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Approach to females with symptoms of vaginitis

Approach to females with symptoms of vaginitis
Author:
Jack D Sobel, MD
Section Editor:
Robert L Barbieri, MD
Deputy Editor:
Kristen Eckler, MD, FACOG
Literature review current through: Feb 2022. | This topic last updated: May 25, 2021.

INTRODUCTION — Vaginitis is the general term for disorders of the vagina caused by infection, inflammation, or changes in the normal vaginal flora. Symptoms include vaginal discharge, odor, pruritus, and/or discomfort. The initial evaluation typically consists of a history, physical examination, microscopy, and cervical tests for sexually transmitted infections. Women whose initial evaluation confirms a diagnosis then receive targeted treatment. Women who remain without a diagnosis, or whose symptoms recur, then go through a more detailed evaluation process.

This topic will discuss the approach to women who present with symptoms of vaginitis from an unknown cause. Detailed reviews of specific causes of vaginitis are presented separately:

(See "Candida vulvovaginitis: Clinical manifestations and diagnosis".)

(See "Bacterial vaginosis: Clinical manifestations and diagnosis".)

(See "Trichomoniasis".)

PATHOGENESIS

Vaginal ecosystem – The nonkeratinized stratified squamous epithelium of the vagina in normally estrogenized premenopausal women is rich in glycogen. Glycogen from sloughed cells is the substrate for Döderlein lactobacilli, which convert glucose into lactic acid, thereby creating an acidic vaginal environment (pH 4.0 to 4.5). This acidity helps maintain the normal vaginal flora and inhibits growth of pathogenic organisms. Disruption of the normal ecosystem can lead to conditions favorable for development of vaginitis. Some of these potentially disruptive factors include sexually transmitted diseases, antibiotics, foreign body, estrogen level, use of hygienic products, pregnancy, sexual activity, and contraceptive choice.

Etiology – Vaginitis is often the result of infectious agents. The most common infections, bacterial vaginosis, Candida vulvovaginitis, and trichomoniasis, account for over 90 percent of infections [1]. Cervicitis, typically from sexually transmitted infections gonorrhea, chlamydia, and mycoplasma, can also present as nonspecific vaginal symptoms.

(See "Bacterial vaginosis: Clinical manifestations and diagnosis".)

(See "Candida vulvovaginitis: Clinical manifestations and diagnosis".)

(See "Trichomoniasis".)

(See "Screening for sexually transmitted infections".)

Noninfectious etiologies include vaginal atrophy/atrophic vaginitis in postmenopausal women, foreign body (eg, retained tampon or condom), irritants and allergens (eg, vaginal washes or douches), and several rarer entities including some systemic medical disorders (eg, rheumatoid arthritis and systemic lupus).

Epidemiology – In a telephone survey of random women in the United States, 8 percent of White women and 18 percent of African American women reported an episode of vaginal symptoms of any severity in the previous year [2]. A health care professional was consulted in 55 and 83 percent of cases, respectively, and most women purchased an over-the-counter antifungal preparation to treat their symptoms, whether or not they saw a physician.

PATIENT PRESENTATION — Women with vaginitis typically present with one or more of the following nonspecific vulvovaginal symptoms:

Change in the volume, color, or odor of vaginal discharge

Pruritus

Burning

Irritation

Erythema

Dyspareunia

Spotting

Dysuria

Vaginal discharge is a prominent symptom of vaginitis but may be difficult to distinguish from normal vaginal discharge. In reproductive-aged women, normal vaginal discharge consists of 1 to 4 mL fluid (per 24 hours), which is white or transparent, thick or thin, and mostly odorless. This physiologic discharge is formed by mucoid endocervical secretions in combination with sloughing epithelial cells, normal vaginal flora, and vaginal transudate. The discharge may become more noticeable at times ("physiological leukorrhea"), such as at midmenstrual cycle close to the time of ovulation or during pregnancy or use of estrogen-progestin contraceptives. Diet, sexual activity, medication, and stress can also affect the volume and character of normal vaginal discharge. Although normal discharge may be yellowish, slightly malodorous, and accompanied by mild irritative symptoms [3], it is not accompanied by pruritus, pain, burning or significant irritation, erythema, local erosions, or cervical or vaginal friability. The absence of these signs and symptoms helps to distinguish normal vaginal discharge from discharge related to a pathological process, such as vaginitis or cervicitis. (See 'Leukorrhea' below.)

OUR APPROACH — Based on a literature review, the author and other experts follow six steps in assessing female patients who present with vulvovaginal complaints [4]:

Identify the anatomic site of discomfort – Vulva, clitoris, vestibule, vagina, cervix, and/or pelvis. (See 'Physical examination' below.)

Consider that more than one condition may be present. (See 'Common diagnoses' below.)

Evaluate each symptom, including vaginal discharge, itching, and/or pain, separately. (See 'History' below.)

Evaluate vaginal secretions with both pH and wet mount. (See 'Diagnostic studies' below.)

Schedule a follow-up visit for two to four weeks after initial intervention to assess response.

In patients whose symptoms persist despite treatment, reevaluate for additional causes and perform a biopsy if no other etiologies are identified. (See 'Women without a diagnosis after initial evaluation' below.)

Given the nonspecific nature of vaginitis symptoms (table 1), laboratory documentation of the etiology of vaginitis is mandatory before initiating therapy [5]. Diagnostic testing enables targeted treatment, increases therapeutic compliance, and increases the likelihood of partner notification [6]. Empiric therapy based on history and physical examination alone should be avoided because of frequent misdiagnosis and inappropriate therapy [7,8]. In one study of over 300 symptomatic individuals, 47 percent of those with a laboratory diagnosis (81 out of 170) received one or more inappropriate prescriptions [9].

The main steps in the initial evaluation of women with symptoms of vaginitis are:

Obtain a history and perform a physical examination – The history often leads the clinician toward a particular diagnosis (table 2), which must be confirmed in the office by examination of vaginal secretions. During physical examination, vaginal pH is determined as that will drive the subsequent diagnostic process. (See 'History' below and 'Physical examination' below.)

Test for vaginal and cervical infections – The vaginal infections bacterial vaginosis (BV), vulvovaginal candidiasis, and trichomoniasis account for over 90 percent of vaginitis in premenopausal women and can be diagnosed by pH testing, microscopy, and/or culture or rapid antigen and nucleic acid amplification tests [1,10]. A literature review concluded that the initial office evaluation (history and physical examination; pH, wet mount microscopy, and whiff test of vaginal discharge) correctly diagnosed 60 percent of candidal vulvovaginitis, 70 percent of trichomoniasis, and 90 percent of BV [11].

For sexually active women, we also test for sexually transmitted cervical infections (eg, gonorrhea and chlamydia) as coinfections can be present. (See 'Diagnostic studies' below.)

Treat.

Infection – Targeted antimicrobial treatment as indicated by tests.

Vulvovaginal atrophy – Begin topical treatment for vulvovaginal atrophy if present on physical examination. If an infection is also present, topical vaginal estrogen therapy (cream, tablet, or ring) or nonhormonal vaginal moisturizers can be started once the vaginal infection has been treated. (See 'Special populations' below.)

Reassess after targeted treatment.

For women in whom an etiology is identified and whose symptoms resolve after initial targeted treatment, no further evaluation is needed. (See 'Initial findings' below.)

For women in whom an etiology is not identified, we proceed to evaluate for less common and rare causes of vaginitis. Twenty-five to 40 percent of patients with genital symptoms will not have a specific cause identified on initial diagnostic evaluation [12]. These women tend to have a noninfectious etiology of symptoms as discussed below. (See 'Women without a diagnosis after initial evaluation' below.)

For women who are diagnosed and treated but continue to exhibit symptoms, we repeat testing for vaginal and cervical infections. The causes of recurrent symptoms are complex and depend on pathogen or causal mechanisms. Sexual partners can cause recurrence of cervicitis or vaginitis resulting from sexually transmitted infection pathogens (eg, trichomonas or N. gonorrhea). (See 'Special populations' below.)

