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Bacterial vaginosis: Clinical manifestations and diagnosis

Bacterial vaginosis: Clinical manifestations and diagnosis
Literature review current through: Jan 2024.
This topic last updated: Dec 07, 2023.

INTRODUCTION — Bacterial vaginosis (BV) is a clinical condition characterized by a shift in vaginal microbiota away from Lactobacillus species toward more diverse bacterial species, including facultative anaerobes. The altered microbiome causes a rise in vaginal pH and symptoms that range from none to very bothersome (eg, abnormal vaginal discharge and odor). Future health implications of BV include, but are not limited to, increased susceptibility to other sexually transmitted infections (STIs), including HIV, and preterm birth.

This topic will discuss the pathogenesis, clinical presentation, and treatment of BV. Related topics on the treatment of BV, evaluation of vaginitis, and cervicitis are presented separately.

(See "Bacterial vaginosis: Initial treatment".)

(See "Vaginitis in adults: Initial evaluation".)

(See "Acute cervicitis".)

In this topic, when discussing study results, we will use the terms "woman/en" or "patient(s)" as they are used in the studies presented. However, we encourage the reader to consider the specific counseling and treatment needs of transgender and gender diverse individuals.

DEFINITION — BV is characterized by three alterations in the vaginal environment [1]:

A shift in vaginal microbiota from Lactobacillus species to one of high bacterial diversity, including facultative anaerobes.

Production of volatile amines by the new bacterial microbiota and reduced lactic acid production [2].

Resultant rise in vaginal pH to >4.5 (normal vaginal pH of estrogenized females typically ranges from 4.0 to 4.5). (See "Vaginitis in adults: Initial evaluation", section on 'Normal vaginal discharge'.)

EPIDEMIOLOGY — BV is the most common cause of abnormal vaginal discharge in females of childbearing age, accounting for 40 to 50 percent of vaginitis cases [3-5]. In the United States, the National Health and Nutrition Examination Survey (NHANES), which included results from self-collected vaginal swabs from over 3700 women, estimated the prevalence of BV was 29 percent in the general population of women aged 14 to 49 years and 50 percent in African American women [6]. This included both symptomatic and asymptomatic infection. Worldwide, a meta-analysis of studies from seven regions of the world found that the prevalence of Nugent-diagnosed BV was 23 to 29 percent among women of reproductive age, with small variations according to the population studied [7,8]. The health consequences of BV infection are presented below. (See 'Clinical consequences of BV' below.)

PATHOGENESIS AND MICROBIOLOGY — Processes that contribute to clinical BV include a shift in vaginal microbiota from hydrogen peroxide-producing lactobacillus to anaerobic bacteria, release of amines, and production of a protective biofilm.

Altered vaginal microbiota and dysbiosis – BV represents a complex change in the vaginal microbiota characterized by a reduction in concentration of the normally dominant lactobacilli, which produce hydrogen peroxide and lactic acid, and an increase in concentration of other organisms, especially anaerobic Gram-negative rods [9-13]. Ethnicity and age are additional factors that appear to impact the vaginal microbial community [14]. The absence of clinical signs of inflammation is the basis for the term "vaginosis" rather than "vaginitis." Some authors use the term "dysbiosis" to reflect the microbial imbalance in the vaginal microbiota that can ultimately impact vaginal function and lead to negative health consequences [15,16]. (See 'Clinical consequences of BV' below.)

Commonly associated bacteria – The major bacteria detected in females with BV are Gardnerella vaginalis, Prevotella species, Porphyromonas species, Bacteroides species, Peptostreptococcus species, Mycoplasma hominis, and Ureaplasma urealyticum, as well as Mobiluncus, Megasphaera, Sneathia, and Clostridiales species [9,17,18]. Fusobacterium species and Atopobium vaginae (now renamed Fannyhessea vaginae) [19] are also common.

Bacteria identified with ribosomal DNA probes – The difference in vaginal microbiota between those with and without BV was illustrated in a study that used broad range ribosomal DNA probes to determine the vaginal microbiota of 27 women with BV and 46 controls [1]. Overall, 35 bacterial phylotypes were identified in women with BV, including 16 that were newly recognized. Women with BV had a mean of 12.6 phylotypes (range 9 to 17) per sample compared with 3.3 phylotypes (range 1 to 6) per sample in women without BV. The organisms newly identified by polymerase chain reaction include fastidious bacteria termed "BV-associated bacteria 1, 2, and 3" in the Clostridiales order, which appear to be specific indicators of BV [20]. Subsequent studies have documented several other bacterial species in the human vagina, including the novel strains Peptoniphilaceae DNF01163 and Prevotellaceae DNF00733 [21-24].

Production of amines – Hydrogen peroxide-producing lactobacilli appear to be important in preventing overgrowth of the anaerobes normally present in the vaginal microbiota. With the loss of lactobacilli, pH rises and massive overgrowth of vaginal anaerobes occurs. These anaerobes produce large amounts of proteolytic carboxylase enzymes, which break down vaginal peptides into a variety of amines that are volatile, malodorous, and associated with increased vaginal transudation and squamous epithelial cell exfoliation, resulting in the typical clinical features observed in patients with BV (see 'Clinical features' below). The rise in pH also facilitates adherence of G. vaginalis to the exfoliating epithelial cells.

Role of biofilm – Increasing evidence suggests that G. vaginalis is a key player in the pathogenesis of BV and the development of a biofilm may be an essential component of this process, in addition to the gradual overgrowth of resident anaerobic vaginal microbiota [25-31]. In this model, a cohesive form of G. vaginalis adheres to the vaginal epithelium and then becomes the scaffolding to which other species adhere [32].

Biopsy data – The biofilm hypothesis is supported by a study of microbiota on the epithelial surfaces of vaginal biopsy specimens from individuals with BV that showed a biofilm adhered to part or all of the epithelium, and G. vaginalis comprised 90 percent of bacteria in the biofilm, while Atopobium vaginae accounted for most of the remainder [25]. Subsequent desquamation of these epithelial cells would result in the classic clue cells diagnostic of the disorder (see 'Diagnostic evaluation' below). By contrast, most healthy controls had unstructured accumulations of bacteria within secretions loosely attached to epithelial surfaces.

Role of extracellular DNA (eDNA) – Extracellular DNA (eDNA) is a factor in the structural stability of biofilms in a variety of bacterial species and appears to play an important role in the establishment and maintenance of the G. vaginalis biofilm in BV [33]. The presence of a biofilm may make it difficult to eradicate BV and increase the rate of recurrence, but discovery of the role of eDNA has led to the hypothesis that a DNase might be able to destroy the eDNA that helps to maintain the BV biofilm.

Impact of gender-affirming therapy – The impact of hormonal and surgical gender-affirming treatment on the microbiota of the vagina and neovagina are not yet well understood.

Estrogen-dominant neovagina – Transfeminine individuals may elect gender-affirming surgery with creation of a neovagina. Scrotal and penile skin is typically used and may require an extension with colon or skin graft. Individuals with neovaginas who use estrogen therapy have reported symptoms of vaginal discharge and malodor [34]. In one study comparing the microbiome of 5 individuals with neovaginas with 32 individuals with vaginas, the most common taxa in the neovaginas were Porphyromonas (30.2 percent), Peptostreptococcus (9.2 percent), Prevotella (9.0 percent), Mobiluncus (8.0 percent), and Jonquetella (7.2 percent) compared with Lactobacillus and Gardnerella in the vaginas [35]. Of the patients with neovaginas, four had penile inversion/scrotal graft with sigmoid colon graft and one had penile inversion/scrotal graft only.

