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Vaginitis
is infectious or noninfectious inflammation of the vaginal mucosa,
sometimes with inflammation of the vulva. Symptoms include vaginal
discharge, irritation, pruritus, and erythema. Diagnosis is by in-office
testing of vaginal secretions. Treatment is directed at the cause
and at any severe symptoms.
Vaginitis is one of the most common gynecologic disorders. Some of its causes affect the vulva alone (vulvitis) or in addition (vulvovaginitis).
Etiology
The most common causes vary by patient age.
Children:
In children, vaginitis usually involves infection with GI tract flora (nonspecific vulvovaginitis). A common contributing factor in girls aged 2 to 6 yr is poor perineal hygiene (eg, wiping from back to front after bowel movements; not washing hands after bowel movements; fingering, particularly in response to pruritus). Chemicals in bubble baths or soaps may cause inflammation. Foreign bodies (eg, tissue paper) may cause nonspecific vaginitis with a bloody discharge. Sometimes childhood vulvovaginitis is due to infection with a specific pathogen (eg, streptococci, staphylococci, Candida sp; occasionally, pinworm).
Women of reproductive age:
In these women, vaginitis is usually infectious. The most common types are bacterial vaginosis (see Vaginitis and Pelvic Inflammatory Disease (PID): Bacterial Vaginosis), candidal vaginitis (see Vaginitis and Pelvic Inflammatory Disease (PID): Candidal Vaginitis), and trichomonal vaginitis (see Sexually Transmitted Diseases (STD): Trichomoniasis), which is sexually transmitted. Normally in women of reproductive age, Lactobacillus sp is the predominant constituent of normal vaginal flora. Colonization by these bacteria keeps vaginal pH in the normal range (3.8 to 4.2), thereby preventing overgrowth of pathogenic bacteria. Also, high estrogen levels maintain vaginal thickness,
bolstering local defenses. Factors that predispose to overgrowth
of bacterial vaginal pathogens may include the following:
Postmenopausal
women:
Usually, a marked decrease in estrogen causes vaginal thinning, increasing vulnerability to infection and inflammation. Some treatments (eg, oophorectomy, pelvic radiation, certain chemotherapy drugs) also result in loss of estrogen. Decreased estrogen predisposes to atrophic vaginitis. Poor hygiene (eg, in patients who are incontinent or bedridden) can lead to chronic vulvar inflammation due to chemical irritation from urine or feces or due to nonspecific infection. Bacterial vaginosis, candidal vaginitis, and trichomonal vaginitis are uncommon among postmenopausal women but may occur in those with risk factors.
Women of all ages:
At any age, conditions that predispose to vaginal or vulvar infection include fistulas between the intestine and genital tract, which allow intestinal flora to seed the genital tract, and pelvic radiation or tumors, which break down tissue and thus compromise normal host defenses. Noninfectious vulvitis accounts for up to 30% of vulvovaginitis cases. It may result from hypersensitivity or irritant reactions to hygiene sprays or perfumes, menstrual pads, laundry soaps, bleaches, fabric softeners, fabric dyes, synthetic fibers, bathwater additives, toilet tissue, or, occasionally, spermicides, vaginal lubricants or creams, latex condoms, vaginal contraceptive rings, or diaphragms.
Symptoms and Signs
Vaginitis causes vaginal discharge, which must be distinguished from normal discharge. Normal discharge is common when estrogen levels are high—eg, during the first 2 wk of life, because maternal estrogen are transferred before birth (slight bleeding often occurs when estrogen levels abruptly decrease), and during the few months before menarche, when estrogen production increases. Normal vaginal discharge is commonly milky white or mucoid, odorless, and nonirritating; it can result in vaginal wetness that dampens underwear. Discharge due to vaginitis is accompanied by pruritus, erythema, and sometimes burning, pain, or mild bleeding. Pruritus may interfere with sleep. Dysuria or dyspareunia may occur. In atrophic vaginitis, discharge is scant, dyspareunia is common, and vaginal tissue appears thin and dry. Although symptoms vary among particular types of vaginitis, there is much overlap (see Table 1: Vaginitis and Pelvic Inflammatory Disease (PID): Common Types of Vaginitis ).
