How to Get Rid of Bv Naturally When Pregnant

Bacterial vaginosis (BV) is a complex, extremely common vaginal condition and the primary cause of lower-genital complaints, primarily malodorous vaginal discharge and odor [1]. Not a reportable condition, the prevalence of BV among nonpregnant women ranges from 15–30%, with up to 50% of pregnant women found to be BV-positive [2–5]. BV has been related to many adverse gynecological conditions and complications of pregnancy, including: pelvic inflammatory disease, posthysterectomy vaginal cuff cellulites, postabortal endometritis, postpartum endometritis, amniotic-fluid infection, preterm delivery, preterm labor, preterm premature rupture of the membranes (PPROM) and spontaneous abortion [6–11].

The anaerobic organisms characteristic of BV have been shown to ascend from the lower genital tract to the endometrium and invade the placenta, but the complete impact of this migration in terms of initial and sustained placental growth, inflammation, infection and early fetal development are unclear [12]. Furthermore, the impact of BV may be complicated by multiple and possibly synergistic pathways. For example, ascension of BV-associated organisms has been related to an increased potential for other vaginal pathogens to gain access to the upper genital tract, an increased level of enzymes that restrict leukocyte ability to reduce infection, and an increased level of vaginal endotoxins that stimulate cytokine and prostaglandin production and inflammation of the placenta [13–18]. The purpose of this article is to review the diagnosis and epidemiology of BV, current BV management and treatment during pregnancy, and the role of BV in adverse pregnancy outcomes.

Pathogenesis of bacterial vaginosis

BV is a polymicrobial superficial lower genital tract condition involving a reduction in the normal amount of hydrogen peroxide (H₂O₂)-producing Lactobacillus spp. and an overgrowth of anaerobic and Gram-negative or -variable bacteria [19–20]. In a healthy lower genital tract, Lactobacilli spp. constitute 95% of the bacteria present and, in the vast majority of cases of BV, a significantly reduced amount of H₂O₂-producing Lactobaccilus spp. are found [19]. As characteristic in cases of BV, the reduced number or absence of H₂O₂-producing Lactobacillus spp. promotes the overgrowth of anaerobic bacteria, including Gardnerella vaginalis, Mycoplasma hominis, Bacteroides spp., Mobiluncus spp. and Ureaplasma urealyticum [20–21]. Although most of these organisms are present in small numbers within a healthy lower genital tract, Mobiluncus is rarely found and can be a sensitive diagnostic marker for BV [22]. In fact, one study comparing BV-positive and -negative women reported that Mobiluncus spp. occurred only in the lower genital tracts of women with BV and that Mobiluncus spp. was present in 97% of the women with BV [23].

The initial cause of this alteration in normal vaginal flora is not well understood; however, disturbances in the normal vaginal ecosystem through changes in vaginal PH, purportedly through hormonal changes occurring during pregnancy, vaginal douching, stress or antibiotic use, may play a role [24]. More recently, investigators have begun to examine subsets of BV-positive women categorized by the type and amount of BV-associated organisms present. For example, Pereira and colleagues compared the clinical and sociodemographic profiles of BV-positive women with and without Mobiluncus and found BV-positive/Mobiluncus-positive women were more likely to be non-Hispanic black, older and to have had more lifetime sexual partners [25]. Whether this subset of BV-positive women have a greater risk of gynecological and reproductive outcomes is not known. An interesting recent article reported higher median levels of glycosulfatase and glycoprotein sialidase activity, enzymes involved in mucin degradation, among BV-positive compared with BV-negative women, suggesting that the organisms characteristic of BV degrade the vaginal mucins in order to colonize the lower genital tract and replace the normal H₂O₂-producing Lactobacilli spp. [26].

Epidemiology & risk factors for bacterial vaginosis

The currently known, consistently documented risk factors for BV have been limited to black race, higher-risk sexual activity (i.e., early age of sexual intercourse, new or multiple sexual partners) and frequent vaginal douching [27–31]. African–American women have an almost threefold increased risk of BV, and Ness and colleagues continued to report an increased risk of BV among African–American women after adjustment for a variety of concurrent risk factors for BV including lower socioeconomic status, higher sexual activity and frequent vaginal douching [32]. Among both pregnant and nonpregnant women, lower socioeconomic status and higher self-reported levels of psychosocial stress also increase the risk of BV [33]. Culhane and colleagues assessed the role of chronic maternal stress and found that, independent of sociodemographic and behavioral factors, chronic maternal stress remained a significant predictor of BV among pregnant women [34]. In addition, another study suggested that a reduction in stress among nonpregnant women may be involved in the spontaneous resolution of BV [35].

