Immunoprophylaxis and Immunotherapy of S. Epidermidis
For a long time, the detection of S. epidermidis in blood or tissue samples was considered as contamination. Indeed, as part of the commensal flora, S. epidermidis rarely infects healthy people and may even exert a probiotic function against pathogens such as Staphylococcus aureus. Without intentional disruption of epithelial or mucosal layers, S. epidermidis is only occasionally the cause of skin infection, sepsis, endocarditis and osteomyelitis. In particular, low-weight neonates, elderly and immuno-compromised patients are prone to such S. epidermidis infections.
Despite this low pathogenicity, during the last decade, S. epidermidis has emerged as an important opportunistic pathogen frequently causing infections linked to medical devices such as intravascular catheters, ventricular shunts, prosthetic heart valves, artificial lenses and orthopedic implants. The infection starts with adherence of S. epidermidis to the biomaterial, followed by colonization of the device surface and formation of a biofilm. In contrast to a planktonically grown culture, the bacteria embedded in a biofilm constitute an interactive community containing genetically and phenotypically different subpopulations. This differentiation allows bacteria to cope better with surrounding conditions. However, the sessile lifestyle, the importance of which in many human diseases has only recently been recognized (reviewed in), necessitates a totally different treatment approach. Although planktonic cells may be responsive to a specific antimicrobial agent, their sessile counterparts may not be inhibited by the same compound. In addition, biofilm-embedded bacteria are better protected against host immune responses compared with planktonic cells.
An S. epidermidis biofilm on a medical device leads to a persistent, predominantly chronic infection and often requires the removal of the medical device. Although not life-threatening, these infections increase the duration of hospitalization and thus increase costs. Furthermore, S. epidermidis cells may disperse from this biofilm to other body niches. Immunocompromised, long-term hospitalized and intensive care patients are most vulnerable to those secondary infections, including bloodstream infection, endocarditis, osteomyelitis and abscesses. The latter complications are not only accompanied with prolonged hospital stays, but significantly increase morbidity and mortality. As a result of population aging and the widespread use of indwelling devices in modern medicine, the incidence of S. epidermidis infections is growing alarmingly.
Nowadays, S. epidermidis infections pose several challenges to clinicians. First, it remains difficult to distinguish invasive from contaminating strains in clinical samples, but the growing insights in S. epidermidis epidemiology and improved techniques to identify epidemic clonal lineages by means of genetic markers help. Second, the number of antibiotic-resistant S. epidermidis strains has increased over the years and even exceeds that of S. aureus. Approximately 70% of clinical S. epidermidis isolates have acquired methicillin resistance, and the majority of isolates are resistant to other antimicrobial classes as well. Moreover, it is postulated that coagulase-negative staphylococci (CoNS) may serve as a reservoir of antibiotic resistance genes for other pathogens, including S. aureus. Third, treatment of an S. epidermidis infection, the origin of which is mostly a biofilm, becomes difficult because the effect of antimicrobials and immune responses on biofilm-embedded bacteria is diminished or even nullified compared with planktonic cells.
Thus, the ability of S. epidermidis to switch from a harmless commensal to an opportunistic pathogen, which is closely linked to its capacity to form a biofilm, increases its clinical importance.
Changing Paradigms: Increasing Clinical Importance of Staphylococcus epidermidis
For a long time, the detection of S. epidermidis in blood or tissue samples was considered as contamination. Indeed, as part of the commensal flora, S. epidermidis rarely infects healthy people and may even exert a probiotic function against pathogens such as Staphylococcus aureus. Without intentional disruption of epithelial or mucosal layers, S. epidermidis is only occasionally the cause of skin infection, sepsis, endocarditis and osteomyelitis. In particular, low-weight neonates, elderly and immuno-compromised patients are prone to such S. epidermidis infections.
Despite this low pathogenicity, during the last decade, S. epidermidis has emerged as an important opportunistic pathogen frequently causing infections linked to medical devices such as intravascular catheters, ventricular shunts, prosthetic heart valves, artificial lenses and orthopedic implants. The infection starts with adherence of S. epidermidis to the biomaterial, followed by colonization of the device surface and formation of a biofilm. In contrast to a planktonically grown culture, the bacteria embedded in a biofilm constitute an interactive community containing genetically and phenotypically different subpopulations. This differentiation allows bacteria to cope better with surrounding conditions. However, the sessile lifestyle, the importance of which in many human diseases has only recently been recognized (reviewed in), necessitates a totally different treatment approach. Although planktonic cells may be responsive to a specific antimicrobial agent, their sessile counterparts may not be inhibited by the same compound. In addition, biofilm-embedded bacteria are better protected against host immune responses compared with planktonic cells.
An S. epidermidis biofilm on a medical device leads to a persistent, predominantly chronic infection and often requires the removal of the medical device. Although not life-threatening, these infections increase the duration of hospitalization and thus increase costs. Furthermore, S. epidermidis cells may disperse from this biofilm to other body niches. Immunocompromised, long-term hospitalized and intensive care patients are most vulnerable to those secondary infections, including bloodstream infection, endocarditis, osteomyelitis and abscesses. The latter complications are not only accompanied with prolonged hospital stays, but significantly increase morbidity and mortality. As a result of population aging and the widespread use of indwelling devices in modern medicine, the incidence of S. epidermidis infections is growing alarmingly.
Nowadays, S. epidermidis infections pose several challenges to clinicians. First, it remains difficult to distinguish invasive from contaminating strains in clinical samples, but the growing insights in S. epidermidis epidemiology and improved techniques to identify epidemic clonal lineages by means of genetic markers help. Second, the number of antibiotic-resistant S. epidermidis strains has increased over the years and even exceeds that of S. aureus. Approximately 70% of clinical S. epidermidis isolates have acquired methicillin resistance, and the majority of isolates are resistant to other antimicrobial classes as well. Moreover, it is postulated that coagulase-negative staphylococci (CoNS) may serve as a reservoir of antibiotic resistance genes for other pathogens, including S. aureus. Third, treatment of an S. epidermidis infection, the origin of which is mostly a biofilm, becomes difficult because the effect of antimicrobials and immune responses on biofilm-embedded bacteria is diminished or even nullified compared with planktonic cells.
Thus, the ability of S. epidermidis to switch from a harmless commensal to an opportunistic pathogen, which is closely linked to its capacity to form a biofilm, increases its clinical importance.
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