- Author: Philippe H Girerd, MD; Chief Editor: Michel E Rivlin, MD more...
Bacterial vaginosis (BV), or nonspecific vaginitis, was named because bacteria are the etiologic agents and an associated inflammatory response is lacking. Many studies have demonstrated the relation of Gardnerella vaginalis with other bacteria in causing BV, such as Lactobacillus, Prevotella, and anaerobes, including Mobiluncus, Bacteroides, Peptostreptococcus, Fusobacterium, Veillonella, and Eubacterium. Mycoplasma hominis, Ureaplasma urealyticum,Streptococcus viridans, and Atopobium vaginae have also been associated with BV.
Signs and symptoms
Typical symptoms of BV include the following:
- Vaginal odor (the most common, and often initial, symptom of BV); often recognized only after sexual intercourse
- Mildly to moderately increased vaginal discharge
- Vulvar irritation (less common)
- Dysuria or dyspareunia (rare)
Risk factors that may predispose patients to BV include the following:
- Recent antibiotic use
- Decreased estrogen production of the host
- Wearing an intrauterine device (IUD)
- Sexual activity that could lead to transmission (eg, having a new sexual partner or a recent increase in the number of sexual partners)
Physical findings in BV may include the following:
- Gray, thin, and homogeneous vaginal discharge, which adheres to the vaginal mucosa
- Increased light reflex of the vaginal walls, but typically with little or no evidence of inflammation
- Normal-appearing labia, introitus, cervix, and cervical discharge
- In some case, evidence of cervicitis
See Clinical Presentation for more detail.
In addition to the history and vaginal examination, microscopic examination is vital to the clinical diagnosis of BV.
On microscopic examination of the discharge, demonstration of 3 of the following 4 Amsel criteria is considered necessary to diagnose BV most accurately :
- Demonstration of clue cells on a saline smear (the most specific diagnostic criterion)
- A pH greater than 4.5 (up to 90% of patients)
- Characteristic thin, gray, and homogeneous discharge
- Positive whiff test (up to 70% of patients)
Nugent’s criteria may be used to quantify or grade bacteria via Gram staining of vaginal samples. These criteria evaluate the following 3 types of bacteria and assign scores to each as shown:
- Lactobacillus (score, 0-4)
- Bacteroides/Gardnerella (score, 0-4)
- Mobiluncus (score, 0-2)
Total scores are calculated and interpreted as follows:
- 0-3: Normal
- 4-6: Intermediate bacterial count
- 7-10: BV
See Workup for more detail.
General principles of treatment of BV include the following:
- Antibiotics are the mainstay of therapy
- Data on the efficacy of dietary supplementation with Lactobacillus (acidophilus) are conflicting
- Asymptomatic women with G vaginalis colonization do not need treatment
- BV occurring in pregnant women should be treated
- Treatment before cesarean delivery, total abdominal hysterectomy, or insertion of an IUD is also recommended
- Uncomplicated cases typically resolve after standard antibiotic treatment
- BV that does not resolve after one course of treatment may be cured by giving a second course of the same agent or by switching to another agent (eg, from metronidazole to clindamycin or from clindamycin to metronidazole)
- Some women with recurrent BV may benefit from evaluation or treatment of G vaginalis colonization in their sexual partner (controversial)
- Patients should be advised to stop douching or using bubble bath or any other over-the-counter vaginal hygiene products
- Patients should wash only with hypoallergenic bar soaps or no soap at all and should avoid liquid soaps and body washes
- Surgery is not indicated
- Testing for other infections (eg, N gonorrhoeae, C trachomatis, or herpes simplex virus [HSV]-1) may be appropriate
- Therapy with metronidazole or clindamycin may alter the vaginal flora and predispose the patient to development of vaginal candidiasis
See Treatment and Medication for more detail.
Gardnerella vaginalis is a facultatively anaerobic gram-variable rod. It has been demonstrated to cause a wide variety of infections; however, it is most commonly recognized for its role as one of the organisms responsible for bacterial vaginosis (BV).
Bacterial vaginosis (BV), formerly known as nonspecific vaginitis, was named because bacteria are the etiologic agent in this infection and an associated inflammatory response is lacking.
