Introduction
Vulvovaginitis is one of the most common problems seen by gynecologists and other primary care practitioners. Due to the nonspecific nature of symptoms, empiric therapy has remained the mainstay of treatment by many physicians despite frequent misdiagnoses. With all the various over-the-counter treatments also available to women, frequent self-diagnosis and therapy have led to inappropriate treatment in many cases. A wide array of microbes, ranging from the normal vaginal flora to sexually transmitted pathogens, cause these genital infections. Bacterial vaginosis, trichomoniasis, and candidal infections are responsible for over 90% of infections. The cardinal symptom is abnormal vaginal discharge. If the vulva is involved, the patient may also complain of pruritus, burning, dysuria, and dyspareunia. The correct diagnosis involves a thorough history and physical examination, vaginal pH, whiff test, and microscopy. Even with all these tools, diagnosis of bacterial vaginosis, trichomoniasis, and candidal infections will be made only 60–90% of the time.
Normal vaginal discharge ranges from 1 to 4 mL per day. The vagina is acidic (pH 3.5–4.5) because of the lactic acid produced by Doderlein’s bacillus (Lactobacillus acidophilus), which are dominant bacteria in a healthy vaginal ecosystem. Lactic acid, produced by L. acidophilus, suppresses the growth of the gram-positive and gram-negative facultative and obligate anaerobes, maintains a normal pH, and inhibits bacteria from adhering to vaginal epithelial cells. In addition, the hydrogen peroxide produced by these organisms is toxic to a wide variety of microbes. Normal vaginal flora consist of many bacterial organisms, including potential pathogens that exist in symbiosis. Cervical mucus, semen, menstrual blood, overgrowth of other organisms of the vaginal flora, and progesterone all raise the vaginal pH and favor the growth of trichomonads and Gardnerella vaginalis.
A vaginal discharge can be physiologic when due to mucus secretion from the endocervix at mid-cycle or to desquamation of epithelial cells premenstrually. Other factors that contribute to vulvovaginitis are poorly cornified vaginal epithelium, as seen in prepupertal girls and postmenopausal women, fecal contamination from the anus, sexual intercourse, vaginal douching, pregnancy, and excessive local heat and moisture. In addition, broad-spectrum antibiotic therapy sufficient to destroy the normal bacterial flora, and co-existing systemic disease, such as diabetes, can result in recurrent infections.
In assessing the patient for vulvovaginitis, the history should include accounts of any previous vaginal infections and their treatment, as well as hygienic, contraceptive, and sexual practices. During the pelvic examination, attention should be paid to the appearance of the vulva, as well as the pH, color, consistency, and odor of the vaginal discharge. Abnormal discharge may be white, gray or green-yellow in color; the consistency may be homogeneous, “cottage-cheese” like or frothy in appearance. Microscopic examination of a wet smear will help to differentiate among infections due to fungi, trichomonads, and bacteria. Cultures for Candida and trichomoniasis should be done in symptomatic patients who have a negative microscopy due to the low sensitivity of microscopy for Candida (22%) and trichomoniasis (62%).
The emotional state of a patient suffering from recurrent vulvovaginitis should not be overlooked, as dealing with these infections can be frustrating. In addition to the symptoms, simply the sense of having a discharge can make sexual activity quite uncomfortable and embarrassing for the woman and may at times lead to stress in personal relationships.
Bacterial vaginosis (BV) is the most common type of vulvovaginitis irrespective of age. Various terms have been used in the past to describe this entity, including nonspecific vaginitis (NSV). The term BV has been proposed for this condition since bacteria are involved but without leukocytes. In the majority of these cases, however, the infection is due to a specific, though unidentified, bacterium.
The microbiologic picture of BV consists of the presence of gram-variable coccobacilli, consistent with G. vaginalis (found in 40% of women normally), together with numerous anerobic organisms. The latter are thought to be responsible for the production of aromatic amines with names such as putrescine, cadavarine, and trimethylamines, which are volatilized by the addition of 10% potassium hydroxide, resulting in the characteristic fishy odor (positive “whiff test”) associated with this disorder. Clue cells (stratified squamous cells with a granular appearance due to a coating of micro-organisms) may be visualized when saline is mixed with the vaginal fluids; however, it is not pathognomonic for this condition.
