Vaginal infections: diagnosis and management

Vaginal infections: diagnosis and management

Barbara D. Reed

Vaginal symptoms are among the most common reasons that women consult primary care physicians. Several diagnostic choices, methods of evaluation and treatment protocols are possible. Women also may treat themselves for vaginal symptoms, using over-the-counter remedies. The availability of these products implies that diagnosis of vaginal symptoms is straightforward; however, evidence suggests that diagnosis without careful attention to specific criteria is less accurate than a coin toss.[1,2] Specific evaluation of vaginal symptoms and directed therapies are essential if treatment is to be appropriate and potentially serious infections are to be recognized.

Most vaginal symptoms are caused by one of three common infections: bacterial vaginosis, Candida vulvovaginitis and Trichomonas vaginitis. This article reviews the diagnosis and management of these infections in primary care.

Diagnosis

The evaluation of women with vaginal symptoms requires a directed history, a physical examination and in-office laboratory testing in all cases. The components of the evaluation are outlined in Table 1. [TABULAR DATA OMITTED]

BACTERIAL VAGINOSIS

Bacterial vaginosis (or vaginal bacteriosis) has previously been referred to as nonspecific vaginitis or anaerobic vaginosis, or identified by the causative organism (e.g., Haemophilus vaginalis, Corynebacterium vaginalis and Gardnerella vaginalis).

Bacterial vaginosis represents an ecologic disturbance of the vaginal microbial flora, the etiology of which is unclear. It is thought to result from overgrowth of bacteria, especially various anaerobes and gram-negative bacilli, with a concomitant decrease in the normally predominant peroxide-producing lactobacilli. Metabolic products of this altered flora include aromatic amines, which increase the vaginal pH from the normal range of 3.8 to 4.4. These products result in a “fishy” odor that is frequently more noticeable after intercourse.

Patients with bacterial vaginosis often complain of a vaginal discharge and an unpleasant vaginal odor. In contrast, approximately 50 percent of women with microbiologic findings suggestive of bacterial vaginosis are asymptomatic, and studies suggest that spontaneous resolution of laboratory-proven bacterial vaginosis occurs in the majority of asymptomatic women.[3]

Although bacterial vaginosis infrequently leads to systemic consequences, it has been associated with adnexal tenderness, pelvic inflammatory disease, postpartum endometritis, urinary tract infections, pelvic abscesses and cuff cellulitis following abdominal hysterectomy.[4] An association between bacterial vaginosis and preterm labor, premature rupture of the membranes and chorioamnionitis has been reported,[5,6] but further study is needed to determine whether treatment of bacterial vaginosis improves pregnancy outcome.[4]

Factors associated with bacterial vaginosis include a history of multiple sexual partners,[2] use of an intrauterine device or lack of contraception,[7] and the presence of a sexually transmitted disease.[7] Although G. vaginalis is more common in children who have been sexually abused, it may also be found in asymptomatic girls without a history of sexual abuse and, thus, the presence of this organism is not considered proof of sexual exposure.[4]

The diagnosis of bacterial vaginosis is based on clinical criteria[7]; at least three of the four components shown in Table 2 are required, all of which can be assessed readily in the family physician’s office (Figure 1). [TABULAR DATA OMITTED]

Culture of vaginal discharge is rarely indicated because of the polymicrobial nature of the infection. Although most patients with bacterial vaginosis have positive cultures for G. vaginalis, identification of this organism is not required for diagnosis. Gram-stain diagnosis of bacterial vaginosis, demonstrating the absence of large gram-negative rods (lactobacilli) and an overabundance of other flora, is fairly accurate and may be used instead of the wet mount if desired.[4,8]

CANDIDA VULVOVAGINITIS

Candida vulvovaginitis is the second most common diagnosis in women with vaginal symptoms. Although it can be caused by various types of Candida fungi, 85 percent of clinical cases are caused by Candida albicans. This organism is also found in more than 25 percent of asymptomatic women, and the factors resulting in symptomatic infection are unclear. Numerous risk factors have been suggested for Candida vulvovaginitis, including diabetes mellitus, dietary practices, intestinal colonization by Candida, tight clothing, sexual transmission, specific immunologic defects and the use of oral contraceptives or antibiotics.[9]

Symptoms and signs associated with this infection, such as marked itching, a thick discharge and vulvar or vaginal erythema, are not accurate predictors of confirmed Candida infection[2]; therefore, each patient should be assessed by laboratory testing to ensure accurate diagnosis (Table 2).