-(See "Gender-affirming surgery: Male to female".)

-(See "Transgender women: Evaluation and management".)

Testosterone-dominant vagina – For transmasculine individuals with a vagina who are taking testosterone therapy, one study of 28 individuals reported diverse anaerobic taxa for most patients and three with Lactobacillus-dominant microbiota [36]. In this study, the microbiota were more similar to those of postmenopausal females than those with BV. (See "Transgender men: Evaluation and management".)

RISK FACTORS

Sexual activity – While the majority of epidemiologic data support the hypothesis that BV is a sexually transmitted infection (STI), it is not yet classified as such because of lack of a single causative agent and absence of a clear disease counterpart in males [17,37-41]. In addition, early studies reported mixed results on the impact of treatment of the male sexual partner [42-47]. However, a subsequent review of early negative or inconclusive studies reported that these studies lacked sufficient power to detect reasonable effect sizes, had deficient or inadequately reported randomization methods, and lacked information on adherence to therapy [48]. However, in contrast to trichomoniasis, chlamydial, or gonococcal infection, there is also a high rate of symptomatic recurrence of BV in the absence of sexual activity or reinfection.

Studies including male and female sexual partners – Sexual activity is a risk factor for BV, and most experts believe that BV does not occur in individuals who have never had sexual contact of any type, including receptive oral sex [49-51].

-Impact of first sexual encounter – An observational study including 400 Kenyan females age 16 to 21 years reported BV prevalence (Nugent score ≥7) increased from 2.8 percent to 13.7 percent in the time period from before first sex to after first sex [51]. First sex was associated with more than two-fold increased risk of BV in both adjusted analysis (adjusted hazard ratio [aHR] 2.44, 95% CI 1.25-4.76) and a generalized estimating equations model (aHR 1.92, 95% 1.12-3.31).

-Epidemiologic data – Epidemiologic studies are strongly supportive of sexual transmission of BV pathogens [52].

-Impact of male partner treatment – A trial evaluating male partner treatment with seven days of oral metronidazole was stopped early after interim analysis reported similar BV recurrence rates in both treatment (81 percent) and placebo (80 percent). However, in a subset analysis, women who stated that their partners had higher adherence to the course of metronidazole had a lower risk for BV recurrence [53].

-Impact of sexual contact – In a systematic review and meta-analysis of 43 observational studies, sexual contact with new and multiple male and female partners was associated with an increased risk of BV, while condom use was associated with a decreased risk [37].

-Male penile microbiome – Many BV-associated species have been isolated from the male penile skin, semen, urethra, and urine specimens, and the penile microbiome has been reported to correlate with incident BV infections [54-57].

Studies of same-sex female partnerships – BV is highly prevalent (25 to 50 percent) in females who have sex with females and is associated with increasing numbers of female sexual partners, a female partner with symptomatic BV, and various sexual practices, suggesting sexual transmission is an important factor [58-63]. However, in one study, sexually active monogamous female same-sex partnerships over six months tended to have concordant, stable, vaginal microbiota, which was most concordant for normal microbiota [60]. This suggests that longer duration, sexually active partnerships led to stability and alignment of a favorable vaginal microbiota in the couples. Accordingly, the majority of investigators believe that BV, as an original or first infection or occurrence, is sexually transmitted.

Infection with sexually transmitted infections – The presence of other STIs appears to be associated with an increased prevalence of BV. In a systematic review and meta-analysis of studies evaluating the association between BV infection and herpes simplex virus (HSV) type 2 infection, women infected with HSV-2 had a 55 percent higher risk of BV infection compared with women who were HSV-2 uninfected [64]. Similarly, a five-year prospective cohort study reported that BV was both more prevalent and more persistent among HIV-infected women compared with those without HIV [65]. Conversely, BV may also be a risk factor for HIV and other STI acquisition [66-71]. (See "HIV and women", section on 'Bacterial vaginosis, genital ulcers, and pelvic inflammatory disease'.)

Race and ethnicity – While higher rates of BV have been reported in some populations, it is not clear if this finding reflects genetic, socioeconomic, behavioral, or other differences [6,14,72,73]. In the United States National Health and Nutrition Examination Survey (NHANES) 2001 to 2004 study, the rates of BV based on self-collected swabs were 51 percent for African American women, 32 percent for Mexican-American women, and 23 percent for White women [6]. By contrast, in a small study comparing the vaginal microbiota of White women and Black women by both cultivation-dependent and cultivation-independent methods, there were no differences in colonization and density of bacterial species by race once women with BV by Nugent criteria were removed [74].

Other – In addition to sexual and infectious risk factors, most studies indicate that douching and cigarette smoking are risk factors for acquisition of BV among sexually active females [3,4,60,75-80]. Other risk factors may include:

Diet – One questionnaire study reported an association between high fat diets and BV as well as an inverse relationship for BV with the intakes of folate, vitamin E, and calcium [81]. A diet high in fiber has been associated with higher likelihood of a Lactobacillus-dominant vaginal microbial community [82]. While these dietary factors were associated with differences in the vaginal microbiota, further studies are needed to determine causality.

Body mass index – One study that evaluated Nugent scores for nearly 6000 women reported that overweight (body mass index [BMI] 25.0 to 29.9 kg/m2) and obese (BMI ≥30 kg/m2) women had higher Nugent scores and rates of BV compared with women of normal BMI (BMI 18.5 to 24.9 kg/m2) [73]. The prevalence rates of BV were 21, 30, and 35 percent for lean, overweight, and obese BMIs, respectively.

No increased risk – BV is not associated with chronic medical conditions (eg, diabetes) or immunosuppressive states. Although some degree of genetic susceptibility to BV is likely, no association between a gene polymorphism and BV has been established [83] .

CLINICAL FEATURES — Individuals can present with classic symptoms, symptoms that suggest multiple etiologies of vaginal discharge, or be asymptomatic.

Classic symptoms – Symptomatic individuals typically present with vaginal discharge and/or vaginal odor [49,84,85]. The discharge is off-white, thin, and homogeneous; the odor is an unpleasant "fishy smell" that may be more noticeable after sexual intercourse and during menses [86,87].

Although supporting data are limited, in our experience, in the absence of microscopy, a lack of fishy odor (negative whiff test) makes the diagnosis of BV less likely [88-92].

Mixed vaginitis – BV alone typically does not cause dysuria, dyspareunia, pruritus, vulvovaginal burning, or vaginal/vulvar inflammation (erythema, edema) [84,85]. The presence of these symptoms suggests mixed vaginitis (symptoms due to two pathogens) [93]. However, symptoms are poorly predictive of diagnosis; thus, all symptomatic individuals should undergo examination and evaluation [94].

Cervicitis – Although BV does not involve the cervix, the disorder may be associated with acute cervicitis (endocervical mucopurulent discharge or easily induced cervical bleeding) [95]. (See "Acute cervicitis".)

Asymptomatic – Up to fifty to 70 percent of females with BV are asymptomatic [49,84,85]. Small studies with a follow-up durations of 28 to 40 days have reported that 12 to 18 percent of asymptomatic patients will go on to develop symptoms [78,96,97].

CLINICAL CONSEQUENCES OF BV — Presence of BV increases the risk of poor obstetric and gynecologic outcomes as well as risk of acquisition of HIV and other sexually transmitted infections (STIs).