The diagnosis of bacterial vaginosis requires three of the following:
- a thin, homogeneous, white noninflammatory discharge with the appearance of skim milk
- presence of clue cells on microscopic examination (greater than 20% of epithelial cells)
- pH of vaginal sidewall or fluid > 4.5
- a fishy odor before or after adding KOH (positive “whiff test”).
Gram stain of vaginal secretions is also a reliable mode of diagnosing BV (93% sensitive, 70% specific), but it is not commonly used since it requires laboratory processing and delays diagnosis. Cultures for G. vaginalis are not useful in diagnosing BV because they are positive in 40–60% of asymptomatic women.
Bacterial vaginosis will resolve spontaneously in up to one-third of women. Treatment should be given to nonpregnant women with symptomatic infection. Numerous drugs (oral vs intravaginal) are available to treat BV. Intravaginal clindamycin (one applicator 2% cream before bedtime for 7 nights or 100 mg vaginal ovule every day for 3 days) and metronidazole (one applicator 0.75% cream before bedtime or twice a day for 5 days) are commonly used, and are comparable in their efficacy in the nonpregnant state. Oral therapies with clindamycin (300 mg twice a day for 7 days) or metronidazole (500 mg twice a day for 5 days) are alternatives as primary treatment or in recurrent infections. A single dose of Clindesse vaginal cream has been shown to be as effective as a 7-day course of Cleocin, which can lead to increased user reliability. Other antibiotic therapies such as ampicillin and erythromycin may eradicate G. vaginalis but since they also kill Lactobacillus, they raise the vaginal pH and facilitate reinfection. Poor efficacy has been observed also with the use of triple-sulfa creams, tetracycline, and povidone-iodine vaginal douches. Unprotected intercourse has also been shown to predict recurrence after initial improvement, so condoms should be advocated after treatment.
In pregnancy, early infection with BV is a strong risk factor for preterm delivery and spontaneous abortion. This risk can be attributed to BV being linked to chorio-amnionitis. However, a Cochrane review of 15 trials [1] reported no clear decrease in the odds of preterm birth with treatment of asymptomatic pregnant women in the general population. But when women with prior preterm birth were looked at separately, a significant reduction in the rate of preterm premature rupture of membranes and low birthweight was seen. Earlier diagnosis and treatment in the first trimester has been shown to be more effective for prevention of preterm birth than in the second trimester and beyond. Therefore, screening and treatment of BV in women with previous preterm birth should be considered at the first prenatal visit. In the first trimester, intravaginal clindamycin treats the infection locally and limits fetal exposure. After the first trimester, oral or intravaginal metronidazole can be used [2].
Causal relations have also been established between BV and upper genital tract infections, postpartum fevers, posthysterectomy vaginal cuff cellulitis, and postabortion infections. If BV is identified in the preoperative evaluation of a patient undergoing hysterectomy, appropriate therapy as listed above should be used to reduce the chance of postoperative surgical site infectious complications.
Vulvovaginitis due to Candida is usually caused by the species C. albicans, a dimorphic fungus that forms yeastlike buds, pseudohyphae, and hyphae. This ubiquitous organism is frequently found as a saprophyte on the skin and in the bowel, oropharynx, and vagina. Twenty percent of women are normally colonized with candidal species. Seventy-five percent of women will have at least one episode of vulvovaginal candidiasis during their lifetime. Approximately half experience more than one episode and approximately 5% experience a relapse and recurrence during a period of many years. When the host defenses are impaired, it becomes a pathogen. Certain predisposing conditions are responsible for recurrent candidal infections. These include pregnancy, uncontrolled diabetes, immunocompromised states such as AIDS, and chronic systemic steroid use. In addition, using antibiotics and oral contraceptives with high estrogen levels is associated with recurrent infections in some women. Vulvovaginal candidiasis is not considered a sexually transmitted disease since it occurs in celibate women; however, there is an increased frequency at the time most women begin regular sexual activity.
Candida albicans is currently the most common cause of vaginitis during the reproductive years. However, an increasing frequency of other candidal species, particularly C. glabrata, has been reported, possibly due to the widespread use of over-the-counter drugs that are more selective in eradicating C. albicans.
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