Epidemiological studies have found that higher-risk sexual activity, as measured by early sexual activity, a high number of lifetime sexual partners, a new sexual partner and/or a history of a sexually transmitted disease (STD), also increases the risk for BV [36–38]. Although STDs and BV commonly coexist, particularly trichomoniasis and BV, and sexually activity is related to the risk of BV, BV is not considered a STD for a variety of reasons [39–44]. First, BV has been diagnosed among women without sexual experience. For example, BV rates among school-age girls have been found to be similar between virgins and nonvirgins (12 and 15%, respectively), and case studies have reported recurrent BV among virgin adolescents [40,45]. In addition, the treatment of male sexual partners who culture positive for the organisms associated with BV is not an effective method to reduce the future occurrence of BV among their female partners [46]. Second, a more recent study also located possible endogenous intestinal tract reservoirs for BV pathogens and identified the mode of spread of BV-associated organisms, adding further evidence that organisms associated with BV do not necessarily spread sexually, but colonize within the lower genital tract from endogenous intestinal tract sites [23].

Interestingly, women having sex with women are at a higher risk of B V. One study reported a 20-fold increased risk of BV among monogamous lesbian women whose partners were BV positive (odds ratio [OR]: 19.7; 95% confidence interval [CI]: 2.1–588.0), suggesting the transmission of BV through vaginal secretions [41]. In fact, lesbians have consistently reported a high prevalence of BV, ranging from 30–50%, illustrating the potential spread of BV through the exchange of cervicovaginal fluid and direct mucosal contact [47–49].

Some behaviors, such as frequent vaginal douching and cigarette smoking, have been examined as potential risk factors for BV. Frequent vaginal douching may change the vaginal flora, reduce the amount of H₂O₂-producing Lactobacillus spp., and create an environment promoting excessive anerobic growth [50,51]. However, the act of douching may also be in response to symptomatic BV (malodor and discharge). A study among adolescent women found that douching after menses was the strongest predictor of BV (OR: 5.11; 95% CI: 1.99–13.15) [50–53]. No studies have been published to date examining the role of douching and BV development among pregnant women, although a more recent article reported that subclinical iron deficiency in early pregnancy (9.2 ± 2.6 weeks) is a strong predictor of BV development [54].

Diagnostic considerations

There are two commonly used diagnostic tests for BV (Box 1 & Table 1). The Amsel criteria, the test most commonly used in the clinical setting, involves an assessment of four clinical conditions, with the existence of three or more conditions corresponding to a diagnosis of BV. These conditions include: an elevated vaginal pH (>4.5), an amine or fishy odor when vaginal fluid is prepared with 10% potassium hydroxide solution (called the 'whiff test'), the presence of clue cells on saline wet mount and a homogeneous, white, adherent vaginal discharge [55]. The updated Amsel criteria specify that at least 20% of epithelial cells should be clue cells [6,56]. In addition, a recent report suggested that any two of the four clinical criteria could be used without a change in sensitivity or specificity; with vaginal pH the most sensitive criterion (89%) and amine odor the most specific (93%) [57].

Table 1. Nugent scoring system for Gram-stained vaginal smears.

The second diagnostic test for BV involves a Gram stain of vaginal fluid and the use of Nugent criteria to identify a case of BV. This method of diagnosis is most commonly used in research settings. A vaginal swab is obtained, spread on a glass slide, air dried and, at a later time, Gram stained. The amount of three morphotypes characteristic of BV are quantified and scored: Lactobacillus spp., Mobiluncus spp. and G. vaginalis. For Lactobacillus spp., scores range from 0–4, with 0 indicating that 30 or more organisms were found and 4 indicating that no organisms were found in the sample. In contrast, for G. vaginalis, a score of 0 indicates that no organisms were found and the highest score, 4, indicates that 30 or more organisms were found. For Mobiluncus spp., the scores range from 0–2, with a score of 2 indicating that 5 or more organisms were identified in the sample. The Nugent criteria have been shown to have a high sensitivity and specificity compared with Amsel's criteria (89 and 83%, respectively) [58,59]. A summary BV score ranging from 0–10 is computed and this score can be dichotomized, with values of 7 and over indicating a case of BV. In addition, an intermediate stage of BV has been developed, as indicated by a score of 4–6 [60].

