Bacterial Vaginosis in Postmenopausal Women

Abstract

Purpose of Review:

Bacterial vaginosis (BV) is the most common vaginal infection worldwide, but most research has been conducted in premenopausal women. After menopause, endogenous estrogen production decreases, often leading to the genitourinary syndrome of menopause (GSM), characterized by vulvovaginal dryness and irritation. The estrogen-deficient postmenopausal state results in an elevated vaginal pH and depletion of vaginal lactobacilli. Use of traditional BV diagnostics (Amsel criteria, Nugent score) is difficult in post-menopausal women, especially those not on estrogen replacement therapy, as these methods were originally developed in premenopausal women. In this review, we discuss recent clinical data on BV in postmenopausal women, difficulties in diagnosis using traditional methods, the role of BV molecular diagnostics, and our current expert opinion for managing BV in this population.

Recent Findings:

BV prevalence has been found to range between 2%-57% among postmenopausal women per Amsel and Nugent criteria. This is likely an over-estimate of the true prevalence due to limitations in these criteria which were only validated in pre-menopausal women. Despite increasing diagnostic options for BV in recent years, including highly sensitive and specific BV nucleic acid amplification tests (NAATs), the physiologic changes of menopause and limited inclusion of postmenopausal women in clinical studies, diagnosis is difficult in this population. Recent studies utilizing 16s rRNA gene sequencing suggest that the vaginal microbiota of premenopausal and postmenopausal women is quite different, even if BV is not present. Data also suggest that obese postmenopausal women have significantly lower rates of BV compared to non-obese postmenopausal women, although further research is needed in this area. Multiple treatment options exist for vaginal atrophy and BV in this population.

Summary:

Data are limited regarding optimal diagnostic approaches for BV in postmenopausal women; BV NAATs and 16s rRNA gene sequencing may have a role for diagnosing BV in symptomatic women although further studies are needed. Menopausal women with characteristic vaginal symptoms and an elevated vaginal pH should be initially treated for estrogen deficiency prior to considering a diagnosis of BV; subsequent treatment for BV should be driven by symptoms.

Introduction

Bacterial vaginosis (BV) is the most common vaginal infection among reproductive-age women worldwide.(1) It is a vaginal dysbiosis characterized by a reduction in lactic acid and hydrogen peroxide-producing lactobacilli and increases in facultative and strict anaerobic bacteria (i.e., Gardenerella spp, Prevotella spp, Fannyhessea vaginae (previously Atopobium vaginae), etc.) in the vaginal microbiota.(2) Despite extensive research, the etiology of BV remains unknown although a hypothetical model has been proposed.(3, 4) Nevertheless, epidemiological data strongly suggest that BV is sexually transmitted.(5-7) Common BV symptoms include a thin, homogeneous white-grayish vaginal discharge, vaginal odor often described as “fishy”, and less frequently, vaginal irritation.(8, 9) Many patients with BV, though, are asymptomatic, as noted in prior U.S. National Health and Nutrition Examination Survey (NHANES) data among reproductive age (14-49 years old) women.(10) BV has been associated with multiple adverse obstetric and gynecologic health outcomes including adverse birth outcomes (preterm birth, chorioamnionitis, low birth weight, postpartum endometritis, etc.)(11), pelvic inflammatory disease (PID)(12), infertility(13), post-hysterectomy infections, including vaginal cuff cellulitis and deep infections, and an increased risk of human immunodeficiency virus (HIV) and other sexually transmitted infections (STIs).(14-19)

Traditionally, BV has been diagnosed clinically using the Amsel criteria or microbiologically by determining the Nugent Score from a vaginal Gram stain. The Amsel criteria include a thin, homogeneous grayish-white vaginal discharge; vaginal pH >4.5; positive whiff test (a fishy, amine odor after KOH is mixed with vaginal secretions); and presence of ≥20% clue cells/high power field on a wet mount of vaginal secretions.(20) The presence of three or four Amsel criteria are used to make a clinical diagnosis of BV.(20) The Nugent score is calculated from a vaginal Gram stain by assessing for the presence of large Gram-positive rods (Lactobacillus morphotypes; decrease in Lactobacillus spp. scored as 0 to 4), small Gram-variable rods (G. vaginalis morphotypes; scored as 0 to 4), and curved Gram-variable rods (Mobiluncus spp. morphotypes; scored as 0 to 2) and can range from 0 to 10.(21) A score of 0-3 is consistent with optimal vaginal microbiota, 4-6 with intermediate vaginal microbiota, and 7-10 with BV. More recently, highly sensitive and specific BV molecular diagnostics have become available with several Food and Drug Administration (FDA)-approved nucleic acid amplification tests (NAATs) available for use in symptomatic women.(22, 23)

