Vulvovaginitis

VULVOVAGINITIS

Background

Vulvovaginitis is the most common gynecologic condition seen by practitioners rendering primary care to women. The term vulvovaginitis is a semantic compromise that categorizes many vaginal infections as vulvovaginitis because the 2 are interrelated. Discharge, burning, and pruritus are the most common symptoms, accompanied by signs of vulvar irritation such as erythema and excoriation of the vulvar skin.

Traditionally, the 3 classic entities of vaginitis include bacterial vaginosis, Trichomonas infection, and candidiasis. However, this article focuses on topics that are primarily inflammatory disorders and affect the vulvar region.

Pathophysiology

The vulva, the external genitalia of the female, includes the labia majora and minora, the clitoris, and the vestibule of the vagina. During the reproductive years of a healthy woman's life, the vagina maintains a moist environment that is in constant fluctuation. The secretion of an alkaline transudate from the vaginal epithelium and cervical glands maintains this moist environment with a pH ranging from 3.8-4.5. In addition, the vagina and its microflora form a unique balanced environment that can change under pressure from external stimuli but returns to normal with removal of the stimuli. It can vary in degree during the menstrual cycle, pregnancy, and sexual activity.

The vaginal epithelium consists of 3 cell layers: superficial, intermediate, and basal. These cells are capable of storing glycogen under the influence of estrogen. Glycogen is available in the fully mature cells in the superficial layer of the epithelium. With elevated levels of either exogenous or endogenous estrogen, all levels of the epithelium thicken as a result of glycogen storage. With diminishing levels of estrogen, the layers become thin and atrophic.

In an adult woman's reproductive years, the bacterial flora of the healthy vagina contains numerous microorganisms, including aerobic and anaerobic gram-positive and gram-negative bacteria. Lactobacillus and Corynebacterium predominate over other bacteria such as Streptococcus, Bacteroides, Staphylococcus, and Peptostreptococcus. Both Lactobacillus and Corynebacterium produce lactic and acetic acid from glycogen, thus maintaining the low vaginal pH. Additional bacteria are kept in check by the acid-producing bacteria and are rarely pathogenic, but they may become pathogenic if the environmental balance is affected.

The skin of the vulva is sensitive to the vaginal environment and hormonal, metabolic, and allergic influences. It is composed of stratified squamous epithelium that contains hair follicles, sebaceous sweat glands, and apocrine glands.

Differential Diagnosis

The focus of this article includes Candida vulvovaginitis, atrophic vaginitis, contact dermatitis, pediatric vulvovaginitis, and vulvar vestibulitis.

The complete differential includes the following:

• Allergic reaction

• Physiologic leukorrhea

• Atopic dermatitis

• Lichen simplex chronicus

• Lichen sclerosus

• Paget disease

• Psoriasis

• Vulvodynia

In prepubertal girls with vaginal discharge, the following should be considered:

• Anatomic abnormality

• Foreign bodies

• Neoplasm

• Sexual abuse

• Hygiene

Vulvovaginal Candidiasis

In the United States, estimates indicate that approximately 50% of college-aged women will have an episode of vulvovaginal candidiasis. At some point in their lifetime, nearly 75% of all women experience an attack of Candida vulvovaginitis. Approximately half of these women have more than 1 episode, and a few have frequent relapses.

Etiology

Vulvovaginal candidiasis can be an acute, chronic, recurrent, or persistent condition that can involve the vulva, vagina, and adjacent crural areas. The specific causative agent belongs to the genus Candida. These organisms are found in almost all humans and many animals. An estimated 10-50% of reproductive-aged American women are considered opportunistic carriers. Candida albicans is identified approximately 85-90% of the time. Recently, an increased frequency of other Candida species, such as Candida glabrata, Candida tropicalis, and Candida krusei, has been reported. The emergence of these other Candida species may possibly be due to widespread use of over-the-counter drugs, long-term use of suppressive azoles, and the use of frequent short courses of antifungal drugs.