BV is the most common cause of vaginitis and the most common infection encountered in the outpatient gynecologic setting. An increase in vaginal discharge and vaginal malodor caused by a change in the vaginal flora characterizes BV. The vaginal discharge of BV is characteristically described as a thin, gray, homogeneous fluid that is adherent to the vaginal mucosa.
Many studies have demonstrated the relationship of Gardnerella vaginalis with other bacteria in causing BV. BV is known to be a synergistic polymicrobic infection. Some of the associated bacteria include Lactobacillus species, Prevotella, and anaerobes, including Mobiluncus, Bacteroides, Peptostreptococcus, Fusobacterium, Veillonella, and Eubacterium species. Mycoplasma hominis, Ureaplasma urealyticum, and Streptococcus viridans may also play a role in BV. Atopobium vaginae is now recognized as a pathogen associated with BV.
Evidence in support of a synergistic relationship includes the following: (1) Gardner and Dukes inoculated pure cultures of G vaginalis into the vaginas of healthy women and failed to produce BV symptoms; (2) inoculation of vaginal discharge fluid from BV patients into the vaginas of healthy women produced symptoms of BV; (3) treatment for BV, an antianaerobic antibiotic (metronidazole), is ineffective against G vaginalis; and (4) the volatile products elaborated from the whiff test are products of anaerobes and not of G vaginalis.
In BV, the vaginal flora becomes altered through known and unknown mechanisms, causing an increase in the local pH. This may result from a reduction in the hydrogen peroxide–producing lactobacilli. Lactobacilli are large rod-shaped organisms that help maintain the acidic pH of healthy vaginas and inhibit other anaerobic microorganisms through elaboration of hydrogen peroxide. Normally, lactobacilli are found in high concentrations in the healthy vagina. In BV, the lactobacilli population is reduced greatly, while populations of various anaerobes and G vaginalis are increased.
G vaginalis forms a biofilm in the vagina. Some studies show that this biofilm may be resistant to some forms of medical treatment. This predominant G vaginalis biofilm has been shown to survive in hydrogen peroxide (H2 O2), lactic acid, and high levels of antibiotics. When the biofilm was subjected in the laboratory to enzymatic dissolution, susceptibility to H2 O2 and lactic acid were restored. These findings may lead to future development of novel therapies involving enzymatic degradation of biofilms. No such products are currently on the market.
In a study published by Fredricks et al, G vaginalis was detected by PCR in 96% of subjects with BV and 70% of those without BV. Multiple other bacterial species were found by PCR in this study. Fredricks' study confirms the polymicrobial nature of BV and the presence of G vaginalis as one of the causative agents.
Although BV is not considered a sexually transmitted disease, sexual activity has been linked to development of this infection. Observations in support of this include the following: (1) incidence of BV increases with an increase in the number of recent and lifetime sexual partners, (2) a new sexual partner can be related to BV, and (3) male partners of women with BV may have urethral colonization by the same organism, but the male is asymptomatic. Evidence that does not support an exclusive sexually transmitted role of BV is its occurrence in virginal females and its colonization of the rectum in virginal boys and girls.
More recent studies indicated that BV is associated with changes in select soluble immune mediators, an increase in HIV target cells, and a reduction in endogenous antimicrobial activity, which may contribute to the increased risk of HIV acquisition.
Bacterial vaginosis is a polymicrobic synergistic infection. As described in Pathophysiology, the normally predominant lactobacilli population is reduced in the vagina, while populations of Gardnerella vaginalis and other anaerobes are increased.
G vaginalis is the only member of its genus. Originally, it was known as Haemophilus vaginalis and then as Corynebacterium vaginale. It is a nonmotile, nonflagellated, nonsporeforming, facultative anaerobic, and nonencapsulated bacteria.
Although G vaginalis appears microscopically as a gram-variable rod, it is officially categorized as a gram-negative rod.
Other factors associated in the development of BV include douching, tub bathing (particularly with bubble bath), use of over-the-counter intravaginal hygiene products, multiple sexual partners, high frequency of intercourse, the use of an IUD and the presence of other sexually transmitted diseases. The theory for why these factors contribute to the development of BV is that they disrupt the normal vaginal flora. Some evidence shows that hormonal contraception (both combined estrogen/progestin and progestin only) is protective for the development of BV. Recurrent BV may be attributable to previous colonization of the oral cavity or anus with BV-associated bacteria.