The majority of BV research focuses on women of reproductive age; the estimated global prevalence of BV among premenopausal women is 23%-29% across regions.(1) The estimated global prevalence of BV in postmenopausal women is not known as a much smaller body of data exists in this age group. A recent systematic review of the literature and meta-analysis including 13 English-language peer-reviewed studies (with significant heterogeneity between studies and considerable variability in terms of quality) found that BV prevalence ranged between 2%-57% among postmenopausal women, with an overall BV prevalence of 16.9% (95% CI 8.45-27.4%; I²=97.9%;p<0.01).(24) BV prevalence was higher in studies using the Nugent score than in studies using the Amsel criteria for BV diagnosis; this may be an over-estimate of BV prevalence in postmenopausal women as these diagnostic methods were only validated in pre-menopausal women.(20, 21) In a subgroup analysis of this study, BV was noted to be most prevalent among HIV-positive postmenopausal women (25.1%; 95% CI 7.49-48.27; I²=94.6;p<0.01), although the reason(s) behind this finding are unknown. Data on the incidence of BV among post-menopausal women are even more limited and the time to the first episode of BV among post-menopausal women is unknown. The physiological changes associated with menopause can perturb the vaginal microbiota in ways that can result in unfavorable shifts in Lactobacillus-dominance. Postmenopausal women, particularly those who are receiving estrogen replacement therapy and are sexually active, continue to be at risk for BV.

In this article, we review the normal physiologic changes that occur in the vaginal microbiota during menopause and how these changes can influence the risk of BV in postmenopausal women, especially among those receiving estrogen replacement therapy. In addition, we review the most recent clinical data on BV in postmenopausal women, including difficulties in diagnosis using traditional methods (Amsel and Nugent), the role of BV molecular diagnostics, the role of body mass index (BMI), and the effect of topical vaginal estrogen use. We conclude by providing our current expert opinion on the management of symptomatic BV in postmenopausal women as well as identifying gaps in the literature which should be the focus of future research.

Normal Physiologic Changes in the Vaginal Microbiota During Menopause

Typically occurring in women between the ages of 49-52 years,(25) menopause is generally defined as the cessation of spontaneous menses for 12 months. It is the result of declining endogenous ovarian estrogen and progesterone production.(26) Estrogen levels can fluctuate as perimenopause and menopause progress, leading to dynamic hormonal changes that differ from woman to woman. Clinically, this leads to hypoestrogenic changes to the vulva, labia, vestibule, vagina, urethra, and/or bladder in up to 60% of postmenopausal women.(27, 28) These changes can result in symptoms such as vaginal dryness, burning, and irritation as well as dysuria and dyspareunia that can negatively impact a woman’s quality of life.(29) This syndrome was previously called vulvovaginal atrophy (VVA), but in 2014 the term was replaced with the more inclusive term genitourinary syndrome of menopause (GSM).(30)

Differentiating between GSM and BV in some women can be difficult, as genital irritation and elevated vaginal pH can occur in both conditions.(8, 31) Mixed vaginitis syndromes where ≥2 vaginal infections are present can occur in some women (32) however it is very unusual for vaginal atrophy and BV to be present in post-menopausal women concurrently. The hypoestrogenic state of menopause can directly impact the vaginal microbiota; low levels of estrogen in the setting of menopause have been associated with decreased glycogen deposition, as well as reduced epithelial proliferation and turnover in the vaginal mucosa, leading to a reduction in free glycogen.(33) These changes can result in lower levels of vaginal Lactobacillus spp. and higher levels of facultative and strict anaerobic bacteria (i.e., Anaerococus, Peptoniphilus, and Prevotella spp, etc.), many of which can be found in BV.(34, 35) Notably, the resultant Lactobacillus-deficient state can manifest with elevated vaginal pH levels >4.5 and a decreased ability of the vaginal microenvironment to protect against colonization by potential pathogenic micro-organisms (i.e., F. vaginae).(36)

