Introduction
Vulvovaginal inflammation is a common, frequently curable cause of dyspareunia (Table 15.1). The purpose of this chapter is to review infectious causes of vulvovaginitis while excluding cervicitis and upper genital tract inflammation, both of which can cause sexual pain, especially deep dyspareunia.
Transient vaginal symptoms, which are temporary and mild, are extremely common. More severe and persistent symptoms usually prompt some action on the part of the woman; she may either visit a health care provider or self-treat with topical over-the-counter (OTC) symptom-relieving agents or a topical antimycotic without having received a medical evaluation or diagnosis. Vulvovaginal symptoms, including vaginal discharge, are among the 25 most common reasons for a physician in a private office to receive a consultation in the United States [1]. As indicated in Table 15.1, vulvovaginitis is only found in approximately 40% of women with vulvovaginal symptoms and in over 25% of women attending sexually transmitted infection (STI) clinics.
While the mechanism of dyspareunia encountered in the presence of vulvovaginal disease usually results from friction, pressure, and irritation of sensitized and inflamed nerve fibers, other mechanisms undoubtedly exist. In virtually all women with vulvovaginitis, symptoms of burning and irritation may either begin or continue after intercourse and may last for hours or days. Vulvovaginitis may also be associated with pelvic floor dysfunction (see Chapter 13), a factor frequently missed by practitioners.
It should be emphasized that “reasonable expectations” should be addressed with the patient at the initial visit. Given that many vulvovaginal disorders are long-standing and multifactorial in their etiology, they will most likely not be resolved immediately and in some cases may never be completely resolved. Symptoms of severe vulvovaginitis, especially due to Candida species, do not disappear in a matter of a day or two but may take up to 2 weeks to dissipate, especially with regards to intercourse.
Recurrent vaginitis (more than four episodes per year), especially candidiasis, can result in frequent, painful sexual relations with each “flare,” followed by a progressive healing period until the patient’s baseline subjective feelings and comfort are restored. Not surprisingly, frequent vaginitis results in frequent pain/discomfort which can stress an intimate relationship. Thus, for many reasons, breaking the vicious cycle of repeated recurrent infections is a major goal of treatment. Unfortunately, some women never return to their baseline function and represent a major challenge in pain management. Complete control of the underlying infection is often not achieved due to inadequate treatment measures.
Epidemiology
Bacterial vaginosis (BV) is the most common cause of vaginitis in women of childbearing age [2]. BV has been diagnosed in 17–19% of women who seek gynecologic care in family practice or student health care settings [2]. It has also been observed in 16–29% of pregnant women, and its prevalence increases considerably among symptomatic women in STI clinics, ranging from 24% to 37% [2]. Although Gardnerella vaginalis, one of the predominant organisms found in BV, has been found in 10–31 % of virgin adolescent girls, it is still found significantly more often among sexually active women, reaching a prevalence of 50–60% in some populations at risk for infection [3], Epidemiologie study has revealed that intrauterine devices, intravaginal pessaries, smoking, and douches were found to be more common in women with BV. BV is significantly more common in blacks and lesbians, and in women with a multiple number of sexual partners in the prior 12 months [2],
Infectious Vulvovaginitis |
Vulvovaginal candidiasis |
Bacterial vaginosis |
Trichomoniasis |
Mixed infections |
Genital herpes |
Group A streptococcus |
Desquamative inflammatory vaginitis (DIV) (??) |
Vaginal fistula (rectovaginal, vesicovaginal) |
Noninfectious |
Estrogen deficiency |
atrophic vaginitis |
atrophic vestibulitis |
Desquamative inflammatory vaginitis |
Erosive lichen planus |
Lichen simplex chronicus |
Contact dermatitis /chemical irritant |
Allergic vaginitis/vulvitis |
Dermatosis |
eczema |
psoriasis |
Pemphigus/pemphigoid syndromes |
Idiopathic vestibulitis syndrome |
Cytolytic vaginosis (??) |
* Does not include causes of cervicitis
(??) indicates that controversy exists for these conditions
Pathogenesis
BV is the result of massive overgrowth of mixed, predominantly anaerobic flora, including peptostreptococci, Bacteroides, Gardnerella vaginalis, Mobiluncus, and genital mycoplasmas [4]. With BV, there is little inflammation; the disorder represents a disturbance of the vaginal microbial ecosystem rather than a true infection of the tissues. The overgrowth of mixed flora is associated with a loss of the normal Lactobacillus-dominated vaginal flora. No single bacterial species is responsible for BV.
Two factors support the role of sexual transmission of BV: (1) the higher prevalence of BV among sexually active young women than among sexually inexperienced women, and (2) the observation that BV-associated microorganisms are isolated more often from the urethras of male partners of women with BV [2]. On the other hand, treatment of male partners does not result in reduced recurrence of BV in females.
The cause of the anaerobic overgrowth–including Gardnerella, Mycoplasma, and Mobiluncus species–that results in BV is unknown. Theories include increased substrate availability, increased pH, and loss of the restraining effects of the predominant Lactobacillusüom in the vagina. Women without BV are colonized by hydrogen peroxide-producing strains of lactobacilli, whereas women with BV have reduced numbers of lactobacilli, and the lactobacillus species that are present lack the ability to produce hydrogen peroxide [4, 5]. The hydrogen peroxide produced by lactobacilli may inhibit the pathogens associated with BV.
