Vaginal bacteria responsible for recurrent urinary tract infections

Photo - Urinary tract infection-Optimized
The vaginal bacteria Gardnerella vaginalis damages cells on the surface of the bladder, causing dormant E. coli to emerge from those cells and start multiplying again. In the image above, a bladder cell (blue) that has been exposed to G. vaginalis is dying and detaching from its neighbouring cells (teal), revealing immature cells below (purple). – Photo: Matthew Joens, James Fitzpatrick and Nicole Gilbert

For  the first time, researchers have found that recurrent urinary tract infections are not caused by repeated infections by E. coli but due to the bladder being exposed transiently to a vaginal bacterium —Gardnerella vaginalis. The vaginal bacteria, which get into the bladder from the vagina, do not cause infection directly but trigger E. coli, which is in a dormant state after a previous infection, to cause a reinfection. When exposed to vaginal bacteria, a few cells of the bladder lining get killed and removed causing dormant E. coli to emerge from those cells and start multiplying again to cause a recurrent infection.

The results were published on March 30 in the journal PLOS Pathogens.

This is the reason why nearly 25% of women who experience acute urinary tract infection experience a recurrence within six months; about 1% worldwide experience as many as six recurrent infections in a year. The same strain of E. coli is responsible for causing nearly 50% of recurrent infections in women.

Several studies have shown that the bladder is regularly exposed to vaginal bacteria; this is likely to occur during sexual activity in many women. So a team led by Amanda L. Lewis from the Washington University School of Medicine, St. Louis hypothesised that certain vaginal bacteria were triggering the emergence of E. coli from the bladder reservoirs to cause a recurrent infection.

To test this, the researchers infected the urinary tract of mice with E. coli. Vaginal bacteria — G. vaginalis and Lactobacillus crispatus —  were introduced into the urinary tract of mice that did not shed E. coli in urine after four weeks of infection. Mice were exposed to the vaginal bacteria twice, one week apart.

Though the G. vaginalis bacteria did not permanently colonise the urinary tract, even its transient presence was sufficient to trigger E. coli to reappear in the urine. The amount of E. coli present in the urine was more after a second exposure to the vaginal bacteria, linking frequent sexual activity to “increased risk” of urinary tract infection. In contrast, exposure to L. crispatus did not lead to E. coli emergence.

Further evidence of the emergence of E. coli on exposure to G. vaginalis vaginal bacteria came from the reduced E. coli titters in the mice bladder tissue compared with mice exposed to L. crispatus or saline water. Mice exposed to G. vaginalis also had higher levels of E. coli bacteria in urine.

Also, the severity and/or duration of the first E. coli infection is a key determinant of recurrent infection when exposed to vaginal bacteria again. Researchers also observed G. vaginalis-exposed bladders showing patches of cells killed and removed from the lining.

These results indicate the first plausible trigger of recurrent urinary tract infections from dormant E. coli in the bladder. They also explain the previously found links between vaginal bacteria species, sexual activity, and risk of recurrent infections in women.

“Our findings suggest that targeting specific members [G. vaginalis] of the vaginal community may be an effective strategy for treating recurrent urinary tract infections,” they write.

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