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Table 1
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Common Types of Vaginitis
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Disorder
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Typical Symptoms and Signs
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Criteria for Diagnosis
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Microscopic Findings
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Differential Diagnosis
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Bacterial vaginosis
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Gray, thin, fishy-smelling discharge, often with pruritus and irritation; no dyspareunia
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Three of the following: gray discharge, pH > 4.5, fishy odor, and clue cells
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Clue cells, decreased lactobacilli, increased coccobacilli
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Trichomonal vaginitis
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Candidal vaginitis
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Thick, white discharge; vaginal and sometimes vulvar pruritus with or without burning, irritation, or dyspareunia
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Typical discharge, pH < 4.5, and microscopic findings*
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Budding yeast, pseudohyphae, or mycelia; best examined with 10% K hydroxide diluent
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Contact irritant or allergic vulvitis
Chemical irritation
Vulvodynia
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Trichomonal vaginitis
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Profuse, malodorous, yellow-green discharge; dysuria; dyspareunia; erythema
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Identification of causative organism by microscopy* (occasionally by culture)
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Motile, flagellated protozoa, increased PMNs
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Bacterial vaginosis
Inflammatory vaginitis
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Inflammatory vaginitis
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Purulent discharge, vaginal dryness and thinning, dyspareunia, dysuria; usually in postmenopausal women
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pH > 6, negative whiff test, and characteristic microscopy findings
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Increased PMNs, parabasal cells, and cocci; decreased bacilli
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Erosive lichen planus
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*Culture is needed if microscopic findings are negative or symptoms persist.
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Vulvitis can cause erythema, pruritus, and sometimes tenderness and discharge from the vulva.
Diagnosis
Vaginitis is diagnosed using clinical criteria and in-office testing. First, vaginal secretions are obtained with a water-lubricated speculum, and pH paper is used to measure pH in 0.2 intervals from 4.0 to 6.0. Then, secretions are placed on 2 slides with a cotton swab and diluted with 0.9% NaCl on one slide (saline wet mount) and with 10% K hydroxide on the other (KOH wet mount). The KOH wet mount is checked for a fishy odor (whiff test), which results from amines produced in trichomonal vaginitis or bacterial vaginosis. The saline wet mount is examined microscopically as soon as possible to detect trichomonads, which can become immotile and more difficult to recognize within minutes after slide preparation. The KOH dissolves most cellular material except for yeast hyphae, making identification easier. If clinical criteria and in-office test results are inconclusive, the discharge may be cultured for fungi or trichomonads.
Other causes of discharge are ruled out. If children have vaginal discharge, a vaginal foreign body is suspected. Cervical discharge due to cervicitis (eg, due to pelvic inflammatory disease [PID]) can resemble that of vaginitis; abdominal pain, cervical motion tenderness, or cervical inflammation suggests PID. Discharge that is watery, bloody, or both may result from vulvar, vaginal, or cervical cancer; cancers can be differentiated from vaginitis by examination and Papanicolaou (Pap) tests. Vaginal pruritus and discharge may result from skin disorders (eg, psoriasis, tinea versicolor), which can usually be differentiated by history and skin findings.
If children have trichomonal vaginitis, evaluation for sexual abuse is required. If they have unexplained vaginal discharge, cervicitis, which may be due to a sexually transmitted disease, should be considered. If women have bacterial vaginosis or trichomonal vaginitis (and thus are at increased risk of sexually transmitted diseases), cervical tests for Neisseria gonorrhoeae and Chlamydia trachomatis, common causes of sexually transmitted PID, are done.
Treatment
The vulva should be kept as clean as possible. Soaps and unnecessary topical preparations (eg, feminine hygiene sprays) should be avoided. Intermittent use of ice packs or warm sitz baths with or without baking soda may reduce soreness and pruritus.
If symptoms are moderate or severe or do not respond to other measures, drugs may be needed. For pruritus, topical corticosteroids (eg, topical 1% hydrocortisone bid prn) can be applied to the vulva but not in the vagina. Oral antihistamines decrease pruritus and cause drowsiness, helping patients sleep.
