How lactobacilli fight E. faecalis

Author: Jessica Lloyd
Senior Naturopath | BHSc(N) | ISSVD, ISSWSH, BSSM, ATMS

Last reviewed: April 9, 2026

If you have had a vaginal microbiome test come back showing Enterococcus faecalis, you might be wondering what it is, why it is there, and what you can do about it.

Importantly, can one of our best weapons, probiotics, actually fight Enterococcus faecalis vaginal infections?

E. faecalis is a bacterium normally found in the gut, but when it sets up shop in the vagina, it can cause aerobic vaginitis (AV) and contribute to persistent, difficult-to-treat infections. One of E. faecalis‘ most annoying tricks is forming biofilms – sticky, protective structures that shield it from your immune system and from antimicrobial treatments.

The good news? A growing body of research shows that probiotic lactobacilli – particularly Lactobacillus crispatus – can actively fight E. faecalis and disrupt its biofilms. Here is what we know so far.

What is Enterococcus faecalis and why does it matter?

Enterococcus faecalis is a bacteria that belongs in your intestines, not your vagina. When it turns up in vaginal microbiome tests, it is typically associated with aerobic vaginitis – a distinct inflammatory condition that differs from bacterial vaginosis (BV).

Unlike the strictly anaerobic bacteria associated with BV, E. faecalis is what’s known as a facultative anaerobe – it can survive with or without oxygen, but it particularly thrives in aerobic (oxygen-rich) conditions. In the vagina, it can cause significant inflammation, discharge, and discomfort.

What makes E. faecalis particularly stubborn is its ability to form biofilms. These are structured communities of bacteria encased in a self-produced matrix of sugars and proteins. Once a biofilm is established, the bacteria inside become dramatically more resistant to both antibiotics and your immune defences. This is a major reason why E. faecalis infections can keep coming back even after antibiotic treatment.

How does Lactobacillus crispatus fight E. faecalis?

L. crispatus is considered the gold standard of protective vaginal bacteria. It dominates what researchers call community state type I (CST-I), a classification system for vaginal microbiome profiles. CST-I is the type most strongly associated with vaginal health. And when it comes to E. faecalis, L. crispatus does not just sit there looking pretty. It actively kills it.

Touch-free killing powers

A 2025 genome-wide analysis published in the Journal of Bacteriology demonstrated that L. crispatus eradicates E. faecalis in a contact-independent manner. That means it secretes substances that kill E. faecalis without needing physical contact – the chemical weapons work at a distance.

The study looked at which E. faecalis genes help it survive against L. crispatus. They found that certain mutants with disruption in the dltABCD operon – which controls how E. faecalis modifies the electrical charge on its surface – were significantly more susceptible to being killed.

In other words, E. faecalis needs to actively defend itself against the assault from L. crispatus, and when those defences are compromised, it does not survive.

Multiple strains are effective

A separate study in Microbiology Spectrum found that the majority of L. crispatus strains tested – from both human and poultry ecological niches – inhibited E. faecalis. There was some strain-to-strain variation in how potent the killing was, but the overall picture is clear: most L. crispatus strains have this antimicrobial capacity built in.

The weapons include secreted proteins

The same study’s proteomic analysis suggests that the killing activity is mediated at least in part by proteins that form a crystalline outer coat on L. crispatus cells (S-layer secreted proteins). The antimicrobial effect is also pH-dependent, which makes sense given that L. crispatus produces large amounts of lactic acid that acidify the vaginal environment.

Other lactobacilli that fight E. faecalis biofilms

While L. crispatus has the strongest direct evidence for killing E. faecalis, other probiotic lactobacilli bring complementary anti-biofilm mechanisms to the table.

Lipoteichoic acid, the biofilm buster

One of the most clearly defined anti-biofilm mechanisms involves lipoteichoic acid (LTA) – a component of the lactobacillus cell wall. A study published in the Journal of Microbiology showed that purified LTA from Lactobacillus plantarum inhibited E. faecalis biofilm formation in a dose-dependent manner, targeting the early stages of biofilm development without actually killing the bacteria outright.

Even more impressively, LTA could also disrupt preformed biofilms – meaning it can break apart the sticky structures once they have already been established.