TRICHOMONAS VAGINITIS

Trichomonas vaginitis is caused by Trichomonas vaginalis, a flagellated anaerobic protozoan that is usually acquired through sexual contact, although fomite transmission is theoretically possible. Trichomoniasis in women is often associated with a profuse discharge and vaginal or vulvar irritation but may also be associated with vaginal itching, dysuria, dyspareunia or an abnormal vaginal odor.[10] The infection is asymptomatic in approximately 50 percent of women and 90 percent of men.[10]

On physical examination, the discharge may be white or discolored (yellow, gray or green) and is occasionally frothy or foamy. Less common physical findings are the classic colpus macularis (“strawberry cervix”), or redness of the vagina, perineum or inner thigh.

Laboratory findings in patients with Trichomonas vaginitis include an elevated pH (greater than 5.0) and more than 10 white blood cells per high-power field on a normal saline preparation. These findings, although suggestive of specific infections, are insufficient for diagnosis (Table 2).

Improving Diagnostic Accuracy

The diagnosis of both Candida vulvovaginitis and Trichomonas vaginitis requires identification of the causal organism (Figures 2 and 3). When hyphae, budding yeasts or motile trichomonads are identified on saline or potassium hydroxide (KOH) preparation, the diagnosis is reliable; however, several studies have documented that results of microscopic examinations are false-negative in 37 to 81 percent of patients with Candida vulvovaginitis[2,11] and 23 to 58 percent of patients with Trichomonas vaginitis in nonreferral settings.[12,13] The diagnosis of Trichomonas vaginitis by Papanicolaou smear is unreliable and should not be the basis of the diagnosis of a sexually transmitted disease.[14] Other diagnostic modalities offer improved accuracy in these cases.

Rapid in-office tests (requiring three to five minutes) for Candida antigens in vaginal discharge are now commercially available. They appear to be more sensitive than the KOH preparation in the outpatient setting,[15] but they lack the accuracy of culture. Solid agar cultures for Candida (Sabouraud’s or Nickerson’s agar) also improve diagnostic accuracy and are easy to perform in the office.

Immunologic tests for Trichomonas infection have been developed for laboratory use,[16] but further evaluation is needed before tests designed for primary care settings can be generally recommended. Commercial liquid media (i.e., modified Diamond) are now available for incubation of Trichomonas and have been shown to have a sensitivity of 90 percent for the identification of T. vaginalis, compared with 64 percent for wet mount.[17] In our office, these media also have a sensitivity of more than 95 percent for Candida species.

Because of cost and patient comfort considerations, presumptive treatment may be instituted at the initial visit if desired, but the level of certainty of the diagnosis should be clearly documented, and cultures should be obtained following treatment failure or recurrence of symptoms.

OTHER DIAGNOSES CAUSING VAGINAL SYMPTOMS

In approximately one-third of patients with vaginal symptoms, no laboratory evidence of bacterial vaginosis, Candida vulvovaginitis or Trichomonas vaginitis can be found. In addition, patients who have one vaginal pathogen are at increased risk of infection with multiple organisms. Careful evaluation, including history, physical examination and laboratory testing, is indicated to search for other causes of the vaginal symptoms, such as multiple infections, cervicitis, allergic reactions or vulvodynia.

Treatment

BACTERIAL VAGINOSIS

The treatment of bacterial vaginosis is directed toward reestablishing the normal balance of bacteria in the vagina. Therapeutic options[18] are listed in Table 3. Metronidazole (Flagyl, Protostat), 500 mg orally twice daily for seven days, is the initial recommended treatment. This regimen is effective in more than 90 percent of cases. However, approximately 18 percent of patients have clinical evidence of bacterial vaginosis at least 29 days after the beginning of therapy.[19] A single 2-g dose of metronidazole for bacterial vaginosis has initial cure rates ranging from 67 to 92 percent, with several studies showing cure rates comparable to those achieved with five- or seven-day therapy.[20] [TABULAR DATA OMITTED]

Oral metronidazole may be accompanied by adverse gastrointestinal effects, including nausea, heartburn and a metallic taste in the mouth. These effects are dose-related and are usually self-limited.[21] Peripheral neuropathy, seizures and other complications have rarely been reported. Patients should be informed about the potential side effects and cautioned about the emetic effect of metronidazole in combination with alcohol.

Metronidazole readily crosses the placental barrier and, although advocated for use in pregnancy by some physicians, is officially contraindicated in the first trimester of pregnancy because of a small teratogenic potential. Risks in the second and third trimesters of pregnancy are minimal, and the drug is commonly used during that period, but the theoretic increased risk of childhood malignancies following fetal exposure to metronidazole has not yet been completely excluded.

Two new intravaginal products are available for treatment of bacterial vaginosis. Both clindamycin (Cleocin) 2 percent vaginal cream[22,23] and metronidazole vaginal gel (MetroGel-Vaginal.)[24,25] are reported to have efficacy rates similar to those obtained with oral administration of the same drugs. Systemic absorption is low for each drug (less than 5 percent).

