REVIEW

EDUCATIONAL OBJECTIVE: Readers will diagnose the cause of vaginal symptoms and treat it appropriately

OLUWATOSIN GOJE, MD, MSCR, FACOG JESSIAN L. MUNOZ, MD, PhD

Regional Obstetrics and Gynecology and Center for OB/GYN and Women’s Health Institute,
Specialist Women’s Health, Women’s Health Institute, Cleveland Clinic
Cleveland Clinic; Committee on Gynecologic Practice,
American Society for Colposcopy and Cervical Pathology,
American College of Obstetricians and Gynecologists

Vulvovaginitis:
Find the cause to treat it
ABSTRACT
Vulvar and vaginal disorders are among the most com-
A lthough vulvovaginitis has several
possible causes, the typical presenting
symptoms are similar regardless of the cause:
mon problems seen in ambulatory care. The cause is itching, burning, and vaginal discharge. Physi-
usually infectious, but noninfectious causes should also cal examination often reveals atrophy, redness,
be considered, and differentiating them can be challeng- excoriations, and fissures in the vulvovaginal
ing. Accurate diagnosis based on patient history, physical and perianal areas. Determining the cause is
examination, and laboratory testing is necessary so that key to successful treatment.
effective therapy can be chosen. This article reviews the diagnosis and
treatment of many common and less common
KEY POINTS infectious and noninfectious causes of vulvo-
vaginitis, the use of special tests, and the man-
Typical presenting symptoms of vulvovaginitis are itching,
agement of persistent cases.
burning, and abnormal discharge.
■ DIAGNOSIS CAN BE CHALLENGING
Evaluating vaginal secretions with simple office-based Vulvar and vaginal symptoms are most com-
tools is often sufficient for diagnosis, although DNA test- monly caused by local infections, but other
ing is also available. causes must be also be considered, including
several noninfectious ones (Table 1). Chal-
Depending on the cause, vulvovaginitis is generally treat- lenges in diagnosing vulvovaginitis are many
ed with a course of oral or topical antibiotics, antiviral or and include distinguishing contact from al-
antifungal drugs, anti-inflammatory agents, or hormonal lergic dermatitis, recognizing vaginal atrophy,
therapy. and recognizing a parasitic infection. Deter-
mining whether a patient has an infectious
process is important so that antibiotics can be
Cases that do not resolve may require maintenance used only when truly needed.
therapy. Patients who have persistent or unusual symp- Foreign bodies in the vagina should also be
toms should be referred to a specialist. considered, especially in children,1 as should
sexual abuse. A 15-year retrospective review of
prepubertal girls presenting with recurrent vag-
inal discharge found that sexual abuse might
have been involved in about 5% of cases.2
Systemic diseases, such as eczema and psoria-
sis, may also present with gynecologic symptoms.
Heavy vaginal discharge may also be nor-
mal. This situation is a diagnosis of exclusion
but is important to recognize in order to allay
the patient’s anxiety and avoid unnecessary
doi:10.3949/ccjm.84a.15163 treatment.
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 VULVAR AND VAGINAL DISORDERS