Obstetric outcomes

Preterm delivery [98-101] (See "Bacterial vaginosis: Initial treatment", section on 'Pregnant or lactating persons'.)

Postpartum fever (See "Postpartum endometritis".)

Gynecologic complications [102-104]:

Endometrial bacterial colonization and plasma-cell endometritis (See "Endometritis unrelated to pregnancy".)

Posthysterectomy vaginal cuff cellulitis (See "Posthysterectomy pelvic abscess".)

Postabortal infection (See "Septic abortion: Clinical presentation and management".)

Other infections

HIV – Increased risk of both acquisition and transmission [66,105,106].

Sexually transmitted infections – BV is a risk factor for acquisition of herpes simplex virus (HSV) type 2, gonorrhea, chlamydia, and trichomonas infection [107-109]. It has been hypothesized that the increased risk of acquisition of STIs in those with BV may be due to lack of hydrogen peroxide-producing lactobacilli in the vaginal microbiota of affected persons; other factors associated with BV infection, such as local cytokine production, may also play a role. Additionally, BV has been associated with persistence of chlamydia infection (ie, reduces likelihood of spontaneous clearance of chlamydia) [110].

Pelvic inflammatory disease – BV is more common among patients with pelvic inflammatory disease (PID). While it is not clear whether it is a causal factor or an independent risk factor for this disease [111,112], BV-associated organisms have been found in the endometrium in individuals with PID who do not have any other causes identified [113].

HPV and subsequent cervical pathology – BV appears conducive to the persistence of human papillomavirus infection [114,115], which is a contributor to development of cervical lesions and cancer. (See "Cervical intraepithelial neoplasia: Terminology, incidence, pathogenesis, and prevention", section on 'Role of human papillomavirus'.)

DIAGNOSTIC EVALUATION — As symptoms of BV overlap with those of other vaginal infections, accurate diagnosis is needed to correctly guide treatment.

Physical examination — All patients undergo physical examination to assess the vaginal discharge, evaluate for related findings (eg, vulvar excoriations or edema, erythema, cervicitis), and exclude other causes of the patient’s symptoms. Details of physical examination are presented in the algorithm (algorithm 1). (See "Vaginitis in adults: Initial evaluation".)

Approach to test selection

Summary — All patients undergo testing of abnormal vaginal discharge (algorithm 1). Clinician training and test availability drive test selection. Options include laboratory tests, which typically use nucleic acid amplification test (NAAT) technology, clinical evaluation of vaginal discharge with pH testing and microscopy, or gram stain with Nugent criteria (typically in research settings) (table 1). NAAT-based laboratory tests are increasingly used because of their sensitivity and specificity > 90 percent, although they require time for processing that delays diagnosis and treatment. Cervicitis caused by gonorrhea or chlamydia should also be excluded.

The relative advantages, disadvantages, and efficacy of each test approach is briefly presented here and discussed in detail in related content. (See "Vaginitis in adults: Initial evaluation", section on 'Test vaginal discharge'.)

Clinical laboratory tests — Clinical laboratory tests are increasingly used for diagnosing BV because they have improved diagnostic accuracy compared with pH testing and microscopy (ie, greater sensitivity and specificity), are able to identify fastidious bacteria, are easy to use, and can test for multiple infections from the same swab (eg, candidiasis and trichomoniasis) (algorithm 1 and table 1) [52,116-122]. Limitations include the need for clinician education to interpret the tests, time delay for diagnosis, and potential identification of non-pathogenic organisms. (See "Vaginitis in adults: Initial evaluation", section on 'Nucleic acid amplification tests (NAATs)'.)

Nucleic acid amplification tests (NAATs) NAATs are laboratory-based tests that exponentially multiply specific nucleic acid sequences through polymerase chain reactions (PCRs) to identify evidence of various vaginal pathogens, including those specific to the diagnosis of bacterial vaginosis, vaginal candidiasis, and trichomoniasis [116,118,121]. The vaginal swab can be collected by a clinician or patient [121,123]. As noted above, we advise a complete physical examination to guide the differential diagnosis and evaluate for alternative diagnoses. Some of the tests are FDA approved (BD Max vaginal panel, Aptima BV) while other are laboratory-developed tests (NuSwab VG, SureSwab BV, and OneSwab BV panel) that require internal validation prior to use [52]; all have high sensitivity and specificity (ie, >90 percent) [117,119,124]. BV cannot be diagnosed by NAATs that are not specific to BV organisms. (See "Vaginitis in adults: Initial evaluation", section on 'Nucleic acid amplification tests (NAATs)'.)

Details by test type include:

The BD Max vaginal panel (Becton Dickinson) uses quantitative PCR measurement of G. vaginalis, Atopobium vaginae, Megasphaera-1, BV-associated bacteria 2, L. crispatus, L. jensenii, and a proprietary algorithm to provide a positive/negative assessment for the presence of BV [52,125]. In a study of 1763 symptomatic individuals, the sensitivity of the assay compared with a combination of Nugent score and Amsel criteria was 90.5 percent (95% CI 88.3-92.2) and specificity was 85.8 percent (95% CI 83.0-88.3) [121].

The Aptima BV (Hologic) is a NAAT that measures the presence of Lactobacillus, G. vaginalis, and A. vaginae [52,125]. In a study that included 1501 symptomatic women, the sensitivity compared with a combination of Nugent score and Amsel criteria was 95 percent (95% CI 93.1-96.4) and specificity was 89.6 percent (95% CI 87.1-91.6) [123].

NuSwab VG (LabCorp) is a laboratory-developed test that evaluates for Atopobium vaginae, Megasphaera-1, and BV-associated bacterium 2 [52]. Results are reported as positive, negative, or indeterminate.

SureSwab BV (Quest Diagnostics) is a laboratory-developed test that evaluates for Lactobacillus species, G. vaginalis, Atopobium vaginae, Megasphaera-1 and -2, and BV-associated bacterium 2 [52]. Results are reported as supportive of BV, not supportive, or equivocal.

OneSwab BV Panel (MDL) is a laboratory-derived test that uses PCR to assess for G. vaginalis, Atopobium vaginae, Megasphaera-1 and -2, and BV-associated bacteria 2 and uses quantitative PCR for Lactobacillus profiling [52].

Point of care tests – These tests can be done in the office at the time of the physical examination and are to be used in conjunction with physical examination, vaginal pH, and whiff-amine test. All have become less commonly used since the development of NAATs.

OSOM BVBlue – The OSOM BVBlue system is a chromogenic diagnostic test based on the presence of elevated sialidase enzyme activity in vaginal fluid samples [88,126,127].

Affirm VP III – The Affirm VP III test is an automated DNA probe assay for detecting G. vaginalis when present at a high concentration [128].

pH and microscopy using Amsel criteria — When pH testing and microscopy are available, the diagnosis of BV in premenopausal females is usually based upon the presence of at least three Amsel criteria (characteristic vaginal discharge, elevated pH, clue cells seen on microscopy, fishy odor) (figure 1) [87,116,129,130]. Compared with Gram stain for diagnosing BV, reported sensitivity of Amsel criteria for diagnosis of BV is over 90 percent and specificity is 77 percent when used by expert clinicians [131]. However, this approach is limited by availability of microscopy equipment and trained providers; lower sensitivities and specificities have been reported when Amsel criteria are used by general clinicians [117]. Advantages, disadvantages, diagnostic accuracy, and how to perform the vaginal pH and microscopy is reviewed in detail in related content (algorithm 1).

(See "Vaginitis in adults: Initial evaluation", section on 'pH and microscopy'.)

