:198.
13. Paavonen J, Critchlow CW, DeRouen T, et al. Etiology of cervical inflammation. Am J Obstet
Gynecol 1986; 154:556.
14. Kletzel HH, Rotem R, Barg M, et al. Ureaplasma urealyticum: the Role as a Pathogen in
Women's Health, a Systematic Review. Curr Infect Dis Rep 2018; 20:33.
15. Mukherjee S, Nagarsenkar A, Chandra S, et al. Amoebic cervicitis mimicking posterior wall
fibroid: a rare presentation. J Microbiol Immunol Infect 2014; 47:354.
16. Abou M, Dällenbach P. Acute cervicitis and vulvovaginitis may be associated with
Cytomegalovirus. BMJ Case Rep 2013; 2013.
17. Schwebke JR, Weiss HL. Interrelationships of bacterial vaginosis and cervical inflammation.
Sex Transm Dis 2002; 29:59.
19. Gorgos LM, Sycuro LK, Srinivasan S, et al. Relationship of Specific Bacteria in the Cervical
and Vaginal Microbiotas With Cervicitis. Sex Transm Dis 2015; 42:475.
20. Uusküla A, Raukas E. Atypical genital herpes: report of five cases. Scand J Infect Dis 2004;
36:37.
22. Marrazzo JM. Mucopurulent cervicitis: no longer ignored, but still misunderstood. Infect Dis
Clin North Am 2005; 19:333.
23. McClelland RS, Sangare L, Hassan WM, et al. Infection with Trichomonas vaginalis increases
the risk of HIV-1 acquisition. J Infect Dis 2007; 195:698.
26. Baithun M, Freeman-Wang T, Chowdary P, Kadir RA. Ligneous cervicitis and endometritis: A
gynaecological presentation of congenital plasminogen deficiency. Haemophilia 2018;
24:359.
27. Oliveto JM, Muinov L. Cystic Cervicitis: A Case Report and Literature Review of Cystic
Cervical Lesions. J Comput Assist Tomogr 2016; 40:564.
28. Kim MJ, Kim NR, Cho HY, et al. Differential diagnostic features of small cell carcinoma in the
uterine cervix. Diagn Cytopathol 2008; 36:618.
29. Johnson LF, Lewis DA. The effect of genital tract infections on HIV-1 shedding in the genital
tract: a systematic review and meta-analysis. Sex Transm Dis 2008; 35:946.
30. Falk L, Fredlund H, Jensen JS. Signs and symptoms of urethritis and cervicitis among
women with or without Mycoplasma genitalium or Chlamydia trachomatis infection. Sex
Transm Infect 2005; 81:73.
31. Marrazzo JM, Handsfield HH, Whittington WL. Predicting chlamydial and gonococcal cervical
infection: implications for management of cervicitis. Obstet Gynecol 2002; 100:579.
32. Koelle DM, Benedetti J, Langenberg A, Corey L. Asymptomatic reactivation of herpes simplex
virus in women after the first episode of genital herpes. Ann Intern Med 1992; 116:433.
33. Huppert JS, Mortensen JE, Reed JL, et al. Mycoplasma genitalium detected by transcription-
mediated amplification is associated with Chlamydia trachomatis in adolescent women. Sex
Transm Dis 2008; 35:250.
34. Short VL, Totten PA, Ness RB, et al. Clinical presentation of Mycoplasma genitalium Infection
versus Neisseria gonorrhoeae infection among women with pelvic inflammatory disease.
Clin Infect Dis 2009; 48:41.
35. FDA News Release: FDA permits marketing of first test to aid in the diagnosis of a sexually-tr
ansmitted infection known as Mycoplasma genitalium. January 23, 2019. https://www.fda.g
ov/NewsEvents/Newsroom/PressAnnouncements/ucm629746.htm (Accessed on January 2
5, 2019).
36. Reichman O, Sobel J. Desquamative inflammatory vaginitis. Best Pract Res Clin Obstet
Gynaecol 2014; 28:1042.
37. Sobel JD. Desquamative inflammatory vaginitis: a new subgroup of purulent vaginitis
responsive to topical 2% clindamycin therapy. Am J Obstet Gynecol 1994; 171:1215.
38. Kirkcaldy RD, Kidd S, Weinstock HS, et al. Trends in antimicrobial resistance in Neisseria
gonorrhoeae in the USA: the Gonococcal Isolate Surveillance Project (GISP), January 2006-
June 2012. Sex Transm Infect 2013; 89 Suppl 4:iv5.
39. Whittington WL, Kent C, Kissinger P, et al. Determinants of persistent and recurrent
Chlamydia trachomatis infection in young women: results of a multicenter cohort study. Sex
Transm Dis 2001; 28:117.