INITIAL DIAGNOSTIC EVALUATION

History — The initial history questions gather details of the patient's symptoms. However, none of the findings from the history allows a definitive diagnosis since there is considerable overlap in symptoms among the different etiologies of vaginitis (table 1) [3,13]. Our initial evaluation includes questions about the following:

Discharge – If discharge is present, what is the quantity, color, consistency, and odor? Classic descriptions of the vaginal discharge associated with the three most common vaginal infections are as follows:

Bacterial vaginosis (BV) – The discharge of BV is typically malodorous, thin, grey (never yellow), and is a prominent complaint. (See "Bacterial vaginosis: Clinical manifestations and diagnosis".)

Vaginal candidiasis – Vaginal candidiasis typically presents with scant discharge that is thick, white, odorless, and often curd-like. (See "Candida vulvovaginitis: Clinical manifestations and diagnosis".)

Trichomoniasis – Trichomoniasis is characterized by purulent, malodorous discharge, which may be accompanied by burning, pruritus, dysuria, frequency, and/or dyspareunia. (See "Trichomoniasis".)

Burning, irritation, or other discomfortCandida vulvovaginitis often presents with marked inflammatory symptoms (pruritus and soreness). In contrast, BV is associated with only minimal inflammation and minimal irritative symptoms. Burning and irritation can also be a symptom of noninfectious disorders such as vulvodynia. (See "Candida vulvovaginitis: Clinical manifestations and diagnosis" and "Bacterial vaginosis: Clinical manifestations and diagnosis" and "Clinical manifestations and diagnosis of vulvodynia (vulvar pain of unknown cause)".)

Pruritus – General pruritus is suggestive of a diffuse process such as infection, allergy, or dermatosis. Persistent or chronic focal pruritus is suggestive of a localized process such as neoplasia or malignancy. (See 'Pruritus' below.)

Vaginal bleeding – Vaginal bleeding is not consistent with infectious vaginitis. If vaginal bleeding is present, the patient should be evaluated for erosive causes of vaginitis (eg, erosive lichen planus) or a uterine source. (See "Vulvar lesions: Differential diagnosis of vesicles, bullae, erosions, and ulcers", section on 'Erosions, excoriations, and fissures' and "Abnormal uterine bleeding in nonpregnant reproductive-age patients: Evaluation and approach to diagnosis".)

Pain – Women with predominant pain symptoms are evaluated for inflammatory causes of vaginitis or nonvaginal sources, such as pelvic floor myofascial pain or vulvodynia. (See 'Inflammation or irritation' below and "Clinical manifestations and diagnosis of myofascial pelvic pain syndrome in women" and "Clinical manifestations and diagnosis of vulvodynia (vulvar pain of unknown cause)".)

Dysuria or dyspareunia – These symptoms can be suggestive of inflammatory disorders such as infection or allergy as well vulvovaginal atrophy. (See 'Inflammation or irritation' below and "Genitourinary syndrome of menopause (vulvovaginal atrophy): Clinical manifestations and diagnosis".)

Timing of symptoms – Symptoms of candidal vulvovaginitis often occur in the premenstrual period, while symptoms of trichomoniasis and BV often occur during or immediately after the menstrual period. Symptoms that develop soon after sexual intercourse are suggestive of sexually transmitted infections (STIs). Symptoms that develop after gynecologic surgery such as hysterectomy can suggest a vaginal fistula.

Estrogen status – Low estrogen levels can cause genitourinary syndrome of menopause (ie, vulvovaginal atrophy) that presents with symptoms of vaginitis. Other symptoms include vaginal dryness and dyspareunia. In addition to menopausal women, hypoestrogenic women include those who are postpartum, lactating, or taking antiestrogenic drugs. Some women develop relatively low estrogen levels related to contraceptive use. Menopausal women receiving systemic hormone therapy may not have adequate estrogen levels for vaginal health and thus remain prone to atrophic vaginitis. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Clinical manifestations and diagnosis".)

Physical examination — All women with suspected vaginitis should undergo a physical examination and some diagnostic studies. The physical examination assesses the degree of vulvovaginal inflammation, characteristics of the vaginal discharge, and presence of lesions or foreign bodies. Other potentially significant findings include signs of cervical inflammation and pelvic or cervical motion tenderness.

Vulva – Findings of the vulvar examination can help guide further evaluation and diagnosis.

Normal vulva are consistent with BV or leukorrhea.

Erythema, edema, or fissures suggest candidiasis, trichomoniasis, or dermatitis.

Atrophic changes are caused by hypoestrogenemia and suggest the possibility of atrophic vaginitis.

Changes in vulvovaginal architecture (eg, scarring) may be caused by a chronic inflammatory process, such as erosive lichen planus, as well as lichen sclerosus or mucous membrane pemphigoid rather than vaginitis.

Pain with application of pressure from a cotton swab ("Q-tip test") on the labia or at the vaginal introitus may indicate an inflammatory process (candidiasis, dermatosis) or provoked vulvodynia (ie, vulvar pain of unclear etiology).

Speculum examination is performed to evaluate the vagina, any vaginal discharge, and the cervix.

The vagina is examined for the following lesions:

-A foreign body (eg, retained tampon or condom) is easily detected and is often associated with vaginal discharge, intermittent bleeding or spotting, and/or an unpleasant odor due to inflammation and secondary infection. Removal of the foreign body is generally adequate treatment. Antibiotics are rarely indicated.

-Vaginal warts are skin-colored or pink and range from smooth flattened papules to a verrucous, papilliform appearance (picture 1). When extensive, they can be associated with vaginal discharge, pruritus, bleeding, burning, tenderness, and pain. (See "Condylomata acuminata (anogenital warts) in adults: Epidemiology, pathogenesis, clinical features, and diagnosis".)

-Granulation tissue or surgical site infection can cause vaginal discharge or bleeding after hysterectomy or after childbirth.

-Necrotic or inflammatory changes associated with malignancy in the lower or upper genital tract can result in vaginal discharge; spotting is more common in this setting than in infectious vaginitis.

-The presence of multifocal rounded macular erythematous lesions (like a spotted rash or bruise), purulent discharge, and tenderness suggests erosive vulvovaginitis, which can be caused by trichomoniasis or one of several noninfectious inflammatory etiologies (picture 2) [14].

Vaginal discharge – The characteristics of the vaginal discharge may suggest the type of infection, if present (table 1). Trichomoniasis is classically associated with a greenish-yellow purulent discharge; candidiasis with a thick, white, adherent, "cottage cheese-like" discharge; and BV with a thin, homogeneous, "fishy smelling" gray discharge. Inflammation and/or necrosis related to malignancy of the lower or upper genital tract can result in watery, mucoid, purulent, and/or bloody vaginal discharge. However, the appearance of the discharge is unreliable and should never form the basis for diagnosis [3]. A sample of vaginal discharge is collected with a cotton-swab and tested for pH and with microscopy. (See 'Diagnostic studies' below.)

Vesicovaginal and rectovaginal fistulas are rare, can be hard to detect, and are a source of chronic vaginal discharge. At-risk patients include those who are postpartum, posthysterectomy, postsurgery for prolapse, or have a history of inflammatory bowel disease or radiation therapy to the pelvis. (See "Rectovaginal and anovaginal fistulas" and "Urogenital tract fistulas in females".)

Cervix – Cervical inflammation with a normal vagina is suggestive of cervicitis rather than vaginitis. The cervix in women with cervicitis is usually erythematous and friable, with a mucopurulent discharge (picture 3). (See "Acute cervicitis".)

Cervical erythema in cervicitis should be distinguished from ectropion, which represents the normal physiologic presence of endocervical glandular tissue on the exocervix. Ectropion is more common in women taking estrogen-progestin contraceptives and during pregnancy. Ectropion may increase the volume of normal vaginal discharge. (See "Benign cervical lesions and congenital anomalies of the cervix", section on 'Ectropion'.)

Bimanual examination is performed to assess for tenderness and/or abnormal anatomy.

Women with vaginitis who also have pelvic or cervical motion tenderness are further evaluated for pelvic inflammatory disease. (See "Pelvic inflammatory disease: Clinical manifestations and diagnosis".)

