Enterococcus faecalis in the vagina: symptoms explained

Author: Veronica Danger
Qualified Naturopath | BHSc(N)

Last reviewed: July 6, 2026

Enterococcus faecalis is a bacterium that normally lives in the gut, but when it settles into the vagina and overgrows, its metabolic byproducts can drive real, uncomfortable symptoms. Ammonia, biogenic amines, hydrogen sulfide, sticky biofilms and, in some strains, tissue-damaging toxins are what turn a quiet coloniser into a source of odour, irritation, inflammation and stubborn, recurring infection.

These byproducts sit at the centre of aerobic vaginitis (AV) and some urinary tract infections (UTIs). Understanding what E. faecalis actually makes, and why, explains a lot about how symptoms behave, and why they can be so hard to shift once the protective, lactobacilli-led balance is lost.

What is E. faecalis and why is it in the vagina?

Enterococcus faecalis is a hardy, adaptable gut bacterium. It is a facultative anaerobe, which means it can live with or without oxygen and switch its metabolism depending on what fuel is around, whether that is sugars, proteins or amino acids.¹

Finding Enterococcus faecalis in the vagina is not unusual in itself, and in a balanced vagina, protective Lactobacillus species dominate and keep opportunists like E. faecalis in the minority. When those protective bacteria are depleted, by antibiotics, low oestrogen or other disruption, E. faecalis can stick to vaginal and cervical cells, build biofilms and settle in.² Its numbers rise in aerobic vaginitis, where lactobacilli are reduced and visible inflammation is the giveaway that tells AV apart from bacterial vaginosis (BV).³

To see how far this is from a healthy state, it helps to know what a healthy vaginal microbiome looks like and how the different community state types behave. E. faecalis is one of a cluster of byproduct-producing bacteria we cover across the site, alongside Gardnerella and Prevotella.

E. faecalis byproducts of sugar fermentation

Enterococcus faecalis can ferment glucose and other simple sugars in the vaginal environment, often released from glycogen breakdown. Glycogen is more abundant when there is more oestrogen present, which is one reason the whole picture shifts when oestrogen falls.¹

The acids this produces add some acidity, but when Enterococcus faecalis dominates, the overall vaginal pH tends to become less stable, particularly once lactobacilli are depleted.

Lactic acid

Lactic acid is a primary byproduct of glucose fermentation and contributes to an acidic vaginal environment. However, the amount of lactic acid produced by Enterococcus faecalis is often too little to hold the vaginal pH where lactobacilli would keep it.¹

In our clinic, we often find the vaginal pH in aerobic vaginitis is acidic and sitting within what is otherwise considered a ‘healthy’ range of 3.8 to 4.5, which is exactly why a normal-looking pH result can be so misleading when someone is clearly symptomatic. There is more in our guide to vaginal pH.

Acetic acid and formic acid

Acetic and formic acids are weak acids that can slightly acidify the environment, but they are less effective than lactic acid at promoting a protective low pH.¹

Ethanol and carbon dioxide (CO₂)

Ethanol and carbon dioxide are minor byproducts that are understood to have little direct impact on the vaginal environment.

E. faecalis byproducts of protein and amino acid metabolism

When sugars are less available, Enterococcus faecalis shifts to metabolising amino acids and proteins. This tends to happen in dysbiotic conditions, when lactobacilli are depleted and more protein is around, released from host tissue or by bacterial enzymes.¹

The alkaline byproducts this generates, like ammonia and biogenic amines, raise vaginal pH, encourage the overgrowth of anaerobic bacteria and worsen the dysbiosis. Hydrogen sulfide adds tissue irritation and inflammation on top.¹

Ammonia is produced by deamination of amino acids. It is strongly alkaline, raises the vaginal pH and disrupts lactobacilli.¹
Putrescine, cadaverine and other biogenic amines, made from breaking down amino acids like lysine and ornithine, cause the foul odours associated with AV.
Hydrogen sulfide, produced from sulfur-containing amino acids such as cysteine and methionine, causes irritation, inflammation and unpleasant sulfurous ‘fart’ or faeces-like odours from the vagina.

