The female vagina has its own unique microbiome, a collection of microbes very different if compared to the gastrointestinal (GI) microbiome. The vaginal microbiome is a thousand-fold less dense in microbial populations, though still harboring tens to hundreds of billions of microbes per milliliter. While the GI microbiome is composed of >1000 species, the vaginal microbiome harbors a few hundred species, at most. The vaginal microbiome is therefore less complicated, more predictable.
The healthy vaginal microbiome is dominated by Lactobacillus species, especially the unique species, L. crispatus, and contains low numbers of species such as Gardnerella vaginalis and Atopobium. A L. crispatus-dominated vaginal microbiome provides partial protection against vaginal pathogens such as E. coli and other fecal microbes, Candida, HIV, herpes, human papillomavirus, and gonorrhea.
A disrupted vaginal microbiome, “vaginosis,” in which Lactobacilli, especially L. crispatus, are reduced in numbers and Gardnerella, Atopobium, and fecal microbes become dominant, is exceptionally common. Though definitions for vaginosis vary, the most severe form afflicts an astounding 25-30% of the world’s female population—1 in 3 females. Vaginosis increases susceptibility to all the pathogens listed above, fungal, bacterial, and viral. In women of childbearing age, vaginosis also inflames the cervix, causing it to relax, a phenomenon that can lead to premature delivery of a baby, a potentially catastrophic event with increased risk for lifelong complications (impaired neurological maturation, learning disabilities, increased susceptibility to infections due to an impaired immune system, behavioral difficulties, among others).
But it is also becoming clear that the vaginal microbiome can serve as a reservoir for colonization of the urinary tract, i.e., (in ascending order) urethra, bladder, ureters, and kidneys. This poses potentially important implications for urinary health, incontinence, and urinary tract infections (UTIs). While it is not entirely clear how the vaginal microbiome communicates with the urinary microbiome (simple contiguity or is there an additional pathway?), it is clear that vaginosis sets a woman up for urinary dysbiosis that increases susceptibility to urinary tract infections.
While a course of antibiotics such as trimethoprim-sulfamethoxazole eradicates a cause of UTI, it also massively disrupts the vaginal and urinary microbiome of healthy microbes that are no longer able to fend off pathogens. You can therefore appreciate that an antibiotic prescribed for a urinary tract infection leads to vaginosis that, in turn, alters the urinary microbiome, making a woman more susceptible to recurrent UTIs. In conventional circles, it means prescribing course after course of antibiotics that makes the situation worse.
A better solution: address the vaginal microbiome that, in turn, recolonizes the urinary microbiome. Start with our standard efforts to recolonize the GI microbiome: fermented foods such as kimchi, sauerkraut, fermented veggies; selected microbes we ferment in very high counts as yogurt such as L. reuteri and Bacillus coagulans; plentiful prebiotic fibers and related compounds from vegetable matter; vitamin D that has impressive ability to reverse vaginosis. Consider a probiotic containing L. crispatus or, even better, make yogurt with this species to obtain high bacterial counts.