Staphylococcus aureus has the ability to cause a wide variety of human diseases: from superficial abscesses and wound infections to deep and systemic infections such as osteomyelitis, endocarditis and septicaemia. S. aureus invasion might be involved in some of the unique pathogenic manifestations of this bacterium, including long-term colonization. The ability to cause disease is a result of presence of virulence factors. Virulence factors are synthesized in response to the specific needs during the infectious process. The molecular mechanism and the precise role of invasion in S. aureus pathology are not known. S. aureus expresses many potential virulence factors: surface proteins, invasins (leukocidin, kinases hyaluronidase), inhibitors of phagocytic engulfment (capsule, Protein A), factors enhancing bacterial survival in phagocytes ( carotenoids, catalase production), immunological disguises (Protein A, coagulase, clotting factor), membrane- damaging toxins (hemolysins, leukotoxin, leukocidin) and exotoxins (SEA-G, TSST, ET).
The pathogenicity of S. aureus infections is related to surface components including those recognizing adhesive matrix molecules (e.g., clumping factor and fibronectin binding protein) and to extracellular proteins [e.g., coagulase, hemolysins, enterotoxins, toxic-shock syndrome (TSS) toxin, exfoliatins, and Panton-Valentine leukocidin (PVL)]. In general, the precise roles of individual staphylococcal factors in invasive infections are difficult to assess.