The Effect of Menopause on the Composition of the Vaginal Microbiota

Typically, the optimal vaginal microbiota of premenopausal women is characterized by abundant Lactobacillus spp. and very low levels of BV-associated bacteria (i.e., G. vaginalis, P. bivia, F. vaginae, etc.), though this may fluctuate based on age, race, sexual activity, menses, antibiotic use, concomitant STI infection, and other factors.(37, 38) The effect of menopause on the composition of the vaginal microbiota has been studied over the past several decades, initially using cultivation-dependent methods (i.e., bacterial culture) and, more recently, using cultivation-independent methods (i.e., 16S ribosomal RNA (rRNA) gene sequencing). In a 1997 study of 73 postmenopausal women not on estrogen replacement therapy, the vaginal microbiota was investigated using bacterial culture; none of these women had BV by Nugent score.(39) Lactobacilli were detected in 49% of the women (although at a lower concentration than in premenopausal women); hydrogen peroxide-producing lactobacilli were only detected in a minority (38%) of women. Anaerobic gram-negative rods (89%; including P. bivia at 33%) and gram-positive cocci (including any Peptostreptococcus spp. at 88%) were the most frequent bacterial spp. identified, although many were at lower concentrations than from other published studies of reproductive-age women (i.e., G. vaginalis at 27%). In another study of 100 postmenopausal women using Nugent score, 18% had BV while 21% had “apparent absence of, or very scanty, vaginal bacteria.”(40) In a 2004 case report of a postmenopausal woman with asymptomatic BV (Nugent score 9), 16S rRNA gene sequencing was used to examine the composition of her vaginal microbiota; sequences from F. vaginae were the most commonly detected.(41) In a survey of 35 additional postmenopausal women in this study, this BVAB was detected in 5/10 (50%) of women with BV but not in any participants with a normal Nugent score.(41)

More recently, Brotman et al compared the vaginal microbial community composition of pre- (n=30), peri- (n=29), and postmenopausal (n=28) women using 16S rRNA gene sequencing, categorizing the microbial communities via community state types (CSTs).(42) In this study, the bacterial communities clustered into 6 CSTs, of which 4 were dominated by L. crispatus, L. gasseri, L. iners, or L. jensenii and 2 were dominated by Streptococcus spp. and Prevotella spp. (CST-IV-A) and Fannyhessea spp. (CST-IV-B), respectively. Premenopausal women were more likely to have CSTs dominated by L. crispatus and L. iners. Peri-menopausal women were more likely to be classified as the L. gasseri CST or CST IV-A. Postmenopausal women were more likely to be classified as CST IV-A. Nineteen women had signs of mild or moderate VVA. Compared to women with no VVA, the vaginal microbiota of women with VVA had 25-fold greater odds of being classified as CST IV-A vs. L. crispatus CST (aOR: 25.89; 95% CI: 2.98-406.79). Overall, this study found significant associations between vaginal bacterial composition, menopause stage, and signs of vaginal atrophy however, additional research is necessary to extend these findings in larger populations of women.

A recent study by Mitchell et al compared the relative abundance of specific bacterial taxa using 16S rRNA gene sequencing to Nugent score in both pre- and postmenopausal women. They found 33 bacterial taxa in 220 premenopausal women that were significantly correlated with a high Nugent score, including BV-associated bacteria such as Gardnerella, Fannyhessea, Sneathia, Megasphaera, and Prevotella. Conversely, the postmenopausal group (n=114) had 11 taxa that were significantly associated with a high Nugent score of 7-10, including Prevotella spp, but not other common BV-associated bacteria (i.e. Gardnerella, Megasphaera, Fannyhessea, and Sneathia).(43) The authors of this study concluded that high Nugent scores should not be used to infer a diagnosis of BV in postmenopausal women. Vaginal Gram stain scoring is based on morphologic assessment and bacterial assignments may not be as accurate in postmenopausal women.(43)

Difficulties in Diagnosing BV Using the Amsel Criteria and Nugent Score in Postmenopausal Women