In clinical studies, side effects resulting in discontinuation of clindamycin and metronidazole gel were low (4 percent and 1 percent, respectively). Development of symptomatic vulvovaginitis (primarily Candida) was the most common side effect with clindamycin (16 percent). Candida vulvovaginitis and gastrointestinal symptoms each occurred in approximately 6 percent of patients using metronidazole gel. Because the mineral oil base may weaken latex or rubber, patients should be instructed to avoid condoms and contraceptive diaphragms for 72 hours after using clindamycin cream.

Persistent Cases. Recurrent and persistent cases of bacterial vaginosis should be reevaluated. Bacterial vaginosis is commonly associated with other genital infections, including Trichomonas vaginitis and other sexually transmitted diseases.[26] Careful evaluation for multiple pathogens and appropriate treatment of each is required.

The most successful alternative oral regimen for persistent bacterial vaginosis is clindamycin, 300 mg orally twice daily for seven days. Cure rates with this regimen are similar to those achieved with metronidazole.[27] As clindamycin is not known to have teratogenic or oncogenic potential, this alternative may be useful for pregnant patients.[21]

Other promising oral agents include ciprofloxacin (Cipro), amoxicillin plus clavulanic acid (Augmentin) and cephalexin (Keflex). Agents such as tetracycline, ampicillin, triple sulfa cream and erythromycin are ineffective against bacterial vaginosis. Ampicillin is no longer recommended in the treatment of bacterial vaginosis because of the prevalence of resistant organisms, as well as its ability to decrease the lactobacilli in the vagina, thereby inhibiting the return to normal vaginal flora.[28]

Other intravaginal treatments are meant to eliminate bacterial vaginosis by improving the “ecological balance” of the vaginal microflora. Estrogen creams and acetic acid jelly (such as Aci-Jel) are not effective against bacterial vaginosis.[29] Although it seems reasonable to reconstitute the normal lactobacillus flora of the vagina with commercially available acidophilus preparations, this effort is rarely effective. Chlorhexidine suppositories[30] and povidoneiodine (Betadine) suppositories[31] have been found to be curative in 79 percent and 76 percent of cases, respectively, although the rate of resolution in the placebo group in clinical studies was also substantial.[31]

Sexual Partners. The advantage of treating the sexual partners of patients with bacterial vaginosis is controversial. Most investigators have not found treatment of partners to be superior to treating only the woman,[32] although one study demonstrated an increased rate of cure when the male partner was treated with a single 2-g oral dose of metronidazole.[33] Based on current data, treatment of sexual partners should only be considered in persistent or recurrent cases.

Pregnancy. The risks and benefits of treatment for bacterial vaginosis during pregnancy are unclear. Although bacterial vaginosis is associated with chorioamnionitis and preterm rupture of the membranes resulting in low-birth-weight infants,[5,34] bacterial vaginosis is associated with other genital infections that may also increase risk to the pregnancy, and the individual contribution of bacterial vaginosis to pregnancy complications is unclear. The risk of metronidazole to the fetus is small, but universal metronidazole treatment of pregnant patients with bacterial vaginosis is controversial. Treatment with clindamycin may be a reasonable alternative for persistent disease in pregnant patients.

CANDIDA VULVOVAGINITIS

Candida vulvovaginitis can be successfully treated with a variety of vaginal preparations.[35] The imidazole and triazole preparations have superior clinical efficacy compared with the polyene preparations, such as nystatin (Mycostatin, Nilstat), and are preferred to polyene medications. Most imidazole antifungal vaginal preparations, such as miconazole (Monistat), clotrimazole (Gyne-Lotrimin, Mycelex-G) and butoconazole (Femstat) eradicate Candida species from the vagina in approximately 85 percent of patients with acute Candida vulvovaginitis. This efficacy rate is found with tablet or cream formulations and with treatment periods ranging from one to seven days.[5] Little comparative data are available to recommend one over the others (Table 4). [TABULAR DATA OMITTED]

Individual treatment recommendations for each patient should be based on several factors, such as severity, duration and location of symptoms, and patient preference.[36] Severe symptoms and chronic infections may respond better to longer courses of treatment. Extensive vulvar involvement may respond better to a cream than to a suppository preparation.

Terconazole (Terazol), a newer triazole antifungal vaginal preparation, forms a firmer and longer lasting link with fungal cytochrome P-450 than the imidazole preparations.[37] From 5 to 16 percent of the active agent is absorbed systemically, occasionally causing flu-like symptoms.[37] Terconazole has been compared with the imidazoles in European and American studies and has been found to be equivalent or superior to treatment with miconazole or clotrimazole cream (seven-day regimen) or a 500-mg clotrimazole tablet (one-time treatment).

