Staphylococcus aureus organisms are pyogenic, nonmotile, Gram-positive cocci that form grapelike clusters. These bacteria cause a myriad of skin lesions (boils, carbuncles, impetigo, and scalded skin) and also cause osteomyelitis, pneumonia, endocarditis, food poisoning, and toxic shock syndrome (TSS).
Pathogenesis
S. aureus and other virulent staphylococci possess a multitude of virulence factors, which include surface proteins involved in adherence, secreted enzymes that degrade proteins, and secreted toxins that damage host cells. Staphylococci are distinguished by their large number of plasmids, which encode proteins involved in antibiotic resistance and other virulence factors.
S. aureus expresses surface receptors for fibrinogen (called clumping factor), fibronectin, and vitronectin, and uses these molecules as a bridge to bind to host endothelial cells.
Staphylococci infecting prosthetic valves and catheters have a polysaccharide capsule that allows them to attach to the artificial materials and to resist host cell phagocytosis.
The lipase of S. aureus degrades lipids on the skin surface, and its expression is correlated with the ability of the bacteria to produce skin abscesses.
Staphylococci also have protein A on their surface, which binds the Fc portion of immunoglobulins.
S. aureus produces multiple membrane-damaging (hemolytic) toxins, including ?-toxin, which is a pore-forming protein that intercalates into the plasma membrane of host cells and depolarizes them; ?-toxin, a sphingomyelinase; and ?-toxin, which is a detergent-like peptide. Staphylococcal ?-toxin and leukocidin lyse erythrocytes and phagocytic cells, respectively.
Cutaneous bullous lesions
The exfoliative toxins produced by S. aureus are serine proteases that split the skin by cleaving the protein desmoglein-1 (DSG1), which is part of the desmosomes that hold epidermal cells tightly together.
This can cause the superficial epidermis to split away from the deeper skin, making the patient vulnerable to secondary infections.
Exfoliation can occur at the site of staphylococcal skin infection (bullous impetigo) or can be widespread, when secreted toxin from a localized infection causes disseminated loss of the superficial epidermis (staphylococcal scalded-skin syndrome or SSSS).
Superantigens
Superantigens produced by S. aureus cause food poisoning and, of more concern, toxic shock syndrome (TSS). TSS came to public attention because of its association with the use of hyperabsorbent tampons, which became colonized with S. aureus during use. It is now clear that TSS can be caused by growth of S. aureus at many sites, most commonly the vagina and infected surgical sites.
TSS is characterized by hypotension (shock), renal failure, coagulopathy, liver disease, respiratory distress, a generalized erythematous rash, and soft tissue necrosis at the site of infection. If not promptly treated, TSS can be fatal. TSS can also be caused by Streptococcus pyogenes.
Superantigens bind to conserved portions of MHC molecules and to relatively conserved portions of TCR ? chains. In this manner, superantigens may stimulate up to 20% of T lymphocytes. The stimulation of so many T lymphocytes leads to massive T-lymphocyte proliferation and cytokine release. The high levels of cytokines can lead to capillary leak and shock and may cause vomiting by affecting the nervous system in the gut or the central nervous system.