These factors haven't an evident virulence but concur in thwarting host defence mechanisms. Most of S. aureus strains show a thin polysaccharide external layer that forms a capsule visualized only by electron microscopy after antibody labelling, whose function apparently is to prevent phagocytosis, though, in vitro, this occur only in the absence of the complement and the polysaccharide production ends. Meanwhile, polysaccharide expression is associated with a lesser capability in colonizing damaged heart valves and causing endocarditis, probably leading to adhesins masking. Between surface components Protein A plays an important role in blocking phagocytosis (lacking Protein A mutant strains are more efficiently opsonized and engulfed in vitro) specifically binding Ig-G (G type immunoglobulin) by the Fc region in a wrong site and impeding the development of the immune response. Also Leukocidin produces a toxin whose target is polymorphonucleate leukocytes and inhibits phagocytosis. Inhibiting bacterial carotenoid production, responsible of the typical yellow glow surrounding the growing colonies, allows a higher efficiency in phagocytosis by both human and animal neutrophils. The yellow pigmentation is also a defence against oxidizing agents as hydrogen peroxide.