Oral Antifungal Agents. Many women prefer oral medications to intravaginal preparations for the treatment of vaginal infections.[38] Currently there are two oral regimens for treatment of resistant or recurrent Candida vulvovaginitis.

Oral ketoconazole (Nizoral), 400 mg per day for five to 14 days, is effective in the treatment of Candida vulvovaginitis.[39] The risk of mild, reversible hepatitis from ketoconazole treatment is approximately 5 to 10 percent, and the risk of symptomatic, potentially serious hepatitis is one in 15,000. Therefore, this drug should only be considered for resistant, recurrent cases of Candida vulvovaginitis, such as in women with human immunodeficiency virus (HIV) infection.[40]

Fluconazole (Diflucan) and itraconazole (Sporanox) are new oral triazole antifungal agents that have been used extensively in immunosuppressed patients with systemic Candida infections and have been shown to be effective against Candida vulvovaginitis. Side effects are usually mild, consisting of nausea and diarrhea (2 to 6 percent of patients),[41,42] or occasional headache. Isolated allergic reactions have been reported with each.

Results of studies comparing oral fluconazole to intravaginal clotrimazole are variable, with some studies suggesting similar clinical response rates (84 percent or greater).[41] Other studies show superior long-term (greater than 27 days) clinical cure rates over a one-month period and more rapid symptom relief with a single dose of fluconazole, compared with three-day treatment with clotrimazole.[43] Acute vulvovaginitis resolved in 75 percent of patients treated with oral itraconazole, 200 mg daily for three days, but comparisons with other agents are lacking.[42] To date, studies comparing oral agents and vaginal treatments have not shown that systemic treatment decreases the rate of long-term recurrence.[44,45]

Other Treatment Possibilities. A recent report suggests that prophylaxis with dietary yogurt containing live lactobacillus may decrease episodes of Candida vulvovaginitis.[46] Preparations containing this organism are commercially available. Prophylaxis with dietary yogurt should be individualized and discontinued if ineffective.

Other treatment modalities for persistent Candida vulvovaginitis are less commonly employed, possibly because of inconvenience. These modalities include boric acid suppositories, 600 mg in gelatin capsules used intravaginally twice daily, and gentian violet painted on the vaginal walls. Although little is written about the efficacy of these agents compared with other vaginal preparations, these remedies are suggested as alternatives for recurrent or persistent infections.

Pregnancy. Studies of clotrimazole and miconazole in pregnant patients have shown no increase in congenital defects. Teratogenicity has not been reported with terconazole, but limited data are available. None of the imidazoles are recommended for use in the first trimester of pregnancy unless the severity of symptoms precludes delay of treatment. The use of fluconazole in pregnancy has not yet been studied extensively. Fluconazole, itraconazole and ketoconazole should not be used for localized disease in pregnant patients.

Recurrences. Approximately 40 percent of adult women experience more than one lifetime episode of Candida vulvovaginitis. If recurrences are spaced widely in time, and if treatment with vaginal antifungal creams is effective, no alteration in the evaluation or management of the patient is needed. However, if symptoms do not resolve completely with treatment, or if they recur within a two- to three-month period, further evaluation is indicated. Reexamination (and possibly culture) is necessary despite previous documentation of the etiology. Misdiagnoses do occur and in many cases, treatment for Candida may “unmask” the presence of previously unidentified genital infections.

Other Factors. Other characteristics potentially increasing the risk for Candida vulvovaginitis have been identified in various populations. These characteristics include the use of oral contraceptives, the presence of diabetes, increased dietary intake of milk products or artificial sweeteners, Candida carried in the gastrointestinal tract and Candida carried by a sexual partner.[9] However, alteration of these factors does not consistently alter recurrence rates and cannot be routinely recommended.[9] If such modifications are recommended to a patient, pre- and postalteration recurrence rates should be documented so that unsuccessful modifications can be discontinued as indicated. Prophylactic Treatment. Several protocols for prevention of recurrences of vaginal infections by prophylactic treatment have been evaluated. When compared with placebo, the following alternatives decreased recurrences of Candida vulvovaginitis over the short term, but no long-term benefit was shown: clotrimazole, one 500-mg suppository monthly; miconazole, one or two suppositories weekly, or ketoconazole, 400 mg orally daily for five days each month during menses or 100 mg every day.[44,47]

Prophylactic fluconazole may be preferable to prophylactic ketoconazole, because of its lower toxicity. Data suggest that 150 mg of oral fluconazole taken once monthly decreases the recurrence rate by approximately 50 percent, but this regimen may be less effective than daily ketoconazole prophylaxis.[48]

Weekly dosage intervals of fluconazole or intravaginal clotrimazole appear to lower recurrence rates dramatically, but these regimens have not yet been studied in randomized trials. Further research on the safety and efficacy of various prophylactic treatment regimens is needed.