Predisposing agents

Any host factor that affects the vaginal environment or vaginal secretions can play a role in the initiation of Candida vulvovaginitis. Pregnancy is one of the most common predisposing factors. Studies have demonstrated that up to one third of pregnant women worldwide on any day can be affected. The high levels of reproductive hormones and an increase in the glycogen content in the vaginal environment create a favorable environment for Candida species. In combination, these 2 changes provide an abundant source of carbon for candidal growth, germination, and adherence. Furthermore, the acidity of the pregnant vaginal flora can suppress the growth of other microorganisms that are naturally inhibitory to Candida. Although the initial attachment of the organism occurs more readily at high pH values (6-7), the germ tube formation and the development of mycelia are favored by a low vaginal pH (< 5).

Older studies of women using high-dose estrogens in oral contraceptives found an increase in vaginal colonization by Candida. The mechanism is believed to be similar to that found in pregnancy. However, the newer oral contraceptives with a lower estrogen dose do not seem to predispose the patient to Candida vulvovaginitis.

Disorders associated with an altered immune response, such as acquired immunodeficiency syndrome (AIDS) and diabetes mellitus, also predispose to Candida vulvovaginitis.

Antimicrobials are thought to predispose a patient to Candida by reducing the number of protective resident vaginal bacteria. The most common offenders are broad-spectrum agents such as tetracycline, cephalosporins, and ampicillin-like agents.

A study by Horowitz et al in 1987 demonstrated Candida species in ejaculate fluid of partners of patients with recurrent Candida infections. They suggested that the carrier rate might be low.[1] Traditionally, vulvovaginal candidiasis is not considered a sexually transmitted disease because it occurs in celibate women, and Candida itself is considered part of the normal vaginal flora.

Clinical

In acute vulvovaginal candidiasis, vulvar pruritus and burning are the main symptoms. Patients commonly complain of both symptoms after intercourse or upon urination. Dyspareunia may develop and become severe enough to lead to intolerance of intercourse. Physical findings include erythema and edema of the vestibule and labia majora and minora. The rash may extend to the thighs and to the perineum. Thrush patches are usually found loosely adherent to the vulva. A thick, white, curdlike vaginal discharge is usually present.

The clinical picture of chronic persistent candidiasis differs in that it includes marked edema and lichenification of the vulva with poorly defined margins. Often, a grayish sheen made up of epithelial cells and organism covers the area. Symptoms include severe pruritus, burning, irritation, and pain. This patient group is usually older, obese, and often has long-standing diabetes mellitus.

Diagnosis

The diagnosis depends both on the demonstration of a species of Candida and the presence of clinical symptoms. Diagnostic tests include a positive wet-mount test or potassium hydroxide preparation. Vaginal pH usually remains normal in vulvovaginal candidiasis.

The wet-mount test involves microscopic examination of vaginal discharge or scrapings from vulvar lesions mixed with physiological saline under both low-power and high-power magnifications. Under microscopic viewing, the spores and conidia are visible. The presence of yeast blastospores or pseudohyphae can be detected in approximately 30-50% of patients with symptomatic vulvovaginal candidiasis. Adding 10% potassium hydroxide to the solution lyses white blood cells, red blood cells, and vaginal epithelial cells, making the alkali-resistant branching budding hyphae of Candida easier to see. This method may increase the sensitivity; however, at least one third of patients with symptomatic candidiasis have negative findings with this method. Nevertheless, positive results from these 2 tests, in combination with a normal vaginal pH, are helpful in confirming the diagnosis.

Most studies demonstrate that 85-90% of vaginal isolates are C albicans. As a result, fungal cultures have not been used by most clinicians as part of the initial evaluation. The rationale is thought to be that using fungal cultures will be too sensitive and will detect yeast that may be colonizing the patient, but not causing the symptoms.

Treatment

The cell wall of the organism is a complex glycoprotein that depends on the biosynthesis of ergosterol. Azole compounds found in antimycotic drugs are believed to block this step in biosynthesis. Topical antimycotic drugs can achieve cure rates in excess of 80%. The only oral azole agent approved for this indication by the US Food and Drug Administration (FDA) is fluconazole, which also achieves a high rate of cure. It achieves therapeutic concentrations in vaginal secretions for at least 72 hours after the ingestion of a single 150-mg tablet.[2]

In considering treatment, distinguishing between sporadic or recurrent episodes of vulvovaginitis is of great importance. Uncomplicated

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