41. Nyirjesy P. Nongonococcal and Nonchlamydial Cervicitis. Curr Infect Dis Rep 2001; 3:540.
42. Dunlop EM, Garner A, Darougar S, et al. Colposcopy, biopsy, and cytology results in women
with chlamydial cervicitis. Genitourin Med 1989; 65:22.
43. Paavonen J, Vesterinen E, Meyer B, Saksela E. Colposcopic and histologic findings in cervical
chlamydial infection. Obstet Gynecol 1982; 59:712.
44. Dehon PM, Hagensee ME, Sutton KJ, et al. Histological Evidence of Chronic Mycoplasma
genitalium-Induced Cervicitis in HIV-Infected Women: A Retrospective Cohort Study. J Infect
Dis 2016; 213:1828.
45. Rubinstein E. The copper-7 device in chronic and IUD-induced acute cervicitis treated with
oral estriol. Contraception 1974; 10:673.
46. Erol O, Simavlı S, Derbent AU, et al. The impact of copper-containing and levonorgestrel-
releasing intrauterine contraceptives on cervicovaginal cytology and microbiological flora: a
prospective study. Eur J Contracept Reprod Health Care 2014; 19:187.
47. Mena LA, Mroczkowski TF, Nsuami M, Martin DH. A randomized comparison of azithromycin
and doxycycline for the treatment of Mycoplasma genitalium-positive urethritis in men. Clin
Infect Dis 2009; 48:1649.
48. Schwebke JR, Rompalo A, Taylor S, et al. Re-evaluating the treatment of nongonococcal
urethritis: emphasizing emerging pathogens--a randomized clinical trial. Clin Infect Dis 2011;
52:163.
49. Jensen JS, Cusini M, Gomberg M, Moi H. 2016 European guideline on Mycoplasma
genitalium infections. J Eur Acad Dermatol Venereol 2016; 30:1650.
50. Mattson SK, Polk JP, Nyirjesy P. Chronic Cervicitis: Presenting Features and Response to
Therapy. J Low Genit Tract Dis 2016; 20:e30.
Topic 5460 Version 29.0
GRAPHICS
Odds ratio
Infection
(95% CI)
Chlamydia trachomatis
at 24 weeks 2.2 (1.03-4.78)
at 28 weeks 0.95 (0.36-2.47)
Data from: Klein LL, Gibbs RS. Use of microbial cultures and antibiotics in the prevention of infection-associated preterm birth. Am J Obstet
Gynecol 2004; 190:1493.
Mucopurulent discharge is visible coming from the os in a patient with Chlamydia cervicitis.
The cervix is erythematous and friable.
Reproduced from: Sexually Transmitted Diseases: STD Clinical Slides. Centers for Disease Control and Prevention.
Available at: http://www.cdc.gov/std/training/clinicalslides/slides-dl.htm (Accessed on April 24, 2014).
Reproduced with permission from: www.visualdx.com. Copyright VisualDx. All rights reserved.
Vulvovaginal
Parameter Normal findings Bacterial vaginosis Trichomoniasis
candidiasis
Symptoms None or mild, transient Pruritus, soreness, Malodorous discharge, Malodorous discharge,
dyspareunia no dyspareunia burning, postcoital
bleeding, dyspareunia,
dysuria
Signs Normal vaginal Vulvar erythema and/or Off-white/gray thin Thin green-yellow
discharge consists of 1 edema Discharge may discharge that coats the discharge, vulvovaginal
to 4 mL fluid (per 24 be white and clumpy vagina erythema
hours), which is white or and may or may not
transparent, thin or adhere to vagina
thick, and mostly
odorless
Saline microscopy PMN:EC ratio <1; rods PMN:EC ratio <1; rods PMN:EC <1; loss of PMN ++++; mixed flora;
dominate; squames +++ dominate; squames rods; increased motile trichomonads
+++; pseudohyphae coccobacilli; clue cells (present in
(present in comprise at least 20% approximately 60% of
approximately 40% of of epithelial cells patients)
patients); budding yeast (present in >90% of
for nonalbicans Candida patients)
Low (A) and high (B) power microscopy of vaginal discharge reveals parabasal cells and a
marked increase in inflammatory cells (primarily polymorphonuclear leukocytes).
Drugs of choice
Metronidazole 500 mg orally twice daily for 7 days OR
Metronidazole gel 0.75% 5 g* (one full applicator) intravaginally once daily for 5 days OR
Alternatives
Clindamycin 300 mg orally twice daily for 7 days OR
Clindamycin ovule (vaginal suppository) 100 mg intravaginally once daily for 3 days OR
Although data are limited, metronidazole 750 mg extended release tablets once daily for 7 days OR a single vaginal dose of
clindamycin 2% bioadhesive cream (United States trade name: Clindesse) 5 g ¶, one full applicator, also appear to be effective.
Adapted from: Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015.
MMWR Recomm Rep 2015; 64:1.
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