United States statistics
BV occurs in one third of adult women in the United States, which represents approximately 21 million women. Each year, women make 10 million office visits for vaginal discharge. An increased prevalence is associated with cigarette smoking, obesity, being single/never married, prior pregnancy, and a history of induced abortion.
Gardnerella vaginalis has been reported to occur in up to 100% of women with signs and symptoms of BV and in up to 70% of women with no signs or symptoms of BV.
G vaginalis has been isolated in up to 80% of the urethras of male sexual partners of women with BV. However, treatment of male partners is not recommended as it has not been shown to alter rates of BV in their female partners.
The incidence of BV in patients attending obstetric clinics is 10-25% and may be as high as 30-65% in patients attending sexually transmitted disease clinics.
Race-, sex-, and age-related demographics
Some studies have shown that bacterial vaginosis appears to occur more commonly among African American women than non-Hispanic white women. The reasons for this are not entirely clear.
G vaginalis colonization and/or infection predominantly occurs in women. Men rarely develop infections with G vaginalis; however, the urethras of men whose sexual partners have symptoms of BV are frequently colonized with the same strain of G vaginalis. A recent study by Bradshaw et al found that G vaginalis is not associated with nongonococcal urethritis.
G vaginalis infections typically occur in women of reproductive age. Studies have documented G vaginalis colonization in prepubertal and/or virginal girls and boys and cases of BV occurring in prepubertal and/or virginal girls.
Uncomplicated cases of bacterial vaginosis (BV) typically resolve after the standard antibiotic treatment.
The prognosis for uncomplicated cases of bacterial vaginosis is generally excellent. Uncomplicated bacterial vaginosis that is assessed promptly typically resolves with standard antibiotic treatment.
The prognosis for complicated cases of bacterial vaginosis leading to other infections varies depending on the particular infectious process. Note the following:
- Long-standing or untreated BV may lead to more serious sequelae, such as endometritis, salpingitis, pelvic inflammatory disease, or complications of pregnancy, including premature rupture of membranes, premature labor, chorioamnionitis, and postpartum endometritis.
- Postgynecologic procedure infections, such as vaginal cuff cellulitis (status posthysterectomy) and postabortion infection may also occur.
- Suspect concomitant infections (such as candida vaginitis) or newer, resistant organisms (Atopobium vaginae) in patients whose symptoms do not resolve after treatment of BV. See Treatment.
Bacterial vaginosis (BV) may lead to an increased risk of salpingitis and/or endometritis, postsurgical infections (eg, postcesarean endometritis, posthysterectomy vaginal cuff cellulitis), and adverse outcomes in pregnancy, including premature rupture of membranes, premature labor, chorioamnionitis, and postpartum endometritis.
Mixed infections with Trichomonas and yeast can occur among patients with BV.
Gardnerella vaginalis bacteremia occurs much more commonly in women than in men and occurs most commonly in postpartum and postgynecologic procedure infections (eg, postpartum endometritis, chorioamnionitis, septic abortion) but is rare.
SPS, the anticoagulant used in blood culture media, is toxic to G vaginalis and inhibits its growth unless a neutralizing gelatin is added to counteract this effect. Routine blood cultures, therefore, may not grow G vaginalis, leading to underdiagnosis and underrecognition of this organism as the etiologic agent in these types of infections.
Although G vaginalis urinary tract infections (UTI) occur much more frequently in women than in men, the overall occurrence of G vaginalis as a causative etiology in this infection is low (< 0.6%). However, the overall frequency may be underestimated because of a lack of optimal laboratory growth conditions (eg, aerobic incubation, short anaerobic growth period, urine not properly refrigerated prior to being cultured) and absence of associated pyuria occurring in women with concomitantly positive urine cultures.
In men, infections caused by G vaginalis are uncommon. Infection of the prostate and urinary bladder have been documented, although this occurs rarely and probably arises as a result of ascending spread of the organism from the colonized urethra. Balanoposthitis from G vaginalis has also been described.
Other infections caused by G vaginalis include chorioamnionitis, endometritis, cervicitis, pelvic inflammatory disease, vaginal cuff cellulitis following hysterectomy, and bacteremia.
Case reports include disc space infection (lumbar spine), vaginitis emphysematosa, liver abscess (postcesarean), neonatal meningitis, and neonatal cellulitis/skin abscess.