Adnexal masses could represent a cyst or malignancy.

While bimanual examination can also identify pelvic muscle spasm and tenderness reflecting pelvic muscle dysfunction, these entities are not usually associated with abnormal vaginal discharge. (See "Clinical manifestations and diagnosis of myofascial pelvic pain syndrome in women".)

Diagnostic studies — Examining the vaginal discharge for pH, fishy amine odor, and microscopic evidence of infection can lead to a definitive diagnosis (table 1) [3,15].

Vaginal pH — Measurement of vaginal pH is the single most important finding that drives the diagnostic process and should always be determined. A pH test stick (or pH paper if available) is applied for a few seconds to the vaginal sidewall (to avoid contamination by blood, semen, or cervical mucus, which pool in the posterior fornix and distort results). Alternatively, the vaginal sidewall can be swabbed with a dry swab and then the swab rolled onto pH paper (if available). The pH of the specimen is stable for approximately two to five minutes at room temperature. The swab should not be premoistened, as the moistening liquid can affect pH.

Narrow range pH paper (4.0 to 5.5) is easier to interpret than broad range paper (4.5 to 7.5). An elevated pH in a premenopausal woman suggests infections such as BV (pH>4.5) or trichomoniasis (pH 5 to 6), and helps to exclude Candida vulvovaginitis (pH 4 to 4.5) (table 1).

The pH of the normal vaginal secretions in premenopausal women is 4.0 to 4.5 because these women have relatively high estrogen levels. Under the influence of estrogen, the normal vaginal epithelium cornifies and produces glycogen, which is the substrate for lactic acid production by lactobacilli. In premenarchal and postmenopausal women in whom estrogen levels are low, the pH of the normal vaginal secretions is ≥4.7. The higher pH is due to less glycogen in epithelial cells, reduced colonization of lactobacilli, and reduced lactic acid production. Thus measurement of pH for diagnosis of BV, trichomoniasis, or candidiasis is less useful at the extremes of age. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Clinical manifestations and diagnosis".)

Vaginal pH may be altered (usually to a higher pH) by contamination with lubricating gels, semen, blood, douches, and intravaginal medications. In pregnant women, leakage of amniotic fluid raises vaginal pH.

Microscopy

Steps — A sample of the patient's vaginal discharge is obtained with a cotton swab, smeared onto a slide, and evaluated under a microscope with both saline and potassium hydroxide in the steps below. Subsequent treatment is determined by the findings of the microscopic evaluation.

Saline wet mount – Vaginal discharge is generally sampled with a plastic or wood vaginal/cervical scraper or a cotton-tipped swab. The sample of vaginal discharge is mixed with one to two drops of 0.9 percent normal saline solution at room temperature on a glass slide. Cover slips are then placed on the slides, which are examined under a microscope at low and high power. Microscopy should be performed within 10 to 20 minutes of obtaining the sample to reduce the possibility of loss of motility of any trichomonads. (See "Trichomoniasis".)

Microscopic examination of normal vaginal discharge reveals a predominance of squamous epithelial cells, rare polymorphonuclear leukocytes (PMNs), and Lactobacillus species morphotype (table 1 and figure 1). The primary goal of the examination is to look for candidal buds (picture 4) or hyphae (picture 5), motile trichomonads (picture 6), epithelial cells studded with adherent coccobacilli (clue cells (picture 7 and picture 8)), and increased numbers of PMNs. Clue cells may be accompanied by Mobiluncus species (movie 1).

Excess PMNs without evidence of yeast, trichomonads, or clue cells suggest cervicitis or noninfectious or inflammatory vaginitis. (See "Acute cervicitis".)

The presence of parabasal epithelial cells suggests vaginal atrophy (picture 9).

Potassium hydroxide wet mount – The addition of 10 percent potassium hydroxide (KOH) to the wet mount of vaginal discharge destroys cellular elements, thus it is helpful for identifying hyphae and budding yeast for the diagnosis of candidal vaginitis (picture 4 and picture 5). (See "Candida vulvovaginitis: Clinical manifestations and diagnosis".)

Amine test – Smelling ("whiffing") the slide immediately after applying KOH is useful for detecting the fishy (amine) odor of BV. (See "Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Diagnosis'.)

If microscopy is negative — If microscopy is negative but yeast is suspected, additional testing by culture or nucleic acid amplification test (NAAT) for Candida species is important because microscopy is not sufficiently sensitive to exclude Candida in symptomatic patients. Similarly, a diagnostic test using NAAT, if available, is strongly advised if BV or trichomoniasis is suspected [10]. In one study, the sensitivity of microscopy for diagnosis of Candida species and Trichomonas vaginalis was only 22 and 62 percent, respectively, using Gram stain as the standard [5]. Sensitivity of microscopy is 50 percent compared with a standard of NAAT for trichomoniasis or culture for Candida species.

Bacterial cultures are rarely indicated in women with vaginal discharge. In fact, they are frequently misleading since a large variety of bacterial species colonize the vagina and are not vaginal pathogens [16]; identification of these bacteria may lead to unnecessary antibacterial therapy. Apart from Group A Streptococcus, a clear causal relationship between any bacteria and vaginitis has not been established in adults.

If microscopy is not available — If microscopy is not available, commercial diagnostic testing methods (eg, rapid antigen, NAATs, and polymerase chain reaction [PCR]) are used for confirming the clinical suspicion of BV, vaginal candidiasis, or trichomonas vaginitis [10,17]. A cross-sectional study of over 1700 women with vaginitis symptoms reported high sensitivity and specificity for detection of BV, candidiasis, and trichomoniasis by NAAT compared with traditional culture methods [10]. A different cross-sectional study of over 1500 individuals tested with a single-use, point-of-care PCR device reported sensitivities and specificities of over 96 percent for the detection of Neisseria gonorrhoeae, Chlamydia trachomatis, and T. vaginalis [17]. (See "Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Commercial tests' and "Trichomoniasis", section on 'Rapid antigen and DNA hybridization probes' and "Candida vulvovaginitis: Clinical manifestations and diagnosis".)

Microscopy is not sufficiently sensitive for diagnosis of Candida species; a culture for Candida species must be obtained. (See "Candida vulvovaginitis: Clinical manifestations and diagnosis", section on 'Office evaluation'.)

Cervical tests for STI — The STIs N. gonorrhoeae, C. trachomatis, and T. vaginalis must always be considered in sexually active individuals with vaginitis since females with STIs may go on to develop pelvic inflammatory disease and its potential complications. In a study of 581 vaginal specimens evaluated with molecular-based testing, one-quarter of the specimens positive for BV or Candida vulvovaginitis also tested positive for an STI (N. gonorrhoeae, C. trachomatis, or T. vaginalis) [18]. Any woman with new or multiple sexual partners, a symptomatic sexual partner, or an otherwise unexplained cervical or vaginal discharge that contains a high number of PMNs should be tested for these organisms by culture or an alternative sensitive test.

The presentation and diagnosis of these infections is presented in detail elsewhere:

(See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents".)

(See "Clinical manifestations and diagnosis of Chlamydia trachomatis infections".)

INITIAL FINDINGS

Alarm findings — Rarely, physical examination reveals an atypical cause of vaginitis that warrants a change in the diagnostic evaluation. Examples include an obvious vulvar, vaginal, or cervical cancer; probable pelvic inflammatory disease; purulent vaginitis; vulvovaginal ulceration; and vaginal fistulae. These women should be immediately referred for specialty evaluation and care.

(See "Vulvar cancer: Epidemiology, diagnosis, histopathology, and treatment".)

(See "Vaginal cancer".)

(See "Invasive cervical cancer: Epidemiology, risk factors, clinical manifestations, and diagnosis".)

(See "Pelvic inflammatory disease: Clinical manifestations and diagnosis".)

(See "Vulvar lesions: Differential diagnosis of vesicles, bullae, erosions, and ulcers", section on 'Ulcers'.)

(See "Urogenital tract fistulas in females".)