TABLE 1 thelial cells, blood cells, “clue” cells (ie, epithe-

lial cells with borders studded or obscured by
Common causes of vulvovaginitis bacteria), and motile trichomonads.
10% KOH whiff test and microscopy.
Infectious
To a second vaginal sample, a small amount
Bacterial vaginosis of 10% potassium hydroxide should be added,
Vulvovaginal candidiasis and the examiner should sniff it. An amine or
fishy odor is a sign of bacterial vaginosis.
Trichomoniasis
The sample should next be examined
Herpes simplex virus infection under a microscope for fungal elements (Fig-
Cervicitis ure 2). However, not finding trichomonads
or fungal elements by either saline or 10%
Noninfectious KOH microscopy does not rule out such in-
Desquamative inflammatory vaginitis fections.
If pH paper, KOH, and a microscope are
Atrophic vaginitis unavailable, other point-of-care tests can be
Aphthous ulcers (“canker sores”) used for specific conditions as discussed be-
Urogenital manifestation of Behçet disease low.
Lichen planus, lichen sclerosus ■ INFECTIOUS CAUSES
Contact, chemical, or radiation dermatitis
Infectious causes of vulvovaginitis include
Vulvar and vaginal malignancies bacterial vaginosis, candidiasis, trichomonia-
Vulvar intraepithelial neoplasia sis, and herpes simplex virus (HSV) infection.
Parasitic infestation
■ BACTERIAL VAGINOSIS
Vulvodynia (ie, chronic vulvar pain of unknown
etiology) Bacterial vaginosis is the most common vagi-
Vulvovaginitis nal disorder worldwide. It has been linked to
Foreign body (eg, tampon) preterm delivery, intra-amniotic infection,
typically Vulvar dermatoses endometritis, postabortion infection, and vag-
presents with Eczema inal cuff cellulitis after hysterectomy.3 It may
itching, burning, also be a risk factor for human immunodefi-
Psoriasis
ciency virus (HIV) infection.4
and discharge Plasma cell vulvitis The condition reflects a microbial imbal-
ance in the vaginal ecosystem, characterized
by depletion of the dominant hydrogen per-
oxide-producing lactobacilli and overgrowth
■ SIMPLE OFFICE-BASED ASSESSMENT
of anaerobic and facultative aerobic organ-
A thorough history and physical examination isms such as Gardnerella vaginalis, Mycoplasma
are always warranted. hominis, Atopobium vaginae, and Prevotella and
Simple tests of vaginal secretions can often Mobiluncus species.
determine the diagnosis (Table 2). Vaginal se-
cretions should be analyzed in the following Diagnosis of bacterial vaginosis
order: The Amsel criteria consist of the following:
Testing the pH. The pH can help deter- • pH greater than 4.5
mine likely diagnoses and streamline further • Positive whiff test
testing (Figure 1). • Homogeneous discharge
Saline microscopy. Some of the vaginal • Clue cells.
discharge sample should be diluted with 1 or Three of the four criteria must be present for a
2 drops of normal saline and examined under diagnosis of bacterial vaginosis. This method
a microscope, first at × 10 magnification, then is inexpensive and provides immediate results
at × 40. The sample should be searched for epi- in the clinic.
216 C LEV ELA N D C LINIC J OURNAL OF MEDICINE VOL UME 84 • NUM BE R 3 M ARCH 2017
 GOJE AND MUNOZ

TABLE 2
Vaginal secretion test results for common causes of vulvovaginitis
Condition pH Saline microscopy ± 10% KOH 10% KOH Other test Gold standard
Normal < 4.5 Normal flora, lactobacillus present, some Not Clinical None
white blood cells (WBCs) may be present applicable diagnosis
Candidiasis < 4.5 Hyphae, blastophores may be seen Fungal Vaginal DNA Fungal culture
elements probe a
WBCs may be abundant
Bacterial > 4.5 Clue cells, lactobacillus may be absent Positive Vaginal DNA Gram stain
vaginosis or reduced whiff probe (Nugent score)
Coccobacillary flora

Trichomoniasis Normal Trichomonads may be seen Variable Vaginal DNA Polymerase chain
or > 4.5 probe a reaction test for
WBCs may be abundant Trichomonas vaginalis
Trichomonas
culture
Atrophic > 4.5 Parabasal cells, decreased flora, some- Not Vaginal Vaginal Maturation
vaginitis times decreased vaginal epithelial cells applicable Maturation Index
Index
Desquamative > 4.5 Parabasal cells, sheets of WBCs, mixed Not Clinical Clinical diagnosis
inflammatory flora applicable diagnosis
vaginitis
a
Vaginal DNA probe is the nonculture, nonamplified test (Affirm VPIII).

