Trichomonas vaginalis

Trichomonas vaginalis is a flagellated protozoan slightly larger than a leukocyte. It may be found in the lower urogenital tract of both men and women. Humans appear to be its only host, and sexual transmission appears to be its primary mode of dissemination. Trichomonas does not invade tissues and rarely causes serious complications. The most common symptom is leukorrhea associated with itching and burning. The discharge is frequently malodorous, greenish yellow, and frothy. The “strawberry cervix” with punctate hemorrhages is found in only a small percentage of patients with Trichomonas infection. Trichomonads grow optimally at a pH of 5.5 to 5.8.⁹ Thus, conditions that elevate the pH, such as increased progesterone, will favor overgrowth of Trichomonas. Conversely, a vaginal pH of 4.5 in a woman with vaginitis is suggestive of an agent other than Trichomonas. A saline wet mount of fresh vaginal fluid demonstrates the presence of small motile organisms to confirm the diagnosis in 80% to 90% of symptomatic carriers.^10,11

Candida albicans

Both the relative frequency and the total incidence of candidal vaginitis have risen dramatically, 2.5-fold, in the past 20 years. This increase parallels a declining incidence of gonorrhea and trichomoniasis.¹² Several factors have contributed to this increased incidence, chief among them being the greater use of antibiotics. The alterations that antibiotics make in both intestinal and vaginal ecology favor the growth of Candida. In the 1970s, Miles et al¹¹ found a 100% correlation between genital and gastrointestinal Candida cultures, leading to the suggestion that significant intestinal colonization with Candida may be the single most significant predisposing factor in vulvovaginal candidiasis. However, this suggestion has not been confirmed by adequate research.

Steroids, oral contraceptives, and the continuing rise in incidence of diabetes mellitus all contribute to the problem. Candida is 10 to 20 times more common during pregnancy owing to the elevated vaginal pH, increased vaginal epithelial glycogen, elevated blood glucose, and intermittent glycosuria. Yeast infections are three times more prevalent in women wearing pantyhose than those wearing cotton underwear because the pantyhose prevent drying of the area.¹³

A woman who has four or more episodes of vulvovaginal candidiasis within 1 year is classified as having recurrent disease. Many cases of recurrent yeast infections may be caused by non-albicans strains of Candida. These resistant strains have become more problematic in recent years as women have been using more and more antifungal agents (see Box 213-1). There are three main theories to explain why women have recurring yeast vaginitis: (1) the intestinal reservoir theory, which hypothesizes that a patient’s reinoculation is due to Candida populating in the gastrointestinal tract and migrating into the vagina; (2) the sexual transmission theory, which points to the possibility that the sex partner is the source of the recurrence; and (3) the vaginal relapse theory, which maintains that some women retain small numbers of yeasts, even after treatment, that later cause a resurgence of symptoms. A considerable body of research supports this last theory.^14,15 These studies include immunologic research suggesting that women with recurrent infections have an abnormal immune response to infection, which leaves them susceptible to further episodes.¹⁶

The primary symptom of candidal vaginitis is vulvar itching, which can be severe. Burning of the vulva may also be experienced and can be exacerbated by urination or vaginal sexual activity. It is also common to have an increase or change in the consistency of the vaginal discharge. In a classic case, this is associated with the presence of a thick, curdy, or “cottage cheese” discharge that adheres to the vaginal walls. The presence of such a discharge is strong evidence of a yeast infection, but its absence does not rule out Candida. Fewer than 20% of symptomatic patients with candidal infection actually display classic thrush patches. Other clues to a candidal etiology are the presence of erythema of the vulva and excoriations due to scratching. The vaginal pH is not usually altered. Neither the character of the discharge nor the symptomatology is sufficient alone to make a diagnosis of Candida. A wet mount in saline or 10% KOH should always be performed and the presence of mycelia confirmed. Budding forms of yeast may be found in both normal and symptomatic vaginas, but the mycelial stage is found only in symptomatic women.

