Bacterial vaginosis (BV) happens when the balance of bacteria inside the vagina shifts. Normally, beneficial bacteria called lactobacilli dominate the vaginal environment and keep it slightly acidic, with a pH between 3.8 and 4.5. In BV, those protective bacteria drop dramatically in number, and a mix of other bacteria that were previously a small minority overgrow and take their place. This isn’t an infection you “catch” from a single germ. It’s a disruption of an entire ecosystem.
How the Vaginal Ecosystem Normally Protects Itself
A healthy vagina is dominated by lactobacilli, with one species in particular, Lactobacillus crispatus, considered the strongest marker of vaginal health. These bacteria maintain their territory through several overlapping defenses. They produce lactic acid, which keeps the vaginal pH acidic enough to suppress harmful organisms. They release hydrogen peroxide, a natural antimicrobial that kills off competing bacteria. They also produce compounds called bacteriocins, which function like targeted antibiotics against unwanted microbes. On top of all that, they produce an enzyme that starves certain harmful bacteria of an amino acid they need to grow.
When hydrogen peroxide and lactic acid work together, they’re especially effective at killing off both urogenital and intestinal pathogens. The lactobacilli also help regulate the local immune response, keeping inflammation low. Women whose vaginal microbiome is dominated by L. crispatus tend to have the most stable, resilient bacterial communities. Another common species, Lactobacillus iners, is less protective and more prone to giving way to the kind of imbalance that leads to BV.
What Changes When BV Develops
In BV, lactobacilli numbers plummet and are replaced by a diverse mix of anaerobic bacteria, organisms that thrive in low-oxygen environments. The key players include Gardnerella vaginalis, Atopobium vaginae, Prevotella, Mobiluncus, Mycoplasma hominis, and several others that are difficult to grow in a lab and were only recently identified through DNA sequencing.
Gardnerella species play a particularly important role in getting the process started. They attach to the cells lining the vaginal wall and form a biofilm, a sticky, structured layer of bacteria that’s difficult for the immune system (or antibiotics) to penetrate. As this biofilm matures, Gardnerella facilitates the incorporation of other BV-associated bacteria into higher layers of the structure, essentially building a scaffold that supports an entire community of harmful organisms.
Once lactobacilli are displaced, the chemical environment of the vagina changes. Without lactic acid production, the pH rises above 4.5, sometimes significantly. This more alkaline environment favors the anaerobic bacteria and makes it even harder for lactobacilli to reestablish themselves. The result is a self-reinforcing cycle: the loss of protective bacteria creates conditions that favor the overgrowth, and the overgrowth further suppresses the protective bacteria.
Risk Factors That Trigger the Shift
No single cause of BV has been identified. Instead, several factors increase the likelihood that the vaginal microbiome will tip out of balance.
Douching is one of the most well-documented triggers. It directly disrupts the hydrogen peroxide and lactobacilli-based defense system. Women who douche at least once a month have a 1.4 times higher risk of developing BV or an intermediate disruption of vaginal flora. For women who had douched within the past week, the risk jumps to 2.1 times higher. Douching essentially washes away the protective bacteria and the acidic environment they create, giving anaerobes an opening.
Having multiple sexual partners also increases risk, and BV occurs most often in sexually active people. That said, BV is not classified as a sexually transmitted infection. It can develop in people who have never had sex. Among female sexual partners, BV can be transmitted between them, but treating male sexual partners has not been shown to reduce a woman’s risk of BV or its recurrence.
Other factors associated with increased risk include a new sexual partner, lack of condom use, and use of an intrauterine device (IUD). Anything that disrupts the vaginal pH or reduces lactobacilli populations can potentially set the stage.
Symptoms and How BV Is Identified
Many people with BV have no symptoms at all. When symptoms do appear, the most common is a thin, grayish-white discharge with a milklike consistency that coats the vaginal walls. A fishy odor is characteristic, often more noticeable after sex. There’s typically no itching or significant irritation, which helps distinguish BV from yeast infections.
Clinicians diagnose BV using a set of criteria that look for at least three of four signs: the characteristic thin discharge, a vaginal pH above 4.5, a fishy smell when a chemical solution is applied to a sample of the discharge, and the presence of “clue cells” under a microscope (vaginal cells coated in a layer of adherent bacteria). A lab-based scoring system can also confirm the diagnosis by evaluating the ratio of lactobacilli to BV-associated bacteria in a stained sample of vaginal fluid.
Why BV Keeps Coming Back
One of the most frustrating aspects of BV is its recurrence rate. Standard antibiotic treatment clears the infection initially, but the numbers tell a sobering story. In a study tracking women after oral antibiotic therapy, 23% had a recurrence within one month. By three months, that figure rose to 43%. By 12 months, 58% of women had experienced at least one recurrence.
The biofilm that Gardnerella and its associated bacteria form on the vaginal wall is a major reason antibiotics often provide only temporary relief. The biofilm structure shields bacteria from full antibiotic exposure, so while the symptoms resolve, the underlying bacterial community isn’t fully eradicated. Once the antibiotic course ends, the surviving organisms can repopulate.
Recurrence is also tied to the difficulty of reestablishing a lactobacilli-dominant environment. If L. crispatus or other protective species don’t return in sufficient numbers after treatment, the vaginal pH stays elevated and conditions remain favorable for another round of anaerobic overgrowth. Women whose baseline microbiome leans toward L. iners rather than L. crispatus are especially vulnerable to this cycle.
BV and Sexual Partners
The relationship between BV and sexual activity is complicated and still not fully understood. BV occurs far more often in sexually active people, and having a new partner is a consistent risk factor. Yet it doesn’t behave like a classic STI. It can develop without any sexual contact, and treating male partners doesn’t prevent recurrence.
The picture is different for women who have sex with women. BV can be shared between female partners, likely because vaginal bacteria are exchanged directly during sexual contact. Female couples often develop concordant vaginal microbiomes, meaning they tend to share the same bacterial communities, including BV-associated ones. This is one area where partner treatment may actually matter, though guidelines are still evolving on exactly how to approach it.