What is Enterococcus faecalis?
Enterococcus faecalis is a gram-positive bacterium that lives as a normal part of the human gastrointestinal tract in most people. E. faecalis is an opportunistic pathogen, harmless in the gut environment, but capable of causing infection when it ends up elsewhere in the body, including the urinary tract, bloodstream, or heart valves.
Enterococcus species cause an estimated 110,000 UTIs annually in the United States, and E. faecalis accounts for the large majority of those. E. faecalis represents roughly 70–75% of enterococcal urinary isolates, with the closely related Enterococcus faecium responsible for most of the remainder1. The two species are often discussed together, but they behave differently enough, especially around antibiotic resistance, that it’s worth keeping them distinct.
What causes an Enterococcus faecalis UTI?
Like most UTI-causing bacteria, E. faecalis is thought to reach the urinary tract primarily by migrating from the gastrointestinal tract. Contamination around the urethra by gut bacteria is considered an important route of infection, and this shows up in clinical data: recurrent UTI patients, particularly premenopausal women, have been found to have a higher frequency of infections caused by their own endogenous gut microbes2. Beyond the urinary tract specifically, E. faecalis has a few recognized portals of entry into the body: the gastrointestinal tract itself (via translocation through the intestinal lining, often after surgery or illness), the urinary tract (via catheterization or the ascending route just described), and the bloodstream (via central lines)3.
It’s disproportionately involved in complicated UTIs. A few groups of patients experience E. faecalis infection more often:
- People who use urinary catheters, both short- and long-term
- People who are hospitalized or in long-term care, particularly with multiple prior UTIs or antibiotic courses
- People with structural or functional urinary tract abnormalities, including urinary retention or recent urologic instrumentation or surgery
- Older adults
Risks and complications
UTIs caused by E. faecalis carry some distinct risks compared with more typical gram-negative infections.
Biofilm and catheter persistence
E. faecalis isn’t especially aggressive at invading healthy tissue, its strategy is closer to “squatter’s rights.” When a catheter is placed, the body deposits a protein called fibrinogen onto its surface as part of a normal wound-response reaction. E. faecalis uses a structure called a pilus (Ebp) to bind to the fibrinogen, anchoring itself to the catheter and building a protective biofilm from there4. Once established, bacteria embedded in that biofilm are considerably harder for antibiotics to reach.
Antibiotic resistance
The Clinical and Laboratory Standards Institute (CLSI) the standards body that defines U.S. laboratory antibiotic susceptibility testing, specifically warns that for Enterococcus species, cephalosporins, low-level aminoglycosides, clindamycin, and trimethoprim-sulfamethoxazole may appear active in a susceptibility test but aren’t effective clinically and shouldn’t be reported as susceptible, regardless of the in vitro result5. Unlike its relative E. faecium, most E. faecalis remains ampicillin-susceptible, and while vancomycin-resistant enterococcus (VRE) draws significant attention, surveillance data consistently show the large majority of VRE isolates are E. faecium, not E. faecalis67.
Bloodstream spread
E. faecalis can reach the bloodstream by more than one route: directly from the gut, when illness, surgery, or broad-spectrum antibiotics compromise the intestinal lining, or from the urinary tract itself, if an infection ascends to the kidneys. Either route can lead to bacteremia, a more serious systemic infection distinct from an uncomplicated UTI3.
How is Enterococcus faecalis infection detected?
Unlike fastidious organisms such as Aerococcus species, E. faecalis isn’t inherently difficult to grow. It typically grows readily in isolation. In practice, though, detecting it accurately is not always straightforward.
Polymicrobial infections
E. faecalis frequently appears as part of a polymicrobial infection alongside gram-negative bacteria like E. coli. Standard culture protocols aren’t always set up to fully characterize every organism present in a mixed sample, and semi-quantitative reporting thresholds can cause a real but lower-abundance pathogen to go unreported.
Detection gaps in standard culture
In our peer-reviewed clinical validation performed at Biotia’s NYS-CLIA/CLEP-certified laboratory, the BIOTIA-ID Urine Test identified E. faecalis as one of the organisms most frequently missed by standard culture8. This isn’t unique to sequencing-based methods: enhanced quantitative urine culture (EQUC), a method that plates larger urine volumes under a wider range of incubation conditions, has independently shown that standard culture detects only a fraction of the non-E. coli uropathogens present in symptomatic urine, with E. faecalis among the organisms most inconsistently recovered between the two techniques9. The most likely explanation in both cases is how often E. faecalis shows up in polymicrobial samples and at lower relative abundance, rather than any inherent difficulty growing the organism itself.