The Nugent score, based on seeing cer- the test has a sensitivity of 87.7% to 95.2%
tain bacteria from a vaginal swab on Gram and a specificity of 81% to 99.1% for bacte-
stain microscopy, is the diagnostic standard rial vaginosis.7
for research.5 In 323 symptomatic women, a poly-
DNA tests. Affirm VPIII (BD Diagnos- merase chain reaction (PCR) assay for
tics, Sparks, MD) is a nonamplified nucleic bacterial vaginosis was 96.9% sensitive
acid probe hybridization test that detects and 92.6% specific for bacterial vaginosis,
Trichomonas vaginalis, Candida albicans, and and Affirm VPIII was 90.1% sensitive and
G vaginalis. Although it is more expensive 67.6% specific, compared with a reference
than testing for the Amsel criteria, it is com- standard incorporating Nugent Gram-stain
monly used in private offices because it is scores and Amsel criteria.8 The test is com-
simple to use, gives rapid results, and does mercially available.
not require a microscope.6 Insurance pays for
it when the test is indicated, but we know Management of bacterial vaginosis
of a patient who received a bill for approxi- Initial treatment. Bacterial vaginosis can be
mately $500 when the insurance company treated with oral or topical metronidazole,
thought the test was not indicated. oral tinidazole, or oral or topical clindamy-
In a study of 109 patients with symp- cin.9 All options offer equivalent efficacy as
toms of vulvovaginitis, the Affirm VPIII was initial treatments, so the choice may be based
found comparable to saline microscopy when on cost and preferred route of administration.
tested on residual vaginal samples. Com- Treatment for recurrent disease. Women
pared with Gram stain using Nugent scoring, who have 3 or more episodes in 12 months
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 VULVAR AND VAGINAL DISORDERS

Symptoms and examination indicate vulvovaginitis

Check vaginal pH

Normal pH Abnormal pH (> 4.5)

Infectious causes Noninfectious causes Infectious causes Noninfectious causes

Vulvovaginal candidiasis a Vulvodynia Bacterial vaginosis Blood
Herpes simplex virus Physiologic leukorrhea Trichomoniasis Semen
infection
Dermatosis Cervicitis Cervical mucus
Dermatitis Amniotic fluid
Desquamative
inflammatory vaginitis
Vaginal atrophy
Lichen planus
a
Candidal infections are usually acidic, with pH < 4.0, but pH paper does not measure this.

FIGURE 1. Using pH as a diagnostic tool in vulvovaginitis.

should receive initial treatment each time as ■ VULVOVAGINAL CANDIDIASIS

described above and should then be offered Vulvovaginal candidiasis is the second most
additional suppressive therapy with 0.75% common cause of vaginitis.
metronidazole intravaginal gel 2 times a week
Simple for 4 months. A side effect of therapy is vulvo- Diagnosis can be clinical
vaginal candidiasis, which should be treated Vulvovaginal candidiasis can be clinically
laboratory diagnosed on the basis of cottage cheese-like
as needed.
evaluation In a multicenter study, Sobel et al10 ran- clumpy discharge; external dysuria (a burning
of secretions domized patients who had recurrent bacterial sensation when urine comes in contact with
vaginosis to twice-weekly metronidazole gel or the vulva); and vulvar itching, pain, swelling,
can often and redness. Edema, fissures, and excoriations
placebo for 16 weeks after their initial treat-
determine ment. During the 28 weeks of follow-up, re- may be seen on examination of the vulva.
(Figure 3).
the diagnosis currences occurred in 51% of treated women
Saline microscopy (Figure 2) with the addi-
vs 75% of those on placebo.
tion of 10% KOH may reveal the characteristic
Another option for chronic therapy is oral
fungal elements, but its sensitivity is only 50%.
metronidazole and boric acid vaginal supposi- Fungal culture remains the gold standard
tories. for diagnosis and is needed to determine the
Reichman et al11 treated women with oral sensitivity of specific strains of Candida to
metronidazole or tinidazole 500 mg twice a therapy.12
day for 7 days, followed by vaginal boric acid DNA tests can also be helpful. In a study
600 mg daily for 21 days. This was followed by of patients with symptomatic vaginitis, Affirm
twice-weekly vaginal metronidazole gel for 16 VPIII detected Candida in 11% of samples,
weeks. At follow-up, the cure rate was 92% whereas microscopy detected it in only 7%.13
at 7 weeks, dropping to 88% at 12 weeks and Another study7 found that Affirm VPIII pro-
50% at 36 weeks. duced comparable results whether the sample
Patients with recurrent bacterial vaginosis was collected from residual vaginal discharge
despite therapy should be referred to a vulvo- found on the speculum or was collected in the
vaginal or infectious disease specialist. traditional way (by swabbing).
218 C LEV ELA N D C LINIC J OURNAL OF MEDICINE VOL UME 84 • NUM BE R 3 M ARCH 2017
 GOJE AND MUNOZ