Amsel criteria for diagnosis of BV (at least three criteria must be present) (table 2) [116]:

Homogeneous, thin, grayish-white discharge that smoothly coats the vaginal walls.

Vaginal pH >4.5.

Positive whiff-amine test, defined as the presence of a fishy odor when a drop of 10 percent potassium hydroxide (KOH) is added to a sample of vaginal discharge.

Clue cells on saline wet mount (picture 1A-B and figure 1). Clue cells are vaginal epithelial cells studded with adherent coccobacilli that are best appreciated at the edge of the cell (picture 2). For a positive result, at least 20 percent of the epithelial cells on wet mount should be clue cells. The presence of clue cells diagnosed by an experienced microscopist is the single most reliable predictor of BV [132].

However, these criteria are not exclusive to BV; the first three findings are sometimes also present in patients with trichomoniasis (table 3). Mobiluncus species may be noted on microscopy as well (movie 1).

Gram stain with Nugent criteria — Gram stain of vaginal discharge is the gold standard for diagnosis of BV (picture 3A-B) [133], but is mostly performed in research studies because it requires more time, resources, and expertise than Amsel criteria [116,134-136]. The Gram-stained smear is evaluated using Nugent criteria (table 4) or Hay/Ison criteria (table 5). When clinical criteria are used to define infection, the reported sensitivity of Gram stain scoring ranges from 62 to 100 percent [137].

Approaches to avoid — The following methods are unreliable for the diagnosis of BV and therefore are not advised.

Diagnosis without speculum examination – BV has been diagnosed using a swab of vaginal discharge obtained by the patient or clinician without physical examination. However, omission of the speculum examination results in under-diagnosis and should be avoided. Additionally, a speculum examination facilitates evaluation for alternative or concurrent diagnoses, such as cervicitis, pelvic inflammatory disease (PID), or retained objects.

In one study of 131 individuals who tested a self-collected vaginal swab for pH and sialidase, self-test pH had a sensitivity of 73 percent and specificity of 67 percent and self-sialidase was 40 percent sensitive and 90 percent specific compared with clinical diagnosis of BV [138].

In another study of the diagnostic accuracy for BV, clinician-performed clinical examination with speculum examination was more likely to result in a correct diagnosis of BV compared with examination of a self-obtained vaginal swab (90 in 125 versus 68 in 125) [139]. Over-diagnosis/over-treatment occurred in 15 patients (105 positive diagnoses versus 61 positive diagnoses).

Diagnosis without testing – In settings where neither microscopy nor commercial tests are available, diagnosis is based upon findings on clinical examination (characteristic vaginal discharge, elevated vaginal pH, fishy odor). In a 2020 study evaluating 303 symptomatic individuals in eight clinics affiliated with an academic medical center, all participants were evaluated for presence of vaginal discharge but pH was assessed in 15 percent and whiff test in 21 percent [140]. As a result, 30 percent of participants with BV diagnosed by the study gold standard received inadequate treatment and 23 percent of participants without BV received inappropriate treatment.

Culture – As BV represents complex changes in the vaginal microbiota, vaginal culture has no role in diagnosis. Although cultures for G. vaginalis are positive in almost all females with symptomatic infection, the organism is detected in up to 50 to 60 percent of healthy asymptomatic individuals; thus, its presence alone, no matter how identified, is not diagnostic of BV.

Cytology – The Papanicolaou smear is not reliable for diagnosis of BV (sensitivity 49 percent, specificity 93 percent) [141]. No information is available on the sensitivity and specificity of liquid-based cervical cytology screening methods. If a cytology smear suggests BV (ie, shift in microbiota from predominantly lactobacilli to predominantly coccobacilli with or without clue cells), the patient should be asked about symptoms, and if symptomatic, she should undergo standard diagnostic testing for BV and treatment, if appropriate. Treatment of asymptomatic individuals is not routinely indicated. (See "Bacterial vaginosis: Initial treatment", section on 'Asymptomatic nonpregnant'.)

DIAGNOSIS — BV is diagnosed when laboratory or clinical tests find evidence of altered vaginal flora in patients with suggestive physical examination findings. Symptoms may or may not be present.  

DIFFERENTIAL DIAGNOSIS — BV is usually suspected because of high vaginal pH (>4.5). Other causes of increased pH include trichomoniasis, atrophic vaginitis, and desquamative inflammatory vaginitis. These four entities are easily distinguishable by clinical and microscopic features (table 3).

Dyspareunia and/or vaginal inflammation – Individuals with BV generally do not have dyspareunia or signs of vaginal inflammation; by contrast, those with atrophic vaginitis, desquamative inflammatory vaginitis, and trichomoniasis usually have these signs and symptoms.

Additional microscopy findings

Parabasal cells – Both atrophic vaginitis and desquamative inflammatory vaginitis are associated with an increased number of parabasal cells on microscopy, which is not observed in individuals with BV.

White blood cells – Large numbers of white blood cells, specifically polymorphonuclear leukocytes (PMNs), on microscopy are characteristic of desquamative inflammatory vaginitis, trichomoniasis, and atrophic vaginitis with infection, but not BV.

Trichomonads – Visualization of trichomonads readily makes the diagnosis of trichomoniasis in the setting of an elevated pH; in the absence of visible trichomonads or if microscopy is not available, we suggest using more sensitive and specific diagnostic tests to diagnose or exclude trichomoniasis. (See "Trichomoniasis: Clinical manifestations and diagnosis", section on 'Diagnosis'.)

Mixed infections – Mixed infections with BV and a second pathogen, either T. vaginalis or Candida species, are not infrequent, with clinical and laboratory findings reflecting features of both entities.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Bacterial vaginosis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Bacterial vaginosis (The Basics)")

Beyond the Basics topics (see "Patient education: Bacterial vaginosis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Definition and epidemiology – Bacterial vaginosis (BV) is characterized by a shift in vaginal microbiota, production of volatile amines, and resultant rise in vaginal pH. BV is the most common cause of vaginitis in females of childbearing age. (See 'Definition' above and 'Epidemiology' above.)

Pathogenesis – BV represents a complex change in the vaginal microbiota characterized by a reduction in concentration of the normally dominant hydrogen peroxide- and lactic acid-producing lactobacilli and an increase in concentration of other organisms, particularly anaerobic and highly specific fastidious BV-associated bacteria. Vaginal wall biofilms, comprised predominantly of Gardnerella vaginalis, appear to play a role in pathogenesis. (See 'Pathogenesis and microbiology' above.)

Risk factors for BV – The most common risk factor for BV is sexual activity (male and/or female sexual partners). While BV is likely a sexually transmitted infection (STI), it is not yet classified as such because of lack of a single causative agent and absence of a clear disease counterpart in males. Infection with another STI also increases risk of BV. The impact of race and ethnicity are unclear. (See 'Risk factors' above.)

Clinical features – Symptomatic individuals often present with an off-white, thin, homogeneous, and "fishy smelling" vaginal discharge that is more noticeable after coitus and during menses. However, up to 50 to 75 percent of individuals with BV are asymptomatic. (See 'Clinical features' above.)

Clinical sequelae – Sequelae of BV can include an increased risk of preterm birth, plasma-cell endometritis, postpartum fever, posthysterectomy vaginal cuff cellulitis, postabortal infection, pelvic inflammatory disease (PID), and acquisition of other STIs. (See 'Clinical consequences of BV' above.)