Resistance profiling
Knowing an infection involves E. faecalis immediately rules out cephalosporins, per CLSI guidance5. If the infection progresses to bacteremia, combination therapy with ampicillin, penicillin, or vancomycin plus an aminoglycoside is often used, so labs run a dedicated high-level aminoglycoside resistance (HLAR) screen ahead of time, typically a high-concentration gentamicin and streptomycin disk or agar screen defined by CLSI standards510. Documented high-level resistance to both drugs rules out that combination strategy entirely, so getting a fuller picture of resistance markers can help guide antibiotic selection before it’s needed.
Virulence factors
Virulence factors are characteristics or evolutionary strategies of a pathogen that enable it to more efficiently infect a host, evade the immune system, and cause disease. Clinical metagenomic-based tests can identify specific virulence factors a given isolate carries, though more research is needed to know how their presence should change treatment. Virulence factors of E. faecalis are listed in the table below.
| Virulence Factor | Role in Infection |
|---|---|
| Ebp pilus (EbpA) | Surface fiber that binds host fibrinogen deposited on catheters, anchoring the bacteria as a first step toward biofilm formation |
| Gelatinase (GelE) | Breaks down host tissue proteins; also implicated in breaching gut epithelial tight junctions, a step in how E. faecalis translocates out of the GI tract |
| Aggregation substance | Helps bacterial cells clump together, enhancing adherence to host tissue and catheter surfaces |
| Enterococcal surface protein (Esp) | Supports adherence to the urothelium and catheter surfaces, contributing to biofilm formation |
| Cytolysin | A toxin that damages host cells, including red blood cells, increasing tissue injury |
How is an E. faecalis UTI treated?
E. faecalis is treated with antibiotics, but susceptibility testing, not assumptions about the species, should drive the choice. Ampicillin or amoxicillin is typically a first-line option for susceptible E. faecalis, since it usually remains ampicillin-susceptible, unlike E. faecium. Nitrofurantoin is another option for uncomplicated cases, though it isn’t appropriate for pyelonephritis or complicated UTI due to poor tissue penetration. For complicated UTI specifically, levofloxacin is FDA-approved as an alternative option, though rising fluoroquinolone resistance in E. faecalis means susceptibility should be confirmed before relying on it11. For more severe infections requiring combination therapy, labs test specifically for high-level aminoglycoside resistance (HLAR), since its presence rules out that strategy.
Catheter-associated and other complicated infections may require additional intervention beyond antibiotics alone. Persistent or recurrent symptoms combined with consistent E. faecalis detection may point to an entrenched biofilm, in which case treatment may include replacing the urological device entirely.
The bottom line
UTIs caused by Enterococcus faecalis are common, particularly for people with catheters, recent hospitalization, or a history of complicated UTI. It typically reaches the urinary tract the same way most UTI-causing bacteria do, traveling from its normal home in the gastrointestinal tract. Once in the urinary tract, its survival strategy relies on biofilm persistence rather than aggressive tissue invasion, which is what makes catheter-associated infections so stubborn. While standard culture usually identifies E. faecalis without difficulty in isolation, Biotia’s own validation data for the BIOTIA-ID Urine Test show it’s still one of the organisms most often missed by urine culture in real-world specimens relative to next-generation sequencing, and when it is found, it’s often part of a polymicrobial infection that benefits from a fuller diagnostic picture.
The BIOTIA-ID Urine Test uses next-generation sequencing to identify over 40 urogenital pathogens, including Enterococcus faecalis, alongside antibiotic resistance markers to help guide treatment.
Frequently asked questions
Is Enterococcus faecalis dangerous?
It can cause real, sometimes hard-to-clear infections, particularly in catheterized, hospitalized, or otherwise vulnerable patients, but it's generally less acutely aggressive than some gram-negative uropathogens. Its main risk is persistence via biofilm rather than rapid tissue invasion.
How does Enterococcus faecalis get into the urinary tract?
It typically travels from its normal home in the gastrointestinal tract, contaminating the area around the urethra before ascending into the bladder, the same general route responsible for most UTIs, including those caused by E. coli.
How is Enterococcus faecalis UTI treated?
Treatment should be guided by the specific strain’s antibiotic resistance profile. Ampicillin or amoxicillin is typically a first-line option for susceptible E. faecalis, since this species usually remains ampicillin-susceptible, unlike E. faecium. Nitrofurantoin is another option for uncomplicated cases, though it isn't appropriate for pyelonephritis or complicated UTI.
Is Enterococcus faecalis contagious or sexually transmitted?
No. It's a normal inhabitant of the human gut, and infection typically results from the bacteria moving from their usual location to the urinary tract, not from person-to-person transmission in the way an STI would spread.
Can Enterococcus faecalis cause a UTI in an otherwise healthy person?