Cartwright et al8 compared the perfor-

mance of a multiplexed, real-time PCR assay
and Affirm VPIII in 102 patients. PCR was
much more sensitive (97.7% vs 58.1%) but
less specific (93.2% vs 100%), with culture
serving as the gold standard.
Management of candidiasis
Uncomplicated cases can be managed with
prescription or over-the-counter topical or
oral antifungal medications for 1 to 7 days,
depending on the medication.9 However,
most of the common antifungals may not be
effective against non-albicans Candida.
In immunosuppressed patients and diabet-
ic patients, if symptoms do not improve with FIGURE 2. Potassium hydroxide 10% added to a vaginal
regular treatment, a vaginal sample should be sample and microscopy performed at × 40 magnification
cultured for C albicans. If the culture is positive, reveals yeast.
the patient should be treated with fluconazole
150 mg orally every 3 days for 3 doses.14
Patients with recurrent episodes (3 or more
in 12 months) should follow initial treatment
with maintenance therapy of weekly flucon-
azole 150 mg orally for 6 months.15
Non-albicans Candida may be azole-
resistant, and fungal culture and sensitivity
should be obtained. Sobel et al13 documented
successful treatment of non-albicans Candida
using boric acid and flucytosine. Phillips16
documented successful use of compounded
amphotericin B in a 50-mg vaginal supposi-
tory for 14 days. Therefore, in patients who
have Candida species other than C albicans,
treatment should be one of the following:
• Vaginal boric acid 600 mg daily for 14 to
21 days
• Flucytosine in 15.5% vaginal cream, intra-
vaginally administered as 5 g for 14 days
• Amphotericin B 50 mg vaginal supposito-
ries for 14 days.
Boric acid is readily available, but flucyto-
sine vaginal cream and amphotericin B vagi-
nal suppositories must usually be compounded
by a pharmacist.
Of note: All that itches is not yeast. Pa-
tients with persistent itching despite treat-
ment should be referred to a specialist to
search for another cause.

■ TRICHOMONIASIS
The incidence of T vaginalis infection is FIGURE 3. Erythema, excoriation, and fissures of vulvovagi-
higher than that of Neisseria gonorrhoeae and nal candidiasis.

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 VULVAR AND VAGINAL DISORDERS

tients diagnosed with T vaginalis by conven-

tional Pap smear should have a second test
performed. The liquid-based Pap test is more
accurate for microscopic diagnosis, and its
results can be used to determine if treatment
is needed (sensitivity 60%–90%; specificity
98%–100%).22,23
Culture. Amplification of T vaginalis in
liquid culture usually provides results within
3 days.24 It is more sensitive than microscopy
but less sensitive than a nucleic acid ampli-
fication test: compared with a nucleic acid
amplification test, culture is 44% to 75%
sensitive for detecting T vaginalis and 100%
specific.19 Culture is the preferred test for re-
sistant strains.
Non–culture-based or nucleic acid tests
do not require viable organisms, so they allow
for a wider range of specimen storage tem-
peratures and time intervals between collec-
tion and processing. This quality limits them
for testing treatment success; if performed too
early, they may detect nonviable organisms. A
2-week interval is recommended between the
end of treatment and retesting.25
Nonamplified tests such as Affirm VPIII
and the Osom Trichomonas Test (Sekisui Di-
agnostics, Lexington, MA) are 40% to 95%
sensitive, depending on the test and reference
standard used, and 92% to 100% specific.26,27
Nucleic acid amplification tests are usually
FIGURE 4. Primary herpes simplex virus infection, with clas-
not performed as point-of-care tests. They are
sic vesicles and pustules crusting over and edema of vulva.
more expensive and require special equipment
with trained personnel. Sensitivities range
Chlamydia trachomatis combined, with an esti-
from 76% to 100%, making these tests more
mated 7.4 million new cases occurring in the
suitable for screening and testing of asymp-
year 2000 in the United States.17 Infection tomatic women, in whom the concentration
increases the sexual transmission of HIV.18–20 of organisms may be lower.
It is often asymptomatic and so is likely un-
derdiagnosed. Treatment of trichomoniasis
Treatment is a single 2-g oral dose of metroni-
Diagnosis of trichomoniasis dazole or tinidazole.9
Vaginal pH may be normal or elevated (> 4.5). If initial treatment is ineffective, an addi-
Direct microscopy. Observation by saline tional regimen can be either of the following:
microscopy of motile trichomonads with their • Oral metronidazole 500 mg twice a day for
characteristic jerky movements is 100% spe- 7 days
cific but only 50% sensitive. Sensitivity is re- • Oral metronidazole or tinidazole, 2 g daily
duced by delaying microscopy on the sample for 5 days.
by as little as 10 minutes.21 Patients allergic to nitroimidazoles should
The incidental finding of T vaginalis on be referred for desensitization.
a conventional Papanicolaou (Pap) smear If these treatments are unsuccessful, the
has poor sensitivity and specificity, and pa- patient should be referred to an infectious dis-
220 C LEV ELA N D C LINIC J OURNAL OF MEDICINE VOL UME 84 • NUM BE R 3 M ARCH 2017
 GOJE AND MUNOZ