TRICHOMONAS VAGINITIS

Standard treatment for Trichomonas vaginitis consists of oral metronidazole, 2 g in a single dose, for both the patient and any sexual partners, examination for coexistent sexually transmitted diseases, and condom use or sexual abstinence until completion of therapy[18] (Table 5). The side effects and toxicity of metronidazole are discussed in the section on treatment of bacterial vaginosis. Intrauterine devices may be left in place in all patients except those with severe (upper reproductive tract) infections. [TABULAR DATA 5 OMITTED]

Alternate regimens include oral metronidazole, 500 mg twice daily for seven days,[18] or 250 mg three times daily for seven days.[49] When both partners are treated, cure rates approach 100 percent.[49]

Persistent Cases. When initial therapy is unsuccessful, complicating factors must be considered. The most common reasons for treatment failure are noncompliance and reinfection, but the possibilities of metronidazole resistance, inaccurate diagnosis and infection with multiple sexually transmitted diseases must also be entertained.

A careful sexual and medication history will identify treatment failures caused by lack of completion of the prescribed medication, and reexamination will clarify the persistence of the organism. Because infection with T. vaginalis is often associated with bacterial vaginosis and other sexually transmitted infections, careful evaluation for multiple infections is required.[7] If persistence of the trichomonal organism is confirmed, retreatment of the patient and partners is indicated, using standard dosages.

Although most patients respond to standard treatment, metronidazole resistance sometimes occurs. Higher dosages of metronidazole may be effective in these cases: 2 g orally each day for three days[18] or 500 g orally twice daily for 14 days, accompanied by vaginal povidone-iodine,[50] or intravaginal metronidazole gel. The sexual partner(s) should also be retreated.

Patients with multiple trichomonal recurrences have been evaluated for malabsorption of metronidazole, but serum and vaginal levels have been found to be in the usual therapeutic range in these individuals. Metronidazole may be administered intravenously to patients who are unable to tolerate the oral preparation because of vomiting.

Alternative Treatments. When continued metronidazole resistance is suspected, despite appropriate dosing, antibiotic sensitivity testing of T. vaginalis cultures can be performed. It is estimated that a small percentage of trichomonal isolates are metronidazole-resistant, but this resistance is relative, not all or none.[20]

Although systemic treatment of vaginal trichomoniasis is usually necessary because of the capacity of the organism to remain viable in the periurethral and Skene’s glands and the upper reproductive tract, local therapy may be beneficial in resistant cases or in patients for whom metronidazole is contraindicated. Local agents that may be helpful include metronidazole vaginal gel,[51] or povidone-iodine as a douche or suppositories (Table 5). Clotrimazole cream and intravaginal acetic acid solution may also decrease symptoms.

Pregnancy. Recent studies suggest that infection with T. vaginalis is associated with premature delivery, low birth weight and postpartum endometritis.[52] Whether this is a causal relationship is not known, and hence difficult decisions must be made regarding the risk of treating pregnant patients with metronidazole after the first trimester versus delaying treatment until after delivery. Recommendations about the need to treat pregnant women after the first trimester vary from treating all women[10] to treating rarely.[18] Intravaginal metronidazole should not be used during the first trimester of pregnancy. Povidone-iodine is also not recommended during pregnancy because of the small risk of neonatal hypothroidism.

Symptomatic relief may be obtained with clotrimazole vaginal cream. Lactating women may be treated with a single, 2-g oral dose of metronidazole. Breast feeding should be discontinued for 24 hours after treatment.[18]

Additional Considerations. In patients for whom the preceding diagnostic and therapeutic techniques are not effective, or who experience multiple recurrences of vaginal symptoms, further investigation must be undertaken. Unrecognized cervical infections or sources of reinfection, vulvodynia and allergic responses represent additional etiologies of vaginal discomfort that should be excluded.

A patient information handout on vaginal infections is provided on page 1817.

Vaginal Infections

What is a vaginal infection?

The vagina normally contains large numbers of organisms (germs) called Lactobacillus (or acidophilus). Vaginal infections happen when other organisms grow and change the normal balance of organisms in the vagina. Most women have a vaginal infection now and then, and many women have them often. You may have a vaginal infection if your normal vaginal discharge changes color, becomes heavier or smells different, or if you notice itching, burning, swelling or redness around the vagina.

What is a normal vaginal discharge?

A normal discharge usually does not smell bad and is not accompanied by redness, swelling or itching of the vaginal area. Most vaginal discharges are normal. You may notice a vaginal discharge on your panties at some stages of your menstrual cycle. This discharge may be most noticeable at the middle of the cycle, which is close to the time of ovulation. Some women have a discharge on most days, and some women must use sanitary pads because of the amount of discharge.