(See "Anorectal fistula: Clinical manifestations, diagnosis, and management principles".)

Common diagnoses — Of women who present for the evaluation of vaginitis, approximately 70 percent will be diagnosed with one of three vaginal infections: bacterial vaginosis (40 to 50 percent), Candida vulvovaginitis (20 to 25 percent), or trichomoniasis (15 to 20 percent) [3,19]. The sexually transmitted cervical infections gonorrhea and chlamydia are also commonly diagnosed causes of vaginitis in sexually active women. Lastly, in addition to infectious etiologies, hypoestrogenic women can have concomitant vulvovaginal atrophy. Women with a specific diagnosis receive treatment targeted to the etiology.

(See "Bacterial vaginosis: Treatment".)

(See "Candida vulvovaginitis: Treatment".)

(See "Trichomoniasis".)

(See "Treatment of uncomplicated Neisseria gonorrhoeae infections".)

(See "Treatment of Chlamydia trachomatis infection".)

(See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Treatment".)

Women who remain without a clear diagnosis after the initial evaluation continue with a more detailed evaluation. We avoid empiric therapy, as this can aggravate symptoms without benefit. (See 'Women without a diagnosis after initial evaluation' below.)

When to refer for specialty evaluation — We advise referral to a specialist in vulvovaginal disease for women whose symptoms persist in the absence of abnormal diagnostic tests and women who experience persistent symptoms or frequent symptom recurrence following diagnostic test-directed therapy (assuming lack of compliance has been excluded).

WOMEN WITHOUT A DIAGNOSIS AFTER INITIAL EVALUATION — As discussed above, 25 to 40 percent of patients with genital symptoms do not have a specific cause identified on initial diagnostic evaluation [12].

Secondary approach — Upon completion of the initial diagnostic evaluation above, some women remain without an identified cause of their symptoms. For women in whom Candida vaginitis, bacterial vaginosis (BV), and trichomoniasis have been excluded, and no other source of vaginitis has been identified, we take the following approach:

If the patient had minimal symptoms at the time of initial evaluation and the evaluation was nondiagnostic, we repeat the steps of the initial evaluation at a future visit when she is symptomatic. When symptoms persist without a clear diagnosis, the author advises biopsy of the symptomatic site [4].

Avoid empiric blind therapy, which often aggravates symptoms. Vaginitis symptoms are extremely common and frequently lead to self-diagnosis and therapy, which can further complicate the diagnostic process as the patient may have a partially treated infection or a reaction to a previous treatment [20].

Repeat the vaginal pH, as it helps guide the differential diagnosis:

If pH is increased, consider noninfectious causes of vaginal symptoms, such as vaginal atrophy, atrophic vaginitis, erosive lichen planus, lichen sclerosus, desquamative inflammatory vaginitis, and pemphigoid syndromes.

If pH is normal, the vagina is likely to be normal with normal microbiome, so focus on the most common vulvar and external causes of vulvovaginal symptoms, such as contact or irritant dermatitis, seborrheic or eczematoid dermatitis, psoriasis, or vulvodynia.

If the pH is decreased, some evaluate for cytolytic vaginosis. (See 'Pruritus' below.)

Obtain information on the duration of symptoms (acute versus chronic disease), site of symptoms (vulva versus vagina), and whether there has been a recent change in sexual partner, as this information is also helpful in forming a differential diagnosis.

Detailed secondary history — For women who remain without a diagnosis after the initial history and evaluation above, we then perform a more detailed history in attempt to identify the cause of the patient's symptoms.

Acuity and timing of symptoms – Are the symptoms acute, chronic, or recurrent? An acute process is likely to have an infectious etiology; a chronic process is more likely from inflammation unrelated to infection.

Associated symptoms – Does the patient have pelvic pain or systemic symptoms (eg, fever, nausea)? Pelvic pain is suggestive of pelvic inflammatory disease (PID) and suprapubic pain is suggestive of cystitis, although both are rare with vaginitis. The common causes of vaginitis are not associated with systemic symptoms. (See "Pelvic inflammatory disease: Clinical manifestations and diagnosis" and "Acute simple cystitis in women".)

Sexual practices – For individuals with undiagnosed vaginitis, we obtain a detailed sexual history. Females who have sex with females and females who have sex with both females and males are at increased risk of BV [21]. Those with a new sexual partner have an increased risk of acquiring sexually transmitted infections such as T. vaginalis or cervicitis related to N. gonorrhoeae or C. trachomatis. (See "Screening for sexually transmitted infections".)

Medication history – What medications (prescription and nonprescription) are being used? Antibiotics predispose to candidal vulvovaginitis; estrogen-progestin contraceptives can increase physiologic discharge; pruritus and burning unresponsive to antifungal agents may be due to vulvovaginal dermatitis. (See "Vulvar dermatitis".)

Hygienic practices – What are the patient's hygienic practices? Mechanical, chemical, or allergic irritation may cause vulvovaginal symptoms (pruritus, burning) mistakenly attributed to an infectious source. Vaginal symptoms can result from irritants (eg, scented panty liners, spermicides, povidone-iodine, soaps and perfumes, and some topical drugs) and allergens (eg, latex condoms, topical antifungal agents, seminal fluid, chemical preservatives) that produce acute and chronic hypersensitivity reactions, including contact dermatitis. For women from the developing world, it is important to ask about vaginal practices using traditional products and medicines, as these can have adverse effects [22].

Careful assessment of the woman's personal practices is the best way to detect potential irritants and allergens in her environment and habits unhealthy for the vulvar skin. Patient symptom/contact diaries may be helpful. (See "Vulvar dermatitis".)

Medical history – Does the patient have a history of an oral mucosal, ocular, cutaneous, or systemic disease that could affect the vulvovaginal area? As examples:

Herpes simplex virus and Behçet syndrome can cause vulvovaginal ulcers. (See "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection" and "Clinical manifestations and diagnosis of Behçet syndrome", section on 'Urogenital lesions'.)

Women with diabetes are prone to vulvovaginal candidiasis. (See "Susceptibility to infections in persons with diabetes mellitus".)

Women with human immunodeficiency virus (HIV) are prone to vaginal infections. (See "HIV and women" and "HIV and women", section on 'Gynecologic issues'.)

After transplantation, graft versus host disease can cause vaginal irritation, discharge, ulceration, and stenosis [23,24]. (See "Clinical manifestations and diagnosis of chronic graft-versus-host disease".)

Stevens-Johnson syndrome and toxic epidermal necrolysis have potentially severe vulvovaginal sequelae [25]. (See "Stevens-Johnson syndrome and toxic epidermal necrolysis: Pathogenesis, clinical manifestations, and diagnosis".)

Surgical history – Has the patient had recent transvaginal surgery or repair of perineal lacerations from childbirth? Vaginal symptoms may be related to a foreign body, bacterial infection, granulation tissue, or vaginal fistula.

Continued evaluation by dominant symptom

Inflammation or irritation — Women whose vaginitis complaint is associated with significant irritation or inflammation are further evaluated for dermatitis and desquamative inflammatory vaginitis.

Vulvar dermatitis – Vulvar dermatitis, an allergic or chemical-induced irritative dermatitis, is the most common noninfectious etiology of vulvovaginal itching, irritation, or burning associated with inflammatory changes. Vaginal pH is normal in these patients. Allergens/irritants include soaps, creams, microbicides, toilet paper, detergents, and sanitary pads. Diagnosis and management involves identifying and eliminating the offending agent by taking a thorough history and systematically removing potential irritants and allergens from the urogenital environment (table 3). Patient symptom/contact diaries may be helpful. (See "Vulvar dermatitis".)

Corticosteroid therapy is indicated to control inflammation and relieve symptoms. We use a medium potency fluorinated topical steroid two to three times per day, as needed, until symptoms resolve (table 4). (See "Irritant contact dermatitis in adults" and "Topical corticosteroids: Use and adverse effects".)