ease specialist or gynecologist who specializes

in vulvovaginal disorders. Treatment failure is
uncommon and is usually related to noncom-
pliance, reinfection, or metronidazole resis-
tance.28 The US Centers for Disease Control
and Prevention offers testing for resistance by
request.
Reportedly successful regimens for refrac-
tory trichomoniasis include 14 days of either:
• Oral tinidazole 500 mg 4 times daily plus
vaginal tinidazole 500 mg twice daily29 Parabasal cell
• Oral tinidazole 1 g 3 times daily plus com-
pounded 5% intravaginal paromomycin 5
g nightly.30 Vaginal White blood cell
epithelial
■ HERPES SIMPLEX VIRUS INFECTION cell
HSV (HSV-1 and HSV-2) causes lifelong
infection. About 50 million people in the
United States are infected with HSV-2, the
most common cause of recurrent infections.31 FIGURE 5. On saline microscopy, desquamative inflam-
Owing to changes in sexual practices, an in- matory vaginitis shows the classic findings of leukorrhea,
creasing number of young people are acquiring epithelial cells, and parabasal cells (× 40).
anogenital HSV-1 infection.32,33
Diagnosis of herpes
Diagnosis may be difficult because the pain-
ful vesicular or ulcerative lesions (Figure 4)
may not be visible at the time of presentation.
Diagnosis is based on specific virologic and
serologic tests. Nonspecific tests (eg, Tzanck
smear, direct immunofluorescence) are neither
sensitive nor specific and should not be relied
on for diagnosis.34 HSV culture or HSV-PCR
testing of a lesion is preferred. The sensitivity
of viral culture can be low and is dependent
on the stage of healing of a lesion and obtain-
ing an adequate sample.
Accurate type-specific HSV serologic as-
says are based on HSV-specific glycoprotein
G1 (HSV-1) and glycoprotein G2 (HSV-2).
Unless a patient’s serologic status has already FIGURE 6. Atrophic vaginitis. Parabasal cells and a few im-
been determined, serologic testing should be mature squamous epithelial cells, rounded, with a large
done concurrently with HSV culture or PCR nucleus-to-cytoplasm ratio.
testing. Serologic testing enables classification
of an infection as primary, nonprimary, or re- specific and may be positive during recurrent
current. For example, a patient with a positive genital or oral episodes of herpes.35
HSV culture and negative serology most like-
ly has primary HSV infection, and serologic Treatment of herpes
study should be repeated after 6 to 8 weeks to In general, antiviral medications (eg, acyclo-
assess for seroconversion. vir, valacyclovir, famciclovir) are effective for
Immunoglobulin M (IgM) testing for managing HSV.12 Episodic or continuous sup-
HSV-1 or HSV-2 is not diagnostic or type- pression therapy may be needed for patients
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 VULVAR AND VAGINAL DISORDERS