What are common causes of vaginal infections?

The most common form of vaginal infection is called bacterial vaginosis. Women with this infection have a large number of organisms called Gardnerella vaginalis, as well as many other organisms, in their vagina. If you have this infection, you may notice a different vaginal smell that is strongest after sexual intercourse, and perhaps an increased amount of thin vaginal discharge, which may be white or discolored.

A yeast infection, or Candida vaginitis, is another common type of vaginal infection. If you have this kind of infection, you may notice larger amounts of thick, white discharge, or no discharge at all. Other common symptoms include itching, swelling, irritation or redness around the vaginal area.

Trichomonas vaginitis, which is sometimes called “trick,” is the third most frequent vaginal infection. Like bacterial vaginosis, this infection often causes an increased amount of discharge, which may be discolored. Sometimes the discharge smells different. Itching may be present but is less likely than with a yeast infection.

How can the cause of the vaginal symptoms be determined?

It is very hard to know the cause of vaginal symptoms unless your doctor talks with you, does a pelvic examination and looks at any vaginal discharge through a microscope. If these steps are taken, a fairly accurate diagnosis can be made most of the time, and the right medicine can be started. If the cause of the symptoms is still unclear, a sample of the vaginal discharge can be sent to a laboratory for testing to find out the right medicine to use.

How can vaginal symptoms be treated?

The treatment for vaginal symptoms depends on the cause. Bacterial vaginosis is often treated with a prescription medicine called metronidazole (Flagyl, Protostat). This medicine is taken by mouth. Sometimes it causes an upset stomach or nausea. If you drink alcohol while taking this drug, you may have nausea and vomiting. There are other medicines that may be taken by mouth for this infection, such as clindamycin (Cleocin), and there are also vaginal creams or gels.

A yeast infection is usually treated with creams or suppositories that are placed in the vagina. The length of treatment may vary from one to seven days. Some of these medicines are now available without prescription, such as miconazole (Monistat) and clotrimazole (Gyne-Lotrimin or Mycelex-G), and you may use them when you know you have a yeast infection. If the infection doesn’t get better or comes back soon, you should see your doctor to make sure of the diagnosis and treatment. When the infections are frequent or when they are hard to cure, your doctor may prescribe medicine to be taken by mouth.

Trichomonas vaginitis is also treated with metronidazole, taken by mouth. However, because this infection is often passed back and forth between sexual partners, your sexual partner also ought to take the medicine, to stop your infection from coming back.

What if the symptoms aren’t caused by one of these common infections?

In about one of every three women with vaginal symptoms, the cause of the symptoms may be harder to find. Another type of infection, such as gonorrhea, chlamydia or herpes, may be present. Low hormone levels, related to menopause, or an allergy may also cause vaginal symptoms. Sometimes no cause for the symptoms can be found.

Even with medical treatment, some women keep having vaginal irritation or discharge. We still don’t know all the causes of vaginal symptoms, and scientists are still investigating. If you continue to have problems with vaginal symptoms, ask your doctor about new treatments.

This information provides a general overview on vaginal infections and may not apply in each indiv case. Consult your physician to determine whether this information can be applied to your personal s and to obtain additional information.

