While nosocomial infections by Staphylococcus epidermidis have gained much attention, this skin colonizer has apparently not evolved to cause disease, but maintain the commonly benign relationship with its host. Accordingly, S. epidermidis does not produce aggressive virulence determinants. Rather, factors that normally sustain the commensal lifestyle of S. epidermidis seem to rise to additional benefit during infection. Furthermore, we are beginning to comprehend the roles of S. epidermidis in balancing the epithelial microflora and serving as a reservoir of resistance genes. In this review, the molecular basis of the commensal and infectious lifestyles of S. epidermidis will be discussed.
Whereas previously only regarded as an innocuous commensal microorganism on the human skin, Staphylococcus epidermidis is nowadays seen as an important opportunistic pathogen. It is now the most frequent cause of nosocomial infections, at a rate about as high as that due to its more virulent cousin Staphylococcus aureus1. In particular, S. epidermidis represents the most common source of infections on indwelling medical devices. This likely stems from the fact that S. epidermidis is a permanent and ubiquitous colonizer of human skin, and the resulting high probability of device contamination during insertion2. While S. epidermidis infections only rarely develop into life-threatening diseases, their frequency and the fact that they are extremely difficult to treat represent a serious burden for the public health system. The costs related to vascular catheter-related bloodstream infections caused by S. epidermidis amount to an estimated $ 2 billion annually in the United States alone3–5. Treatment is complicated by specific antibiotic resistance genes and the formation of biofilms, multicellular agglomerations that have intrinsic resistance to antibiotics and mechanisms of host defense3. Furthermore, recent investigation has identified specific molecular determinants facilitating S. epidermidis immune evasion and ability to cause chronic disease. Interestingly, many of these determinants are believed to have original functions in the non-infectious lifestyle of this microorganism, emphasizing the accidental nature of S. epidermidis infections. A better understanding of S. epidermidis physiology not only during infection, but also in its commensal status is urgently needed to evaluate therapeutic strategies against S. epidermidi