LTAs from Lactobacillus acidophilus, Lactobacillus casei, and Lactobacillus rhamnosus showed similar biofilm-inhibiting effects. Among these, LTA from Lacticaseibacillus rhamnosus GG was the most effective.

Probiotic supernatants outperform conventional treatments

Cell-free supernatants – essentially the liquid that remains after probiotic bacteria are filtered out, containing all their secreted metabolites – have shown impressive activity against E. faecalis. A study in BMC Oral Health compared supernatants from L. plantarum, L. rhamnosus, and L. acidophilus against calcium hydroxide (a standard antimicrobial used in dentistry). All three probiotic supernatants were more effective than calcium hydroxide at killing E. faecalis.

A separate study found that while sodium hypochlorite (a standard clinical irrigant) failed to fully eradicate E. faecalis biofilm cells, conditioned media from L. plantarum and L. casei fully prevented the regrowth of treated biofilms. The probiotic metabolites succeeded where the conventional approach fell short.

Switching off virulence genes

Perhaps the most interesting recent finding involves postbiotics (the metabolic byproducts of probiotics) and their effect on E. faecalis gene expression. A study examining cell-free supernatants from L. plantarum found they significantly downregulated three key virulence genes in E. faecalis:

efaA – the endocarditis antigen gene, involved in adhesion to host cells
asa – the aggregation substance gene, which helps bacteria clump together
ace – the collagen adhesin gene, which helps bacteria stick to tissue surfaces

By dialling down these genes, probiotic metabolites interfere with the fundamental machinery E. faecalis uses to attach, aggregate, and form biofilms. This is not just physical disruption – it is genetic sabotage.

How lactobacilli fight E. faecalis: a multi-pronged attack

What makes lactobacilli so effective against E. faecalis is that they do not rely on a single mechanism. The research shows multiple complementary strategies working together:

Lactic acid production that drops the pH below the range E. faecalis prefers
Secreted antimicrobial proteins (including S-layer proteins from L. crispatus) that kill E. faecalis at a distance
Lipoteichoic acid that specifically disrupts biofilm formation and breaks apart existing biofilms
Biosurfactants that compete for attachment sites on vaginal tissue
Postbiotic metabolites that switch off virulence and biofilm genes
Hydrogen peroxide production that creates an inhospitable environment

This multi-pronged approach is exactly why probiotics can succeed where single-target antibiotics sometimes fail. Antibiotics typically attack one bacterial process; lactobacilli attack several simultaneously, making it much harder for E. faecalis to develop resistance.

What this means for AV

If your vaginal microbiome test shows E. faecalis, the research supports a treatment approach that combines targeted antimicrobials with vaginal probiotics to restore protective vaginal bacteria. The evidence is particularly strong for L. crispatus-based strategies, given its demonstrated ability to directly kill E. faecalis through multiple mechanisms.

Biofilm disruption is also a key consideration. Because E. faecalis biofilms protect the bacteria from treatment, breaking down that biofilm layer first or alongside antimicrobial treatment (which AV Rescue does) may improve outcomes. The research on lipoteichoic acid and probiotic supernatants suggests that the metabolites produced by lactobacilli can help with this process.

A combination of approaches – tackling the bacteria directly, disrupting its biofilms, and simultaneously introducing protective lactobacilli – gives you the best shot at clearing E. faecalis and preventing it from coming back. This is precisely My Vagina’s method, using non-drug strategies.

Frequently asked questions

Can probiotics alone clear an E. faecalis vaginal infection?

While the research shows lactobacilli can kill E. faecalis and disrupt its biofilms, probiotics typically work best as part of a combined approach.

Think of them as one arm of your treatment strategy – they help create an environment that is hostile to E. faecalis and support long-term vaginal health, but a significant active infection usually benefits from antimicrobial and systemic support as well. In our experience, most AV is driven by an underlying factor rather than just a localised infection.

Which probiotic species is most effective against E. faecalis?

L. crispatus has the strongest direct evidence for killing E. faecalis, with studies showing contact-independent eradication across most strains tested. L. rhamnosus GG appears most effective for biofilm disruption via lipoteichoic acid, and L. plantarum has the best evidence for downregulating E. faecalis virulence genes.

A multi-strain approach covers the most bases.

How long does it take for probiotics to affect E. faecalis?

