Gene symbols: agr, accessory gene regulator; aur, auroelysin; cap, capsular polysaccharide synthesis; JhbA, fibronectin binding protein A; hla, a-toxin; hlb, fi-toxin; isaA, immunodominant staphylococcal antigen; kdpABC, potassium-transporting ATPase A, B, C chain homologue; IrgA, holin-lilce protein LrgA; IrgB, holin-lilce protein LrgB; lukSF, Pantone-Valentine leulcocidin components S and F; lytM, peptidoglycan hydrolase; murZ, UDP-N-acetylglucosamine 1-carboxylvinyl transferase 2; pbp2, penicillin binding protein 2; seb, staphylococcal enterotoxinB; sgtB, hypothetical protein, similar to penicillin-binding protein 1A/1B; spa, staphylococcal protein A; spl, serin protease; ssa, staphylococcal secretory antigen; tst, toxic shock syndrome toxin-1. n.d., not defined; n.p., not present.

has been suggested that the presence of the collagen binding protein (cna) may be associated with more virulent strains as many predominant lineages express cna [51, 52]. Likewise, many MSCRAMMs (microbial surface components recognizing adhesive matrix molecules) including clumping factor (ClfA and ClfB), fibro-nectin binding protein A (FnbA), and protein A, which binds the Fc part of antibodies, were found in most S. aureus strain [19, 20]. However, strains in which one or even more of those adhesins are lacking are also able to cause diseases. Interestingly, for some adhesins like clfA, clfB, fnbB, sdrC, and sdrD allelic variants due to a variable number of repeats have been described [20, 53]. This observation might be important in the light of antigenic variations of these adhesins by which the pathogen escapes immune defense mechanisms of the host. Most of the surface proteins of S. aureus carry a conserved C-terminal LPXTG motif by which the adhesins are attached to the cell wall by an enzyme named sortase. Both the cell wall attachment motif and the sortase enzyme seem to be conserved in all grampositive pathogens [54, 55].

Importantly, all S. aureus strains investigated so far encode the intercellular adhesin (ica) locus which is important for biofilm formation [56]. In contrast to S. epidermidis, where ica is predominantly associated with nosocomial isolates, in S. aureus the ica gene cluster is also found in carrier strains [19, 57]. Although most S. aureus isolates carry the sequence of the ica locus, only a few strains express the icaABCD genes and form a biofilm in vitro. Obviously, environmental stimuli as well as unknown regulatory elements control the ica expression in a different way from S. epidermidis.

Exoenzymes of S. aureus including lipase (geh), coagulase (coa), serine proteases (splC, splD), V8 protease (V8), aureolysin (aur), and hyaluronidase (hysA) are found in most strains and can therefore be regarded as part of the core genome [17, 19]. In contrast, many toxins, especially superantigenic toxins, are located on mobile genetic elements such as pathogenicity islands or bacteriophages, consequently being part of the accessory genome (for more details see below). Only some hemolysins such as a-toxin and c-hemolysin are present in most isolates, indicating a significant function for survival of S. aureus in its ecological niche.

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