Desquamative inflammatory vaginitis – Desquamative inflammatory vaginitis is an uncommon, chronic clinical syndrome of unknown etiology that usually occurs in perimenopausal women. Patients present with purulent vaginal discharge, vulvovaginal burning or irritation, dyspareunia, and vulvar and vaginal erythema. (See "Desquamative inflammatory vaginitis".)

The diagnosis requires all of the following criteria:

At least one of the following symptoms: vaginal discharge, dyspareunia, pruritus, burning, irritation

Vaginal inflammation (spotted ecchymotic rash, erythema, focal or linear erosion)

Vaginal pH >4.5

Saline microscopy showing increased parabasal and inflammatory cells (ie, leukocyte to epithelial cell ratio greater than 1:1)

Pruritus — Pruritus unrelated to infection can occur anywhere in the lower genital tract: the vagina, vestibule, vulva, perineum, or perianal area. It may be unilateral or bilateral. Often women are unable to localize the site or source. Infrequent, transient, mild vulvovaginal pruritus is relatively common and may be normal. Evaluation is indicated in women with persistent, chronic, or severe pruritus. Candida is the most common infectious cause of vulvovaginal pruritus, followed by trichomoniasis and, uncommonly, BV. Once infection has been excluded, noninfectious etiologies of vaginal discharge associated with pruritus include vulvar dermatitis, other vulvar dermatoses, and cytolytic vaginitis. Rarely, vulvar or vaginal malignancy can present with pruritus as the main symptom.

Evaluation of women with pruritus involves taking a detailed history, which often takes a considerable amount of time, and performing a thorough physical examination, with laboratory tests guided by clinical findings. Tissue biopsy can be necessary to make the diagnosis. Treatment often begins with a local "drug holiday" (ie, removing potential causes of pruritus from daily life). Empiric drug therapy should be avoided. Targeted drug therapy is administered when a specific cause is identified.

Vulvar dermatitis – Vulvar dermatitis, the most common vulvar dermatosis, can present as vaginitis with complaints of pain and/or itching as well as the finding of inflammation on physical examination. (See 'Inflammation or irritation' above.)

Other vulvar dermatoses – Women whose chief complaint is vaginitis associated with pruritus, without infection or vulvar dermatitis, are further evaluated for other disorders of the vulvar skin. Biopsy can be required to diagnose other vulvar conditions. (See "Vulvar lesions: Differential diagnosis of vesicles, bullae, erosions, and ulcers" and "Vulvar lesions: Diagnostic evaluation".)

Inflammatory vulvar dermatoses include lichen sclerosus, lichen planus, and lichen simplex chronicus. (See "Vulvar lichen sclerosus" and "Vulvar lichen planus".)

Other common skin conditions that may present with external pruritus include psoriasis, eczema, and seborrheic dermatitis. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis" and "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis" and "Seborrheic dermatitis in adolescents and adults".)

Malignancy – Although malignancy is uncommon in women presenting with vaginitis, vulvar pruritus is the most common complaint among symptomatic women with vulvar intraepithelial neoplasia; other presentations include a visible lesion, a palpable abnormality, perineal pain or burning, or dysuria. Malignancy, while rare, is more likely in menopausal women. (See 'Special populations' below.)

Cytolytic vaginosis – Cytolytic vaginosis refers to a rare controversial syndrome of vaginal hyperacidity due to overgrowth of lactobacilli, although the existence of this entity is debated. It is characterized by pruritus, dyspareunia, vulvar dysuria, and cyclical increase in symptoms during the luteal phase [26,27]. The cyclic symptoms are thought to reflect the higher levels of lactobacilli that occur in the luteal phase.

Diagnostic criteria include presence of white vaginal discharge, pH between 3.5 and 4.5, Gram stain showing large numbers of lactobacilli, paucity of white blood cells, evidence of cytolysis (bare nuclei, shreds of cytoplasm), and most importantly exclusion of candidal infection by culture.

Sodium bicarbonate douches have been used for treatment. A solution of one rounded teaspoon of sodium bicarbonate in 600 mL of water is used for irrigating the vagina, once per day for 7 to 14 days. There are no data to support longer courses of therapy.

Pain

Acute onset of purulent discharge and pain – Women who present with acute pelvic pain and purulent discharge are evaluated for pelvic inflammatory disease (PID). (See "Pelvic inflammatory disease: Clinical manifestations and diagnosis".)

Women whose evaluation is negative for PID may have Group A Streptococcus (Streptococcus pyogenes [GAS]), although this infection is an uncommon cause of vulvovaginitis in adults [28,29]. In one series of almost 7000 pregnant women, only 0.03 percent were colonized with GAS [28]. GAS vulvovaginitis typically occurs in prepubertal girls and in mothers whose children suffer from active GAS infection or who serve as GAS carriers. Carriage or exposure to a carrier is an important source of recurrent GAS infection. GAS can colonize and be transmitted from skin (especially in individuals with chronic dermatological conditions), nasopharynx, and the gastrointestinal tract (including the perianal area) [30].

Clinical features include acute onset of frankly purulent discharge accompanied by pruritus, soreness and irritation, erythema, labial edema, and possibly dysuria from burning of the skin with voiding. Vaginal pH can be normal or mildly increased. Microscopy of the discharge reveals a marked increase in polymorphonuclear leukocytes and Gram stain shows chains of gram-positive cocci.

Penicillin treatment after confirmation of the diagnosis by culture rapidly leads to cure. We use Penicillin VK 500 mg four times daily for 10 to 14 days or clindamycin cream 2% vaginally for 7 to 10 days.

Serosanguinous discharge and pelvic pain – Women with serosanguinous discharge and pelvic symptoms (eg, pain and/or bloating) and a negative initial vaginitis evaluation are assessed for fallopian tube carcinoma. Women with fallopian tube carcinoma typically present in the fifth or sixth decades with vague complaints, although the incidence of this cancer is very low. The type and frequency of so-called "classic" symptoms and signs associated with this malignancy are: serosanguinous vaginal discharge (50 to 60 percent), pelvic pain (30 to 50 percent), and a pelvic mass (12 to 61 percent); however, the full triad (Latzko triad) is noted in fewer than 15 percent of patients. Hydrops tubae profluens, which refers to intermittent discharge of clear or blood-tinged fluid spontaneously or on pressure followed by shrinkage of the adnexal mass, has been described as pathognomonic of the disease. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Clinical features and diagnosis", section on 'Subacute presentation'.)

Chronic introital pain – Vestibulodynia refers to spontaneous or induced pain on penetration of the introitus and tenderness provoked by focal vestibular pressure. These symptoms should be present for at least three to six months and other causes of vestibular pain, such as infectious vaginitis, should be excluded before making the diagnosis. Vaginal discharge and vaginal inflammation are typical features of vaginitis but are not part of the clinical spectrum of vestibulodynia. Candidal vulvovaginitis may mimic localized, provoked vulvodynia and may also be an initial trigger for this condition. (See "Clinical manifestations and diagnosis of vulvodynia (vulvar pain of unknown cause)".)

Postcoital vulvovaginal pruritus and pain – Seminal plasma allergy or hypersensitivity is a rare disorder characterized by postcoital vulvovaginal itching, burning, edema, and erythema with or without systemic signs and symptoms. Vaginal discharge is not a typical feature. Complaints occur immediately or within one hour after contact with seminal plasma. Most affected women are under age 40 years and have a family history of atopy.

The diagnosis is based on absence of symptoms with condom use and on positive skin testing with a pooled sample of seminal fluid. (See "Allergic reactions to seminal plasma".)

Vulvar lesions — While a wide variety of lesions can develop on the vulva, most are not associated with vaginitis in the absence of infection. Vulvar lesions can be grouped by appearance and then further evaluated with examination and biopsy, as indicated. The differential and diagnosis of vulvar lesions is presented in detail separately.

(See "Vulvar lesions: Differential diagnosis of vesicles, bullae, erosions, and ulcers".)

(See "Vulvar lesions: Diagnostic evaluation".)