REFERENCES

[1.] Berg AO, Heidrich FE, Fihn SD, et al. Establishing the cause of genitourinary symptoms in women in a family practice. Comparison of clinical examination and comprehensive microbiology. JAMA 1984;251:620-5. [2.] Reed BD, Huck W, Zazove P. Differentiation of Gardnerella vaginalis, Candida albicans, and Trichomonas vaginalis infections of the vagina. J Fam Pract 1989;28:673-80. [3.] Bump RC, Zuspan FP, Buesching WJ 3d, Ayers LW, Stephens TJ. The prevalence, six-month persistence, and predictive values of laboratory indicators of bacterial vaginosis (nonspecific vaginitis) in asymptomatic women. Am J Obstet Gynecol 1984;150:917-24. [4.] Spiegel CA. Bacterial vaginosis. Clin Microbiol Rev 1991;4:485-502. [5.] Gravett MG, Nelson HP, DeRouen T, Critchlow C, Eschenbach DA, Holmes KK. Independent associations of bacterial vaginosis and Chlamydia trachomatis infection with adverse pregnancy outcome. JAMA 1986;256: 1899-903. [6.] McGregor JA, French JI, Richter R, et al. Antenatal microbiologic and maternal risk factors associated with prematurity. Am J Obstet Gynecol 1990;163(5 Pt 1):1465-73. [7.] Amsel R, Totten PA, Spiegel CA, Chen KC, Eschenbach D, Holmes KK. Nonspecific vaginitis. Diagnostic criteria and microbial and epidemiologic associations. Am J Med 1983;74:14-22. [8.] Spiegel CA, Amsel R, Holmes KK. Diagnosis of bacterial vaginosis by direct gram stain of vaginal fluid. J Clin Microbiol 1983;18:170-7. [9.] Reed BD. Risk factors for Candida vulvo-vaginitis. Obstet Gynecol Surv 1992;47:551-60. [10.] Thomason JL, Gelbart SM. Trichomonas vaginalis. Obstet Gynecol 1989;74(3 Pt 2):536-41. [11.] Bergman JJ, Berg AO, Schneeweiss R, Heidrich FE. Clinical comparison of microscopic and culture techniques in the diagnosis of Candida vaginitis. J Fam Pract 1984;18:549-52. [12.] Schaaf VM, Perez-Stable EJ, Borchardt K. The limited value of symptoms and signs in the diagnosis of vaginal infections. Arch Intern Med 1990;150:1929-33. [13.] Krieger JN, Tam MR, Stevens CE, et al. Diagnosis of trichomoniasis. Comparison of conventional wet-mount examination with cytologic studies, cultures, and monoclonal antibody staining of direct specimens. JAMA 1988;259:1223-7. [14.] Perl G. Errors in the diagnosis of Trichomonas vaginalis infections as observed among 1199 patients. Obstet Gynecol 1972; 39:7-9. [15.] Reed BD, Pierson CL. Evaluation of a latex agglutination test for the identification of Candida species in vaginal discharge. J Am Board Fam Pract 1992;5:375-80. [16.] Yule A, Gellan MC, Oriel JD, Ackers JP. Detection of Trichomonas vaginalis antigen in women by enzyme immunoassay. J Clin Pathol 1987;40:566-8. [17.] Schmid GP, Matheny LC, Zaidi AA, Kraus SJ. Evaluation of six media for the growth of Trichomonas vaginalis from vaginal secretions. J Clin Microbiol 1989;27:1230-3. 18. 1989 Sexually Transmitted Diseases Treatment Guidelines. MMWR Morb Mortal Wkly Rep 1989;38(Suppl 8):143 [Published erratum appears in MMWR Morb Mortal Wkly Rep 1989;38(38):664]. [19.] Eschenbach DA, Critchlow CW, Watkins H, et al. A dose-duration study of metronidazole for the treatment of nonspecific vaginosis. Scand J Infect Dis Suppl 1983;40:73-80. [20.] Lugo-Miro VI, Green M, Mazur L. Comparison of different metronidazole therapeutic regimens for bacterial vaginosis. JAMA 1992;268:92-5. [21.] Lossick JG. Treatment of sexually transmitted vaginosis/vaginitis. Rev Infect Dis 1990;12 (Suppl 6):S665-81. [22.] Thomason JL, Gelbart SM, Livengood CH III, Hill GB, Faro S. Does clindamycin vaginal cream cure bacterial vaginosis? [Abstract] Programs and abstracts of the twenty-eighth Interscience Conference on Antimicrobial Agents and Chemotherapy. Washington, D.C.: American Society for Microbiology, 1988:262. [23.] Hillier S, Krohn MA, Watts DH, Wolner-Hanssen P, Eschenbach D. Microbiologic efficacy of intravaginal crindamycin cream for the treatment of bacterial vaginosis. Obstet Gynecol 1990;76(3 Pt 1):407-13. [24.] Bistoletti P, Fredricsson B, Hagstrom B, Nord CE. Comparison of oral and vaginal metronidazole therapy for nonspecific bacterial vaginosis. Gynecol Obstet Invest 1986;21:144-9. [25.] Brenner WE, Dingfelder JR. Metronidazole-containing vaginal sponges for the treatment of bacterial vaginosis. Adv Contracept 1986; 2:363-9. [26.] Fleury FJ. Adult vaginitis. Clin Obstet Gynecol 1981;24:407-38. [27.] Greaves WL, Chungafung J, Morris B, Haile A, Townsend JL. Clindamycin versus metronidazole in the treatment of bacterial vaginosis. Obstet Gynecol 1988;72:799-802. [28.] Bayer