Diagnostic evaluation As symptoms of BV overlap with those of other vaginal infections (table 3), accurate diagnosis is needed to correctly guide treatment (algorithm 1). All patients undergo physical examination; the selection of further diagnostic tests is determined by clinical suspicion and test availability. (See 'Diagnostic evaluation' above.)

Clinical laboratory tests – Clinical laboratory tests for diagnosing BV are increasingly used because of improved diagnostic accuracy compared with clinical diagnosis by Amsel criteria, ability to identify fastidious bacteria, and ease of use. In addition to diagnosing BV, nucleic acid amplification tests (NAATs) can identify vaginal candidiasis and trichomonas vaginitis as well as cervicitis caused by gonorrhea and chlamydia. (See 'Clinical laboratory tests' above.)

Microscopy with Amsel criteria – When microscopy is available, the diagnosis of BV is based on the presence of at least three of the following four Amsel criteria. Compared with Gram stain for diagnosing BV, the sensitivity of Amsel criteria for diagnosis of BV is over 90 percent and specificity is 77 percent. However, this approach is limited by availability of microscopy equipment and trained providers (see 'pH and microscopy using Amsel criteria' above):

Amsel criteria include:

-Homogeneous, thin, grayish-white discharge that smoothly coats the vaginal walls.

-Vaginal pH greater than 4.5.

-Positive whiff-amine test, defined as the presence of a fishy odor when 10 percent potassium hydroxide (KOH) is added to a sample of vaginal discharge.

-Clue cells on saline wet mount, comprising at least 20 percent of epithelial cells (picture 1A and picture 1B).

Gram stain with Nugent or Hay/Ison criteria – The Gram-stained smear made from the patient's vaginal discharge is evaluated using Nugent criteria (table 4) or Hay/Ison criteria (table 5). If clinical criteria are used to define infection, then reported sensitivity ranges from 62 to 100 percent. Although Gram stain of vaginal discharge has been the gold standard for diagnosis of BV, it is mainly used in research settings as it requires more time, training, and expertise compared with other methods. (See 'Gram stain with Nugent criteria' above.)

Diagnostic approaches to avoid – Diagnosis of BV should not be made based on history alone or without a speculum examination. Vaginal culture and cytology are not useful for diagnosing BV. (See 'Approaches to avoid' above.)

