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Case Report

Suspected Heterosexual Transmission of Bacterial Vaginosis Without Seminal Fluid Exposure

Muzny, Christina A. MD; Schwebke, Jane R. MD

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Sexually Transmitted Diseases: January 2014 - Volume 41 - Issue 1 - p 58-60
doi: 10.1097/OLQ.0000000000000057
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Bacterial vaginosis (BV) is the most common vaginal infection worldwide.1 Microbiologically, BV is characterized by depletion of H2O2-producing lactobacilli that compromise the normal vaginal flora and increases in facultative (ie, Gardnerella vaginalis) and strict anaerobic (ie, Prevotella species, Mycoplasma hominis, Bacteroides spp., Peptostreptococcus spp., Fusobacterium spp., Mobiluncus spp., Atopobium vaginae, etc) bacteria.1 Bacterial vaginosis is a known risk factor for the acquisition of HIV and sexually transmitted infections.2–4 Currently, the pathogenesis of BV is not well known, although there is considerable evidence that it is sexually transmitted.5,6 Seminal fluid is thought to play an important role in the pathogenesis of BV among heterosexuals.7 We report a case of suspected heterosexual transmission of BV to an otherwise healthy woman from a male sexual partner who had undergone radical prostatectomy 2 years before. The most likely method of heterosexual transmission in this case was through contact with infected desquamated epithelial cells from the male sexual partner’s distal urethra or coronal sulcus.


A 51-year old-white woman on oral estrogen replacement therapy participating in a prospective study of changes in vaginal flora complained of new-onset vaginal irritation for 1 day. She denied discharge, pruritus, or odor and had not recently douched. She was sexually active with one partner, a 58-year-old white man who had undergone a radical prostatectomy 2 years before for prostate cancer. Her last unprotected vaginal intercourse with this male partner occurred 3 days before the onset of symptoms, and before that, she had been abstinent for 6 weeks. Of note, the study involved frequent vaginal Gram stains, and a slide obtained the day before her sexual exposure had a Nugent score of 0 (lactobacilli only; Fig. 1). On examination, minimal vaginal discharge was noted; pH was 4.7. A subsequent vaginal Gram stain revealed BV with a Nugent score of 8 (Fig. 2). The patient was treated for BV with intravaginal metronidazole during a 5-day course with resolution of her vaginal irritation and normalization of her vaginal flora. Upon further questioning of her male sexual partner, she learned that he had had unprotected sex 6 days before with another female sexual partner. A vaginal Gram stain obtained from the other female sexual partner approximately 48 hours after the onset of the patient’s symptoms also revealed BV with a Nugent score of 7 (Fig. 3). Written permission from all participants described in this report was obtained.

Figure 1:
Patient’s vaginal Gram stain obtained the day before sexual exposure with her male sexual partner demonstrating a predominance of lactobacilli (Nugent score 0).
Figure 2:
Patient’s vaginal Gram stain obtained 3 days after sexual exposure, consistent with BV (Nugent score 8).
Figure 3:
Vaginal Gram stain from the man’s other female sexual partner, obtained approximately 48 hours after the onset of the patient’s symptoms, also consistent with BV (Nugent score 7).


To our knowledge, this is the first report documenting suspected heterosexual transmission of BV to a woman from a male sexual partner who had undergone a radical prostatectomy. Taking into account the onset of the patient’s symptoms in the context of her sexual history, it seems that the incubation period for the development of BV in the patient was approximately 72 hours, similar to that of other bacterial sexually transmitted infections such as Neisseria gonorrhoeae.8 In addition, it is interesting to note that the patient’s presenting symptom of vaginal irritation was atypical for BV, which usually presents with a vaginal discharge and malodor.1 Future research should investigate whether this may be an early, unrecognized symptom of this infection.

It has been postulated that semen may be integral in the pathogenesis of BV among heterosexuals. A study by Gallo et al.7 also found that the sole correlate of incident BV among women was the detection of spermatozoa on vaginal Gram stain, a marker of semen exposure. In addition, G. vaginalis and other BV-associated microorganisms have frequently been isolated from the semen of asymptomatic men who had abstained from sexual intercourse for a minimum of 3 days before collection, suggestive of colonization of the male genital tract.9 It is possible that the alkaline nature (pH 7.2) of seminal fluid10 could alter the normal lactobacillus-predominant vaginal milieu, promoting the overgrowth of BV-associated microorganisms and the subsequent development of the BV syndrome. Correspondingly, it has been found that exposure to semen in the female reproductive tract elicits a localized inflammatory response with cytokine expression,11 although it is unknown whether this contributes to BV development.