the vulva may be erythematous, friable, and

tender to the touch. The vagina may have ec-
chymoses, be diffusely erythematous, and have
linear lesions. Mucoid or purulent discharge
may be seen.
The vaginal pH is greater than 4.5.
Saline microscopy shows increased para-
basal cells and leukorrhea (Figure 5).
Diagnosis is based on all of the following:
• At least 1 symptom (ie, vaginal discharge,
dyspareunia, pruritus, pain, irritation, or
burning)
• Vaginal inflammation on examination
• pH higher than 4.5
• Presence of parabasal cells and leukorrhea
on microscopy (a ratio of leukocytes to
vaginal epithelial cells > 1:1).36
Treatment involves use of 2% intravagi-
nal clindamycin or 10% intravaginal com-
pounded hydrocortisone cream for 4 to 6
weeks. Patients who are not cured with single-
agent therapy may benefit from compounded
clindamycin and hydrocortisone, with estro-
gen added to the formulation for hypoestro-
genic patients.
Atrophic vaginitis
Atrophic vaginitis is often seen in meno-
pausal or hypoestrogenic women. Presenting
symptoms include vulvar or vaginal pain and
FIGURE 7. Biopsy-proven lichen sclerosus. The patient pre- dyspareunia.
sented with intense pruritus and pain. Diagnosis. On physical examination, the
vulva appears pale and atrophic, with nar-
experiencing more than four outbreaks in 12 rowing of the introitus. Vaginal examination
months. Patients who do not respond to treat- may reveal a pale mucosa that lacks elasticity
ment should be referred to an infectious dis- and rugation. The examination should be per-
ease specialist and undergo a viral culture with formed with caution, as the vagina may bleed
sensitivities. easily.
The vaginal pH is usually elevated.
■ NONINFECTIOUS CAUSES Saline microscopy may show parabasal
cells and a paucity of epithelial cells. (Figure
Desquamative inflammatory vaginitis 6).
Desquamative inflammatory vaginitis is a The Vaginal Maturation Index is an in-
chronic vaginal disorder of unknown cause. dicator of the maturity of the epithelial cell
It is a diagnosis of exclusion, and some pa- types being exfoliated; these normally include
tients may have a superimposed bacterial in- parabasal (immature) cells, intermediate, and
fection. It occurs mostly in perimenopausal superficial (mature) cells. A predominance
woman and is often associated with low es- of immature cells indicates a hypoestrogenic
trogen levels. state.
Diagnosis. Patients may report copious Infection should be considered and treated
green-yellow mucoid discharge, vulvar or vag- as needed.
inal pain, and dyspareunia. On examination, Treatment. Patients with no contraindi-
222 C LEV ELA N D C LINIC J OURNAL OF MEDICINE VOL UME 84 • NUM BE R 3 M ARCH 2017
 GOJE AND MUNOZ

cation may benefit from systemic hormone

therapy or topical estrogen, or both.
Contact dermatitis
Contact dermatitis is classified into two types:
Irritant dermatitis, caused by the destruc-
tive action of contactants, eg, urine, feces,
topical agents, feminine wipes
Allergic dermatitis, also contactant-in-
duced, but immunologically mediated.
If a diagnosis cannot be made from the pa-
tient history and physical examination, biopsy
should be performed.
Treatment of contact dermatitis involves
removing the irritant, hydrating the skin with
sitz baths, and using an emollient (eg, petro-
leum jelly) and midpotent topical steroids
until resolution. Some patients benefit from
topical immunosuppressive agents (eg, tacro-
limus). Patients with severe symptoms may be
treated with a tapering course of oral steroids
for 5 to 7 days. Recalcitrant cases should be
referred to a specialist.
Lichen planus
Vulvovaginal lichen planus, a subtype of li-
chen planus, is characterized by erosive, papu-
lar, or hypertrophic lesions on the vulva, with
or without vaginal involvement.
Lichen sclerosus is a benign, chronic, pro-
gressive dermatologic condition characterized
by marked inflammation, epithelial thinning, FIGURE 8. Biopsy-proven lichen sclerosus and lichen planus
and distinctive dermal changes accompanied at various areas of the vulva.
by pruritus and pain (Figures 7 and 8).
Treatment. High-potency topical ste- processes, superimposed infections (mostly
roids are the mainstay of therapy for lichen bacterial and fungal) may also be present and
disease. Although these are not infectious should be treated. ■

