Pathogenesis

The beta-hemolytic Gram-positive Streptococcus agalactiae, Group B Streptococcus (GBS) is encountered in 10 – 30 % of women. Gastrointestinal and rectal carriage is likely to provide a reservoir from which GBS can colonise the vagina. GBS adapt to a range of host environments including shifts from near neutral pH to acidic pH of the healthy vagina (3.6 – 4.5) and fluctuating levels of nutrient availability. Colonisation involves surface proteins that facilitate adherence to the vaginal extracellular matrix and metallopeptidases that aid tissue invasion. These events culminate in the loss of the protective acidic lactobacillus-dominant vaginal environment. This displacement if overlooked may lead to Aerobic vaginitis (AV), a dysbiosis distinct from bacterial vaginosis. Clinical signs and symptoms include vaginal inflammation, an itching or burning sensation, dyspareunia, yellowish discharge and an increase in vaginal pH > 4.5, and inflammation with leukocyte infiltration. Severe, persistent, or chronic forms of AV can also be referred to as desquamative inflammatory vaginitis (DIV).

The literature is dominated by the rare but devastating effects GBS can have in the obstetric environment but when it occurs outside this demographic, the evidence for its pathogenicity is thin. It first appeared on my clinical radar nestled in a complex case. It presented in a routine swab organised by a fertility clinic. It was dismissed as insignificant by the consulting specialist. In the ensuing months, it raged on until repeat swabs for a persistent discharge and excoriating symptoms revealed GBS again (along with a Candida parapsilosis – another story). So when GBS now appears on a patient swab or in their history, obstetric or not, it requires consideration.

Evidence & treatment considerations

So what is the evidence for GBS in the non-obstetric population? The oral probiotic containing L. rhamnosus GR-1 and L. reuteri RC-14 changed GBS colonisation from positive to negative in 42.9% of women in the probiotic group of a trial (compared to18% of women in the placebo group)… and that’s about it for anything resembling trial evidence.

There is documentation (via a letter to the editor) of eight different women over a four year period, who successfully resolved GBS symptoms by using half a freshly cut clove of garlic inserted vaginally overnight for 3–6 weeks followed by maintenance doses of once every 2–4 days. All cases were previously unresolved by course(s) of oral antibiotics. Apart from the fact, this cannot be considered quality evidence, there were no details as to how long the maintenance phase was or how long the patients themselves were monitored post-treatment and most importantly there was no confirmation of clearance with swabs, however the change in inflammatory symptoms (attributed to GBS) was a significant outcome.

An interesting case report from the obstetric population, discusses the administration of lactoferrin in a patient with recurring preterm delivery and resultant pregnancy loss. GBS and concurrent lactobacillus absence was consistently observed on swabs. A month after the commencement of lactoferrin (700mg/day) lactobacillus was detected and gradually became dominant. The patient achieved (and maintained a full term) pregnancy 3 months after commencement of the intervention.

In vitro studies have demonstrated that GBS forms biofilm-like structures that assist its colonisation in multiple sites. With current evidence for N-acetylcysteine’s mode of action, it becomes a worthy consideration for a GBS prescription.

In addition to a positive culture for GBS, of equal importance are the remaining details on the vaginal swab such as the presence/absence of lactobacillus and other markers such as the presence of gram positive bacilli, epithelial cells and leucocytes. Checking the pH with specialised low pH strips is also an important step in assessment and management.

In the absence of quality evidence, do not ignore a positive GBS culture. In some cases it may not be the cause of symptoms such as discharge but at the very least, it is likely to be a strong sign of dysbiosis.

References

1. Rosini, R., & Margarit, I. (2015). Biofilm formation by Streptococcus agalactiae: influence of environmental conditions and implicated virulence factors. Frontiers in cellular and infection microbiology, 5, 6

2. Yang, Q., Porter, A. J., Zhang, M., Harrington, D. J., Black, G. W., & Sutcliffe, I. C. (2012). The impact of pH and nutrient stress on the growth and survival of Streptococcus agalactiae. Antonie Van Leeuwenhoek, 102(2), 277-287

3. Patras, K. A., Rösler, B., Thoman, M. L., & Doran, K. S. (2015). Characterization of host immunity during persistent vaginal colonization by Group B Streptococcus. Mucosal immunology, 8(6), 1339

4. Leclair, C. M., Hart, A. E., Goetsch, M. F., Carpentier, H., & Jensen, J. T. (2010). Group B streptococcus: prevalence in a non-obstetric population. Journal of lower genital tract disease, 14(3), 162

5. Aerobic Vaginitis: Abnormal Vaginal Flora That Is Distinct From BacterialVaginosis.

6. Ho, M., Chang, Y. Y., Chang, W. C., Lin, H. C., Wang, M. H., Lin, W. C., & Chiu, T. H. (2016). Oral Lactobacillus rhamnosus GR-1 and Lactobacillus reuteri RC-14 to reduce group B Streptococcus colonization in pregnant women: a randomized controlled trial. Taiwanese Journal of Obstetrics and Gynecology, 55(4), 515-518

7. Cohain, J. S. (2009). Long-term symptomatic group B streptococcal vulvovaginitis: eight cases resolved with freshly cut garlic. European Journal of Obstetrics and Gynecology and Reproductive Biology, 146(1), 110-111

8. Otsuki, K., Tokunaka, M., Oba, T., Nakamura, M., Shirato, N., & Okai, T. (2014). Administration of oral and vaginal prebiotic lactoferrin for a woman with a refractory vaginitis recurring preterm delivery: appearance of lactobacillus in vaginal flora followed by term delivery. Journal of Obstetrics and Gynaecology Research, 40(2), 583-585

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