Bacterial vaginosis (BV) develops when the balance of bacteria inside the vagina shifts. Normally, beneficial bacteria called lactobacilli dominate the vaginal environment, keeping it slightly acidic and inhospitable to harmful microbes. When those protective bacteria decline and are replaced by an overgrowth of other organisms, the result is BV. It affects roughly 29% of women of reproductive age in the United States, making it the most common vaginal infection in that group.
What Happens Inside the Vagina
A healthy vagina is home to large numbers of lactobacilli. These bacteria do three important things: they produce lactic acid that keeps vaginal pH below 4.5, they release antimicrobial compounds that punch holes in the membranes of harmful microbes, and they physically occupy binding sites on the vaginal wall so other bacteria can’t latch on. That last point matters because attachment to the vaginal lining is the first step any pathogen needs to establish an infection.
When lactobacilli numbers drop, the vaginal pH rises above 4.5, and the environment becomes friendlier to a range of organisms that normally exist only in small numbers. The most significant of these is Gardnerella vaginalis, which multiplies rapidly in the less acidic environment. As Gardnerella grows, other bacteria begin clinging to it and multiplying alongside it. The result is a sharp shift from a lactobacillus-dominated community to one crowded with diverse anaerobic bacteria, organisms that thrive in low-oxygen conditions.
The Biofilm Problem
One of the most important discoveries about BV is that Gardnerella doesn’t just float freely in vaginal fluid. It forms a biofilm: a structured colony of bacteria that anchors to the vaginal lining and encases itself in a self-made protective shell of carbohydrates, proteins, and genetic material. This biofilm shelters Gardnerella and other BV-associated bacteria from the body’s natural defenses. Unlike free-floating bacteria, the biofilm is resistant to both lactic acid and hydrogen peroxide, the very substances a healthy vagina uses to keep harmful organisms in check.
The biofilm also helps explain why BV is notoriously difficult to get rid of for good. Standard antibiotics struggle to penetrate the deeper layers of the biofilm, and bacteria buried inside it have slower metabolisms, which makes them less vulnerable to drugs designed to kill actively growing cells. Even when antibiotics clear the symptoms, remnants of the biofilm can survive on the vaginal wall and eventually regrow, reigniting the infection. Some bacteria within the biofilm also develop outright antibiotic resistance over time. Research published in Frontiers in Microbiology found that bacteria embedded in biofilms required at least double the antibiotic concentration to be affected compared to free-floating bacteria, and even very high concentrations could not fully eradicate established biofilms.
What Triggers the Shift
No single cause explains every case of BV. The CDC states plainly that researchers still don’t know exactly what initiates the bacterial shift. What is known is a set of factors that reliably increase the risk.
Sexual activity is the strongest association. BV rarely occurs in people who have never had sex. Having new or multiple sexual partners increases risk, and BV can spread between female sexual partners. Yet researchers still can’t explain the precise mechanism by which sex disrupts the vaginal microbiome, and treating a male partner has not been shown to reduce recurrence. This means BV is not classified as a sexually transmitted infection, even though sexual activity clearly plays a role.
Douching is one of the most well-documented triggers. Washing the inside of the vagina with water, vinegar, or antiseptic solutions directly kills lactobacilli and raises vaginal pH, creating exactly the conditions that allow harmful bacteria to multiply. Some antiseptic douching products contain antimicrobial agents that are specifically toxic to lactobacilli. Ironically, many people begin douching to treat the odor or discharge caused by BV, which only worsens the underlying imbalance.
Not using condoms is another risk factor identified by the CDC. Exposure to semen, which has a pH around 7 to 8, temporarily raises vaginal pH after unprotected intercourse. Repeated exposure without barrier protection may create a more sustained shift in the vaginal environment.
How BV Affects Local Immunity
BV doesn’t just change which bacteria live in the vagina. It also reshapes the local immune environment in ways that can have broader health consequences. Research comparing vaginal tissue from people with and without BV found significantly higher levels of inflammatory immune cells and at least 23 elevated inflammatory signaling molecules in those with BV. At the same time, certain protective immune signals were reduced.
This altered immune landscape is one reason BV increases vulnerability to other infections. Immune cells in the cervix of people with BV showed higher levels of the receptor that HIV uses to enter cells (roughly 75% of certain immune cells carried this receptor in BV-positive individuals versus 59% in BV-negative individuals). The chronic, low-grade inflammation created by BV essentially keeps the vaginal immune system in a state of heightened but misdirected activity, making it easier for other pathogens to gain a foothold.
Why BV Keeps Coming Back
Recurrence is the defining frustration of BV. After successful antibiotic treatment, the infection returns in a large proportion of cases. Three factors drive this pattern. First, the biofilm on the vaginal wall is extremely hard to fully eliminate with standard antibiotics. Even when symptoms resolve, surviving bacteria within the biofilm can repopulate the vagina. Second, some of the non-Gardnerella species sheltered inside the biofilm are naturally resistant to the antibiotics used for treatment, and they can shield more vulnerable species from drug exposure. Third, reinfection from a sexual partner or re-exposure to the same environmental triggers (like douching) can restart the cycle from scratch.
The biofilm is central to all three of these mechanisms. It acts as a reservoir, a shield, and a platform for regrowth. Until the biofilm itself is disrupted, the conditions that caused BV in the first place remain embedded in the vaginal lining.
How BV Is Identified
Diagnosis typically relies on a set of bedside findings. A healthcare provider looks for at least three of four signs: a thin, uniform, grayish-white discharge; vaginal pH above 4.5; a fishy odor when a chemical solution is added to a sample of the discharge; and the presence of “clue cells” under a microscope (these are vaginal lining cells so heavily coated in bacteria that their edges appear blurred). A lab-based method scores a stained vaginal smear on a scale of 0 to 10 based on the relative numbers of lactobacilli versus Gardnerella and other organisms. A score of 7 or higher confirms BV, while 0 to 3 is negative.
Many people with BV have no symptoms at all. When symptoms do appear, the most common are a noticeable fishy smell (often stronger after sex) and a thin, off-white or grayish discharge. BV does not typically cause itching, burning, or significant irritation, which can help distinguish it from yeast infections.