Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of immunoglobulins, impairing opsonization.
After attachment, S. aureus deploys multiple factors to evade immunity and promote colonization. Coagulase activates prothrombin, leading to conversion of fibrinogen to fibrin, cloaking bacterial colonies from phagocytosis. Leukocidins lyse neutrophils and other leukocytes, reducing immune clearance. These actions enable persistent infection and tissue injury. Clinically significant methicillin-resistant S. aureus (MRSA) strains pose additional therapeutic challenges.
Cutaneous infections include folliculitis, which causes erythematous, pus-filled papules around hair follicles. Deeper infections produce furuncles—painful nodules containing necrotic tissue and pus. Coalescing furuncles form carbuncles, which involve the deeper dermis and subcutaneous tissue and are often accompanied by fever or malaise.
Some strains produce exfoliative toxins A and B, serine proteases that cleave desmoglein-1, a cadherin essential for keratinocyte adhesion in the stratum granulosum. This causes staphylococcal scalded skin syndrome (SSSS), marked by widespread erythema, fragile blisters, and superficial epidermal desquamation, with mucous membranes typically spared. SSSS mainly affects neonates and young children but may also occur in immunocompromised adults.
The combination of potent adhesins, immune evasion molecules, tissue-damaging toxins, and antibiotic resistance makes S. aureus one of the most clinically important pathogens in dermatology, capable of causing both localized and systemic disease.
Staphylococcus aureus, a Gram-positive bacterium, is part of the skin surface microbiota but can cause skin infection when the skin barrier is breached.
S. aureus uses surface adhesins such as clumping factor B and SasG to attach to host proteins loricrin and cytokeratin, present on skin cells.
This attachment allows the bacteria to persist locally and initiate bacterial infection.
As the infection progresses, coagulase, a S. aureus virulence factor, forms a protective fibrin clot, which helps localize the infection by shielding it from phagocytosis.
It also produces leukocidin, a toxin that destroys white blood cells.
S. aureus invasion causes localized skin infections, such as pimples or folliculitis. These appear as red, raised bumps filled with pus.
When the infection spreads deeper, it leads to the formation of a furuncle.
Carbuncles are clusters of furuncles that extend into the deeper dermis and subcutaneous tissue.
Staphylococcal scalded skin syndrome is characterized by blistering and peeling of the outer skin layer, caused by exfoliative toxins of S. aureus.
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