Educate patients regarding the basic pathophysiology, natural history, and risk factors of the bacterial vaginosis. BV is not considered a sexually transmitted disease, although sexual contact may predispose patients to development of this process in some cases.
For patient education resources, see Women's Health Center and Pregnancy Center, as well as Sexually Transmitted Diseases (STDs), Trichomoniasis, Birth Control Overview, and Birth Control Methods.
Brocklehurst P, Gordon A, Heatley E, Milan SJ. Antibiotics for treating bacterial vaginosis in pregnancy. Cochrane Database Syst Rev. 2013 Jan 31. 1:CD000262. [Medline].
Amsel R, Totten PA, Spiegel CA, Chen KC, Eschenbach D, Holmes KK. Nonspecific vaginitis. Diagnostic criteria and microbial and epidemiologic associations. Am J Med. 1983 Jan. 74(1):14-22. [Medline].
Schuyler JA, Mordechai E, Adelson ME, Sobel JD, Gygax SE, Hilbert DW. Identification of intrinsically metronidazole-resistant clades of Gardnerella vaginalis. Diagn Microbiol Infect Dis. 2015 Oct 8. [Medline].
Tabrizi SN, Fairley CK, Bradshaw CS, Garland SM. Prevalence of Gardnerella vaginalis and Atopobium vaginae in virginal women. Sex Transm Dis. 2006 Nov. 33(11):663-5. [Medline].
Patterson JL, Girerd PH, Karjane NW, Jefferson KK. Effect of biofilm phenotype on resistance of Gardnerella vaginalis to hydrogen peroxide and lactic acid. Am J Obstet Gynecol. 2007 Aug. 197(2):170.e1-7. [Medline]. [Full Text].
Fredricks DN, Fiedler TL, Thomas KK, Oakley BB, Marrazzo JM. Targeted PCR for detection of vaginal bacteria associated with bacterial vaginosis. J Clin Microbiol. 2007 Oct. 45(10):3270-6. [Medline]. [Full Text].
Meriwether KV, Rogers RG, Craig E, Peterson SD, Gutman RE, Iglesia CB. The effect of hydroxyquinoline-based gel on pessary-associated bacterial vaginosis: a multicenter randomized controlled trial. Am J Obstet Gynecol. 2015 Nov. 213 (5):729.e1-9. [Medline].
Payne SC, Cromer PR, Stanek MK, Palmer AA. Evidence of African-American women's frustrations with chronic recurrent bacterial vaginosis. J Am Acad Nurse Pract. 2010 Feb. 22(2):101-8. [Medline].
Marrazzo JM, Fiedler TL, Srinivasan S, et al. Extravaginal reservoirs of vaginal bacteria as risk factors for incident bacterial vaginosis. J Infect Dis. 2012 May 15. 205(10):1580-8. [Medline]. [Full Text].
Coughlin G, Secor M. Bacterial vaginosis: update on evidence-based care. Adv Nurse Pract. 2010 Jan. 18(1):41-4, 53. [Medline].
Alcaide ML, Chisembele M, Malupande E, Arheart K, Fischl M, Jones DL. A cross-sectional study of bacterial vaginosis, intravaginal practices and HIV genital shedding; implications for HIV transmission and women's health. BMJ Open. 2015 Nov 9. 5 (11):e009036. [Medline].
Thurman AR, Kimble T, Herold B, et al. Bacterial Vaginosis and Subclinical Markers of Genital Tract Inflammation and Mucosal Immunity. AIDS Res Hum Retroviruses. 2015 Nov. 31 (11):1139-52. [Medline].
Schwiertz A, Taras D, Rusch K, Rusch V. Throwing the dice for the diagnosis of vaginal complaints?. Ann Clin Microbiol Antimicrob. 2006 Feb 17. 5:4. [Medline]. [Full Text].
Mohanty S, Sood S, Kapil A, Mittal S. Interobserver variation in the interpretation of Nugent scoring method for diagnosis of bacterial vaginosis. Indian J Med Res. 2010 Jan. 131:88-91. [Medline].
West B, Morison L, Schim van der Loeff M, et al. Evaluation of a new rapid diagnostic kit (FemExam) for bacterial vaginosis in patients with vaginal discharge syndrome in The Gambia. Sex Transm Dis. 2003 Jun. 30(6):483-9. [Medline].