  1. Fredricks DN, Fiedler TL, Marrazzo JM. Molecular identification of bacteria associated with bacterial vaginosis. N Engl J Med 2005; 353:1899.
  2. Tachedjian G, Aldunate M, Bradshaw CS, Cone RA. The role of lactic acid production by probiotic Lactobacillus species in vaginal health. Res Microbiol 2017; 168:782.
  3. Joesoef, M, Schmid, G. Bacterial vaginosis. In: Clinical evidence, BMJ Publishing Group, London 2001. p.887.
  4. Morris M, Nicoll A, Simms I, et al. Bacterial vaginosis: a public health review. BJOG 2001; 108:439.
  5. Tolosa JE, Chaithongwongwatthana S, Daly S, et al. The International Infections in Pregnancy (IIP) study: variations in the prevalence of bacterial vaginosis and distribution of morphotypes in vaginal smears among pregnant women. Am J Obstet Gynecol 2006; 195:1198.
  6. Allsworth JE, Peipert JF. Prevalence of bacterial vaginosis: 2001-2004 National Health and Nutrition Examination Survey data. Obstet Gynecol 2007; 109:114.
  7. Kenyon C, Colebunders R, Crucitti T. The global epidemiology of bacterial vaginosis: a systematic review. Am J Obstet Gynecol 2013; 209:505.
  8. Peebles K, Velloza J, Balkus JE, et al. High Global Burden and Costs of Bacterial Vaginosis: A Systematic Review and Meta-Analysis. Sex Transm Dis 2019; 46:304.
  9. Hill GB. The microbiology of bacterial vaginosis. Am J Obstet Gynecol 1993; 169:450.
  10. Ling Z, Kong J, Liu F, et al. Molecular analysis of the diversity of vaginal microbiota associated with bacterial vaginosis. BMC Genomics 2010; 11:488.
  11. Eschenbach DA, Davick PR, Williams BL, et al. Prevalence of hydrogen peroxide-producing Lactobacillus species in normal women and women with bacterial vaginosis. J Clin Microbiol 1989; 27:251.
  12. Lamont RF, Sobel JD, Akins RA, et al. The vaginal microbiome: new information about genital tract flora using molecular based techniques. BJOG 2011; 118:533.
  13. Muzny CA, Schwebke JR. Pathogenesis of Bacterial Vaginosis: Discussion of Current Hypotheses. J Infect Dis 2016; 214 Suppl 1:S1.
  14. Fettweis JM, Brooks JP, Serrano MG, et al. Differences in vaginal microbiome in African American women versus women of European ancestry. Microbiology 2014; 160:2272.
  15. Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nat Rev Immunol 2015; 15:30.
  16. Nelson TM, Borgogna JL, Brotman RM, et al. Vaginal biogenic amines: biomarkers of bacterial vaginosis or precursors to vaginal dysbiosis? Front Physiol 2015; 6:253.
  17. Bradshaw CS, Sobel JD. Current Treatment of Bacterial Vaginosis-Limitations and Need for Innovation. J Infect Dis 2016; 214 Suppl 1:S14.
  18. Plummer EL, Sfameni AM, Vodstrcil LA, et al. Prevotella and Gardnerella Are Associated With Treatment Failure Following First-line Antibiotics for Bacterial Vaginosis. J Infect Dis 2023; 228:646.
  19. Nouioui I, Carro L, García-López M, et al. Genome-Based Taxonomic Classification of the Phylum Actinobacteria. Front Microbiol 2018; 9:2007.
  20. Fredricks DN, Fiedler TL, Thomas KK, et al. Targeted PCR for detection of vaginal bacteria associated with bacterial vaginosis. J Clin Microbiol 2007; 45:3270.
  21. Srinivasan S, Munch MM, Sizova MV, et al. More Easily Cultivated Than Identified: Classical Isolation With Molecular Identification of Vaginal Bacteria. J Infect Dis 2016; 214 Suppl 1:S21.
  22. Diop K, Bretelle F, Fournier PE, Fenollar F. 'Anaerococcus mediterraneensis' sp. nov., a new species isolated from human female genital tract. New Microbes New Infect 2017; 17:75.
  23. Diop K, Diop A, Bretelle F, et al. Olegusella massiliensis gen. nov., sp. nov., strain KHD7(T), a new bacterial genus isolated from the female genital tract of a patient with bacterial vaginosis. Anaerobe 2017; 44:87.
  24. Diop K, Bretelle F, Michelle C, et al. Taxonogenomics and description of Vaginella massiliensis gen. nov., sp. nov., strain Marseille P2517(T), a new bacterial genus isolated from the human vagina. New Microbes New Infect 2017; 15:94.
  25. Swidsinski A, Mendling W, Loening-Baucke V, et al. Adherent biofilms in bacterial vaginosis. Obstet Gynecol 2005; 106:1013.
  26. Swidsinski A, Doerffel Y, Loening-Baucke V, et al. Gardnerella biofilm involves females and males and is transmitted sexually. Gynecol Obstet Invest 2010; 70:256.
  27. Swidsinski A, Mendling W, Loening-Baucke V, et al. An adherent Gardnerella vaginalis biofilm persists on the vaginal epithelium after standard therapy with oral metronidazole. Am J Obstet Gynecol 2008; 198:97.e1.
  28. Alves P, Castro J, Sousa C, et al. Gardnerella vaginalis outcompetes 29 other bacterial species isolated from patients with bacterial vaginosis, using in an in vitro biofilm formation model. J Infect Dis 2014; 210:593.
  29. Patterson JL, Stull-Lane A, Girerd PH, Jefferson KK. Analysis of adherence, biofilm formation and cytotoxicity suggests a greater virulence potential of Gardnerella vaginalis relative to other bacterial-vaginosis-associated anaerobes. Microbiology 2010; 156:392.
  30. Jung HS, Ehlers MM, Lombaard H, et al. Etiology of bacterial vaginosis and polymicrobial biofilm formation. Crit Rev Microbiol 2017; :1.
  31. Marrazzo JM. Vaginal biofilms and bacterial vaginosis: of mice and women. J Infect Dis 2013; 207:1481.
  32. Verstraelen H, Swidsinski A. The biofilm in bacterial vaginosis: implications for epidemiology, diagnosis and treatment. Curr Opin Infect Dis 2013; 26:86.
  33. Hymes SR, Randis TM, Sun TY, Ratner AJ. DNase inhibits Gardnerella vaginalis biofilms in vitro and in vivo. J Infect Dis 2013; 207:1491.
  34. Krakowsky Y, Potter E, Hallarn J, et al. The Effect of Gender-Affirming Medical Care on the Vaginal and Neovaginal Microbiomes of Transgender and Gender-Diverse People. Front Cell Infect Microbiol 2021; 11:769950.
  35. Birse KD, Kratzer K, Zuend CF, et al. The neovaginal microbiome of transgender women post-gender reassignment surgery. Microbiome 2020; 8:61.
  36. Winston McPherson G, Long T, Salipante SJ, et al. The Vaginal Microbiome of Transgender Men. Clin Chem 2019; 65:199.
  37. Fethers KA, Fairley CK, Hocking JS, et al. Sexual risk factors and bacterial vaginosis: a systematic review and meta-analysis. Clin Infect Dis 2008; 47:1426.
  38. Potter J. Should sexual partners of women with bacterial vaginosis receive treatment? Br J Gen Pract 1999; 49:913.
  39. Berger BJ, Kolton S, Zenilman JM, et al. Bacterial vaginosis in lesbians: a sexually transmitted disease. Clin Infect Dis 1995; 21:1402.
  40. Fethers K. Is bacterial vaginosis a sexually transmitted infection. Sex Transm Infect 2001; 77:390.
  41. Bradshaw CS, Morton AN, Garland SM, et al. Higher-risk behavioral practices associated with bacterial vaginosis compared with vaginal candidiasis. Obstet Gynecol 2005; 106:105.
  42. Swedberg J, Steiner JF, Deiss F, et al. Comparison of single-dose vs one-week course of metronidazole for symptomatic bacterial vaginosis. JAMA 1985; 254:1046.
  43. Vutyavanich T, Pongsuthirak P, Vannareumol P, et al. A randomized double-blind trial of tinidazole treatment of the sexual partners of females with bacterial vaginosis. Obstet Gynecol 1993; 82:550.
  44. 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.
  45. 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.
  46. Colli E, Landoni M, Parazzini F. Treatment of male partners and recurrence of bacterial vaginosis: A randomised trial. Genitourin Med 1997; 73:267.
  47. Moi H. Prevalence of bacterial vaginosis and its association with genital infections, inflammation, and contraceptive methods in women attending sexually transmitted disease and primary health clinics. Int J STD AIDS 1990; 1:86.
  48. Mehta SD. Systematic review of randomized trials of treatment of male sexual partners for improved bacteria vaginosis outcomes in women. Sex Transm Dis 2012; 39:822.
  49. Yen S, Shafer MA, Moncada J, et al. Bacterial vaginosis in sexually experienced and non-sexually experienced young women entering the military. Obstet Gynecol 2003; 102:927.
