Bacterial vaginosis (BV) is known to be a polymicrobial infection, with a few key players, many of which are antibiotic-resistant. But this is only part of the reason why treatments so often fail. Without knowing precisely which microorganisms are causing your problem, it’s hard to know which antibiotic to choose, but these microbes build sticky biofilms that prevent penetration by the antibiotics.

Gardnerella vaginialis is the most often cited as the cause, or main contributor, to BV. G. vaginalis is found in about 95 per cent of women with BV, but it is also found in up to 50 per cent of women without BV. It is also found in the digestive systems of men and children. G. vaginalis is known to make biofilms, which means if it gets a foot in the door with special seed cells (it changes form, like many other microbes), it can team up with the other microbes the biofilm supports. They basically make an army of bacteria that make the whole vagina (and beyond in some cases) uninhabitable by friendly bacteria.

All we really know is that high levels of G.vaginalis in the vaignal tract is a good indicator of BV. But, it’s not all. We know the biofilm is resistant to antibiotics, and BV is often recurrent, requiring more new ideas to be put forward as to how to treat the biofilm, instead of just throwing antibiotics at these infections repeatedly. They are only making the problem worse by first, not addressing the true cause of recurrent BV which is the biofilm, but by depleting the body of any friendly microbes it may have had to fight with. It just leaves the biofilm unimpeded, to get stronger.

Culture should not necessarily be used for routine diagnosis of BV – examination of the microbes needs to be more thorough than that. Additionally, treatment of recurrent BV should always include some targeted treatment for the biofilm, typically enzymes or other elements known to break down the biofilm matrix. There are many potential ways to do this, but none are well-studied for BV.

Other bacteria implicated in BV include:

Less-commonly accused – but no less important – microbes include:

  • Fusobacterium spp.
  • Peptostreptococcus
  • Non-viridans group Streptococci

This is what the BV microbial landscape looks like

Normal, and then intermediate, the full-blown BV vaginal flora was studied, and at the intermediate stage, G. vaginalis and Bacteroides were present in moderate amounts. High concentrations of those microbes and M. hominis were not seen until BV had fully developed, indicating that the environment set up by G. vaginalis and Bacteroides was suitable for the new bacteria to colonise.

Gram stains have been used to define abnormal flora (using Nugent scores of 9 or 10). Polymerase chain reaction (PCR) testing (DNA/RNA testing) has detected Mobiluncus spp. in almost 85 per cent of women with BV and 38 per cent of those without BV.

One bacteria produces the food for the others, and vice versa

These unfriendly bacteria are anaerobes, and produce succinic acid rather than lactic acid. (Lactobacilli are acid-loving bacteria and produce lactic acid.)

G. vaginalis and Prevotella bivia have a symbiotic relationship whereby G. vaginalis produces amino acids that are then utilised by P. bivia. P. bivia then produces ammonia, which is then used by G. vaginalis.

Additionally, researchers found that P. bivia made amino acids that were also made available for Peptostreptococcus anaerobius1].

The BV-related bacteria also break down cervical and vaginal mucous in the vagina using enzymes – these are mucinases, sialidases, and neuraminidases. This is the likely reason why the discharge in BV changes. Immune system protections (immunoglobulin A IgA) and IgM) are cleaved (broken into like you would crack open an oyster shell) by certain factors in the vagina produced by the bacteria (known as virulence factors), reducing the capacity of the vagina to defend itself. (Secretory leukocyte protease inhibitor – SLPI – is also reduced.)

How lactobacilli fit in

Lactobacilli also produce substances that are toxic to other bacteria including some other lactobacilli. An acidic vagina is a great defence, along with the hydrogen peroxide produced, which also helps protect against sexually transmitted infections entering the vagina. A low pH inhibits BV-linked bacteria effectively, but higher pHs cause the positive effect to quickly wane. A substance is produced by BV microbes, myeloperoxidase, which breaks down hydrogen peroxide, further weakening the lactobacilli.

Menstrual blood and semen both change the pH and more alkaline, and possibly contribute to the change in flora and BV development. There is a large part of this we’re just not sure about, for example, if enough BV bacteria are deposited into the vagina from someone else’s vagina or penis, will BV develop? Or is it just enough to have a loss of lactobacilli?

Antibiotics do not trigger BV immediately, but may leave women vulnerable down the track if proper populations of lactobacilli aren’t immediately introduced.This is why prompt, effective treatment is required, and women with slight symptoms have their history investigated to see how long it could have been going on for to see what sort of biofilms could potentially be in place.

Bacteria and pH

Common lactobacilli strains in the vagina include Lactobacillus crispatus, followed by L. jensenii and Lactobacillus sp. strain 1086V. In vitro, the rate of acid production by Lactobacillus spp. was measured, keeping the vagina at a pH of between 3.2 and 4.8. BV bacteria like G. vaginalis, P. bivia, and Peptostreptococcus anaerobius reached asymptotic levels at a pH of between 4.7 and 6.0. This is the sort of pH you expect to see in BV.

Semen and pH and BV

Semen was tested – it was determined that 3ml of semen would be acidified at a rate of 0.56 to 0.75 pH units per hour – so would one incident of unprotected sex cause BV by changing the acidity for a short period of time? We don’t know, but having several sex sessions over a 24-hour period may weaken the vaginal flora’s defences enough, if it was already precarious.

Normal semen volume: 1.5 – 3.7ml per ejaculate
Normal semen pH range: 7.1 – 8.0
Acidification rate: 3ml of semen is acidified at a rate of 0.56 – 0.75 pH units per hour

References

Polymicrobial Diseases, Brogden KA, Guthmiller JM, editors. Washington (DC): ASM Press; 2002.

 

  1.  Pybus V., Onderdonk A. B. A commensal symbiosis between Prevotella bivia and Peptostreptococcus anaerobius involves amino acids: potential significance to the pathogenesis of bacterial vaginosis. FEMS Immunol. Med. Microbiol. 1998;22:317–327. [PubMed

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