Reid G, Burton J, Hammond JA, Bruce AW. Nucleic acid-based diagnosis of bacterial vaginosis and improved management using probiotic lactobacilli. J Med Food. 2004 Summer. 7(2):223-8. [Medline].
Masson L, Arnold KB, Little F, et ak. Inflammatory cytokine biomarkers to identify women with asymptomatic sexually transmitted infections and bacterial vaginosis who are at high risk of HIV infection. Sex Transm Infect. 2015 Oct 28. [Medline].
Abramovici A, Lobashevsky E, Cliver SP, Edwards RK, Hauth JC, Biggio JR. Quantitative polymerase chain reaction to assess response to treatment of bacterial vaginosis and risk of preterm birth. Am J Perinatol. 2015 Oct. 32 (12):1119-25. [Medline].
Ya W, Reifer C, Miller LE. Efficacy of vaginal probiotic capsules for recurrent bacterial vaginosis: a double-blind, randomized, placebo-controlled study. Am J Obstet Gynecol. 2010 Aug. 203(2):120.e1-6. [Medline].
De Backer E, Verhelst R, Verstraelen H, et al. Antibiotic susceptibility of Atopobium vaginae. BMC Infect Dis. 2006 Mar 16. 6:51. [Medline]. [Full Text].
Avonts D, Sercu M, Heyerick P, Vandermeeren I, Meheus A, Piot P. Incidence of uncomplicated genital infections in women using oral contraception or an intrauterine device: a prospective study. Sex Transm Dis. 1990 Jan-Mar. 17(1):23-9. [Medline].
Barbone F, Austin H, Louv WC, Alexander WJ. A follow-up study of methods of contraception, sexual activity, and rates of trichomoniasis, candidiasis, and bacterial vaginosis. Am J Obstet Gynecol. 1990 Aug. 163(2):510-4. [Medline].
Berardi-Grassias L, Roy O, Berardi JC, Furioli J. Neonatal meningitis due to Gardnerella vaginalis. Eur J Clin Microbiol Infect Dis. 1988 Jun. 7(3):406-7. [Medline].
Bradshaw CS, Tabrizi SN, Read TR, et al. Etiologies of nongonococcal urethritis: bacteria, viruses, and the association with orogenital exposure. J Infect Dis. 2006 Feb 1. 193(3):336-45. [Medline].
Bump RC, Buesching WJ 3rd. Bacterial vaginosis in virginal and sexually active adolescent females: evidence against exclusive sexual transmission. Am J Obstet Gynecol. 1988 Apr. 158(4):935-9. [Medline].
Carney FE. Hemophilus vaginalis septicemia. Obstet Gynecol. 1973 Jan. 41(1):78-9. [Medline].
Catlin BW. Gardnerella vaginalis: characteristics, clinical considerations, and controversies. Clin Microbiol Rev. 1992 Jul. 5(3):213-37. [Medline]. [Full Text].
Chen KC, Amsel R, Eschenbach DA, Holmes KK. Biochemical diagnosis of vaginitis: determination of diamines in vaginal fluid. J Infect Dis. 1982 Mar. 145(3):337-45. [Medline].
Embree J, Caliando JJ, McCormack WM. Nonspecific vaginitis among women attending a sexually transmitted diseases clinic. Sex Transm Dis. 1984 Apr-Jun. 11(2):81-4. [Medline].
Eschenbach DA. Bacterial vaginosis and anaerobes in obstetric-gynecologic infection. Clin Infect Dis. 1993 Jun. 16 Suppl 4:S282-7. [Medline].
Eschenbach DA, Hillier S, Critchlow C, Stevens C, DeRouen T, Holmes KK. Diagnosis and clinical manifestations of bacterial vaginosis. Am J Obstet Gynecol. 1988 Apr. 158(4):819-28. [Medline].
Ezzell JH Jr, Many WJ Jr. Gardnerella vaginalis: an unusual case of pyogenic liver abscess. Am J Gastroenterol. 1988 Dec. 83(12):1409-11. [Medline].
Gravett MG, Hummel D, Eschenbach DA, Holmes KK. Preterm labor associated with subclinical amniotic fluid infection and with bacterial vaginosis. Obstet Gynecol. 1986 Feb. 67(2):229-37. [Medline].