AS, Chow AW, Concepcion N, Guze LB. Susceptibility of 40 lactobacilli to six antimicrobial agents with broad gram-positive anaerobic spectra. Antimicrob Agents Chemother 1978;14:720-2. [29.] Fredricsson B, Englund K, Weintraub L, Olund A, Nord CE. Bacterial vaginosis is not a simple ecological disorder. Gynecol Obstet Invest 1989;28:156-60. [30.] Ison CA, Taylor RF, Link C, Buckett P, Harris JR, Easmon CS. Local treatment for bacterial vaginosis. Br Med J [Clin Res] 1987;295:886. [31.] Dattani IM, Gerken A, Evans BA. Aetiology and management of non-specific vaginitis. Br J Vener Dis 1982;58:32-5. [32.] Vejtorp M, Bollerup AC, Vejtorp L, et al. Bacterial vaginosis: a double-blind randomized trial of the effect of treatment of the sexual partner. Br J Obstet Gynaecol 1988;95:920-6. [33.] Mengel MB, Berg AO, Weaver CH, et al. The effectiveness of single-dose metronidazole therapy for patients and their partners with bacterial vaginosis. J Fam Pract 1989;28:163-71. [34.] Martius J, Krohn NU, Hillier SL, Stamm WE, Holmes KK, Eschenbach DA. Relationships of vaginal Lactobacillus species, cervical Chlamydia trachomatis, and bacterial vaginosis to preterm birth. Obstet Gynecol 1988;71:89-95. [35.] Van Dyck WA jr. A comparative study of butoconazole, miconazole and placebo J. Reprod Med 1986;31:662-3. [36.] Sobel JD. Individualizing treatment of vaginal candidiasis. J Am Acad Dermatol 1990;23(3 Pt 2):572-6. [37.] Cauwenbergh G, Vanden Bossche H. Terconazole. Pharmacology of a new antimycotic agent. J Reprod Med 1989;34(8 Suppl):588-92. [38.] Tooley PJ. Patient and doctor preferences in the treatment of vaginal candidosis. Practitioner 1985;229:655-60. [39.] Sobel JD. Management of recurrent vulvovaginal candidiasis with intermittent ketoconazole prophylaxis. Obstet Gynecol 1985; 65:435-40. [40.] Lewis JH, Zimmerman HJ, Benson GD, Ishak KG. Hepatic injury associated with ketoconazole therapy. Analysis of 33 cases. Gastroenterology 1984;86:503-13. [41.] Stein GE, Christensen S, Mummaw N. Comparative study of fluconazole and clotrimazole in the treatment of vulvovaginal candidiasis. DICP 1991;25:582-5. [42.] Sanz F, del Palacio Hernanz A. Random comparative trial of three regimens of itroconazole for treatment of vaginal mycoses. Rev Infect Dis 1987;9(Suppl 1):S139-42. A comparison of single-dose oral fluconazole with 3-day intravaginal clotrimazble in the treatment of vaginal candidiasis. Report of an international multicentre trial. Br J Obstet Gynaecol 1989;96:226-32. [44.] Sobel JD. Recurrent vulvovaginal candidiasis. A prospective study of the efficacy of maintenance ketoconazole therapy. N Engl J Med 1986;315:1455-8. [45.] Milne JD, Warnock DW. Effect of simultaneous oral and vaginal treatment on the rate of cure and relapse in vaginal candidosis. Br J Vener Dis 1979;55:362-5. [46.] Hilton E, Isenberg HD, Alperstein P, France K, Borenstein MT. Ingestion of yogurt containing Lactobacillus acidophilus as prophylaxis for candidal vaginitis. Ann Intern Med 1992; 116:353-7. [47.] Sobel JD, Schmitt C, Meriwether C. Clotrimazole treatment of recurrent and chronic candida vulvovaginitis. Obstet Gynecol 1989;73(3 Pt 1):330-4. [48.] Sobel JD. Fluconazole maintenance therapy in recurrent vulvovaginal candidiasis. Int J Gynecol Obstet 1993. In press. [49.] Lossick JG. Treatment of Trichomonas vaginalis infections. Rev Infect Dis 1982;4(suppl):801-18. [50.]. Ahmed-Jushuf IH, Murray AE, McKeown J. Managing trichomonal vaginitis refractory to conventional treatment with metronidazole. Genitourin Med 1988;64:25-9. [51.] Contraceptive Technology Update. Combined therapy helps cure resistant trichomoniasis. STD Quarterly, February, 1992. [52.] Cotch MF, Pastorek JG. Effect of Trichomonas vaginalis carriage on pregnancy outcome [Abstract]. Banff, Canada: International Society for STD Research, 1991:56.

The Authors

BARBARA D. REED, MD., M.S.P.H. is an assistant professor in the Department of Family Practice at the University of Michigan Medical School, Ann Arbor. Dr. Reed graduated from Washington University School of Medicine, Saint Louis, and completed a family practice residency and a faculty training fellowship at the University of Utah School of Medicine, Salt Lake City.

ANN EYLER, M.D. is a clinical instructor and director of predoctoral education in the Department of Family Practice at the University of Michigan Medical School. She completed a family practice residency at University Hospitals, Ann Arbor, Mich.

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