The in vitro studies show effects within hours to days, but restoring a healthy vaginal microbiome is a longer process. Consistent probiotic use, combined with appropriate treatment, typically takes several weeks to months to establish a stable, protective lactobacillus-dominant environment.

Do oral or vaginal probiotics work better for this?

Both routes have value. Vaginal probiotics deliver lactobacilli directly to the site where you need them. Oral probiotics support the gut-vaginal axis – research shows that oral L. crispatus can influence vaginal microbial composition. A combination of both is a reasonable approach.

What about biofilm disruptors – should I use those too?

Given that E. faecalis biofilms are a major reason for treatment failure, combining antimicrobial treatment with biofilm-disrupting agents is a sound strategy. Enzyme-based biofilm disruptors and the EDTA in AV Rescue can help break down the protective matrix, allowing both your immune system and any antimicrobial agents to reach the bacteria more effectively.

What to do next

If your vaginal microbiome test shows E. faecalis, you have several options:

Get a comprehensive vaginal microbiome test if you have not already – you need to know exactly what is going on. See how to get a thorough vaginal microbiome test, or order a Juno comprehensive vaginal microbiome test.
For AV with E. faecalis, use a targeted vaginal antimicrobial like AV Rescue paired with the Oral AV Formula.
Support your protective bacteria with a vaginal probiotic like V-Spot vaginal probiotic and an oral probiotic such as Life-Space Women’s Probiotic.
Address biofilms with a biofilm-disrupting enzyme blend like InterFase Plus or NAC.
If your symptoms have been going on for more than a few months or your presentation is complex, book an appointment with one of our practitioners for personalised guidance.

References

Yang S., Meng X., Zhen Y., Baima Q., Wang Y., Jiang X., Xu Z. (2024). Strategies and mechanisms targeting Enterococcus faecalis biofilms associated with endodontic infections: a comprehensive review. Frontiers in Cellular and Infection Microbiology, 14. doi:10.3389/fcimb.2024.1433313
Lam L.N., Savage K., Shakir C., Lemos J. (2025). Genome-wide analysis of Enterococcus faecalis genes that facilitate interspecies competition with Lactobacillus crispatus. Journal of Bacteriology, 207(3). doi:10.1128/jb.00438-24
Argentini C., Fontana F., Alessandri G., Lugli G., Mancabelli L., Ossiprandi M., van Sinderen D., Ventura M., Milani C., Turroni F. (2022). Evaluation of modulatory activities of Lactobacillus crispatus strains in the context of the vaginal microbiota. Microbiology Spectrum, 10(2). doi:10.1128/spectrum.02733-21
Jung S., Park O.J., Kim A.R., Ahn K.B., Lee D., Kum K.Y., Yun C.H., Han S.H. (2019). Lipoteichoic acids of lactobacilli inhibit Enterococcus faecalis biofilm formation and disrupt the preformed biofilm. Journal of Microbiology, 57, 310–315. doi:10.1007/s12275-019-8538-4
Yoon J.Y., Park S., Lee D., Park O.J., Lee W., Han S.H. (2024). Lipoteichoic acid from Lacticaseibacillus rhamnosus GG as a novel intracanal medicament targeting Enterococcus faecalis biofilm formation. Journal of Microbiology, 62, 897–905. doi:10.1007/s12275-024-00165-6
Shaaban S., Hamad G.M., Genena S., Meheissen M.A., Moussa S. (2022). Evaluation of the antibacterial activity of Lactobacilli probiotics supernatants against Enterococcus faecalis (in-vitro study). BMC Oral Health, 22, 407. doi:10.1186/s12903-022-02434-5
Safadi S., Maan H., Kolodkin-Gal I., Tsesis I., Rosen E. (2022). The products of probiotic bacteria effectively treat persistent Enterococcus faecalis biofilms. Pharmaceutics, 14(4), 751. doi:10.3390/pharmaceutics14040751
Saedi S., Nezhadi J., Abedi Soleimani R., Asghari Ozma M., Samadi Kafil H. (2025). Effects of postbiotics derived from Lactobacillus plantarum and Bifidobacterium bifidum on biofilm formation and virulence gene expression of Enterococcus faecalis. Jundishapur Journal of Microbiology, 18(10), e165694. doi:10.5812/jjm-165694