Persistent genital malodor — The normal odor of vaginal secretions cannot be clearly defined but is probably slightly sour due to lactic acid and volatile sulfur compounds. Persistent genital malodor can seriously impair a woman's quality of life; the cause is difficult to identify after readily diagnosable causes have been excluded. The common causes include [31]:

Neglected foreign body (including retained tampon)

BV

Trichomoniasis

Infectious ulcer/pelvic inflammatory disease (PID)

Pelvic fistula (rectovaginal, vesicovaginal, ureterovaginal)

Hidradenitis suppurativa

Chronic constipation

Urinary incontinence

Fecal incontinence

Poor hygiene

Malignant ulcer

Excessive genital perspiration and local bacterial colonization related to obesity

Other potential causes of malodor include metabolic disorders (see "Inborn errors of metabolism: Epidemiology, pathogenesis, and clinical features", section on 'Abnormal odors'), olfactory reference syndrome [32], and olfactory hallucinations. (See "Nonepileptic paroxysmal disorders in adolescents and adults", section on 'Olfactory hallucinations'.)

Management depends on determining a cause. In the absence of poor hygiene, frequent washing and vaginal douching are not helpful and can be harmful. Excessive soaping of the genital area can cause a chemical vulvitis and douching (rinsing of the vagina with vinegar or an antiseptic with the aid of a douche bag) can increase the risk of vaginal and pelvic infection [33,34]. Frequently a cause is not established.

For women with an elevated vaginal pH or lack of lactobacilli on Gram stain of vaginal discharge, a single but not repeated trial of antibiotics for anaerobic infection is reasonable (eg, metronidazole 500 mg orally twice daily for seven days). For women with no identifiable abnormalities, use of a specific medical grade stainless steel douching device (Water Works Douching Device) can be helpful. A randomized trial including 140 women with perceived vaginal odor and no vaginal infection reported significant improvement after douching daily for four weeks with tap water using this device [35]. In the Water Works group, odor intensity scores fell from 7.3 to 1.8 (p<0.001), which was superior to that among women who used a conventional over-the-counter plastic douche bag, 7.2 to 3.4 (p<0.003).

Leukorrhea — After exclusion of pathological causes of vaginal discharge, women with a change in their normal vaginal discharge can be reassured that changes in the volume and character of vaginal discharge are normal and can be due to changes in diet, sexual activity, medication, stress, etc. Although hormonal therapy, such as depot medroxyprogesterone acetate injection every three months or norethindrone acetate 5 mg orally daily, will decrease estrogen levels and thus may decrease physiological leukorrhea; the use of hormonal therapy for this indication alone is rarely appropriate given the side effects and risks associated with these drugs.

Currently no dietary modifications are relevant in management of vaginitis, with the exception of avoiding excessive refined sugars in some women prone to Candida vulvovaginitis. Similarly, probiotics available to women in the United States are not proven to be useful in prevention or control of vaginitis.

Other — The following diagnoses are listed because clinicians sometimes attempt to diagnose and treat women for these conditions. We do not believe they are causes of vaginitis.

Group B streptococcus (GBS) – Group B Streptococcus (GBS) commonly colonizes the vagina: Approximately 20 percent of women are colonized with GBS [28,36]. Whether GBS is a pathogen in vulvovaginitis is controversial. Some clinicians believe it has a pathogenic role in vulvovaginitis and report an ameliorative effect on vulvovaginal symptoms with antibiotic treatment (oral penicillin or clindamycin cream). We and most experts do not believe this organism has a pathogenic role in symptomatic vulvovaginitis and that positive culture results merely reflect colonization, which is facilitated by disruption of the normal vaginal bacterial environment [36]. Therefore, in women with vaginitis, both GBS culture and treatment of positive culture results should be avoided.

Nonspecific bacterial vaginitis (BV) – The concept of nonspecific BV is no longer acceptable. In the past, many women with BV were given the diagnosis of nonspecific vaginitis, but this should no longer occur since clear diagnostic criteria for BV are now available. (See "Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Diagnosis'.)

As discussed above, vaginal bacterial cultures are rarely indicated in women with vaginal discharge and are frequently misleading, leading to unnecessary antibacterial therapy. Apart from GAS, a clear causal relationship between any bacteria and vaginitis has not been established.

Treatment of infectious causes of vulvovaginitis should be targeted to the causative organism. Sulfanilamide cream (eg, triple sulfa or AVC cream) has no role in the treatment of vulvovaginitis, as it is less effective than other therapies (eg, metronidazole for T. vaginalis and BV, fluconazole for Candida vulvovaginitis) [37,38].

SPECIAL POPULATIONS

Prepubertal children – The evaluation of vaginitis in prepubertal children is presented separately:

(See "Overview of vulvovaginal conditions in the prepubertal child".)

(See "Gynecologic examination of the newborn and child".)

Menopausal women – Menopausal women undergo the initial evaluation discussed above. In addition to the performing the initial evaluation, the clinician should assess menopausal women for vulvovaginal atrophy (ie, genitourinary syndrome of menopause) and genital neoplasia and/or malignancy.

Vulvovaginal atrophy – Vulvovaginal atrophy is common in menopausal women and may be present in addition to other causes of vaginitis. Nonspecific signs and symptoms include a watery, white or yellow, and malodorous discharge; vaginal burning or irritation; itching; dyspareunia; and urinary symptoms such as urgency, frequency, and/or leakage. Physical findings include thinning of the vaginal epithelium, loss of elasticity, loss of rugae, pH ≥5, vaginal erosions, and cervicovaginal friability. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Clinical manifestations and diagnosis".)

The wet mount is nonspecific, as similar findings occur in other inflammatory vaginal conditions. It shows parabasal cells, many polymorphonuclear leukocytes, and no lactobacilli, with or without background bacteria. Parabasal cells are immature squamous epithelial cells that are rounded and have a large nucleus-to-cytoplasm ratio; in contrast, mature squamous epithelial cells are larger, cuboidal, with a smaller nucleus-to-cytoplasm ratio, and sometimes folded. The presence of epithelial cells rather than parabasal cells and premenopausal status helps to distinguish bacterial vaginosis from atrophic vaginitis.

Symptomatic response to topical estrogen therapy, which restores the vaginal epithelium, supports the diagnosis. Antibiotics are not needed. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Treatment", section on 'Vaginal estrogen therapy'.)

Intraepithelial neoplasia and malignancy – Neoplasia and malignancy are unusual causes of vaginal discharge but are more common in menopausal women. Tissue biopsy, with or without colposcopy, is generally required for diagnosis.

-Vaginal intraepithelial neoplasia can present with vaginal discharge and/or postcoital spotting, although patients are usually asymptomatic. (See "Vaginal intraepithelial neoplasia".)

-Vulvar intraepithelial neoplasia may cause vulvar pruritus or burning. (See "Vulvar squamous intraepithelial lesions (vulvar intraepithelial neoplasia)".)

-Fallopian tube cancer may present with a serosanguineous vaginal discharge and pelvic pain. (See 'Pain' above.)

Women taking tamoxifen – Women taking tamoxifen are at increased risk of Candida vulvovaginitis. These women are offered maintenance fluconazole therapy. (See "Candida vulvovaginitis: Treatment", section on 'Recurrent treatment'.)

Women with recurrent symptoms – Individuals with continued vaginal symptoms are separated into those with recurrent symptoms (ie, symptoms improve at intervals) and those with chronic, ongoing symptoms. For women with recurrent vaginitis, we look at chart results of past testing. Frequently the wrong diagnosis is provided by false positive tests for organisms (eg, Gardnerella vaginalis). We also inquire as to the type of therapy the patient received and the response to this therapy. We then perform microscopy and repeat testing, as indicated, for BV, candida, trichomonas, sexually transmitted infections (STIs), including herpes simplex virus, and, less commonly, group A streptococcus.

Patients who continue to exhibit symptoms and/or have positive tests for STIs after treatment are most likely to have been reinfected by their sexual partner(s) [39]. Thus, we advise repeating the approach outlined in the initial evaluation above, including repeat testing for STIs. While gonorrhoea and chlamydia are cervical pathogens, infection can result in vaginal discharge. However, neither infection is typically the cause of recurrent vulvovaginal symptoms in the absence of cervicitis. (See 'Initial diagnostic evaluation' above.)

