Pregnancy and oestrogen promotion 
of vaginal Lactobacilli

Composition of the vaginal microbiota can be dynamic and capable of rapid shifts within a short period of time (e.g. < 24 hours), although more stable in many women during different physiologic states such as pregnancy. Vaginal microbial communities of pregnant women are more stable and have higher relative abundance of lactobacilli than non-pregnant women.^1,2 The most common lactobacillus species of the vaginal microbiota observed in healthy pregnant women in the late first trimester were L. crispatus and L. gasseri (>50%), followed by L. jensenii (~20%) and L. rhamnosus (~10%), as well as combinations thereof (~10%).³

Oestrogen is thought to play an important role in promoting a lactobacilli-dominated vaginal microbiota by stimulating accumulation of glycogen in the vaginal epithelial mucosa, which is thought to contribute to the increased lactobacilli predominance and stability of the vaginal microbiota observed in healthy pregnant women.^4,5 Nutrient-containing vaginal secretions and glycogen-containing (as a source of glucose) vaginal epithelial cells that are sloughed and subsequently lyse are thought to be primary nutrient sources for the vaginal microbiota. 

Oestrogen increases the volume of vaginal secretions and induces thickening of the vaginal epithelium along with glycogen accumulation, thought to support growth of glucose-fermenting lactobacilli.⁶ Changes in relative abundance of vaginal lactobacilli are associated with both oestrogen levels and glycogen content across the various life-stages of women (e.g. pre-pubertal, pubertal/reproductive age, postmenopausal).⁷ Additionally, use of oral hormonal contraceptives (i.e. oestrogen) and a decreased prevalence of Bacterial Vaginosis (BV) has been consistently observed in epidemiological studies.

The mother is the main source of microbes, both non-pathogenic and pathogenic, for newborn colonisation. Dysbiotic vaginal microbiota characteristic of BV with marked reductions of lactobacilli increases risk of obstetric complications such as placental insufficiency, premature birth, fetal growth restriction, and postpartum endometritis, which is particularly relevant for women with immunosuppression and herpes simplex virus (HSV).^8-11 The selected probiotic strains were evaluated for efficacy in the complex therapeutic and preventative intervention for pregnant women with HSV.¹² Sixty pregnant women with HSV either received a patented food supplement to restore and support the vaginal microbiota twice daily for one week containing the selected probiotic strains and the prebiotic carbohydrate, fructooligosaccharides (intervention group; n = 30), or only prenatal care (comparator group; n = 30).

Fifty healthy pregnant women without HSV were included as a control group. Intestinal lactobacilli and bifidobacteria were significantly increased in conjunction with significant decreases in pathogenic microbes (haemolytic E. coli, Klebsiella pneumoniae, Staphylococcus aureus, candida yeast species) in the intervention group vs. the comparison group, post-intervention levels which were similar to levels in healthy pregnant women of the control group. Prior to the intervention, 40% of women with HSV complained of symptoms associated with dysbiosis of the intestinal microbiota, namely bloating/abdominal discomfort, constipation, and mucus in the feces, but these complaints were reduced to only 12% of participants in the intervention group.

At the start of the study, vaginal lactobacilli were only detected in 13.3% and 16.7% of participants in the intervention and comparison groups, respectively, which was significantly increased in the intervention group to 46.7% after the one-week intervention, but not significantly different in the comparison group (20%). The percentage of women in the intervention group with a vaginal pH > 4.5, complaining of profuse vaginal discharge, swelling (hyperaemia), and itching (pruritus), and with a positive amine test of vaginal discharge, were significantly decreased in the intervention group and no longer different than healthy pregnant women of the control group, whereas these parameters did not change in the comparison group. The incidence of placental insufficiency and fetal distress were significantly reduced about two-fold in women of the intervention vs. comparison group.

The percentage of aggravated pregnancy was significantly lower in women of the intervention group (33.3%) vs. the comparison group (53.3%). Furthermore, the percentage of women with other pregnancy complications (i.e., threatened miscarriage, threat of premature birth, pre-eclampsia, and pathology of amniotic fluid) was 25-50% fewer in the intervention vs. comparison group, which may be clinically relevant, but was not statistically significantly different in this study. This result was likely due to the small study population and variability and worth investigating in future, larger clinical trials.

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