Hallen A, Pahlson C, Forsum U. Bacterial vaginosis in women attending STD clinic: diagnostic criteria and prevalence of Mobiluncus spp. Genitourin Med. 1987 Dec. 63(6):386-9. [Medline]. [Full Text].
Hay PE, Morgan DJ, Ison CA, et al. A longitudinal study of bacterial vaginosis during pregnancy. Br J Obstet Gynaecol. 1994 Dec. 101(12):1048-53. [Medline].
Hedges SR, Barrientes F, Desmond RA, Schwebke JR. Local and systemic cytokine levels in relation to changes in vaginal flora. J Infect Dis. 2006 Feb 15. 193(4):556-62. [Medline].
Hill LV. Anaerobes and Gardnerella vaginalis in non-specific vaginitis. Genitourin Med. 1985 Apr. 61(2):114-9. [Medline]. [Full Text].
Hillier SL, Krohn MA, Rabe LK, Klebanoff SJ, Eschenbach DA. The normal vaginal flora, H2O2-producing lactobacilli, and bacterial vaginosis in pregnant women. Clin Infect Dis. 1993 Jun. 16 Suppl 4:S273-81. [Medline].
Hodge TW Jr, Levy CS, Smith MA. Disk space infection due to Gardnerella vaginalis. Clin Infect Dis. 1995 Aug. 21(2):443-5. [Medline].
Holst E, Wathne B, Hovelius B, Mardh PA. Bacterial vaginosis: microbiological and clinical findings. Eur J Clin Microbiol. 1987 Oct. 6(5):536-41. [Medline].
Joesoef MR, Wiknjosastro G, Norojono W, et al. Coinfection with chlamydia and gonorrhoea among pregnant women and bacterial vaginosis. Int J STD AIDS. 1996 Jan-Feb. 7(1):61-4. [Medline].
Johnson AP, Boustouller YL. Extra-vaginal infection caused by Gardnerella vaginalis. Epidemiol Infect. 1987 Apr. 98(2):131-7. [Medline]. [Full Text].
Jones BM, Geary I, Alawattegama AB, Kinghorn GR, Duerden BI. In-vitro and in-vivo activity of metronidazole against Gardnerella vaginalis, Bacteroides spp. and Mobiluncus spp. in bacterial vaginosis. J Antimicrob Chemother. 1985 Aug. 16(2):189-97. [Medline].
Josey WE, Campbell WG Jr. Vaginitis emphysematosa. A report of four cases. J Reprod Med. 1990 Oct. 35(10):974-7. [Medline].
Klebanoff MA, Andrews WW, Yu KF, et al. A pilot study of vaginal flora changes with randomization to cessation of douching. Sex Transm Dis. 2006 Oct. 33(10):610-3. [Medline].
Legrand JC, Alewaeters A, Leenaerts L, Gilbert P, Labbe M, Glupczynski Y. Gardnerella vaginalis bacteremia from pulmonary abscess in a male alcohol abuser. J Clin Microbiol. 1989 May. 27(5):1132-4. [Medline]. [Full Text].
Leighton PM, Bulleid B, Taylor R. Neonatal cellulitis due to Gardnerella vaginalis. Pediatr Infect Dis. 1982 Sep-Oct. 1(5):339-40. [Medline].
Lugo-Miro VI, Green M, Mazur L. Comparison of different metronidazole therapeutic regimens for bacterial vaginosis. A meta-analysis. JAMA. 1992 Jul 1. 268(1):92-5. [Medline].
Martius J, Eschenbach DA. The role of bacterial vaginosis as a cause of amniotic fluid infection, chorioamnionitis and prematurity--a review. Arch Gynecol Obstet. 1990. 247(1):1-13. [Medline].
Martius J, Krohn MA, Hillier SL, Stamm WE, Holmes KK, Eschenbach DA. Relationships of vaginal Lactobacillus species, cervical Chlamydia trachomatis, and bacterial vaginosis to preterm birth. Obstet Gynecol. 1988 Jan. 71(1):89-95. [Medline].
McCormack WM, Hayes CH, Rosner B, et al. Vaginal colonization with Corynebacterium vaginale (Haemophilus vaginalis). J Infect Dis. 1977 Dec. 136(6):740-5. [Medline].