Determining a diagnosis of BV using the Amsel criteria (clinical criteria)(44) or the Nugent score (microbiologic criteria)(21) in postmenopausal women can be difficult, given discrepancies in testing results, as evidenced in the Mitchell et al study.(43) In addition, Cauci et al(45) found that the Nugent score system was not accurate for evaluating normal and intermediate vaginal microbiota in women >40 years of age due to a non-pathological absence of lactobacilli and no evidence of Gardnerella or Mobiluncus morphotypes. Both of these diagnostic methods were originally validated in premenopausal women (i.e., the Amsel criteria and Nugent score were developed using data from a college-age and pregnant women, respectively) and did not account for the effect that hypoestrogenism has on the vaginal pH and the composition of the vaginal microbiota in the setting of menopause.(35) Thus, we recommend that clinicians be cautious when using these methods to make a diagnosis of BV in post-menopausal women. Along these lines, we have noted a change in the vaginal odor of some of our menopausal patients over time, which is not necessarily due to BV (i.e. the odor is not fishy). This anecdotal finding has not been systematically evaluated in this population however we believe that the whiff test may not be of great value in diagnosing BV in postmenopausal women.

Use of Molecular Methods to Diagnose BV in Post-Menopausal Women

Although not excluded, postmenopausal women were underrepresented in recent studies investigating the clinical accuracy of currently FDA-approved BV NAAT tests,(22, 23). It is presently unknown if there is merit in using these tests in symptomatic post-menopausal women to make a diagnosis of BV, especially in those who are not on estrogen replacement therapy. These tests are based on detection of specific bacterial nucleic acids with high sensitivity and/or specificity for BV (i.e., G. vaginalis, F. vaginae, BVAB2, and/or Megasphaera spp.) as well as certain lactobacilli (i.e., L. crispatus, L. jensenii, and/or L. gasseri).(46) Regarding FDA-approved assays, the BD MAX Vaginal Panel provides an algorithmic analysis of molecular DNA detection for Lactobacillus spp (L. crispatus and L. jensenii) in addition to G. vaginalis, F. vaginae, BVAB2, and Megasphaera type 1 with results reported as positive or negative for BV.(22) The Hologic Aptima BV detects G. vaginalis and F. vaginae as well as several Lactobacillus spp including L. crispatus, L. jensenii, and/or L. gasseri with results also reported as positive or negative for BV.(23) Diagnosing BV in terms of the composition of the vaginal microbiota by methods such as 16s rRNA gene sequencing or shotgun metagenomic sequencing (i.e., molecular BV), could provide more clarity in symptomatic postmenopausal women on estrogen replacement therapy, however these methods can be costly, time-consuming, and are not currently approved for use in clinical practice. Thus, because the optimal diagnostic approach to BV in postmenopausal women remains unclear, knowledge of the true epidemiologic impact of this infection in postmenopausal women is unknown and treatment must be driven by symptoms.

The Role of BMI and BV in Post-Menopausal Women

In women in general, regardless of menopausal status, there has been interest in exploring the role of being overweight or obese as a risk factor for BV given the established relationship between increased BMI and gut dysbiosis.(47-49) In studies of premenopausal women, higher frequency of BV Nugent scores(50) as well as larger proportions of BV-associated taxa such as L. iners and Prevotella spp.(51, 52) have been noted among obese women compared to non-obese women. Fewer data are available investigating this relationship among postmenopausal women. Interestingly, a secondary analysis of data from the U.S. Women’s Interagency HIV Study (WIHS) found that obese postmenopausal women (body mass index [BMI]>30 kg/m²) had a significantly lower rate of BV (multivariable aOR 0.87 (0.79–0.97), p=0.009) compared to non-obese postmenopausal women (BMI 18.5–24.9 kg/m2), although no difference was noted in premenopausal women. (53) Postmenopausal obese women without HIV had a significantly lower rate of BV, but this was not seen in postmenopausal obese women. The immune system is significantly impacted during infection with HIV which could influence the relationship between BV and obesity and may help to explain this difference.(53) In addition, the hypoestrogenic state of menopause itself is associated with a high risk of obesity, so it may also be difficult to disentangle the relationship between BV and obesity in postmenopausal women.(54) Given these confounding data regarding the relationship between BV, menopause, HIV status, and obesity, further research is needed in this area to clarify the role that obesity plays in age-related vaginal microbiome changes in postmenopausal women with and without HIV.

The Role of Estrogen Replacement Therapy and BV in Postmenopausal Women

There are data to suggest that levels of vaginal Lactobacillus spp. are optimized in postmenopausal women on estrogen replacement therapy.(55) It is thought that estrogen stimulates the proliferation of squamous epithelial cells in the vaginal mucosa, which increases glycogen production. Glucose, maltose, and maltodextrins produced through hydrolysis of glycogen support the proliferation of vaginal lactobacilli.(55-58) Thus, with the proliferation of squamous epithelial cells and increases in vaginal lactobacilli, exposure of vaginal tissue to estrogen creates an environment to modulate and restore vaginal homeostasis.