POSTDIAGNOSTIC MANAGEMENT — Women with a confirmed diagnosis are treated as appropriate. If the woman's symptoms resolve, no further evaluation or treatment is warranted. However, women diagnosed with sexually transmitted infections (STIs) presumably have an infected partner and are at increased risk of reinfection or acquiring other sexually transmitted diseases. Thus, sexual partners of women diagnosed with an STI should be referred for specific testing and treatment. Partner delivered patient medication (PDPM), also known as expedited partner therapy (EPT), is an alternative if evaluation of the sexual partner is not possible or unlikely. (See "Screening for sexually transmitted infections" and "Treatment of Chlamydia trachomatis infection".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Bacterial vaginosis" and "Society guideline links: Gynecologic infectious diseases (non-sexually transmitted)".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Vaginal discharge (The Basics)" and "Patient education: Vulvar itching (The Basics)")

Beyond the Basics topics (see "Patient education: Vaginal discharge in adult women (Beyond the Basics)" and "Patient education: Vaginal yeast infection (Beyond the Basics)" and "Patient education: Bacterial vaginosis (Beyond the Basics)" and "Patient education: Gonorrhea (Beyond the Basics)" and "Patient education: Chlamydia (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Vaginitis is the general term for disorders of the vagina caused by infection, inflammation, or changes in the normal vaginal flora. Clinical signs and symptoms are similar, irrespective of the underlying etiology. (See 'Introduction' above.)

Vaginitis is often the result of infectious agents. The most common infections, bacterial vaginosis (BV), Candida vulvovaginitis, and trichomoniasis, account for over 90 percent of infections. Cervicitis, typically from sexually transmitted infections (STIs) gonorrhea, chlamydia, and mycoplasma, can also present as nonspecific vaginal symptoms. (See 'Pathogenesis' above.)

Women with vaginitis typically present with one or more of the following: change in vaginal discharge, pruritus, burning, irritation, erythema, dyspareunia, spotting, and dysuria. (See 'Patient presentation' above.)

Given the nonspecific nature of vaginitis symptoms (table 1), laboratory documentation of the etiology of vaginitis is mandatory before initiating therapy. The main steps in the initial evaluation of women with symptoms of vaginitis are to obtain a history and perform a physical examination, measure vaginal pH, test for vaginal and cervical infections, treat according to abnormal results, and reassess after targeted treatment. (See 'Our Approach' above.)

Measurement of vaginal pH is the single most important finding that drives the diagnostic process and should always be determined. A pH test stick (or pH paper if available) is applied for a few seconds to the vaginal sidewall. (See 'Vaginal pH' above.)

A sample of the patient's vaginal discharge is obtained with a cotton swab, smeared onto a slide, and evaluated under a microscope with both saline and potassium hydroxide. (See 'Microscopy' above.)

If microscopy is negative, further testing is performed for Candida species and Trichomonas vaginalis; the choice is dictated by the clinical findings. Culture is performed if Candida is suspected but microscopy is negative. Similarly, a diagnostic test using nucleic acid amplification (NAAT), if available, is strongly advised if trichomoniasis is suspected. (See 'If microscopy is negative' above.)

If microscopy is not available, commercial diagnostic testing methods (eg, rapid antigen and NAATs) are used for confirming the clinical suspicion of BV, vaginal candidiasis, or trichomonas vaginitis. (See 'If microscopy is not available' above.)

The STIs Neisseria gonorrhoeae and Chlamydia trachomatis must always be considered in sexually active women with vaginitis since women with STIs may go on to develop pelvic inflammatory disease and its potential complications. (See 'Cervical tests for STI' above.)

Rarely, physical examination reveals an atypical cause of vaginitis that warrants a change in the diagnostic evaluation. Examples include an obvious vulvar, vaginal, or cervical cancer; probable pelvic inflammatory disease; vulvovaginal ulceration; and vaginal fistulae. These women should be immediately referred for specialty evaluation and care. (See 'Alarm findings' above.)

Of women who present for the evaluation of vaginitis, approximately 70 percent will be diagnosed with one of three vaginal infections: BV (40 to 50 percent), Candida vulvovaginitis (20 to 25 percent), or trichomoniasis (15 to 20 percent) [3,19]. Women with a specific diagnosis receive treatment targeted to the etiology. (See 'Common diagnoses' above.)

Approximately 25 to 40 percent of patients with vaginitis symptoms do not have a specific cause identified on initial diagnostic evaluation. These women undergo secondary evaluation. (See 'Women without a diagnosis after initial evaluation' above.)

If the woman had minimal symptoms at the time of initial evaluation and the evaluation was nondiagnostic, the evaluation should be repeated at a second visit when she is symptomatic. In other cases, less common and rare infectious and inflammatory disorders need to be considered. Avoid empiric blind therapy, which often aggravates symptoms. (See 'Women without a diagnosis after initial evaluation' above and 'Secondary approach' above.)

A detailed secondary evaluation is then driven by the patient's dominant symptom(s). (See 'Continued evaluation by dominant symptom' above.)

Special populations that require different evaluation or treatment include prepubertal children, menopausal women, women receiving tamoxifen therapy, and women with recurrent symptoms. (See 'Special populations' above.)

