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CLINICAL PRESENTATION

Local
skin/subcutaneous: impetigo, cellulitis, folliculitis, furuncles, carbuncles
respiratory: pneumonia with cavitations
Systemic
acute endocarditis, meningitis, osteomyelitis, septic arthritis
PATHOBIOLOGY
bacteria colonize skin (following breach) or nasopharynx (following intubation, viral respiratory infection) overgrow
and evade host defenses using:
protein A (binds Fc portion of IgG)
coagulase (forms fibrin coat around organism)
hemolysins, leukocidins (destroy RBCs and WBCs)
neutrophils localize to infection site purulent abscesses form skin/subcutaneous infections or pneumonia
bacteria may more deeply invade and reach bloodstream using:
hyaluronidase (breaks down connective tissue)
staphylokinase (lyses formed clots)
lipase (breaks down fat)
hematogenous spread to visceral organs systemic infection
DIAGNOSIS
blood culture positive: Gram clusters, catalase , coagulase
TREATMENT
antibiotic treatment:
MSSA (methicillin-sensitive S. aureus): penicillinase-resistant penicillins
MRSA (methicillin-resistant S. aureus): vancomycin
QUICK FACTS
Tricuspid valve endocarditis frequently affects IV drug users.
Patients with chronic granulomatous disease (impaired neutrophil function) are vulnerable.
S. aureus is a leading cause of osteomyelitis in children and adults.
Staphylococcus aureus (infections)
011-033_Harpavat_CoreCards_GramPosBacteria.indd 13b 7/10/11 1:15 AM

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