Postmenopausal women receiving treatment with either systemic or topical estrogen have shown an increase in L. crispatus, similar to premenopausal women not receiving estrogen replacement therapy.(59, 60) Based on data from data from the 2002 Women’s Health Initiative demonstrating the risks associated with systemic estrogen (i.e., increased breast cancer risk, thromboembolic events, etc.) (61), it is typically reserved for the treatment of postmenopausal women with systemic vasomotor symptoms while vaginal estrogen replacement therapy is recommended for women with isolated genitourinary symptoms. Studies comparing the vaginal microbiota of postmenopausal women receiving estrogen replacement therapy versus those not on this therapy also support this finding as well as women not receiving estrogen replacement therapy having a higher propensity for vaginal bacterial colonization with diverse anaerobic bacterial species.(62, 63) This intervention appears to also ameliorate the symptoms of GSM. One 2006 study of women treated with systemic conjugated estrogen for three months found significant improvement in vaginal dryness and irritation in the setting of lower vaginal pH and increased amounts of vaginal lactobacilli.(64) More recently, in 2020, Geng et al compared postmenopausal women receiving oral tibolone, a synthetic steroid and estrogen agonist which is not currently available in the U.S., to those who were not by obtaining vaginal specimens and performing 16S rRNA gene sequencing; genital symptom data was also collected from participants. They found that in women receiving tibolone, vaginal microbial diversity was decreased, and Lactobacillus spp. abundance was increased, whereas those not on tibolone had significant amounts of BV-associated bacteria such as Gardnerella spp., Prevotella spp., and Fannyhessea spp. Treated patients also had less vaginal irritation and dryness compared to untreated patients.(55) In summary, these data suggest that vaginal Lactobacillus dominance can be restored and symptoms of GSM can be relieved by estrogen replacement therapy.

Current Recommendations for the Management of BV in Postmenopausal Women

Current first-line and alternative treatment recommendations for BV are summarized in Table 1A. Mainstays of therapy include 5-nitroimidazoles such as metronidazole, tinidazole, and secnidazole as well as the lincosamide, clindamycin. These BV therapies are aimed at restoring a lactobacillus-dominant vaginal microbiota. However, in postmenopausal women, the vaginal mucosa may not support this for an extended period in the absence of concurrent estrogen replacement therapy.(65) Thus, we recommend initially evaluating and treating symptomatic post-menopausal women for estrogen deficiency prior to considering a diagnosis of and initiating treatment for BV. A trial of vaginal estrogen replacement therapy should be given for at least 6-8 weeks in this situation to see if symptoms improve. Laboratory confirmation of menopause by serum estradiol levels is not necessary to initiate treatment in the setting of physical exam findings consistent with vaginal atrophy, even in the absence of GSM symptoms.(66) Topical estrogen therapy is available in numerous formulations, none proven superior to another for treating the patient with GSM or specifically the vaginal changes related to hypoestrogenism. Often a patient’s choice is based on ease of use and insurance coverage. Options include 17β estradiol 0.01% vaginal cream, conjugated estrogen vaginal cream, 17β estradiol vaginal inserts, estradiol vaginal tablets, and a 17β estradiol vaginal ring (Table 1B). Given that there are multiple contraindications to systemic estrogen therapy and that it may necessitate the addition of a systemic progestogen, vaginal estrogen has a more favorable safety profile and would be a superior choice. Oral estrogen therapy should be reserved for patients who also have systemic symptoms of menopause, such as moderate to severe vasomotor symptoms.

Table 1A.

Recommended and Alternative Treatment Regimens for Bacterial Vaginosis

Recommended

Metronidazole 500mg orally twice daily for 7 days

Metronidazole gel 0.75%, one full applicator (5g) intravaginally daily for 5 days

Clindamycin cream 2%, one full applicator (5g) intravaginally nightly for 7 days

Alternative

Clindamycin 300mg orally twice daily for 7 days

Clindamycin ovules 100mg intravaginally nightly at bedtime for 3 days

Secnidazole 2g orally once daily for 2 days

Tinidazole 2g orally once daily for 2 days

Tinidazole 1g orally once daily for 5 days

Additional options

Metronidazole gel 1.3%, one full applicator intravaginally once

Clindamycin phosphate 2% cream, one full applicatory intravaginally once

Sources: 2021 Centers for Disease Control and Prevention Sexually Transmitted Infection Treatment Guidelines; 2020 American College of Obstetrics and Gynecology Practice Bulletin on Vaginitis in Nonpregnant Patients

Table 1B.