REFERENCES

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  2. Foxman B, Marsh JV, Gillespie B, Sobel JD. Frequency and response to vaginal symptoms among white and African American women: results of a random digit dialing survey. J Womens Health 1998; 7:1167.
  3. Anderson MR, Klink K, Cohrssen A. Evaluation of vaginal complaints. JAMA 2004; 291:1368.
  4. Reichman O, Margesson LJ, Rasmussen CA, et al. Algorithms for Managing Vulvovaginal Symptoms-a Practical Primer. Curr Infect Dis Rep 2019; 21:40.
  5. Landers DV, Wiesenfeld HC, Heine RP, et al. Predictive value of the clinical diagnosis of lower genital tract infection in women. Am J Obstet Gynecol 2004; 190:1004.
  6. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.
  7. Zemouri C, Wi TE, Kiarie J, et al. The Performance of the Vaginal Discharge Syndromic Management in Treating Vaginal and Cervical Infection: A Systematic Review and Meta-Analysis. PLoS One 2016; 11:e0163365.
  8. Nwankwo TO, Aniebue UU, Umeh UA. Syndromic Diagnosis in Evaluation of Women with Symptoms of Vaginitis. Curr Infect Dis Rep 2017; 19:3.
  9. Hillier SL, Austin M, Macio I, et al. Diagnosis and Treatment of Vaginal Discharge Syndromes in Community Practice Settings. Clin Infect Dis 2021; 72:1538.
  10. Gaydos CA, Beqaj S, Schwebke JR, et al. Clinical Validation of a Test for the Diagnosis of Vaginitis. Obstet Gynecol 2017; 130:181.
  11. Carr PL, Rothberg MB, Friedman RH, et al. "Shotgun" versus sequential testing. Cost-effectiveness of diagnostic strategies for vaginitis. J Gen Intern Med 2005; 20:793.
  12. Miller JM, Binnicker MJ, Campbell S, et al. A Guide to Utilization of the Microbiology Laboratory for Diagnosis of Infectious Diseases: 2018 Update by the Infectious Diseases Society of America and the American Society for Microbiology. Clin Infect Dis 2018; 67:e1.
  13. Allen-Davis JT, Beck A, Parker R, et al. Assessment of vulvovaginal complaints: accuracy of telephone triage and in-office diagnosis. Obstet Gynecol 2002; 99:18.
  14. Sobel JD. Erosive Vulvovaginitis. Curr Infect Dis Rep 2003; 5:494.
  15. Vaginitis in Nonpregnant Patients: ACOG Practice Bulletin, Number 215. Obstet Gynecol 2020; 135:e1.
  16. Lamont RF, Sobel JD, Akins RA, et al. The vaginal microbiome: new information about genital tract flora using molecular based techniques. BJOG 2011; 118:533.
  17. Morris SR, Bristow CC, Wierzbicki MR, et al. Performance of a single-use, rapid, point-of-care PCR device for the detection of Neisseria gonorrhoeae, Chlamydia trachomatis, and Trichomonas vaginalis: a cross-sectional study. Lancet Infect Dis 2021; 21:668.
  18. Van Der Pol B, Daniel G, Kodsi S, et al. Molecular-based Testing for Sexually Transmitted Infections Using Samples Previously Collected for Vaginitis Diagnosis. Clin Infect Dis 2019; 68:375.
  19. Mulley AG. Appproach to the patient with a vaginal discharge. In: Primary Care Medicine: Office evaluation and managment of the adult patient, Goroll AH, Mulley AG (Eds), Lippincott Williams & Wilkins, Philadelphia 2000. p.702-7.
  20. Kent HL. Epidemiology of vaginitis. Am J Obstet Gynecol 1991; 165:1168.
  21. Olson KM, Boohaker LJ, Schwebke JR, et al. Comparisons of vaginal flora patterns among sexual behaviour groups of women: implications for the pathogenesis of bacterial vaginosis. Sex Health 2018; 15:61.
  22. Hull T, Hilber AM, Chersich MF, et al. Prevalence, motivations, and adverse effects of vaginal practices in Africa and Asia: findings from a multicountry household survey. J Womens Health (Larchmt) 2011; 20:1097.
  23. Zantomio D, Grigg AP, MacGregor L, et al. Female genital tract graft-versus-host disease: incidence, risk factors and recommendations for management. Bone Marrow Transplant 2006; 38:567.
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  25. Kaser DJ, Reichman DE, Laufer MR. Prevention of vulvovaginal sequelae in stevens-johnson syndrome and toxic epidermal necrolysis. Rev Obstet Gynecol 2011; 4:81.
  26. Cibley LJ, Cibley LJ. Cytolytic vaginosis. Am J Obstet Gynecol 1991; 165:1245.
  27. Cerikcioglu N, Beksac MS. Cytolytic vaginosis: misdiagnosed as candidal vaginitis. Infect Dis Obstet Gynecol 2004; 12:13.
  28. Mead PB, Winn WC. Vaginal-rectal colonization with group A streptococci in late pregnancy. Infect Dis Obstet Gynecol 2000; 8:217.
  29. Bray S, Morgan J. Two cases of group A streptococcal vulvovaginitis in premenopausal adults in a sexual health setting. Sex Health 2006; 3:187.
  30. Sobel JD, Funaro D, Kaplan EL. Recurrent group A streptococcal vulvovaginitis in adult women: family epidemiology. Clin Infect Dis 2007; 44:e43.
  31. Subramanian C, Nyirjesy P, Sobel JD. Genital malodor in women: a modern reappraisal. J Low Genit Tract Dis 2012; 16:49.
  32. Begum M, McKenna PJ. Olfactory reference syndrome: a systematic review of the world literature. Psychol Med 2011; 41:453.
  33. Zhang J, Thomas AG, Leybovich E. Vaginal douching and adverse health effects: a meta-analysis. Am J Public Health 1997; 87:1207.
  34. Cottrell BH. An updated review of of evidence to discourage douching. MCN Am J Matern Child Nurs 2010; 35:102.
  35. Hassan S, Chatwani A, Brovender H, et al. Douching for perceived vaginal odor with no infectious cause of vaginitis: a randomized controlled trial. J Low Genit Tract Dis 2011; 15:128.
  36. Leclair CM, Hart AE, Goetsch MF, et al. Group B streptococcus: prevalence in a non-obstetric population. J Low Genit Tract Dis 2010; 14:162.
  37. Rein MF. Current therapy of vulvovaginitis. Sex Transm Dis 1981; 8:316.
  38. duBouchet L, Spence MR, Rein MF, et al. Multicenter comparison of clotrimazole vaginal tablets, oral metronidazole, and vaginal suppositories containing sulfanilamide, aminacrine hydrochloride, and allantoin in the treatment of symptomatic trichomoniasis. Sex Transm Dis 1997; 24:156.
  39. Baron EJ, Miller JM, Weinstein MP, et al. A guide to utilization of the microbiology laboratory for diagnosis of infectious diseases: 2013 recommendations by the Infectious Diseases Society of America (IDSA) and the American Society for Microbiology (ASM). Clin Infect Dis 2013; 57:e22.
Topic 5477 Version 60.0

References

1 : Vulvovaginitis in healthy women.

2 : Frequency and response to vaginal symptoms among white and African American women: results of a random digit dialing survey.

3 : Evaluation of vaginal complaints.

4 : Algorithms for Managing Vulvovaginal Symptoms-a Practical Primer.

5 : Predictive value of the clinical diagnosis of lower genital tract infection in women.

6 : Sexually transmitted diseases treatment guidelines, 2015.

7 : The Performance of the Vaginal Discharge Syndromic Management in Treating Vaginal and Cervical Infection: A Systematic Review and Meta-Analysis.

8 : Syndromic Diagnosis in Evaluation of Women with Symptoms of Vaginitis.

9 : Diagnosis and Treatment of Vaginal Discharge Syndromes in Community Practice Settings.

10 : Clinical Validation of a Test for the Diagnosis of Vaginitis.

11 : "Shotgun" versus sequential testing. Cost-effectiveness of diagnostic strategies for vaginitis.

12 : A Guide to Utilization of the Microbiology Laboratory for Diagnosis of Infectious Diseases: 2018 Update by the Infectious Diseases Society of America and the American Society for Microbiology.

13 : Assessment of vulvovaginal complaints: accuracy of telephone triage and in-office diagnosis.

14 : Erosive Vulvovaginitis.

15 : Vaginitis in Nonpregnant Patients: ACOG Practice Bulletin, Number 215.

16 : The vaginal microbiome: new information about genital tract flora using molecular based techniques.

17 : Performance of a single-use, rapid, point-of-care PCR device for the detection of Neisseria gonorrhoeae, Chlamydia trachomatis, and Trichomonas vaginalis: a cross-sectional study.

18 : Molecular-based Testing for Sexually Transmitted Infections Using Samples Previously Collected for Vaginitis Diagnosis.

19 : Molecular-based Testing for Sexually Transmitted Infections Using Samples Previously Collected for Vaginitis Diagnosis.

20 : Epidemiology of vaginitis.

21 : Comparisons of vaginal flora patterns among sexual behaviour groups of women: implications for the pathogenesis of bacterial vaginosis.

22 : Prevalence, motivations, and adverse effects of vaginal practices in Africa and Asia: findings from a multicountry household survey.

23 : Female genital tract graft-versus-host disease: incidence, risk factors and recommendations for management.

24 : Graft-versus-host disease of the vulva and/or vagina: diagnosis and treatment.

25 : Prevention of vulvovaginal sequelae in stevens-johnson syndrome and toxic epidermal necrolysis.

26 : Cytolytic vaginosis.

27 : Cytolytic vaginosis: misdiagnosed as candidal vaginitis.

28 : Vaginal-rectal colonization with group A streptococci in late pregnancy.

29 : Two cases of group A streptococcal vulvovaginitis in premenopausal adults in a sexual health setting.

30 : Recurrent group A streptococcal vulvovaginitis in adult women: family epidemiology.

31 : Genital malodor in women: a modern reappraisal.

32 : Olfactory reference syndrome: a systematic review of the world literature.

33 : Vaginal douching and adverse health effects: a meta-analysis.

34 : An updated review of of evidence to discourage douching.

35 : Douching for perceived vaginal odor with no infectious cause of vaginitis: a randomized controlled trial.

36 : Group B streptococcus: prevalence in a non-obstetric population.

37 : Current therapy of vulvovaginitis.

38 : Multicenter comparison of clotrimazole vaginal tablets, oral metronidazole, and vaginal suppositories containing sulfanilamide, aminacrine hydrochloride, and allantoin in the treatment of symptomatic trichomoniasis.

39 : A guide to utilization of the microbiology laboratory for diagnosis of infectious diseases: 2013 recommendations by the Infectious Diseases Society of America (IDSA) and the American Society for Microbiology (ASM).