That sulfurous, faecal note is one of the most distressing symptoms people describe, and it has a real biochemical cause rather than anything to do with hygiene. We go deeper into it in understanding sulfur and the vagina.

Byproducts of E. faecalis biofilm formation

Enterococcus faecalis is very good at forming biofilms, particularly in polymicrobial communities alongside other bacteria.

Biofilm stabilises E. faecalis populations, letting them persist in the vaginal environment and resist treatment, which is a large part of why infections recur.² The byproducts of biofilm formation include:

Extracellular polysaccharides, the matrix components of biofilm that shield E. faecalis and its neighbours from the immune system and from antibiotics.
Proteolytic enzymes, which break down host proteins to release amino acids that feed bacterial metabolism and drive further biofilm growth.
Lipoteichoic acids (LTA), cell-wall components that trigger inflammation and immune responses in the vaginal epithelium.

Biofilm is the reason a course of treatment can appear to work and then symptoms return: the surviving bacteria are sheltered inside a matrix that ordinary treatment cannot fully reach. It is the same challenge we see with biofilms in BV, and it is why breaking the biofilm down matters as much as reducing bacterial numbers.

Secondary metabolites and toxins produced by E. faecalis

In certain conditions, Enterococcus faecalis can produce additional toxic metabolites, including cytolysin, superoxide and reactive oxygen species (ROS).

Cytolysin is a pore-forming toxin made by only some strains of E. faecalis. It punches holes in cell membranes and can lyse vaginal epithelial cells, contributing to inflammation and tissue breakdown.⁵ Because only a subset of strains carry it, two people with E. faecalis can have quite different symptom severity.

Superoxide and ROS are byproducts of E. faecalis metabolism that cause oxidative stress, which is damaging to delicate vaginal tissue.¹

Together, these toxic byproducts can drive more severe tissue inflammation, raise susceptibility to secondary infections, and make it harder to restore a healthy vaginal microbiome.

Summary of Enterococcus faecalis metabolic byproducts

Source	Metabolic byproducts	Effect on the vaginal environment
Sugars (e.g. glucose)	Lactic acid, acetic acid, formic acid, CO₂, ethanol	Mild acidity, but not enough to hold a protective pH
Proteins and amino acids	Ammonia, biogenic amines (putrescine, cadaverine), H₂S	Alkaline pH, odour, inflammation and dysbiosis
Biofilm formation	Extracellular polysaccharides, proteolytic enzymes, LTA	Protects E. faecalis, worsens dysbiosis and promotes inflammation
Secondary metabolites and toxins	Cytolysin, ROS	Tissue damage, immune activation and oxidative stress

Clinical implications

The metabolic byproducts of Enterococcus faecalis make it a meaningful contributor to vaginal dysbiosis, particularly in mixed infections or after the lactobacilli-dominated microbiome has been disrupted. Its ability to produce ammonia, biogenic amines and toxins raises pH and inflammation, setting up a self-reinforcing cycle that, without effective intervention, can be tricky to break.⁴

This matters beyond comfort. In pregnancy, aerobic vaginitis and the aerobic bacteria behind it, including E. faecalis, are linked with a higher risk of adverse outcomes, which is why persistent symptoms deserve proper assessment rather than repeated guesswork.⁴

The root-cause picture: why E. faecalis takes hold

Byproducts explain the symptoms, but they do not explain why E. faecalis got the upper hand in the first place. That question usually leads back to the protective microbiome and, often, to oestrogen.

