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      Staphylococcus epidermidis — the 'accidental' pathogen

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      Journal: Nature Reviews Microbiology
      Publisher: Springer Science and Business Media LLC

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          Abstract

          Although nosocomial infections by Staphylococcus epidermidis have gained much attention, this skin-colonizing bacterium has apparently evolved not to cause disease, but to 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 give rise to additional benefits 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, I discuss the molecular basis of the commensal and infectious lifestyles of S. epidermidis.

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          Identification of novel cytolytic peptides as key virulence determinants for community-associated MRSA.

          Rong. Wang, Kevin R Braughton, Dorothee Kretschmer … (2007)
          Methicillin-resistant Staphylococcus aureus (MRSA) remains a major human pathogen. Traditionally, MRSA infections occurred exclusively in hospitals and were limited to immunocompromised patients or individuals with predisposing risk factors. However, recently there has been an alarming epidemic caused by community-associated (CA)-MRSA strains, which can cause severe infections that can result in necrotizing fasciitis or even death in otherwise healthy adults outside of healthcare settings. In the US, CA-MRSA is now the cause of the majority of infections that result in trips to the emergency room. It is unclear what makes CA-MRSA strains more successful in causing human disease compared with their hospital-associated counterparts. Here we describe a class of secreted staphylococcal peptides that have a remarkable ability to recruit, activate and subsequently lyse human neutrophils, thus eliminating the main cellular defense against S. aureus infection. These peptides are produced at high concentrations by standard CA-MRSA strains and contribute significantly to the strains' ability to cause disease in animal models of infection. Our study reveals a previously uncharacterized set of S. aureus virulence factors that account at least in part for the enhanced virulence of CA-MRSA.
          Article 0 comments Cited 335 times – based on 0 reviews     Review now
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            Novel type of staphylococcal cassette chromosome mec identified in community-acquired methicillin-resistant Staphylococcus aureus strains.

            P Chongtrakool, Keiichi Hiramatsu, Mantana Jamklang … (2002)
            We identified a new type of staphylococcal cassette chromosome mec (SCCmec) from two community-acquired methicillin-resistant Staphylococcus aureus (MRSA) strains. The novel element, designated type IV SCCmec, had a unique combination of the class B mec gene complex and the type 2 ccr gene complex and was much smaller in size (21 to 24 kb) than previously identified SCCmec elements of hospital-acquired MRSA. Consistent with the strains' susceptibilities to various non-beta-lactam antibiotics, the type IV SCCmec was devoid of any antibiotic resistance genes other than the mecA gene.
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              The antimicrobial peptide-sensing system aps of Staphylococcus aureus.

              Amer E. Villaruz, Michael Otto, J. CHA … (2007)
              Staphylococcus aureus is a leading cause of hospital-associated and, more recently, community-associated infections caused by highly virulent methicillin-resistant strains (CA-MRSA). S. aureus survival in the human host is largely defined by the ability to evade attacks by antimicrobial peptides (AMPs) and other mechanisms of innate host defence. Here we show that AMPs induce resistance mechanisms in CA-MRSA via the aps AMP sensor/regulator system, including (i) the d-alanylation of teichoic acids, (ii) the incorporation of lysyl-phosphatidylglycerol in the bacterial membrane and a concomitant increase in lysine biosynthesis, and (iii) putative AMP transport systems such as the vraFG transporter, for which we demonstrate a function in AMP resistance. In contrast to the aps system of S. epidermidis, induction of the aps response in S. aureus was AMP-selective due to structural differences in the AMP binding loop of the ApsS sensor protein. Finally, using a murine infection model, we demonstrate the importance of the aps regulatory system in S. aureus infection. This study shows that while significant interspecies differences exist in the AMP-aps interaction, the AMP sensor system aps is functional and efficient in promoting resistance to a variety of AMPs in a clinically relevant strain of the important human pathogen S. aureus.
              Article 0 comments Cited 81 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Nature Reviews Microbiology
                Abbreviated Title: Nat Rev Microbiol
                Publisher: Springer Science and Business Media LLC
                ISSN (Print): 1740-1526
                ISSN (Electronic): 1740-1534
                Publication date Created: August 2009
                Publication date (Print): August 2009
                Volume: 7
                Issue: 8
                Pages: 555-567
                Article
                DOI: 10.1038/nrmicro2182
                PMC ID: 2807625
                PubMed ID: 19609257
                SO-VID: ea183215-a2b0-4ab9-a98a-6e441081c470
                Copyright © © 2009
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                http://www.springer.com/tdm

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