What Causes Bacterial Vaginosis and Why It Keeps Coming Back

Bacterial vaginosis happens when the balance of bacteria inside the vagina shifts. Protective bacteria, primarily Lactobacillus species, decline in number while a mix of other bacteria overgrow and take their place. This isn’t a single infection caused by a single germ. It’s a disruption of an entire ecosystem, and it affects roughly 23% to 29% of women of reproductive age worldwide.

How the Vaginal Ecosystem Normally Works

A healthy vagina is dominated by Lactobacillus bacteria, which ferment sugars into lactic acid. This keeps the vaginal pH between 4.0 and 4.5, acidic enough to suppress the growth of harmful organisms. Lactobacillus species also produce hydrogen peroxide, which adds another layer of defense against invaders.

Not all Lactobacillus species offer the same protection, though. Lactobacillus crispatus is considered the gold standard. It produces two forms of lactic acid and generates hydrogen peroxide through an additional metabolic pathway that other species lack. Lactobacillus iners, by contrast, can only produce one form of lactic acid and cannot make hydrogen peroxide at all. Women whose vaginal bacteria are dominated by L. iners may have a less stable microbial environment and a higher susceptibility to BV.

What Happens When the Balance Shifts

When Lactobacillus populations drop, lactic acid production falls and vaginal pH rises above 4.5. That higher pH creates conditions where anaerobic bacteria (organisms that thrive in low-oxygen environments) can multiply rapidly. The result is a takeover by a diverse mix of species including Gardnerella, Prevotella, Mobiluncus, Atopobium, Mycoplasma, and others.

These bacteria produce their own fatty acids like acetate, butyrate, and succinate, which further alter the vaginal environment and make it even harder for Lactobacillus to reestablish itself. The hallmark signs of this shift are a thin, grayish-white discharge, a fishy odor, and a pH above 4.5.

The Role of Gardnerella Vaginalis

Gardnerella vaginalis is found in 95% to 100% of BV cases and plays a central role in triggering the condition. Unlike many of the other bacteria involved, Gardnerella can tolerate the acidic, oxygenated environment of a healthy vagina. It essentially serves as the first mover: it can survive where strict anaerobes cannot, and once it gains a foothold, it lowers the oxygen levels in the vaginal environment, paving the way for other harmful bacteria to flourish.

Gardnerella adheres to vaginal cells in large clusters and produces a toxin called vaginolysin that damages those cells directly. More importantly, it initiates the formation of a biofilm, a structured community of bacteria that coats the vaginal lining and encases itself in a protective matrix of carbohydrates, proteins, and genetic material.

Why Biofilms Make BV Persist and Recur

Biofilm formation is one of the most important reasons BV is so stubborn. Once bacteria organize into a biofilm, they become far more resistant to both the body’s natural defenses and to antibiotics. Biofilm bacteria tolerate lactic acid and hydrogen peroxide much better than free-floating bacteria do, which means even a partial recovery of Lactobacillus populations may not be enough to clear them.

Standard antibiotic treatments struggle against these biofilms. In laboratory studies, even the highest concentrations of the two most commonly prescribed antibiotics for BV could not fully eradicate established biofilms. A fraction of bacteria within the biofilm survived, which helps explain BV’s notoriously high recurrence rate: up to 69% of women experience a recurrence within 12 months of completing treatment.

Another bacterium called Atopobium vaginae plays a supporting role. It’s rarely found without Gardnerella and is typically embedded in the same biofilm structure. When both Atopobium and Gardnerella are found together in an adherent biofilm, the odds of having a high BV score are roughly 119 times greater than when neither is present. Atopobium also triggers a stronger inflammatory immune response from vaginal cells, which contributes to symptoms.

Risk Factors That Disrupt the Balance

Researchers still don’t fully understand what initiates the very first loss of Lactobacillus in any given case. But several factors consistently increase the risk.

Sexual activity is the strongest association. BV occurs most often in sexually active women, and having new or multiple partners raises risk significantly. The exact mechanism linking sex to BV isn’t well understood, but exposure to new bacteria from a partner, the alkaline pH of semen, and the physical disruption of the vaginal environment during intercourse are all plausible contributors. Using condoms reduces BV risk, which supports the idea that something transferred during unprotected sex plays a role.

Douching is another well-established risk factor. Vaginal washing products disrupt Lactobacillus colonization regardless of their chemical composition. Products at both ends of the pH spectrum (such as baking soda and vinegar solutions) have been shown to harm either vaginal cells or beneficial Lactobacillus, sometimes both. The vagina is self-cleaning, and introducing any external washing product into it works against the bacterial ecosystem that keeps it healthy.

BV Is Not a Simple Infection

One of the most common misconceptions about BV is that it works like a typical infection, where one germ invades and causes disease. BV is better understood as an ecological collapse. The protective community of bacteria fails, a diverse group of opportunistic organisms fills the void, and those organisms reorganize the environment to favor their own survival through biofilm formation and pH manipulation. This is why BV doesn’t respond to treatment the way a straightforward bacterial infection would, and why it comes back so frequently.

The triggers that start this cascade, whether it’s a new sexual partner, douching, or simply having a vaginal microbiome dominated by less-protective Lactobacillus species, all converge on the same outcome: Lactobacillus loses its dominance, acidity drops, and anaerobic bacteria seize the opportunity to establish themselves in a form that’s extremely difficult to reverse.