Oestrogen drives glycogen in the vaginal wall, and glycogen is what feeds protective Lactobacillus species. When local oestrogen is low, glycogen falls, lactobacilli struggle to hold their numbers, and aerobic organisms like E. faecalis find it far easier to move in. Oestrogen deficiency is one of the recognised drivers of aerobic vaginitis, sitting alongside lactobacilli depletion and a heightened inflammatory response.^3,4

The same low-oestrogen picture shows up in more situations than menopause. It appears while breastfeeding, for trans men on testosterone, during IVF down-regulation, and in some cancer treatments. Any time local oestrogen drops, the tissue thins and the microbiome tips the same way, a pattern we describe in atrophic vaginitis. The useful part is that you can support the tissue and the microbiome locally without changing your whole-body oestrogen, which matters when systemic oestrogen is deliberately low or off the table.

Local, non-hormonal support tends to work on a few fronts at once: soothing and rebuilding the tissue with botanicals such as sea buckthorn and fennel; feeding the protective bacteria back with a prebiotic like vaginal lactulose; and re-seeding protective species so lactobacilli can take the territory back. None of these change systemic oestrogen, which is what makes the approach usable across such different situations.

The other front is the biofilm. Because E. faecalis shelters inside a matrix, a naturopathic approach aims both to unpick that biofilm and to lower bacterial numbers. Green tea polyphenols (EGCG) have been shown to eradicate E. faecalis biofilm and switch off several of its virulence genes.⁷ Chelators such as EDTA destabilise biofilm by stripping out the calcium and other cations that hold its scaffolding together, and plant-derived agents and probiotics are among the strategies studied for the same purpose.⁸ Botanicals including Sida acuta, Cryptolepis, uva ursi and juniper are used for their antimicrobial and urinary-tissue-supporting properties. None of this is a substitute for assessment, but it is why the natural toolkit for E. faecalis targets the biofilm and the underlying terrain, not just the bacteria.

Effective treatments for E. faecalis in the vagina

My Vagina has a range of effective treatments for aerobic vaginitis and urinary tract infections involving E. faecalis, built around targeted botanicals that address the biofilm, the overgrowth and the tissue, plus rebuilding the protective microbiome so the result holds.

Because a normal-looking pH or a partial result can be so misleading, the most useful first step for stubborn or recurring symptoms is a comprehensive vaginal microbiome test, so treatment is matched to what is actually there. If symptoms keep coming back, our guide to chronic aerobic vaginitis covers longer-term management.

Our specialist clinic and experienced naturopaths can help resolve E. faecalis, AV and UTIs with targeted, non-drug approaches that do not drive antibiotic resistance. We do not perform physical or internal examinations ourselves, so where a speculum or pelvic exam is needed, we will point you to the right person for that part.

Frequently asked questions

Why does my discharge smell like faeces or sulfur?

A sulfurous, faecal or ‘rotten egg’ odour usually comes from hydrogen sulfide and biogenic amines produced when bacteria like E. faecalis break down amino acids. It is a biochemical process, not a hygiene problem, and washing more will not fix it. Restoring the protective microbiome is what changes the smell. There is more in understanding sulfur and the vagina.

Is E. faecalis a sexually transmitted infection?

No. E. faecalis is a normal gut bacterium that can reach the vagina from the nearby bowel and overgrow when the protective microbiome is depleted. It is not classed as an STI, though it can turn up as part of a mixed picture, so a proper test is worth it if symptoms persist.

Can E. faecalis cause a UTI and vaginal symptoms at the same time?

Yes. E. faecalis is a recognised cause of urinary tract infections as well as aerobic vaginitis, and its metabolic byproducts can reduce the viability of bladder cells.⁶ Because the vagina and urethra sit so close together, an overgrowth can show up in both places at once. Our guide to UTIs has more.

Why does E. faecalis keep coming back?

Recurrence usually comes down to biofilm and terrain. E. faecalis shelters inside a biofilm matrix that ordinary treatment cannot fully reach, so survivors regroup.² If the underlying driver, often low oestrogen or a depleted microbiome, is not addressed, the same conditions that let it overgrow are still there. Breaking the biofilm and rebuilding the protective bacteria together is what tends to stop the cycle.

This article is general information and not a substitute for personalised medical advice. If you have vaginal symptoms that persist, recur or worry you, please see an experienced practitioner.