16.1
Infezioni cutanee stafilococici
Staphylococcus aureus è un cocco Gram-positivo che risiede innocuamente sulla pelle e sulle mucose degli individui sani. Quando la barriera cutanea vi…
Staphylococcus aureus, un batterio Gram-positivo, fa parte del microbiota superficiale della pelle ma può causare infezioni cutanee quando la barriera cutanea viene violata.
S. aureus utilizza adesine superficiali come il fattore di aggregazione B e SasG per attaccarsi alle proteine ospiti loricrina e citocheratina, presenti nelle cellule della pelle.
Questo attacco permette ai batteri di persistere localmente e di innescare infezioni batteriche.
Con il progredire dell'infezione, la coagulasi, un fattore di virulenza di S. aureus , forma un coagulo protettivo di fibrina, che aiuta a localizzare l'infezione proteggendola dalla fagocitosi.
Produce anche leucocidina, una tossina che distrugge i globuli bianchi.
L'invasione di S. aureus causa infezioni cutanee localizzate, come brufoli o follicolite. Questi appaiono come protuberanze rosse e rialzate piene di pus.
Quando l'infezione si diffonde più a fondo, si forma un forno.
I carbuncoli sono gruppi di foruncoli che si estendono nel derme più profondo e nel tessuto sottocutaneo.
La sindrome della pelle scottata da stafilococo è caratterizzata da vesciche e squamamento dello strato esterno della pelle, causato da tossine esfoliative di 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.