Bacterial Vaginosis

The term bacterial vaginosis has now been used most often to describe a shift in flora from a predominance of lactobacilli to a predominance of anaerobes and facultative bacteria, which results in a degradation of the mucins that form a natural gel barrier on the vaginal epithelium. This destruction of the mucin layer causes a vaginal discharge characteristic of BV. In addition, destruction of these mucins exposes the cervical epithelium and allows other organisms to affect the cervix, resulting in the appearance of clue cells. The changes on the epithelial surface also cause immunologic shifts. Women with BV have an upregulation of interleukin-1-beta and a decrease in protectant molecules such as secretory leukocyte protease inhibitor.

Three main factors have been identified to explain how the shift from a lactobacilli-dominant environment to one in which the anaerobes and facultative bacteria dominate and therefore why some women experience BV—sexual activity, douching, and the absence of peroxide-producing lactobacilli in the vagina. A new sex partner and frequent sexual activity are associated with an increased incidence of BV. Overall, sexual transmission of BV is not well understood. It may not be truly sexually transmitted but rather may occur by various mechanisms other than the sexual transmission of pathogens. Routine douching is associated with a loss of vaginal lactobacilli and the occurrence of BV. Women who douche regularly have BV twice as often as women who do not.¹⁷ It is possible that women with an absence of peroxide-producing lactobacilli in the vagina did not have the normal inhabitation of lactobacilli at menarche, or perhaps the lactobacilli were present but were eliminated through the use of broad-spectrum antibiotics.

Other factors have been associated with the development of BV. Cigarette smoking is associated with BV but may be related to the downregulation of the immune response. Racial background has also been associated with BV. Hispanic women are 50% more likely to have BV, and African American women are twice as likely.¹⁸ Although the reasons for these differences are not clear, we do know that African American women practice douching twice as often as white women and that African American women are less likely to have lactobacilli in the vagina.

Examination for BV involves a medical history, observation of the discharge, and determination of vaginal pH. In the woman with symptomatic BV, the vagina has a fishy odor. The characteristic discharge is thin, dark, or dull gray. Itching is not common with BV but may be present if there is a profuse discharge. A whiff test should be performed, and a wet mount test to detect clue cells and observe the vaginal flora. An abundance of various bacteria and the absence or decrease in lactobacilli is consistent with a diagnosis of BV. The numbers of bacteria rise from 100-fold to 1000-fold. For a diagnosis of BV to be made, three of the following four criteria must be met:

The pH is elevated to 5 to 5.5 in most cases, and there appears to be a correlation between elevated pH and the presence of odor.¹⁹

When a patient has four or more BV episodes in a year, her underlying problem is most likely an inability to re-establish a normal vaginal ecosystem with the dominant lactobacilli. There is no definition of recurrent BV, but most clinicians would probably agree that more than four episodes in a year would define the disorder. About 30% of women experience a recurrence of symptomatic BV within 1 to 3 months, and about 70% have a recurrence within 9 months.²⁰ It is not always clear whether the recurrence represents a relapse or a reinfection. Another possibility is that a woman may be asymptomatic at times but, because of the abnormal vaginal ecosystem, she has a chronic underlying condition, so that she is sometimes symptomatic and at other times is not. Women who are asymptomatic yet have no lactobacilli are four times more likely to experience BV. Unfortunately we do not have a proved treatment for asymptomatic women.

There are potential significant consequences of altered vaginal flora in addition to susceptibility to BV. Women with BV and without sufficient lactobacilli are more susceptible to human immunodeficiency virus (HIV) and gonorrhea.^21,22 PID is also associated with BV. There is also now good evidence that the organisms in pregnant women with BV can ascend the genital tract and cause preterm delivery, and such women are more likely to have postpartum endometritis. Women with BV are also at increased risk for infection after gynecologic surgery.

Vitamin A and Beta-Carotene

Both vitamin and beta-carotene are necessary for the normal growth and integrity of epithelial tissues, such as the vaginal mucosa. Vitamin A is essential for adequate immune response and resistance to infection. Secretory IgA, a major factor in resistance to infection, is lower in vitamin A–deficient subjects.²⁵ Beta-carotene is a source of nontoxic vitamin A precursors. In addition, it has been shown to enhance T-cell numbers and to favorably alter their ratios.²⁶ Excessive vitamin A can be toxic and teratogenic. This is of particular concern in women of reproductive age. Total vitamin A intake should be limited to 5000 IU/day. If larger doses of vitamin A are used, patients should be cautioned to be particularly careful about contraception. Mixed carotenoids rather than synthetic beta-carotene should be used.