Any infection or other cause is treated. Foreign bodies are removed. Prepubertal girls are taught good perineal hygiene (eg, wiping front to back after bowel movements and voiding, washing hands, avoiding fingering the perineum). If chronic vulvar inflammation is due to being bedridden or incontinent, better vulvar hygiene may help.
Bacterial
Vaginosis
Bacterial
vaginosis is vaginitis due to a complex alteration of vaginal flora
in which lactobacilli decrease and anaerobic pathogens
overgrow. Symptoms include a gray, thin, fishy-smelling vaginal
discharge and itching. Diagnosis confirmed by testing vaginal secretions.
Treatment is usually with oral or topical metronidazole or topical
clindamycin.
Bacterial vaginosis is the most common infectious vaginitis. The cause is unknown. Anaerobic pathogens that overgrow include Prevotella sp, Peptostreptococcus sp, Gardnerella vaginalis
, Mobiluncus sp, and Mycoplasma hominis, which increase in concentration 10-fold to 100-fold and replace the normally protective lactobacilli. Risk factors include those for sexually transmitted diseases (see Sexually Transmitted Diseases (STD)). However, bacterial vaginosis can occur in virgins, and treating the male sex partner does not appear to affect subsequent incidence in sexually active women. Use of an intrauterine device is also a risk factor.
Bacterial vaginosis, once considered inconsequential, appears to increase risk of pelvic inflammatory disease, postabortion and postpartum endometritis, posthysterectomy vaginal cuff infection, chorioamnionitis, premature rupture of membranes, preterm labor, and preterm birth.
Symptoms,
Signs, and Diagnosis
Vaginal discharge is malodorous, gray, and thin. Usually, a fishy odor is present, often becoming stronger when the discharge is more alkaline—after coitus and menses. Pruritus and irritation are common. Erythema and edema are uncommon.
For the diagnosis, 3 of 4 criteria must be present:
Clue cells (bacteria adherent to epithelial cells obscuring their cell margins) are identified by microscopic examination of a saline wet mount. Presence of WBCs on a saline wet mount suggests a concomitant infection, possibly trichomonal, gonorrheal, or chlamydial cervicitis, and the need for additional testing.
Treatment
(See also the Centers for Disease Control and Prevention practice guideline Sexually transmitted
diseases characterized by vaginal discharge.) Metronidazole 0.75% vaginal gel bid for 5 days or 2% clindamycin vaginal cream once/day for 7 days is the treatment of choice. Oral metronidazole 500 mg bid for 7 days or 2 g po once is effective but can have systemic adverse effects. Women who use clindamycin cream cannot use latex products (ie, condoms or diaphragms) for contraception because the drug weakens latex. Treatment of asymptomatic sex partners is unnecessary.
For vaginitis during the 1st trimester of pregnancy, metronidazole vaginal gel should be used, although treatment during pregnancy has not been shown to lower the risk of pregnancy complications. To prevent endometritis, clinicians may give metronidazole prophylactically before elective abortion to all patients or only to those who test positive for bacterial vaginosis.
Candidal
Vaginitis
Candidal
vaginitis is vaginal infection with Candida sp,
usually C. albicans.
Most fungal vaginitis is caused by C. albicans, which colonizes 15 to 20% of nonpregnant and 20 to 40% of pregnant women (see also Fungal Skin Infections: Candidiasis). Risk factors for candidal vaginitis include the following:
Candidal vaginitis is uncommon among postmenopausal women except among those taking systemic hormone therapy.
Symptoms and Diagnosis
Vaginal vulvar pruritus, burning, or irritation (which may be worse with intercourse) and dyspareunia are common, as is a thick, white, cottage cheese–like vaginal discharge that adheres to the vaginal walls. Symptoms and signs increase the week before menses. Erythema, edema, and excoriation are common. Infected male sex partners may or may not have symptoms. Recurrences after treatment are uncommon.