  50. Fethers KA, Fairley CK, Morton A, et al. Early sexual experiences and risk factors for bacterial vaginosis. J Infect Dis 2009; 200:1662.
  51. Roxby AC, Mugo NR, Oluoch LM, et al. Low prevalence of bacterial vaginosis in Kenyan adolescent girls, and rapid incidence after first sex. Am J Obstet Gynecol 2023.
  52. Muzny CA, Balkus J, Mitchell C, et al. Diagnosis and Management of Bacterial Vaginosis: Summary of Evidence Reviewed for the 2021 Centers for Disease Control and Prevention Sexually Transmitted Infections Treatment Guidelines. Clin Infect Dis 2022; 74:S144.
  53. Schwebke JR, Lensing SY, Lee J, et al. Treatment of Male Sexual Partners of Women With Bacterial Vaginosis: A Randomized, Double-Blind, Placebo-Controlled Trial. Clin Infect Dis 2021; 73:e672.
  54. Nelson DE, Van Der Pol B, Dong Q, et al. Characteristic male urine microbiomes associate with asymptomatic sexually transmitted infection. PLoS One 2010; 5:e14116.
  55. Nelson DE, Dong Q, Van der Pol B, et al. Bacterial communities of the coronal sulcus and distal urethra of adolescent males. PLoS One 2012; 7:e36298.
  56. Mehta SD, Zhao D, Green SJ, et al. The Microbiome Composition of a Man's Penis Predicts Incident Bacterial Vaginosis in His Female Sex Partner With High Accuracy. Front Cell Infect Microbiol 2020; 10:433.
  57. Zozaya M, Ferris MJ, Siren JD, et al. Bacterial communities in penile skin, male urethra, and vaginas of heterosexual couples with and without bacterial vaginosis. Microbiome 2016; 4:16.
  58. Fethers K, Marks C, Mindel A, Estcourt CS. Sexually transmitted infections and risk behaviours in women who have sex with women. Sex Transm Infect 2000; 76:345.
  59. Marrazzo JM, Antonio M, Agnew K, Hillier SL. Distribution of genital Lactobacillus strains shared by female sex partners. J Infect Dis 2009; 199:680.
  60. Bradshaw CS, Walker SM, Vodstrcil LA, et al. The influence of behaviors and relationships on the vaginal microbiota of women and their female partners: the WOW Health Study. J Infect Dis 2014; 209:1562.
  61. Marrazzo JM, Koutsky LA, Eschenbach DA, et al. Characterization of vaginal flora and bacterial vaginosis in women who have sex with women. J Infect Dis 2002; 185:1307.
  62. Vodstrcil LA, Walker SM, Hocking JS, et al. Incident bacterial vaginosis (BV) in women who have sex with women is associated with behaviors that suggest sexual transmission of BV. Clin Infect Dis 2015; 60:1042.
  63. Evans AL, Scally AJ, Wellard SJ, Wilson JD. Prevalence of bacterial vaginosis in lesbians and heterosexual women in a community setting. Sex Transm Infect 2007; 83:470.
  64. Esber A, Vicetti Miguel RD, Cherpes TL, et al. Risk of Bacterial Vaginosis Among Women With Herpes Simplex Virus Type 2 Infection: A Systematic Review and Meta-analysis. J Infect Dis 2015; 212:8.
  65. Jamieson DJ, Duerr A, Klein RS, et al. Longitudinal analysis of bacterial vaginosis: findings from the HIV epidemiology research study. Obstet Gynecol 2001; 98:656.
  66. Myer L, Denny L, Telerant R, et al. Bacterial vaginosis and susceptibility to HIV infection in South African women: A nested case-control study. J Infect Dis 2005; 192:1372.
  67. Atashili J, Poole C, Ndumbe PM, et al. Bacterial vaginosis and HIV acquisition: a meta-analysis of published studies. AIDS 2008; 22:1493.
  68. Brotman RM, Klebanoff MA, Nansel TR, et al. Bacterial vaginosis assessed by gram stain and diminished colonization resistance to incident gonococcal, chlamydial, and trichomonal genital infection. J Infect Dis 2010; 202:1907.
  69. Abbai NS, Reddy T, Ramjee G. Prevalent bacterial vaginosis infection - a risk factor for incident sexually transmitted infections in women in Durban, South Africa. Int J STD AIDS 2016; 27:1283.
  70. Lokken EM, Balkus JE, Kiarie J, et al. Association of Recent Bacterial Vaginosis With Acquisition of Mycoplasma genitalium. Am J Epidemiol 2017; 186:194.
  71. Brusselaers N, Shrestha S, van de Wijgert J, Verstraelen H. Vaginal dysbiosis and the risk of human papillomavirus and cervical cancer: systematic review and meta-analysis. Am J Obstet Gynecol 2019; 221:9.
  72. Goldenberg RL, Klebanoff MA, Nugent R, et al. Bacterial colonization of the vagina during pregnancy in four ethnic groups. Am J Obstet Gynecol 1996; 174:1618.
  73. Brookheart RT, Lewis WG, Peipert JF, et al. Association between obesity and bacterial vaginosis as assessed by Nugent score. Am J Obstet Gynecol 2019; 220:476.e1.
  74. Beamer MA, Austin MN, Avolia HA, et al. Bacterial species colonizing the vagina of healthy women are not associated with race. Anaerobe 2017.
  75. Ness RB, Hillier SL, Richter HE, et al. Douching in relation to bacterial vaginosis, lactobacilli, and facultative bacteria in the vagina. Obstet Gynecol 2002; 100:765.
  76. Schwebke JR, Desmond RA, Oh MK. Predictors of bacterial vaginosis in adolescent women who douche. Sex Transm Dis 2004; 31:433.
  77. Ness RB, Kip KE, Soper DE, et al. Variability of bacterial vaginosis over 6- to 12-month intervals. Sex Transm Dis 2006; 33:381.
  78. Schwebke JR, Desmond RA. A randomized trial of the duration of therapy with metronidazole plus or minus azithromycin for treatment of symptomatic bacterial vaginosis. Clin Infect Dis 2007; 44:213.
  79. Brotman RM, Klebanoff MA, Nansel TR, et al. A longitudinal study of vaginal douching and bacterial vaginosis--a marginal structural modeling analysis. Am J Epidemiol 2008; 168:188.
  80. Klebanoff MA, Nansel TR, Brotman RM, et al. Personal hygienic behaviors and bacterial vaginosis. Sex Transm Dis 2010; 37:94.
  81. Neggers YH, Nansel TR, Andrews WW, et al. Dietary intake of selected nutrients affects bacterial vaginosis in women. J Nutr 2007; 137:2128.
  82. Shivakoti R, Tuddenham S, Caulfield LE, et al. Dietary macronutrient intake and molecular-bacterial vaginosis: Role of fiber. Clin Nutr 2020; 39:3066.
  83. Verstraelen H, Verhelst R, Nuytinck L, et al. Gene polymorphisms of Toll-like and related recognition receptors in relation to the vaginal carriage of Gardnerella vaginalis and Atopobium vaginae. J Reprod Immunol 2009; 79:163.
  84. Amsel R, Totten PA, Spiegel CA, et al. Nonspecific vaginitis. Diagnostic criteria and microbial and epidemiologic associations. Am J Med 1983; 74:14.
  85. Klebanoff MA, Schwebke JR, Zhang J, et al. Vulvovaginal symptoms in women with bacterial vaginosis. Obstet Gynecol 2004; 104:267.
  86. Livengood CH 3rd, Thomason JL, Hill GB. Bacterial vaginosis: diagnostic and pathogenetic findings during topical clindamycin therapy. Am J Obstet Gynecol 1990; 163:515.
  87. Vaginitis in Nonpregnant Patients: ACOG Practice Bulletin, Number 215. Obstet Gynecol 2020; 135:e1. Reaffirmed 2022.
  88. Bradshaw CS, Morton AN, Garland SM, et al. Evaluation of a point-of-care test, BVBlue, and clinical and laboratory criteria for diagnosis of bacterial vaginosis. J Clin Microbiol 2005; 43:1304.
  89. Challa A, Sood S, Kachhawa G, et al. Diagnostic concordance between Amsel's criteria and the Nugent scoring method in the assessment of bacterial vaginosis. Sex Health 2022; 18:512.
  90. Bhujel R, Mishra SK, Yadav SK, et al. Comparative study of Amsel's criteria and Nugent scoring for diagnosis of bacterial vaginosis in a tertiary care hospital, Nepal. BMC Infect Dis 2021; 21:825.
  91. Simoes JA, Discacciati MG, Brolazo EM, et al. Clinical diagnosis of bacterial vaginosis. Int J Gynaecol Obstet 2006; 94:28.
  92. Gutman RE, Peipert JF, Weitzen S, Blume J. Evaluation of clinical methods for diagnosing bacterial vaginosis. Obstet Gynecol 2005; 105:551.
  93. Sobel JD, Subramanian C, Foxman B, et al. Mixed vaginitis-more than coinfection and with therapeutic implications. Curr Infect Dis Rep 2013; 15:104.
  94. Anderson MR, Klink K, Cohrssen A. Evaluation of vaginal complaints. JAMA 2004; 291:1368.
