Coagulase-Negative Staphylococcus Skin and Soft Tissue Infections

The normal microflora of the skin includes staphylococcal species that will induce inflammation when present below the dermis but are tolerated on the epidermal surface without initiating inflammation. Here we reveal a previously unknown mechanism by which a product of staphylococci inhibits skin inflammation. This inhibition is mediated by staphylococcal lipoteichoic acid (LTA), and acts selectively on keratinocytes triggered through Toll-like receptor (TLR) 3. The significance of this is seen by observations that TLR3 activation is required for normal inflammation after injury, and that keratinocytes require TLR3 to respond to RNA from damaged cells with the release of inflammatory cytokines. Staphylococcal LTA inhibits both inflammatory cytokine release from keratinocytes and inflammation triggered by injury through a TLR2-dependent mechanism. These findings show for the first time that the skin epithelium requires TLR3 for normal inflammation after wounding and that the microflora can modulate specific cutaneous inflammatory responses.

Coagulase-negative staphylococci (CNS) are differentiated from the closely related but more virulent Staphylococcus aureus by their inability to produce free coagulase. Currently, there are over 40 recognized species of CNS. These organisms typically reside on healthy human skin and mucus membranes, rarely cause disease, and are most frequently encountered by clinicians as contaminants of microbiological cultures. However, CNS have been increasingly recognized to cause clinically significant infections. The conversion of the CNS from symbiont to human pathogen has been a direct reflection of the use of indwelling medical devices. This article deals with the clinical syndromes, epidemiology, prevention, and management of infections caused by this unique group of organisms.

Coagulase-negative staphylococci (CNS) are normal inhabitants of human skin and mucous membranes. They have long been dismissed as culture contaminants, but now the potentially important role of CNS as pathogens and their increasing incidence has been recognized. Approximately 55-75% of nosocomial isolates is methicillin resistant. CNS were the first organisms in which glycopeptide resistance was recognized. In the immunocompetent host, CNS endocarditis and urinary tract infections with Staphylococcus saprophyticus are the most common CNS infections. Other patients are usually immunocompromised, with indwelling or implanted foreign bodies. CNS account for approximately 30% of all nosocomial blood stream infections. The majority of these concern catheter-related sepsis. Other important infections due to CNS include central nervous system shunt infections, endophthalmitis, surgical site infections, peritonitis in patients with continuous ambulatory peritoneal dialysis and foreign body infections. CNS are rarely associated with mastitis in humans. Staphylococcus lugdunensis is more pathogenic than other CNS as it expresses several potential virulence factors. The distinction between clinically significant, pathogenic and contaminating isolates is a major problem. Several studies show clonal intra and inter hospital spread of Staphylococcus epidermidis strains which suggests that infection control measures may be necessary for multiresistant CNS isolates as for methicillin resistant Staphylococcus aureus. As a result of medical progress, mainly due to the use of invasive and indwelling medical devices, CNS are now a major cause of nosocomial and health-care related infections.