Staphylococcus epidermidis commonly inhabits the skin and mucous membranes of humans without causing harm, acting as part of the normal, healthy flora. Despite this, it has become a leading cause of serious infections acquired in healthcare settings. S. epidermidis transitions into an opportunistic pathogen, especially in patients with compromised immunity or those who have undergone surgery. These resulting infections are a significant burden on the healthcare system, often proving difficult to diagnose and challenging to treat due to the organism’s inherent resistance mechanisms.
The Commensal and Pathogenic Roles
S. epidermidis is a permanent resident of human skin, maintaining a beneficial relationship with its host. As part of the native microbiota, it contributes to skin health and can prevent colonization by more virulent bacteria, such as Staphylococcus aureus, through colonization resistance. This protective role often leads to the organism being dismissed as a contaminant when isolated in a laboratory setting.
The transition to a pathogenic state requires a breach of the body’s natural defenses, such as a break in the skin barrier. This breach provides the bacteria a pathway to deeper, normally sterile body sites. Vulnerable populations include preterm neonates, the elderly, and immunocompromised patients. Once inside the body, the organism’s capacity for survival and persistence offsets its relatively low native virulence.
Biofilm Formation and Device Colonization
The primary mechanism transforming S. epidermidis into a persistent pathogen is its ability to form a biofilm. A biofilm is a complex community of bacteria encased in a self-produced matrix of extracellular polymeric substances. This matrix allows the bacteria to adhere tenaciously to biological tissues and, critically, to the surfaces of foreign materials.
The bacterium exhibits a strong affinity for colonizing indwelling medical devices, which acts as a major catalyst for infection. Devices like catheters, prosthetic joints, vascular shunts, and cardiac pacemakers provide an abiotic surface for the bacteria to attach and proliferate. The protective biofilm shield prevents antibiotics from reaching effective concentrations, rendering standard systemic treatments ineffective. Biofilm communities are also highly resistant to the host’s immune cells, allowing the infection to persist and become chronic.
Severe and Unusual Clinical Manifestations
S. epidermidis can cause systemic, life-threatening disease beyond localized infections at an insertion site. It is one of the most frequent causes of catheter-related bloodstream infections, leading to sepsis in vulnerable patients. This bacteremia occurs when bacteria detach from the colonized device surface and enter the bloodstream.
The bacteria are also a prominent cause of infective endocarditis, an inflammation of the heart’s inner lining. S. epidermidis is responsible for a high percentage of prosthetic valve endocarditis cases, sometimes accounting for up to 40% of these infections. The bacteria colonize the artificial valve surface, forming biofilm masses called vegetations that can impede blood flow or travel to other organs.
Beyond device-related illness, the organism can cause deep-seated infections, despite its low virulence. These manifestations include osteomyelitis (bone infection) and meningitis following the colonization of cerebrospinal fluid shunts. In neonates, who have underdeveloped immune systems, S. epidermidis can cause devastating systemic infections and sepsis. The slow, indolent nature of these infections often complicates diagnosis, as subtle or delayed symptoms can mask the severity of the underlying disease.
Diagnosis and Management of Resistant Strains
Managing these infections is challenging due to the organism’s high rate of antimicrobial resistance, particularly to methicillin. Methicillin-Resistant S. epidermidis (MRSE) strains are common, with resistance rates often reported over 80%. This resistance means that traditional beta-lactam antibiotics, such as penicillin and cephalosporins, are often ineffective.
Diagnosis requires distinguishing a true, invasive infection from skin colonization or laboratory contamination. Clinicians rely on multiple positive blood cultures drawn from separate sites to confirm a systemic infection. Once confirmed, specialized laboratory testing, including genomic analysis and mass spectrometry, is used to identify the strain and determine its antibiotic susceptibility profile.
Empiric therapy for a suspected serious infection must assume methicillin resistance, making intravenous vancomycin the drug of choice. Other options for resistant strains include daptomycin and linezolid, depending on the infection and patient factors. Due to the protective nature of the biofilm, antibiotic therapy alone often fails. Successful treatment commonly requires the surgical removal of the infected medical device to eliminate the source of the persistent bacterial community.