Vaginal pH is < 4.5; budding yeast, pseudohyphae, or mycelia are visible on a wet mount, especially with KOH. If symptoms suggest candidal vaginitis but signs (including vulvar irritation) are absent and microscopy does not detect fungal elements, fungal culture is done. Women with frequent recurrences require culture to confirm the diagnosis and to rule out non-albicans Candida.
Treatment
(See also the Centers for Disease Control and Prevention practice guideline Sexually transmitted
diseases characterized by vaginal discharge.) Keeping the vulva clean and wearing loose, absorbent cotton clothing that allows air to circulate can reduce vulvar moisture and fungal growth. Topical or oral drugs are highly effective (see Table 2: Vaginitis and Pelvic Inflammatory Disease (PID): Drugs for Candidal Vaginitis). Adherence to treatment is better when a one-dose oral regimen of fluconazole 150 mg is used. Topical butoconazole , clotrimazole , miconazole , and tioconazole are available OTC. However, patients should be warned that topical creams and ointments containing mineral oil or vegetable oil weaken latex-based condoms. If symptoms persist or worsen during topical therapy, hypersensitivity to topical antifungals should be considered.
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Table 2
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Drugs for Candidal Vaginitis
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Type
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Drug
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Dosage
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Topical or vaginal
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Butoconazole
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2% cream 5 g once/day for 3 days
Sustained-release preparation of 2% cream
5 g as a single application
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Clotrimazole
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1% cream 5 g once/day for 7 to 14 days
Vaginal tablet 100 mg once/day for 7 days or 200 mg once/day for 3 days or 500 mg once
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Miconazole
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2% cream 5 g once/day for 7 days
Vaginal suppository 100 mg once/day for 7 days or 200 mg once/day for 3 days
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Nystatin
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Vaginal tablet 100,000 units once/day for 14 days
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Terconazole
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0.4% cream 5 g once/day for 7 days or
0.8% cream 5 g once/day for 3 days
Vaginal suppository 80 mg once/day for 3 days
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Tioconazole
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6.5% ointment 5 g once
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Oral
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Fluconazole
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150 mg in a single dose
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Frequent recurrences require long-term suppression with oral drugs ( fluconazole 150 mg weekly to monthly or ketoconazole 100 mg once/day for 6 mo). Suppression is effective only while the drugs are being taken. These drugs may be contraindicated in patients with liver disorders. Patients taking ketoconazole should be monitored periodically with liver function tests.
Inflammatory
Vaginitis
Inflammatory
vaginitis is vaginal inflammation without evidence of the usual
infectious causes of vaginitis.
Etiology may be autoimmune. Vaginal epithelial cells slough superficially, and streptococci overgrow. The major risk factor is estrogen loss, which can result from menopause or premature ovarian failure (eg, due to oophorectomy, pelvic radiation, or chemotherapy). Genital atrophy predisposes to inflammatory vaginitis and increases risk of recurrence.
Symptoms and Diagnosis
Purulent vaginal discharge, dyspareunia, dysuria, and vaginal irritation are common. Vaginal pruritus and erythema may occur. Burning, pain, or mild bleeding occurs less often. Vaginal tissue may appear thin and dry. Vaginitis may recur.
Because symptoms overlap with other forms of vaginitis, testing (eg, vaginal fluid pH measurement, microscopy, whiff test) is necessary. The diagnosis is made if vaginal fluid pH is > 6, whiff test is negative, and microscopy shows predominantly WBCs and parabasal cells.
Treatment
Treatment is with clindamycin vaginal cream 5 g every evening for 1 wk. After treatment with clindamycin , women are evaluated for genital atrophy. Genital atrophy, if present, can be treated with topical estrogens (eg, 0.01% estradiol vaginal cream 2 to 4 g once/day for 1 to 2 wk, followed by 1 to 2 g once/day for 1 to 2 wk, then 1 g 1 to 3 times weekly; estradiol hemihydrate vaginal tablets 25 μg twice/wk; estradiol rings q 3 mo). Topical therapy is usually preferred because of concerns about the safety of oral hormonal therapy; topical therapy may have fewer systemic effects.
Last full review/revision April 2007 by David E. Soper, MD
Content last modified April 2007
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