More recent diagnostic tools, including biochemical profiles and new molecular microbiological methods, are transforming the diagnosis and understanding of BV [61]. One study assessed the validity of microbial DNA hybridization for G. vaginalis, Prevotella bivia, Bacteroides ureolyticus, and Mobiluncus curtisii compared with Gram stain using Nugent criteria, and found that DNA results were significantly associated with Gram-stained results. In addition, as the Nugent score progressed from normal to abnormal flora, the proportion of samples with more than one pathogen identified through DNA hybridization also increased significantly [62].

Two office-based, point-of-care diagnostic options are also currently available for BV diagnosis. The first has two cards, the FemExam pH and Amines TestCard™, and the FemExam G. vaginalis praline aminopepetidase activity TestCard™. This method has been found to have a high sensitivity (91%) and specificity (61.5%) compared with the Nugent criteria among symptomatic BV-positive women [63]. The second option, the BV Blue system^©, detects sialidase activity in vaginal fluid samples with high sensitivity (92.7%) and specificity (97.8%) compared with the Gram stain or Nugent diagnosis of BV [64].

Bacterial vaginosis & the risk of adverse pregnancy outcomes

The vast majority of research designed to examine the role of BV and adverse pregnancy outcomes has focused on the risk of preterm delivery. These studies have demonstrated a twofold increased risk of spontaneous preterm delivery before 37 weeks among women diagnosed with BV [53,65–68]. In other subgroup analyses, BV in early pregnancy was the strongest predictor of preterm delivery, with an over sevenfold risk among women diagnosed with BV prior to 16 weeks and a fourfold increased risk among women diagnosed with BV before 20 weeks gestation [69]. Interestingly, Carey and Klebanoff recently examined the change in vaginal flora and risk of preterm birth and reported that a change to heavy concentrations of Escherichia coli or Klebsiella pneumoniae, adjusting for overall BV status and other covariates, was related to an increased risk of preterm birth [70]. Macones and colleagues attempted to identify individual factors further contributing to the risk of preterm delivery and found a role of tumor necrosis factor (TNF)-α genotype and BV. In this case–control study, pregnant women with the TNF-2 allele, which is associated with higher levels of TNF-α, were at an increased risk of preterm birth (OR: 2.7; 95% CI: 1.7–4.5), and women who had a history of symptomatic BV during the pregnancy and were carriers of the TNF-2 allele were at an even higher risk of preterm delivery (OR: 6.1; 95% CI: 1.9–21) [71]. In fact, among women with BV, cervicovaginal samples demonstrated increased TNF-α secretion and toll-like receptor (TLR)-4 mRNA expression, lending credibility to the role of BV in promoting a localized inflammatory response [72]. Therefore, an examination of other factors, including genetic components, environmental exposures, inflammatory response and/or behavioral factors, in conjunction with BV positivity, may be helpful in explaining why some, but not all, BV-positive women experience adverse pregnancy outcomes.

Box 1. Diagnostic tests for bacterial vaginosis.

Amsel criteria:

• Three or more of these clinical conditions correspond to a diagnosis of bacterial vaginosis:

  • – A homogenous, white, noninflammatory milky discharge that adheres to the vaginal walls

  • – The presence of clue cells upon microscopic examination

  • – Vaginal pH greater than 4.5

  • – Positive 'whiff' test upon the addition of 10% potassium hydroxide to a specimen (i.e., olfactory detection of the 'sharp' smell of amines)

Nugent criteria:

• A total score of 7 or more indicates a case of BV; a score of 4–6 is considered intermediate, and a score of 0 −3 is normal (Table 1).

A smaller number of studies have examined the relationship between BV and the outcomes of premature labor, low birth weight and PPROM. One study, examining several pregnancy outcomes, related BV diagnosed during the first trimester of pregnancy to a 2.6-fold increased risk for preterm labor (95% CI: 1.3–4.9), a 6.9-fold increased risk for preterm delivery (95% CI: 2.5–18.8) and a 7.3-fold increased risk for PPROM (95% CI: 1.8–29.4) [53]. A growing body of literature has begun to suggest an increased risk of spontaneous abortion among pregnant women with BV [73–78]. Studies have reported a three to fivefold increased risk of spontaneous abortion among pregnant women with BV in the first trimester, although these studies are hampered by small sample size [73,76]. Donders and colleagues reported that, after adjusting for covariates such as smoking, age and prior miscarriage, women with BV diagnosed in the first trimester, women with M. hominis and pregnant women with U. urealyticum remained at a high risk of early pregnancy loss [78].

