Enterococcus faecalis is a common bacterium that lives primarily in the intestines of humans and other mammals, where it typically coexists harmlessly with other microbes. As a member of the normal gut flora, this organism plays a role in maintaining the health of the gastrointestinal tract. However, E. faecalis is a well-known opportunistic pathogen, meaning it can cause serious, even life-threatening, infections when it spreads outside of its usual environment. Its danger stems from its ability to infect sterile body sites and its capacity to resist multiple types of antibiotic treatments. This combination of common presence and potent resistance makes it an organism of considerable medical importance, especially in hospital settings.
Commensal Role and Classification
Enterococcus faecalis is scientifically classified as a Gram-positive, facultative anaerobic coccus. This means the bacteria retain the crystal violet stain due to their thick cell walls, are spherical in shape, and can survive with or without oxygen. The name faecalis refers to its primary habitat, the gastrointestinal tract, where it is found in high numbers in feces.
In its natural environment, the organism is considered a commensal, participating in functions like regulating intestinal pH, producing certain vitamins, and helping to metabolize nutrients. This normal state, known as colonization, is distinct from an infection, which occurs only when the bacteria enter normally sterile tissues. The organism is remarkably resilient, capable of surviving in harsh conditions like high temperatures, high pH levels, and the presence of bile salts.
Clinical Manifestations of Infection
The transition from a harmless gut resident to a pathogen often occurs in a healthcare setting, making E. faecalis a leading cause of nosocomial, or hospital-acquired, infections. Infections typically happen when the bacteria breach the physical barrier of the gut or skin and gain access to a sterile site. This is frequently facilitated by the use of medical devices like urinary catheters and central venous lines, which provide surfaces for the bacteria to adhere to and form protective biofilms.
E. faecalis is a common cause of Urinary Tract Infections (UTIs), especially in hospitalized patients with catheters. It also causes significant bloodstream infections, known as bacteremia, which can originate from an untreated UTI or an infected wound. If bacteremia is left untreated, it can quickly lead to life-threatening conditions like sepsis.
The bacterium is also responsible for a notable percentage of endocarditis, a serious infection of the heart’s inner lining or valves. Other common infection sites include surgical and traumatic wounds, particularly those involving the abdominal or pelvic region. Patients who are immunocompromised, have underlying conditions like diabetes or cancer, or who have recently undergone surgery are at the highest risk for these opportunistic infections.
The Challenge of Antibiotic Resistance
The greatest medical concern surrounding E. faecalis is its remarkable ability to resist antibiotic treatment, a feature that is both intrinsic to the species and acquired from other bacteria. The organism possesses natural resistance to several common antibiotic classes, including most cephalosporins and certain penicillins, which limits initial treatment options. This intrinsic resistance is often due to structural differences, such as having penicillin-binding proteins with a low affinity for the drug.
The most significant threat comes from acquired resistance, particularly to the powerful drug vancomycin, resulting in strains known as Vancomycin-Resistant Enterococci (VRE). Vancomycin normally works by binding to a specific structure in the bacterial cell wall, preventing its construction. However, VRE strains acquire genes, such as vanA or vanB, that allow them to alter this structure, which reduces vancomycin’s binding affinity significantly.
VRE strains are significant because they can transfer their resistance genes to other, more virulent bacteria, such as Staphylococcus aureus. The rise of VRE necessitates the use of alternative, and often more toxic, antibiotics like linezolid or daptomycin. Severe infections typically require combination therapy, using two different antibiotics to achieve a bactericidal effect. This escalating resistance complicates treatment, leads to longer hospital stays, and increases mortality rates.