  95. Marrazzo JM, Wiesenfeld HC, Murray PJ, et al. Risk factors for cervicitis among women with bacterial vaginosis. J Infect Dis 2006; 193:617.
  96. Schwebke JR. Asymptomatic bacterial vaginosis: Response to therapy. Am J Obstet Gynecol 2000; 183:1434.
  97. Schwebke JR, Desmond R. Natural history of asymptomatic bacterial vaginosis in a high-risk group of women. Sex Transm Dis 2007; 34:876.
  98. Klebanoff MA, Hillier SL, Nugent RP, et al. Is bacterial vaginosis a stronger risk factor for preterm birth when it is diagnosed earlier in gestation? Am J Obstet Gynecol 2005; 192:470.
  99. Eschenbach DA. Bacterial vaginosis: emphasis on upper genital tract complications. Obstet Gynecol Clin North Am 1989; 16:593.
  100. Flynn CA, Helwig AL, Meurer LN. Bacterial vaginosis in pregnancy and the risk of prematurity: a meta-analysis. J Fam Pract 1999; 48:885.
  101. Hauth JC, Macpherson C, Carey JC, et al. Early pregnancy threshold vaginal pH and Gram stain scores predictive of subsequent preterm birth in asymptomatic women. Am J Obstet Gynecol 2003; 188:831.
  102. Andrews WW, Hauth JC, Cliver SP, et al. Association of asymptomatic bacterial vaginosis with endometrial microbial colonization and plasma cell endometritis in nonpregnant women. Am J Obstet Gynecol 2006; 195:1611.
  103. Oleen-Burkey MA, Hillier SL. Pregnancy complications associated with bacterial vaginosis and their estimated costs. Infect Dis Obstet Gynecol 1995; 3:149.
  104. MacDermott RI. Bacterial vaginosis. Br J Obstet Gynaecol 1995; 102:92.
  105. Martin HL, Richardson BA, Nyange PM, et al. Vaginal lactobacilli, microbial flora, and risk of human immunodeficiency virus type 1 and sexually transmitted disease acquisition. J Infect Dis 1999; 180:1863.
  106. Cohen CR, Lingappa JR, Baeten JM, et al. Bacterial vaginosis associated with increased risk of female-to-male HIV-1 transmission: a prospective cohort analysis among African couples. PLoS Med 2012; 9:e1001251.
  107. Cherpes TL, Meyn LA, Krohn MA, et al. Association between acquisition of herpes simplex virus type 2 in women and bacterial vaginosis. Clin Infect Dis 2003; 37:319.
  108. Wiesenfeld HC, Hillier SL, Krohn MA, et al. Bacterial vaginosis is a strong predictor of Neisseria gonorrhoeae and Chlamydia trachomatis infection. Clin Infect Dis 2003; 36:663.
  109. Balkus JE, Richardson BA, Rabe LK, et al. Bacterial vaginosis and the risk of trichomonas vaginalis acquisition among HIV-1-negative women. Sex Transm Dis 2014; 41:123.
  110. Brown SE, Tuddenham S, Shardell MD, et al. Bacterial Vaginosis and Spontaneous Clearance of Chlamydia trachomatis in the Longitudinal Study of Vaginal Flora. J Infect Dis 2023; 228:783.
  111. Taylor BD, Darville T, Haggerty CL. Does bacterial vaginosis cause pelvic inflammatory disease? Sex Transm Dis 2013; 40:117.
  112. Ness RB, Hillier SL, Kip KE, et al. Bacterial vaginosis and risk of pelvic inflammatory disease. Obstet Gynecol 2004; 104:761.
  113. Haggerty CL, Totten PA, Tang G, et al. Identification of novel microbes associated with pelvic inflammatory disease and infertility. Sex Transm Infect 2016; 92:441.
  114. Guo YL, You K, Qiao J, et al. Bacterial vaginosis is conducive to the persistence of HPV infection. Int J STD AIDS 2012; 23:581.
  115. King CC, Jamieson DJ, Wiener J, et al. Bacterial vaginosis and the natural history of human papillomavirus. Infect Dis Obstet Gynecol 2011; 2011:319460.
  116. Workowski KA, Bachmann LH, Chan PA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021; 70:1.
  117. Broache M, Cammarata CL, Stonebraker E, et al. Performance of a Vaginal Panel Assay Compared With the Clinical Diagnosis of Vaginitis. Obstet Gynecol 2021; 138:853.
  118. Schwebke JR, Gaydos CA, Nyirjesy P, et al. Diagnostic Performance of a Molecular Test versus Clinician Assessment of Vaginitis. J Clin Microbiol 2018; 56.
  119. Danby CS, Althouse AD, Hillier SL, Wiesenfeld HC. Nucleic Acid Amplification Testing Compared With Cultures, Gram Stain, and Microscopy in the Diagnosis of Vaginitis. J Low Genit Tract Dis 2021; 25:76.
  120. Sherrard J. Evaluation of the BD MAX™ Vaginal Panel for the detection of vaginal infections in a sexual health service in the UK. Int J STD AIDS 2019; 30:411.
  121. Gaydos CA, Beqaj S, Schwebke JR, et al. Clinical Validation of a Test for the Diagnosis of Vaginitis. Obstet Gynecol 2017; 130:181.
  122. Morris SR, Bristow CC, Wierzbicki MR, et al. Performance of a single-use, rapid, point-of-care PCR device for the detection of Neisseria gonorrhoeae, Chlamydia trachomatis, and Trichomonas vaginalis: a cross-sectional study. Lancet Infect Dis 2021; 21:668.
  123. Schwebke JR, Taylor SN, Ackerman R, et al. Clinical Validation of the Aptima Bacterial Vaginosis and Aptima Candida/Trichomonas Vaginitis Assays: Results from a Prospective Multicenter Clinical Study. J Clin Microbiol 2020; 58.
  124. Coleman JS, Gaydos CA. Molecular Diagnosis of Bacterial Vaginosis: an Update. J Clin Microbiol 2018; 56.
  125. Nucleic Acid Based Tests. U.S. Food & Drug Administration. April 2022. https://www.fda.gov/medical-devices/in-vitro-diagnostics/nucleic-acid-based-tests (Accessed on May 04, 2022).
  126. Myziuk L, Romanowski B, Johnson SC. BVBlue test for diagnosis of bacterial vaginosis. J Clin Microbiol 2003; 41:1925.
  127. Sumeksri P, Koprasert C, Panichkul S. BVBLUE test for diagnosis of bacterial vaginosis in pregnant women attending antenatal care at Phramongkutklao Hospital. J Med Assoc Thai 2005; 88 Suppl 3:S7.
  128. Briselden AM, Hillier SL. Evaluation of affirm VP Microbial Identification Test for Gardnerella vaginalis and Trichomonas vaginalis. J Clin Microbiol 1994; 32:148.
  129. Sherrard J, Wilson J, Donders G, et al. 2018 European (IUSTI/WHO) International Union against sexually transmitted infections (IUSTI) World Health Organisation (WHO) guideline on the management of vaginal discharge. Int J STD AIDS 2018; 29:1258.
  130. Sherrard J, Wilson J, Donders G, et al. 2023 update to 2018 European (IUSTI/WHO) guideline on the management of vaginal discharge. Int J STD AIDS 2023; 34:745.
  131. Landers DV, Wiesenfeld HC, Heine RP, et al. Predictive value of the clinical diagnosis of lower genital tract infection in women. Am J Obstet Gynecol 2004; 190:1004.
  132. Eschenbach DA, Hillier S, Critchlow C, et al. Diagnosis and clinical manifestations of bacterial vaginosis. Am J Obstet Gynecol 1988; 158:819.
  133. Nugent RP, Krohn MA, Hillier SL. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation. J Clin Microbiol 1991; 29:297.
  134. Schwebke JR, Hillier SL, Sobel JD, et al. Validity of the vaginal gram stain for the diagnosis of bacterial vaginosis. Obstet Gynecol 1996; 88:573.
  135. Tam MT, Yungbluth M, Myles T. Gram stain method shows better sensitivity than clinical criteria for detection of bacterial vaginosis in surveillance of pregnant, low-income women in a clinical setting. Infect Dis Obstet Gynecol 1998; 6:204.
  136. Gratacós E, Figueras F, Barranco M, et al. Prevalence of bacterial vaginosis and correlation of clinical to Gram stain diagnostic criteria in low risk pregnant women. Eur J Epidemiol 1999; 15:913.
  137. Spiegel CA. Bacterial vaginosis. Clin Microbiol Rev 1991; 4:485.
  138. Huppert JS, Hesse EA, Bernard MC, et al. Accuracy and trust of self-testing for bacterial vaginosis. J Adolesc Health 2012; 51:400.
  139. Singh RH, Zenilman JM, Brown KM, et al. The role of physical examination in diagnosing common causes of vaginitis: a prospective study. Sex Transm Infect 2013; 89:185.
  140. Hillier SL, Austin M, Macio I. Diagnosis and treatment of vaginal discharge syndromes in commuity practice settings. Clin Infect Dis 2020.
  141. Greene JF 3rd, Kuehl TJ, Allen SR. The papanicolaou smear: inadequate screening test for bacterial vaginosis during pregnancy. Am J Obstet Gynecol 2000; 182:1048.
Topic 5451 Version 90.0

References

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