■ REFERENCES collected from the speculum to characterize vaginitis in symptom-

1. Van Eyk N, Allen L, Giesbrecht E, et al. Pediatric vulvovaginal disor- atic women. J Low Genit Tract Dis 2014; 18:344–346.
ders: a diagnostic approach and review of the literature. J Obstet 8. Cartwright CP, Lembke BD, Ramachandran K, et al. Comparison of
Gynaecol Can 2009; 31:850–862. nucleic acid amplification assays with BD Affirm VPIII for diag-
2. McGreal S, Wood P. Recurrent vaginal discharge in children. J Pedi- nosis of vaginitis in symptomatic women. J Clin Microbiol 2013;
atr Adolesc Gynecol 2013; 26:205–208. 51:3694–3699.
3. Livengood CH. Bacterial vaginosis: an overview for 2009. Rev Obstet 9. Workowski KA, Bolan GA; Centers for Disease Control and Preven-
Gynecol 2009; 2:28–37. tion (CDC). Sexually transmitted diseases treatment guidelines,
4. Atashili J, Poole C, Ndumbe PM, Adimora AA, Smith JS. Bacterial 2015. MMWR Recomm Rep 2015; 64:1–137.
vaginosis and HIV acquisition: a meta-analysis of published studies. 10. Sobel JD, Ferris D, Schwebke J, et al. Suppressive antibacterial
AIDS 2008; 22:1493–1501. therapy with 0.75% metronidazole vaginal gel to prevent recurrent
5. Money D. The laboratory diagnosis of bacterial vaginosis. Can J bacterial vaginosis. Am J Obstet Gynecol 2006; 194:1283–1289.
Infect Dis Med Microbiol 2005; 16:77–79. 11. Reichman O, Akins R, Sobel JD. Boric acid addition to suppressive
6. Lowe NK, Neal JL, Ryan-Wenger NA, et al. Accuracy of the clinical antimicrobial therapy for recurrent bacterial vaginosis. Sex Transm
diagnosis of vaginitis compared with a DNA probe laboratory stan- Dis 2009; 36:732–734.
dard. Obstet Gynecol 2009; 113:89–95. 12. Carr PL, Felsenstein D, Friedman RH. Evaluation and management
7. Mulhem E, Boyanton BL Jr, Robinson-Dunn B, Ebert C, Dzebo R. of vaginitis. J Gen Intern Med 1998; 13:335–346.
Performance of the Affirm VP-III using residual vaginal discharge 13. Sobel JD, Chaim W, Nagappan V, Leaman D. Treatment of vaginitis

CL E V E L AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 84 • NUM BE R 3 M ARCH 2 0 1 7 223

