Enterococcus faecalis is a bacterium commonly found in the human gastrointestinal tract, where it typically exists without causing harm. Under certain conditions, it can become an opportunistic pathogen, causing infections in hospital settings. Its ability to cause disease is due to its virulence factors, which are molecules or traits that enable the bacterium to infect a host and evade immune responses.
Adhesion and Colonization Factors
Enterococcus faecalis initiates infection by attaching to host tissues using various surface proteins. These proteins act like anchors, allowing the bacteria to bind firmly to cells in the urinary tract or on heart valves. This prevents them from being washed away by bodily fluids and is necessary for establishing a colony.
The Aggregation Substance (AS) is a protein on the bacterial surface that mediates binding to host cell receptors. AS promotes the formation of bacterial clumps, which enhances their ability to adhere and colonize tissues. This clumping also facilitates the transfer of genetic material between cells, contributing to the spread of antibiotic resistance genes.
The Enterococcal Surface Protein (Esp) is a large protein that aids in the initial attachment of E. faecalis to surfaces like catheters and medical implants. By facilitating this attachment, Esp is involved in the early stages of biofilm formation. The presence of Esp is linked to the increased persistence of the bacteria in hospital environments and during infections.
E. faecalis also uses proteins known as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs). These proteins bind to components of the host’s extracellular matrix, such as collagen and fibronectin. This attachment allows the bacteria to secure themselves within tissues, which is important in infections involving heart valves or wounds.
Secreted Factors for Tissue Damage
Once established, E. faecalis releases substances that damage host tissues and allow the infection to spread. One such factor is cytolysin, a toxin that destroys host cells, including red blood cells. This process, known as hemolysis, releases iron that the bacteria can use for growth.
Cytolysin also acts as a bacteriocin, killing competing bacteria to give E. faecalis a competitive advantage. The production of cytolysin is associated with more severe infections because it contributes directly to tissue destruction and inflammation.
E. faecalis also secretes enzymes that break down host tissues, weakening physical barriers and helping the bacteria invade deeper. Gelatinase (GelE) degrades collagen, a protein that gives structure to skin and organs. Serine Protease (SprE) works with GelE to degrade other matrix components, including fibrin, which is involved in blood clotting.
Biofilm Formation
A major virulence trait of E. faecalis is its ability to form biofilms. A biofilm is a community of bacteria attached to a surface and encased in a self-produced matrix of sugars, proteins, and DNA. This matrix acts as a protective shield for the bacteria inside.
Biofilm formation begins with the attachment of bacteria to a surface, often aided by proteins like Esp. The bacteria multiply into small clusters called microcolonies. As the community grows, it produces the matrix material that forms the mature, three-dimensional biofilm structure.
The biofilm’s matrix provides a defense against the host’s immune system, making it difficult for immune cells to reach the bacteria. Bacteria within a biofilm are also more resistant to antibiotics than their free-floating counterparts. This often requires much higher doses for effective treatment.
E. faecalis forms biofilms on medical devices like urinary catheters, IV lines, and prosthetic heart valves. These biofilms can lead to persistent, difficult-to-treat infections with serious consequences for patient health.
Mechanisms of Antibiotic Resistance
Enterococcus faecalis is well-known for its ability to withstand antibiotic treatment. This resilience is partly due to intrinsic resistance, meaning it is naturally resistant to certain antibiotics. For example, it has a low-level resistance to aminoglycosides and is not affected by cephalosporins.
More concerning is its capacity for acquired resistance, where it obtains genes that confer resistance to powerful antibiotics. This often occurs through the transfer of mobile genetic elements, like plasmids and transposons, from other bacteria. These elements are small pieces of DNA that can be passed between bacteria, carrying resistance instructions.
A primary example is Vancomycin-Resistant Enterococci (VRE). Vancomycin is a potent antibiotic used as a last resort for serious infections. Resistance is typically acquired through genes that alter the bacterial cell wall, preventing the antibiotic from binding to its target.
The emergence of VRE poses a challenge in clinical settings, as these infections are difficult to manage and limit treatment options. This high level of antibiotic resistance, combined with its other virulence factors, makes E. faecalis a serious opportunistic pathogen.