McDonald HM, O'Loughlin JA, Vigneswaran R, Jolley PT, McDonald PJ. Bacterial vaginosis in pregnancy and efficacy of short-course oral metronidazole treatment: a randomized controlled trial. Obstet Gynecol. 1994 Sep. 84(3):343-8. [Medline].
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 Feb. 28(2):163-71. [Medline].
Nilsson U, Hellberg D, Shoubnikova M, Nilsson S, Mardh PA. Sexual behavior risk factors associated with bacterial vaginosis and Chlamydia trachomatis infection. Sex Transm Dis. 1997 May. 24(5):241-6. [Medline].
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 Feb. 29(2):297-301. [Medline]. [Full Text].
Pheifer TA, Forsyth PS, Durfee MA, Pollock HM, Holmes KK. Nonspecific vaginitis: role of Haemophilus vaginalis and treatment with metronidazole. N Engl J Med. 1978 Jun 29. 298(26):1429-34. [Medline].
Rein MF. Vulvovaginitis and cervicitis. Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000. 1218-1235.
Sadhu K, Domingue PA, Chow AW, Nelligan J, Cheng N, Costerton JW. Gardnerella vaginalis has a gram-positive cell-wall ultrastructure and lacks classical cell-wall lipopolysaccharide. J Med Microbiol. 1989 Jul. 29(3):229-35. [Medline].
Schnadig VJ, Davie KD, Shafer SK, Yandell RB, Islam MZ, Hannigan EV. The cytologist and bacterioses of the vaginal-ectocervical area. Clues, commas and confusion. Acta Cytol. 1989 May-Jun. 33(3):287-97. [Medline].
Schwebke JR, Hillier SL, Sobel JD, McGregor JA, Sweet RL. Validity of the vaginal gram stain for the diagnosis of bacterial vaginosis. Obstet Gynecol. 1996 Oct. 88(4 Pt 1):573-6. [Medline].
Soper DE, Bump RC, Hurt WG. Bacterial vaginosis and trichomoniasis vaginitis are risk factors for cuff cellulitis after abdominal hysterectomy. Am J Obstet Gynecol. 1990 Sep. 163(3):1016-21; discussion 1021-3. [Medline].
Spiegel CA. Bacterial vaginosis. Clin Microbiol Rev. 1991 Oct. 4(4):485-502. [Medline]. [Full Text].
Spiegel CA. Gardnerella vaginalis and Mobiluncus Species. Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000. 2383-2386.
Spiegel CA, Amsel R, Holmes KK. Diagnosis of bacterial vaginosis by direct gram stain of vaginal fluid. J Clin Microbiol. 1983 Jul. 18(1):170-7. [Medline]. [Full Text].
Sturm AW. Gardnerella vaginalis in infections of the urinary tract. J Infect. 1989 Jan. 18(1):45-9. [Medline].
Swedberg J, Steiner JF, Deiss F, Steiner S, Driggers DA. Comparison of single-dose vs one-week course of metronidazole for symptomatic bacterial vaginosis. JAMA. 1985 Aug 23-30. 254(8):1046-9. [Medline].
Thomason JL, Gelbart SM, Anderson RJ, Walt AK, Osypowski PJ, Broekhuizen FF. Statistical evaluation of diagnostic criteria for bacterial vaginosis. Am J Obstet Gynecol. 1990 Jan. 162(1):155-60. [Medline].
Venkataramani TK, Rathbun HK. Corynebacterium vaginale (Hemophilus vaginalis) bacteremia: clinical study of 29 cases. Johns Hopkins Med J. 1976 Sep. 139(3):93-97. [Medline].
Vontver LA, Eschenbach DA. The role of Gardnerella vaginalis in nonspecific vaginitis. Clin Obstet Gynecol. 1981 Jun. 24(2):439-60. [Medline].
Watson RA. Gardnerella vaginalis: genitourinary pathogen in men. Urology. 1985 Mar. 25(3):217-22. [Medline].
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. 2015 Nov 3. [Medline].
|Clinical Elements||Bacterial Vaginosis||Trichomoniasis||Vaginal Candidiasis|
|Vaginal discharge||Thin, gray, homogenous||Green-yellow||White, curdlike|
|Bubbles in vaginal fluid||+||+/-||-|
|Microscopy||Saline wet mount|