Research Article: The vaginal microbiome and sexually transmitted infections are interlinked: Consequences for treatment and prevention

Date Published: December 27, 2017

Publisher: Public Library of Science

Author(s): Janneke H. H. M. van de Wijgert

Abstract: In a Perspective for our Collection on STI research, Janneke van de Wijgert discusses the latest on how the vaginal microbiota predisposes women to acquisition of STIs and discusses future potential for clinical intervention.

Partial Text: While a cervicovaginal mucosa covered with lactobacilli is still considered the optimal environment, molecular studies have shown that not all lactobacilli are equal [1]. Lactobacillus crispatus only occasionally co-occurs with organisms other than lactobacilli, has been associated with an anti-inflammatory cervicovaginal immune profile, and seems to protect women from developing anaerobic dysbiosis and from the above-mentioned adverse outcomes [1–5]. In contrast, L. iners does not seem to protect women from developing anaerobic dysbiosis and often co-occurs with BV-associated anaerobes, pathobionts (streptococci, staphylococci, or Enterobacteriaceae), or pathogens [1–6]. A vaginal microbiome dominated by L. iners is, however, not associated with a proinflammatory profile, and data on whether it increases the risk of adverse outcomes are conflicting. Vaginal microbiomes with a high relative abundance of the other vaginal lactobacilli are much less prevalent and less well studied [1,7].

While first-line treatment of BV with oral or vaginal metronidazole or clindamycin is typically efficacious in the short term (as defined by Nugent or Amsel criteria), recurrence rates are high [10,11]. Clinical studies have shown that BV recurrence rates can be reduced by longer duration and/or prophylactic use of first-line antibiotics, by (estrogen-containing) hormonal contraception, and by circumcision of male sexual partners, but not by adding other antibiotics (azithromycin or moxifloxacin) to first-line antibiotics or by metronidazole/clindamycin treatment of male sexual partners [11]. Some argue that recurrence is particularly likely when a mucosal biofilm is present. In vitro and in vivo studies have shown that such a biofilm is damaged and suppressed by metronidazole but not completely eliminated [12]. The interrelationships between various urogenital conditions also pose challenges. For example, treatment of anaerobic dysbiosis often leads to VVC [13]. Treatments might be more efficacious in the longer term when they specifically target dysbiosis-associated anaerobes or pathobionts while sparing lactobacilli and are combined with biofilm disrupting agents, systemic or topical estrogen, and/or Lactobacillus-containing vaginal pro- or synbiotics. Estrogen-containing hormonal contraception, and Lactobacillus-containing vaginal pro- or synbiotics if found to be clinically effective, could also be implemented for routine use on a larger scale to prevent vaginal dysbiosis in women at risk.

Source:

http://doi.org/10.1371/journal.pmed.1002478

 

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