Estrogen Therapies for Vaginal Atrophy^**

Type of Estrogen	Starting Dose	Maintenance Dose
Vaginal Estrogen Creams
17β estradiol 0.01%	0.5-1 g/d for 2 weeks	0.5-1 g 1-3 times/week
Conjugated estrogens (0.625 mg/g)	0.5-1 g/d for 2 weeks	0.5-1 g 1-3 times/week
Vaginal Estrogen Inserts/Tablets
17β estradiol inserts	4 or 10 mcg/d for 2 weeks	1 insert twice a week
Estradiol tablets	10 mcg/d for 2 weeks	1 tablet twice a week
Vaginal Estrogen Ring
17β estradiol ring	Releases ~ 7.5 mcg/day	Replace ring every 90 days

^**All formulations have equivalent efficacy

Vaginal or oral probiotics are currently not recommended for the treatment or prevention of vaginal dysbiosis and/or BV in any age group(67), although there have been several previous studies of their use in post-menopausal women.(36)

Given the scarcity of data on the diagnosis and management of BV in postmenopausal women, clinicians should approach this diagnosis with caution, especially in women not yet on estrogen replacement therapy. Vaginitis symptoms in this population are much more likely to be related to estrogen deficiency than to BV. Therefore, as mentioned above, consideration should be given to a trial of vaginal estrogen therapy before pursuing BV treatment. If vaginal symptoms persist despite a 6-8 week trial of vaginal estrogen therapy, antibiotic treatment for BV may be given concurrently, if BV is suspected.

Gaps in the Literature and Future Directions

Clearly, there are gaps in the literature for the diagnosis and management of BV in postmenopausal women. First, the pathogenesis and natural history of BV in postmenopausal women needs further investigation as it may differ from that of premenopausal women.(35, 43) Second, additional research on the optimal BV diagnostic test(s) in postmenopausal women should be conducted as the current diagnosis remains difficult. As mentioned, many of the currently available BV diagnostic tests (i.e., Amsel criteria, Nugent score, BV NAATs) were primarily developed in premenopausal women. Because of the shift in the vaginal microbiota in the setting of a hypoestrogenic state in postmenopausal women, diagnosis of BV in this population can be challenging. Studies specifically evaluating the accuracy of the currently FDA-approved BV NAAT tests as well as 16S rRNA gene sequencing methods in symptomatic postmenopausal women, especially women on estrogen replacement therapy, are essential. Third, studies evaluating the optimal treatment of BV in postmenopausal women, both those with and without symptomatic GSM are needed. Data are also lacking on BV recurrence rates in postmenopausal women with GSM receiving vaginal estrogen replacement therapy. Finally, the role of vaginal estrogen therapy and vaginal and oral probiotics should also be further evaluated in large sample sizes for their utility in preventing and treating BV in postmenopausal women.

Conclusion

The risk of BV continues throughout a woman’s lifespan into the postmenopausal years, particularly among women who are on estrogen replacement therapy and continue to be sexually active. While postmenopausal women are not at risk for the obstetrical complications of BV, they are still at increased risk of PID, post-hysterectomy infections, and HIV/STIs. BV is well studied in premenopausal women; however, the optimal diagnostic method(s) and management of BV in postmenopausal women is not as well established. Currently used BV diagnostic tests have mainly been studied in premenopausal women and have not been well studied in postmenopausal women who have atrophic changes in the vagina. Currently recommended treatments for women with BV include antibiotics with the goal of restoring the vaginal microbiota to an environment that is Lactobacillus-dominant. Overall, these are efficacious in premenopausal women, although recurrence rates after therapy can be high.(68) However, the hypoestrogenic postmenopausal vagina may not be able to maintain this Lactobacillus-dominant environment for a long period of time. Use of vaginal estrogen has been shown to change the vaginal mucosa in a manner that promotes the vaginal microbiota to becoming more Lactobacillus-dominant and likely reduces the incidence of BV in the postmenopausal patient. More rigorous clinical studies focusing on BV in postmenopausal women are needed to elucidate optimal diagnostic and management strategies.