Bacterial vaginosis treatment among pregnant women

Oral treatments

The most common oral treatment for BV among both pregnant and nonpregnant women is metronidazole [79]. Previously, there was concern regarding the use of metronidazole during the first trimester of pregnancy, before the completion of organogenesis; however, a small study examining children exposed in utero to metronidazole suggested no evidence of long-term teratogenic effects [79–81]. The individual cure rate given a 7-day 500 mg twice-daily course of oral metronidazole is 84–96%. The 375 mg dose, compared with the 500 mg dose, of metronidazole has been shown to be equally effective with fewer gastrointestinal side effects [82]. The effectiveness of a 2 g single dose of metronidazole has also been studied; however, this therapy is less than 75% effective when compared with the week-long treatment. Oral therapy can be associated with a variety of side effects including gastrointestinal upset, intolerance to alcohol, metallic taste and, rarely, neurological or hematological reactions. An interesting article recently reported that high concentrations (>5000 μg/ml) of metronidazole in vivo completely suppressed the growth of Lactobacillus, and concentrations of metronidazole between 1000 and 4000 μg/ml significantly inhibited the growth of Lactobacillus spp. [83]. Therefore, the dose of metronidazole may be important in determining both the cure and recurrence rates.

The second available oral treatment for BV is clindamycin. The one clinical trial conducted describing the efficacy of oral clindamycin reported that a 300 mg, twice-daily course of clindamycin for 7 days resulted in a 94% cure rate. Of note, all of the efficacy studies have been conducted among nonpregnant women with the assumption that the cure rate for BV among pregnant woman is similar.

Vaginal gels

Previously, BV-positive pregnant and nonpregnant women were treated with metronidazole 0.75% vaginal gel, which avoided the increased nausea with oral therapy. However, the CDC recently reported that existing data do not support the use of topical agents during pregnancy and evidence from three randomized, controlled trials suggests an increase in adverse events (e.g., prematurity and neonatal infections) after treatment with clindamycin cream [84,85]. Box 2 outlines the current recommended treatment options for BV-positive pregnant women.

The current topical treatments for BV include a twice-daily, 5-day therapy of vaginal metronidazole, which has a 30-day cure rate of 75–81%, and treatment with clindamycin cream, reported to resolve 82–96% of cases of BV [86]. The 3-day and 7-day treatments with clindamycin cream have been found to be equally effective and well tolerated in treating BV among nonpregnant women [87]. In fact, Lamont and colleagues found that pregnant women receiving a 3-day course of clindamycin vaginal cream had a higher cure rate compared with placebo and recurrence rates were 6% at 6 weeks postbaseline and 10% at 28–24 weeks gestation [88]. Importantly, another study suggests that the grade of abnormal vaginal flora consistent with BV influences the response to treatment, with women in the intermediate grade (Nugent BV score ranging from 4 to 6) less likely to respond to clindamycin treatment compared with women in the highest grade (scores of 7 or above) [89]. A randomized clinical trial compared a 5-night course of 0.75% metronidazole gel with ovules containing 500 mg metronidazole and 100,000 U of nystatin and found that the ovules were significantly more effective in BV resolution 2 weeks, 6 weeks and 3 months following the initial BV episode [90]. However, another study recently reported that treatment with clindamycin ovules was associated with the development of antimicrobial-resistant anaerobes. For example, following treatment with clindamycin ovules, nearly 80% of women had at least one clindamycin-resistant anaerobic organism, which lasted up to 90 days following treatment [91]. These topical treatments may result in the temporary resolution of lower genital tract symptoms and recolonization of Lactobacillus spp., but localized treatment options do not affect organisms that have ascended to the upper genital tract and directly influence pregnancy outcome.