Nevertheless, in the case of our female patient, BV was not transmitted through sexual exposure to semen because her male sexual partner had no prostate gland and was unable to ejaculate. It is thus more likely that her male sexual partner became colonized in the distal portion of his urethra or his coronal sulcus with the organism(s) responsible for BV development after having participated in unprotected sex with his other female sexual partner (who also had a diagnosis of BV by Nugent score), subsequently transferring those organisms on desquamated epithelial cells to our female patient during unprotected sex. Of note, in women, BV is an infection of the vaginal epithelium, which is composed of squamous epithelial cells (as opposed to columnar epithelial cells)1; presence of “clue cells,” desquamated squamous epithelial cells coated with vaginal bacteria, is 1 of the 4 Amsel criteria12 for the clinical diagnosis of BV. Thus, it seems likely that it is this type of epithelium (which is located only in the distal portion of the male urethra and the coronal sulcus of the penis),13 which is the site of colonization/infection with BV-associated microorganisms in males. Results of several studies support the plausibility of this potential method of BV transmission among heterosexuals. Swidsinski et al.14 have recently used fluorescence in situ hybridization on urine samples from females and males to demonstrate that G. vaginalis, a well-known BV-associated microorganism, forms a biofilm on desquamated epithelial cells that is sexually transmitted. During this study, sexual transmission of a cohesive G. vaginalis strain between a wife, her current husband, and her husband’s ex-wife was documented using molecular methods. In addition, Piot et al.15 have shown that G. vaginalis isolates from women with BV and from the urethras of their male sex partners belonged to identical biotypes when strains were isolated within the same 24-hour period from both partners (P < 0.005). Correspondingly, Holst16 recovered 4 BV-associated microorganisms (Mobiluncus mulieris, Mobiluncus curtisii, M. hominis, and G. vaginalis) from the urethras and coronal sulci of male partners of women with BV, less than 20 hours after the last sexual intercourse. In this study, these anatomical sites were recultured 2 weeks later (at which time condoms were used during sexual intercourse), and only 1 of 44 men still harbored 1 (M. hominis) of the 4 BV-associated microorganisms in his urethra, suggesting transient colonization of the male genital tract by BV-associated microorganisms, passively acquired from female sexual partner(s) with BV, similar to what may have occurred to our patients described in this report.

By analogy, the plausibility of male to female sexual transmission of BV in the absence of seminal fluid is supported by studies suggesting sexual transmission of BV between female sexual partners (ie, additional situations in which seminal fluid is not present). In a study of 326 women who have sex with women (WSW), Marrazzo et al.17 found that BV was common among participants who did not douche, who did not have concurrent male sexual partners, or who did not have a new sexual partner, suggesting that other risk factors for BV existed. Of 58 couples involved in monogamous sexual partnerships during this study, 95% had a high concordance for the presence or absence of BV, and the presence of BV in 1 woman was strongly associated with the presence of BV in her sexual partner.17 These data support the hypothesis that sexual exchange of infected vaginal secretions is a possible mechanism for the acquisition of BV among WSW. Further data have corroborated these findings by demonstrating that prevalent BV among WSW is associated with sexual practices (ie, sharing of vaginal sex toys) that efficiently transmit vaginal fluid.18

The use of molecular methods to compare BV-associated microorganisms in the vaginal microbiome of our female patient with BV to those potentially present in the distal portion of the urethra or the coronal sulcus of her male sexual partner (or in the vaginal microbiome of the man’s other female sexual partner with BV) could have provided additional evidence supporting the sexual transmission of BV in this case. However, we did not have stored specimens available to do this analysis for all participants. Interpretation of these data would have been complicated, however, given the amount of time elapsed between each of the sexual acts and the diagnoses of BV among participants. Nevertheless, this report suggests suspected heterosexual transmission of BV, without exposure to seminal fluid, commonly thought to be integral in the pathogenesis of BV among heterosexuals. Further studies are necessary to investigate the plausibility of this potential method of BV transmission.


1. Hillier SL, Marrazzo JM, Holmes KK. Bacterial vaginosis. In: Holmes KK, Sparling PF, Mardh PA, et al. eds. Sexually Transmitted Diseases, 4th ed. New York, NY: McGraw-Hill, 2008: 737–768.
2. 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: 1863–1868.
3. 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: 1907–1915.
4. 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: 319–325.
5. Hawes SE, Hillier SL, Benedetti J, et al. Hydrogen peroxide–producing lactobacilli and acquisition of vaginal infections. J Infect Dis 1996; 174: 1058–1063.
6. Schwebke JR, Desmond R. Risk factors for bacterial vaginosis in women at high risk for sexually transmitted diseases. Sex Transm Dis 2005; 32: 654–658.
7. Gallo MF, Warner L, King CC, et al. Association between semen exposure and incident bacterial vaginosis. Infect Dis Obstet Gynecol 2011; 2011: 842652.
8. Hook EW, Handsfield HH. Gonococcal infections in the adult. In: Holmes KK, Sparling PF, Mardh PA, et al. eds. Sexually Transmitted Diseases, 4th ed. New York, NY: McGraw-Hill, 2008: 627–646.
9. Hillier SL, Rabe LK, Muller CH, et al. Relationship of bacteriologic characteristics to semen indices in men attending an infertility clinic. Obstet Gynecol 1990; 75: 800–804.
10. World Health Organization. WHO Laboratory Manual for the Examination and Processing of Human Semen, 5th ed. Geneva, Switzerland: WHO Press, 2010: 16–17.
11. Sharkey DJ, Macpherson AM, Tremellen KP, et al. Seminal plasma differentially regulates inflammatory cytokine gene expression in human cervical and vaginal epithelial cells. Mol Hum Reprod 2007; 13: 491–501.
12. Amsel R, Totten PA, Spiegel CA, et al. Nonspecific vaginitis. Diagnostic criteria and microbial and epidemiologic associations. Am J Med 1983; 74: 14–22.
13. Netter FH. Atlas of Human Anatomy, 5th ed. Philadelphia, PA: Elsevier, 2011.
14. Swidsinski A, Doerffel Y, Loening-Baucke V, et al. Gardnerella biofilm involves females and males and is transmitted sexually. Gynecol Obstet Invest 2010; 70: 256–263.
15. Piot P, Van Dyck E, Peeters M, et al. Biotypes of Gardnerella vaginalis. J Clin Microbiol 1984; 20: 677–679.
16. Holst E. Reservoir of four organisms associated with bacterial vaginosis suggests lack of sexual transmission. J Clin Microbiol 1990; 28: 2035–2039.
17. 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: 1307–1313.
18. Marrazzo JM, Thomas KK, Agnew K, et al. Prevalence and risks for bacterial vaginosis in women who have sex with women. Sex Transm Dis 2010; 37: 335–339.
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