16.1
Staphylococcal Skin Infections
Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier…
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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Q1: How does Staphylococcus aureus attach to skin cells and cause infection?
S. aureus uses surface adhesins like clumping factor B and SasG to bind to host proteins loricrin and cytokeratin on skin cells. This attachment allows bacteria to persist locally and initiate infection when the skin barrier is breached. Protein A further impairs immunity by binding immunoglobulin Fc regions, reducing opsonization and enabling colonization.
Q2: What role does coagulase play in staphylococcal skin infections?
Coagulase is a virulence factor that activates prothrombin, converting fibrinogen to fibrin and forming a protective clot around bacterial colonies. This fibrin shield localizes the infection and shields bacteria from phagocytosis, allowing persistent infection and tissue damage to occur.
Q3: How do leukocidins contribute to S. aureus pathogenesis?
Leukocidins are toxins produced by S. aureus that lyse neutrophils and other white blood cells, reducing immune clearance of the bacteria. By destroying these key immune cells, leukocidins enable persistent infection and allow the bacteria to cause progressive tissue injury.
Q4: What is the difference between folliculitis, furuncles, and carbuncles?
Folliculitis causes erythematous, pus-filled papules around hair follicles. Furuncles are deeper, painful nodules containing necrotic tissue and pus. Carbuncles form when multiple furuncles coalesce, extending into the deeper dermis and subcutaneous tissue, often accompanied by fever or malaise.
Q5: What causes staphylococcal scalded skin syndrome and who is most affected?
Staphylococcal scalded skin syndrome (SSSS) is caused by exfoliative toxins A and B, serine proteases that cleave desmoglein-1, disrupting keratinocyte adhesion in the stratum granulosum. This produces widespread erythema, fragile blisters, and epidermal peeling. SSSS primarily affects neonates and young children but may occur in immunocompromised adults.
Q6: Why is S. aureus considered a commensal organism on healthy skin?
S. aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals as part of normal microbiota. It only becomes pathogenic when the skin barrier is breached, allowing it to shift from commensal to opportunistic pathogen and deploy virulence factors.
Q7: What makes methicillin-resistant S. aureus clinically significant?
Methicillin-resistant S. aureus (MRSA) strains pose additional therapeutic challenges due to antibiotic resistance. Combined with potent adhesins, immune evasion molecules, and tissue-damaging toxins, MRSA makes S. aureus one of the most clinically important pathogens in dermatology, capable of causing both localized and systemic disease.