Colonization and infection of the human host by staphylococci: adhesion, survival and immune evasion.

The natural habitat of Staphylococcus aureus in humans is the moist squamous epithelium of the anterior nares. Several bacterial surface proteins are implicated in promoting adhesion to desquamated epithelial cells. Clumping factor B (ClfB) and iron-regulated surface determinant A both promote nasal colonization in rodent models, and in the case of ClfB, humans. One of the ligands involved in adhesion is cytokeratin 10. Reduction in nasal colonization can be achieved by active and passive immunization. S. aureus is well endowed with secreted and surface components that compromise innate immune responses, particularly the function of neutrophils. S. aureus secretes proteins that reduce migration of neutrophils from the bloodstream to the site of infection by impeding diapedesis and receptors for chemotactic molecules. Several secreted proteins interfere with complement C3 and C5 convertases, thus reducing the level of C3b opsonin and the chemotactic peptide C5a. Host proteases are recruited to the cell surface to enhance destruction of opsonic C3b and IgG. Surface components ClfA, protein A and polysaccharide capsule compromise the recognition of opsonins on the bacterial cell surface. If engulfed by neutrophils the intracellular bacterium can resist reactive oxygen intermediates, nitric oxide radicals, defensin peptides and bactericidal proteins. A prior infection by S. aureus does not induce complete protective immunity. This could be due to immunosuppression caused by expression of superantigen proteins that disrupt normal activation of T cells and B cells during antigen presentation. By studying the molecular pathogenesis of S. aureus infections markers might be found for investigating S. pseudintermedius infections of dogs.