Abstract

Staphylococcus aureus is a normal commensal of the skin and mucous membranes. When either of these two barriers are disrupted, the first and most important line of host defence against S. aureus is gone. Infections caused by S. aureus are a major source of morbidity and mortality in hospital-based practice. Suppuration is the hallmark of staphylococcal disease. The most frequent lesion is a cutaneous abscess or boil (furuncle), which begins as an infection of sebaceous glands or hair shafts. Superficial skin infections are usually self-limiting, while more serious localized infections can rapidly spread to the soft tissues. Via local invasion or intravascular access devices, S. aureus can also gain access to the bloodstream and cause bacteraemia or septicemia. Serious staphylococcal infections occur much more commonly in association with a predisposing condition than they do spontaneously, as seen in patients with a chronic illness, traumatic injury, or burns or in immuno-compromised patients. Because of this, serious infections are mostly seen in hospitalized patients rather than in healthy individuals in the community. S. aureus is equipped with cell-surface proteins that bind fibrinogen, fibronectin, collagen, laminin, plasminogen, thrombospondin, and heparan sulphate. Using these surface proteins, S. aureus (Fig. 1) can adhere and colonize traumatized tissues. S. aureus (like S. epidermidis) can also bind to synthetic material, as is seen in the frequent infections associated with indwelling devices such as intravascular and intraperitoneal catheters, joint prostheses, cardiovascular devices, and artificial heart valves.KeywordsToxic Shock SyndromeAlpha ToxinArtificial Heart ValveGPCR FamilyCrude SupernateThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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