Methicillin-Resistant Staphylococcus epidermidis (MRSE) is a bacterium of concern in clinical environments, particularly hospitals. This bacterium represents a drug-resistant form of a species that typically lives harmlessly on human skin. MRSE is distinct from the more commonly known Methicillin-Resistant Staphylococcus aureus (MRSA), though both share resistance to beta-lactam antibiotics. Its ability to cause infection is primarily opportunistic, exploiting weaknesses in the host’s immune defense or the presence of foreign materials in the body. Infections are often challenging to treat due to the organism’s resistance profile and pathogenic strategies.
The Organism’s Role as Normal Skin Flora
Staphylococcus epidermidis (SE) is one of the most abundant bacterial colonizers of the human skin and mucous membranes. This commensal relationship is generally non-pathogenic, meaning the organism usually lives in harmony with its host without causing disease. The bacteria contribute to the skin’s natural defenses, forming part of the cutaneous immune system.
SE maintains the skin’s homeostasis and prevents colonization by more harmful microbes, a process known as colonization resistance. Specific strains of S. epidermidis can produce antimicrobial peptides that inhibit the growth of pathogenic bacteria, including Staphylococcus aureus. SE also supports wound healing by stimulating certain immune cells in the skin.
The organism is so universally present that it is often considered a contaminant when isolated in a laboratory setting. In healthy individuals, the intact skin barrier effectively keeps the bacteria on the surface, preventing them from entering deeper tissues. It is only when this natural barrier is compromised that the organism can transition from a harmless resident to a serious pathogen.
Understanding Methicillin Resistance
MRSE’s resistance to methicillin and related antibiotics stems from a specific genetic change. Susceptible Staphylococcus epidermidis strains are killed by beta-lactam antibiotics, which target bacterial cell wall synthesis. These antibiotics work by binding to and inactivating penicillin-binding proteins (PBPs), the enzymes necessary for constructing the cell wall.
MRSE has acquired a mobile genetic element known as the Staphylococcal Cassette Chromosome mec (SCCmec). This element carries the mecA gene, the primary determinant of methicillin resistance. The mecA gene codes for a modified enzyme called penicillin-binding protein 2a (PBP2a).
PBP2a is structurally different from native PBPs and has a reduced affinity for beta-lactam antibiotics. Even when methicillin or similar drugs are present, PBP2a continues to perform cell wall construction. This allows the bacterium to synthesize a complete and stable cell wall, effectively evading the lethal action of nearly all beta-lactam drugs. The presence of PBP2a makes the organism resistant to a broad range of antibiotics, including methicillin, oxacillin, and cephalosporins.
Infections Linked to Medical Devices and Immunocompromised Patients
MRSE is an opportunistic pathogen, primarily causing infection in individuals who are immunocompromised or who have foreign objects implanted in their bodies. The presence of a medical device, such as a catheter or prosthesis, provides an ideal surface for the organism to colonize. MRSE is recognized as the most common cause of infections associated with implanted devices.
The organism’s main pathogenic strategy involves forming a complex structure called a biofilm. A biofilm is a slimy, self-produced matrix composed of proteins, polysaccharides, and extracellular DNA that encases the bacteria and allows them to adhere to non-living surfaces. Once established on a device, the biofilm acts as a protective shield, defending the bacteria from the host’s immune system and preventing antibiotics from reaching the underlying cells.
Common clinical manifestations include catheter-related bloodstream infections (CRBSIs), which occur when the organism travels from the catheter surface directly into the patient’s bloodstream. Patients with prosthetic joints, artificial heart valves, or ventriculoperitoneal shunts are at high risk for deep-seated infections. These device-associated infections often become chronic and persistent due to the difficulty of eradicating the biofilm.
Clinical Management and Prevention in Healthcare Settings
Managing an established MRSE infection is complicated by its multidrug resistance and the protection afforded by the biofilm structure. The first line of antibiotic treatment for methicillin-resistant staphylococci often involves non-beta-lactam drugs such as vancomycin or linezolid. The choice of drug depends on the specific strain’s susceptibility profile and the site of the infection.
Antibiotics alone are frequently insufficient when a biofilm is present on a medical device. For many infections, such as those involving prosthetic joints or heart valves, removal and replacement of the infected device is necessary to achieve a cure. This surgical intervention physically removes the colonized surface, which acts as a reservoir for the protected bacteria.
Prevention focuses on stringent infection control practices in healthcare settings. Foundational measures include excellent hand hygiene among all healthcare personnel, the single most effective way to prevent transmission. Hospitals implement contact precautions for patients colonized or infected with MRSE to limit its spread to vulnerable patients. Meticulous attention to sterile technique during the insertion and maintenance of all indwelling medical devices is necessary to prevent the initial colonization that leads to infection.