Yes, though it is less common; E. faecalis UTI is disproportionately associated with catheters, hospitalization, recent urologic procedures, or structural urinary tract abnormalities rather than occurring as a first UTI in an otherwise healthy young adult.
What's the difference between E. faecalis and E. faecium?
They're related species with different resistance profiles. E. faecalis causes the majority of enterococcal UTIs and is usually ampicillin-susceptible. E. faecium is less common overall but carries a much higher rate of ampicillin resistance and accounts for most vancomycin-resistant enterococcus (VRE) cases.
Does Enterococcus faecalis show up on a normal urine culture?
It's not a fastidious, hard-to-grow organism, so it isn't inherently difficult to culture. In practice, though, Biotia's own validation data found E. faecalis was one of the organisms most often missed by standard culture relative to next-generation sequencing, most likely because it commonly shows up as part of a polymicrobial infection, where standard reporting thresholds and selective media can cause it to be underreported even when truly present.
References
- Sharifi Y, Hasani A, Ghotaslou R, Naghili B, Aghazadeh M, Milani M, Bazmani A. Virulence and antimicrobial resistance in enterococci isolated from urinary tract infections. Adv Pharm Bull. 2013;3(1):197-201. doi:10.5681/apb.2013.032. PMID: 24312837. ↩
- Sharon BM, Arute AP, Nguyen A, Tiwari S, Reddy Bonthu SS, Hulyalkar NV, Neugent ML, Palacios Araya D, Dillon NA, Zimmern PE, Palmer KL, De Nisco NJ. Genetic and functional enrichments associated with Enterococcus faecalis isolated from the urinary tract. mBio. 2024;14(6):e0251523. doi:10.1128/mbio.02515-23. ↩
- Archambaud C, Nunez N, da Silva RAG, Kline KA, Serror P. Enterococcus faecalis: an overlooked cell invader. Microbiol Mol Biol Rev. 2024;88(3):e0006924. doi:10.1128/mmbr.00069-24. ↩
- Flores-Mireles AL, Walker JN, Potretzke A, et al. Antibody-based therapy for enterococcal catheter-associated urinary tract infections. mBio. 2016;7(5):e01653-16. doi:10.1128/mBio.01653-16. PMID: 27795399. ↩
- Clinical and Laboratory Standards Institute. Performance Standards for Antimicrobial Susceptibility Testing. 35th ed. CLSI supplement M100. Table 1D (Enterococcus spp.) and Table 3L (Test for Detecting High-Level Aminoglycoside Resistance in Enterococcus spp.). Published 2025. Accessed September 16, 2026. https://clsi.org/shop/standards/m100/ ↩
- StatPearls, NCBI Bookshelf. Vancomycin-resistant enterococci. Published 2023. Accessed September 16, 2026. https://www.ncbi.nlm.nih.gov/books/NBK513233/ ↩
- Pharmacy Times. Treatment of acute, uncomplicated urinary tract infections with ampicillin for vancomycin-resistant Enterococcus species. Accessed September 16, 2026. https://www.pharmacytimes.com/view/treatment-of-acute-uncomplicated-urinary-tract-infections-with-ampicillin-for-vancomycin-resistant-enterococcus-species ↩
- Couto-Rodriguez M, Danko DC, Wells HL, Rey S, Jirau Serrano X, Fidler G, Papciak J, Combs PF, Plourde A, Augenbraun M, Mason CE, Otto C, O'Hara NB, Nagy-Szakal D. Analytical validation of a highly accurate and reliable next-generation sequencing-based urine assay. Microbiol Spectr. 2026;14(6):e0202625. doi:10.1128/spectrum.02026-25. PMID: 42012213. ↩
- Price TK, Dune T, Hilt EE, Thomas-White KJ, Kliethermes S, Brincat C, Brubaker L, Wolfe AJ, Mueller ER, Schreckenberger PC. The clinical urine culture: enhanced techniques improve detection of clinically relevant microorganisms. J Clin Microbiol. 2016;54(5):1216-1222. doi:10.1128/JCM.00044-16. PMID: 26962083. ↩
- ASM Press. Screen tests to detect high-level aminoglycoside resistance in Enterococcus spp. In: Leber AL, Burnham C-AD, eds. Clinical Microbiology Procedures Handbook. 5th ed. Ch. 7.12. Published 2023. Accessed September 16, 2026. https://journals.asm.org/doi/book/10.1128/9781683670438 ↩
- DailyMed, U.S. National Library of Medicine. Levofloxacin tablets, for oral use — prescribing information. Accessed September 16, 2026. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4be13bd5-0c39-43c3-9232-b1226ccd4dbc ↩