Although the cure rate for systemic BV treatment ranges from 75 to 90%, as many as 30% of women treated for BV relapse within 1 month of treatment, with relapse occurring more commonly among women treated with topical compared with systemic therapies [92]. It seems the significant and long-term reduction in H₂O₂-producing Lactobacillus spp., as opposed to the increase in anaerobic BV-associated organisms characteristic of BV, is the most important predictor of treatment failure and recurrent BV [93]. The failure of current BV therapies to re-establish a dominant H₂O₂-producing Lactobacillus spp. environment in the lower genital tract may be the reason why up to a half of women with BV will have at least one future episode [94]. Probiotic or 'bacteriotherapy' has been suggested as a long-term, ongoing treatment option for BV, although these studies have had limited success to date [95]. In particular, recolonization of Lactobacillus spp. via yogurt or capsules shows promise, but many of the complementary and alternative studies conducted to date have been of poor quality and nonrandomized in design [96].

Typically, a cure for BV refers to the resolution of symptoms and perhaps a repeat BV-negative screen. In pregnancy, owing to the high rate of asymptomatic patients, a test of cure is usually performed. In fact, the CDC recommends follow-up evaluation 1 month after completion of treatment for all BV-positive pregnant women. It is known from clinical studies that BV has both a spontaneous resolution and recurrence during pregnancy, but the factors contributing to this resolution or recurrence are unknown [97]. In addition, the behavioral, hormonal or environmental factors predisposing a woman to multiple, recurrent cases of BV are also unclear.

Future, long-term treatment options for BV should ensure that the levels of glycosulfatase and glycoprotein sialidase activity are returned to the normal range in order to promote the recolonization of H₂O₂-producing Lactobacillus spp. Recently, cases of BV with various concentrations of H₂O₂-producing Lactobacillus spp. have been described. In fact, among BV-positive women with a substantial reduction in the amount of H₂O₂-producing Lactobacillus spp., the continued overgrowth of the anaerobic organisms characteristic of BV is more strongly influenced by sexual activity and douching habits compared with BV-positive women with measurable amounts of H₂O₂-producing Lactobacillus spp. These findings describe various strains of BV, dictated by the presence or absence of H₂O₂-producing Lactobacillus spp., and suggest that these strains may have different responses to treatment and relapse rates [99].

Box 2. Current recommended treatment regimens for bacterial vaginosis among pregnant women.

Metronidazole (Flagyl)

• 250 mg orally three-times daily for 7 days

Clindamycin

• 300mg orally twice daily for 7 days

Does treatment for bacterial vaginosis during pregnancy reduce adverse pregnancy outcomes?

Owing to the potentially serious sequelae associated with BV and the high prevalence of asymptomatic BV among pregnant women, universal screening and treatment for BV during pregnancy seems appropriate to reduce adverse outcomes. However, recent clinical trials examining the efficacy of BV treatment to reduce the risk of preterm delivery among symptomatic and asymptomatic women have found no reduction in risk and perhaps an increase in preterm labor or preterm birth among treated asymptomatic, BV-positive pregnant women [100,101]. Thus, clinically, symptomatic, BV-positive pregnant women are treated primarily to alleviate symptoms, with the prevention of adverse events (e.g., preterm birth, preterm labor and PPROM) a desirable but not well documented consequence [83]. Owing to the lack of evidence supporting the decrease in adverse pregnancy outcomes among asymptomatic women during pregnancy, screening and treatment for BV among asymptomatic pregnant women to possibly reduce adverse pregnancy outcomes is currently not recommended by the CDC or the American College of Obstetrics and Gynecology, except among women with a previous preterm delivery. Three previous, separate, placebo-controlled, randomized, clinical trials indicated a reduction in the risk of preterm delivery following treatment with metronidazole only among this small subset of high-risk asymptomatic pregnant women (those with a history of a previous preterm delivery) [102–105]. However, a recent clinical trial did not find a reduction in the occurrence of preterm delivery among either high- or low-risk asymptomatic pregnant women following treatment with oral metronidazole [106]. In addition, a recent systematic review concluded that no evidence currently exists to support the use of antibiotic treatment for BV in pregnancy, among low- or high-risk women, to reduce the risk of preterm birth [107]. In clinical practice, high-risk asymptomatic pregnant women are commonly screened early in the second trimester and treated with oral metronidazole, but the benefit of this therapy in reducing the woman's risk of preterm delivery remains unclear [108]. It seems apparent that, in order to be effective and treat abnormal flora associated with BV, BV therapy during pregnancy should be systemic and administered early in pregnancy, prior to the initiation of the inflammatory response and irreversible placental tissue damage [109].

Papers of special note have been highlighted as either of interest (•) or of considerable interest (••) to readers.
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How to Get Rid of Bv Naturally When Pregnant

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