 VULVAR AND VAGINAL DISORDERS

caused by Candida glabrata: use of topical boric acid and flucyto- tion for detection of Trichomonas vaginalis vaginitis in specimens
sine. Am J Obstet Gynecol 2003; 189:1297–1300. from women with a low prevalence of infection. J Clin Microbiol
14. Sobel JD, Kapernick PS, Zervos M, et al. Treatment of complicated 2008; 46:3467–3469.
Candida vaginitis: comparison of single and sequential doses of 27. Chapin K, Andrea S. APTIMA Trichomonas vaginalis, a transcription-
fluconazole. Am J Obstet Gynecol 2001; 185:363–369. mediated amplification assay for detection of Trichomonas vaginalis
15. Sobel JD, Wiesenfeld HC, Martens M, et al. Maintenance flucon- in urogenital specimens. Expert Rev Mol Diagn 2011; 11:679–688.
azole therapy for recurrent vulvovaginal candidiasis. N Engl J Med 28. Krashin JW, Koumans EH, Bradshaw-Sydnor AC, et al. Trichomonas
2004; 351:876–883. vaginalis prevalence, incidence, risk factors and antibiotic-resistance
16. Phillips AJ. Treatment of non-albicans Candida vaginitis with in an adolescent population. Sex Transm Dis 2010; 37:440–444.
amphotericin B vaginal suppositories. Am J Obstet Gynecol 2005; 29. Sobel JD, Nyirjesy P, Brown W. Tinidazole therapy for metronida-
192:2009–2013. zole-resistant vaginal trichomoniasis. Clin Infect Dis 2001; 33:1341–
17. Weinstock H, Berman S, Cates W Jr. Sexually transmitted diseases
1346.
among American youth: incidence and prevalence estimates, 2000.
30. Nyirjesy P, Gilbert J, Mulcahy LJ. Resistant trichomoniasis: success-
Perspect Sex Reprod Health 2004; 36:6–10.
ful treatment with combination therapy. Sex Transm Dis 2011;
18. Gatski M, Martin DH, Clark RA, Harville E, Schmidt N, Kissinger
38:962–963.
P. Co-occurrence of Trichomonas vaginalis and bacterial vaginosis
31. Bradley H, Markowitz LE, Gibson T, McQuillan GM. Seroprevalence
among HIV-positive women. Sex Transm Dis 2011; 38:163–166.
of herpes simplex virus types 1 and 2—United States, 1999–2010. J
19. Hobbs MM, Seña AC. Modern diagnosis of Trichomonas vaginalis
infection. Sex Transm Infect 2013; 89:434–438. Infect Dis 2014; 209:325–333.
20. McClelland RS, Sangare L, Hassan WM, et al. Infection with Tricho- 32. Roberts CM, Pfister JR, Spear SJ. Increasing proportion of herpes
monas vaginalis increases the risk of HIV-1 acquisition. J Infect Dis simplex virus type 1 as a cause of genital herpes infection in college
2007; 195:698–702. students. Sex Transm Dis 2003; 30:797–800.
21. Kingston MA, Bansal D, Carlin EM. ‘Shelf life’ of Trichomonas vagi- 33. Ryder N, Jin F, McNulty AM, Grulich AE, Donovan B. Increasing role
nalis. Int J STD AIDS 2003; 14:28–29. of herpes simplex virus type 1 in first-episode anogenital herpes in
22. Aslan DL, Gulbahce HE, Stelow EB, et al. The diagnosis of Tricho- heterosexual women and younger men who have sex with men,
monas vaginalis in liquid-based Pap tests: correlation with PCR. 1992-2006. Sex Transm Infect 2009; 85:416–419.
Diagn Cytopathol 2005; 32:341–344. 34. Caviness AC, Oelze LL, Saz UE, Greer JM, Demmler-Harrison GJ.
23. Lara-Torre E, Pinkerton JS. Accuracy of detection of Trichomonas Direct immunofluorescence assay compared to cell culture for the
vaginalis organisms on a liquid-based papanicolaou smear. Am J diagnosis of mucocutaneous herpes simplex virus infections in chil-
Obstet Gynecol 2003; 188:354–356. dren. J Clin Virol 2010; 49:58–60.
24. Hobbs MM, Lapple DM, Lawing LF, et al. Methods for detection 35. Morrow R, Friedrich D. Performance of a novel test for IgM and IgG
of Trichomonas vaginalis in the male partners of infected women: antibodies in subjects with culture-documented genital herpes sim-
implications for control of trichomoniasis. J Clin Microbiol 2006; plex virus-1 or -2 infection. Clin Microbiol Infect 2006; 12:463–469.
44:3994–3999. 36. Bradford J, Fischer G. Desquamative inflammatory vaginitis: differ-
25. Van Der Pol B, Williams JA, Orr DP, Batteiger BE, Fortenberry JD. ential diagnosis and alternate diagnostic criteria. J Low Genit Tract
Prevalence, incidence, natural history, and response to treatment of Dis 2010; 14:306–310.
Trichomonas vaginalis infection among adolescent women. J Infect
Dis 2005; 192:2039–2044. ADDRESS: Oluwatosin Goje, MD, MSCR, FACOG, Women’s Health Insti-
26. Campbell L, Woods V, Lloyd T, Elsayed S, Church DL. Evaluation of tute, A81, Cleveland Clinic, 9500 Euclid Avenue, Cleveland OH 44106;
the OSOM Trichomonas rapid test versus wet preparation examina- gojeo@ccf.org

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