Accompanying the bacterial overgrowth in BV is the increased production of amines by anaerobes. These amines produce the typical fishy odor of BV. It is likely that amines together with the organic acids found in the vagina are cytotoxic, resulting in exfoliation of vaginal epithelial cells, creating the vaginal discharge typical of BV. Gardnerella vaginalis attaches avidly to exfoliated epithelial cells, especially at an alkaline pH. The adherence of Gardnerella organisms results in formation of the pathognomonic clue cells seen on a wet mount.
Clinical Features
As many as 50% of women with BV are asymptomatic. An abnormal malodorous vaginal discharge (often described as “fishy”) is usually detected, the odor often appearing after unprotected coitus. Examination reveals a nonviscous, grayish-white, adherent discharge. Pruritus, dysuria, and dyspareunia are rare.
Until recently, BV had largely been considered only a nuisance. However, there is substantial evidence that serious obstetric and gynecologic sequelae may occur (Table 15.2), even with asymptomatic disease. Untreated BV has been reported to be associated with increased clinical exacerbations of genital herpes and increased HIV transmission [6],
Obstetric |
Chorioamnionitis |
Premature rupture of membranes |
Preterm labor and delivery |
Low birth weight |
Amniotic fluid infections |
Postpartum endometritis |
Gynecologic |
Tubal infertility |
Pelvic inflammatory disease |
Postabortal pelvic inflammatory disease |
HIV transmission/acquisition/susceptibility |
Postsurgical infection |
Urinary tract infection |
Cervical intraepithelial neoplasia |
Mucopurulent endocervicitis |
Strong association with STIs (trichomoniasis, gonorrhea, chlamydia, herpes simplex virus, human papillomavirus) |
Signs and symptoms cannot reliably diagnose BV. The diagnosis is made by the presence of at least three of the following Amsel criteria: (1) an adherent, white, nonfloccular, homogenous discharge; (2) a positive amine test, with release of fishy odor on addition of 10% KOH to vaginal secretions; (3) a vaginal pH > 4.5; and (4) the presence of clue cells on light microscopy (the most reliable predictor). These criteria are simple, reliable, and easy to test.
At least 20% of observed epithelial cells should be clue cells, the exfoliated vaginal squamous epithelial cells covered with G. vaginalis, for this finding to be of diagnostic significance. The fishy odor may be apparent during the physical examination or the “whiff” (i.e., amine) test. A Gram stain of vaginal secretions is valuable in making the diagnosis, with a sensitivity of 93% and specificity of 70% [7].
Although cultures for G. vaginalis are positive in almost all cases of BV, the organism also may be detected in 50–60% of women who do not meet the diagnostic criteria for the disease [7]. Vaginal cultures are not used to diagnose BV.
Poor efficacy has been observed in the treatment of BV with triple sulfa creams, erythromycin, fiuoroquinolone, ampiciHin, tetracycline, acetic acid gel, and providoneiodine vaginal douches [8]. The most successful oral therapy is metronidazole. Multiple divideddose regimens of metronidazole at 800–1200 mg/day for 1 week achieved clinical cure rates in excess of 90% immediately and of approximately 80% at 4 weeks [8]. Although singledose therapy with 2 g of metronidazole achieved similar immediate clinical response rates, higher recurrence rates have been reported. The beneficial effect of metronidazole results primarily from its antianaerobic activity and its hydroxymetabolites.
Topical therapy with 2% clindamycin (once daily for 7 days) cream or suppositories, or metronidazole gel 0.75% (once daily for 5 days) has been shown to be as effective as oral metronidazole in eliminating BV without the side effects of the oral medication. Singledose vaginal clindamycin in a bioadhesive preparation is also available.
In the past, asymptomatic BV was not treated because patients often improved spontaneously over several months. However, the growing evidence linking asymptomatic BV with numerous obstetric and gynecologic complications involving the upper reproductive tract has prompted a reassessment of this policy, especially with the availability of convenient topical therapies [6].
Asymptomatic BV should be treated before pregnancy, in women with cervical abnormalities, and before elective gynecologic surgery. Routine screening and treatment for asymptomatic BV in pregnancy is controversial. Some controlled studies have shown that treatment of BV with topical clindamycin and oral metronidazole may reduce preterm labor and prematurity, but only in women with a past history of preterm labor. At present, this category of women seems most suited for screening [9]. Despite indirect evidence of its sexual transmission, no study has documented reduced recurrence rates of BV in women whose partners have been treated with a variety of regimens, including metronidazole. Accordingly, most clinicians do not routinely treat the male partners of affected women.
After treatment with oral metronidazole, symptoms of BV recur within 3 months in approximately 30% of patients who initially respond [7]. The reasons for such recurrence are unclear; possibilities include reinfection or vaginal relapse due to failure to eradicate the offending organisms and concurrent failure of the Lactobacillus-dominant vaginal flora to reestablish itself. Management of symptoms of acute BV during relapse includes treatment with oral or vaginal metronidazole or topical clindamycin, usually prescribed for a longer (10–14 days) period than the initial treatment regimen.
A recent study found that long-term suppressive maintenance therapy with twice weekly metronidazole gel (0.75%) is an effective prophylaxis, but long-term cure occurred in < 50% [10]. Attempts to prevent relapse by use of exogenous Lađobacilluspiepnmtions have been reasonably successful but remain controversial [11],
Epidemiology
Studies estimate that 3–5 million American women contract trichomoniasis annually, with a worldwide distribution of approximately 180 million cases each year [ 12]. The prevalence of trichomoniasis correlates with the overall level of sexual activity of the group of women studied, with the disease diagnosed in approximately 5% of women in family-planning clinics, 13–25% of women in gynecology clinics, 50–75% of sex workers, and 7–35% of women in STI clinics. Recent surveys indicate a decline in the incidence of trichomoniasis in many industrialized countries [12],