Gram-positiveCocciCatalase-positive

Staphylococcus aureus

Gram-positive, coagulase-positive coccus forming grape-like clusters, responsible for skin and soft-tissue infections, bacteremia, endocarditis, osteomyelitis, and toxin-mediated diseases including toxic shock syndrome.

Organism Card

DomainMust know
Identity
  • G+ve cocci in clusters; catalase +ve, coagulase +ve [1]
  • Facultative anaerobe; non-motile; golden-yellow colonies on agar
  • Normal flora of skin and anterior nares (~30% carriage)
Lab discriminator
  • Coagulase +ve distinguishes S. aureus from CoNS (S. epidermidis, S. saprophyticus, S. lugdunensis) [1]
  • Catalase +ve distinguishes staphylococci from streptococci (catalase −ve)
  • Mannitol salt agar: S. aureus ferments mannitol (yellow colonies); CoNS do not
  • DNase +ve; Protein A on surface (binds IgG Fc → antiphagocytic)
Reservoir / transmission
  • Human skin and nares; ubiquitous environmental contamination
  • Direct contact, fomites, airborne (wound infections, theatre contamination)
  • Healthcare-associated spread: hands of HCW are the key vector for MRSA transmission [2]
  • IVDU: key risk group for S. aureus bacteraemia and right-sided IE [4]
Key virulence
  • Toxins act as superantigens → bind part of TCR shared by many T cells → massive T cell proliferation and cytokine release [3]
  • Exfoliative toxins (ETA, ETB) → cleave desmoglein 1 → SSSS [4]
  • TSST-1 → toxic shock syndrome (menstrual and non-menstrual) [4]
  • Enterotoxins (heat-stable, preformed) → emetic food poisoning within 1–6 h [6]
  • Panton-Valentine leukocidin (PVL) → necrotising pneumonia, skin abscesses (CA-MRSA) [5]
  • Protein A → binds IgG Fc → evades opsonisation
  • Coagulase → clot formation protecting organism; biofilm on prosthetic devices
Clinical syndromes
  • Skin/soft tissue: impetigo (honey-crust), furuncles, carbuncles, wound infection, cellulitis [3]
  • SSSS: flaccid bullae, Nikolsky +ve, split beneath stratum corneum (cf. TEN = full-thickness) [4]
  • TSS: fever, diffuse erythematous desquamating rash, hypotension, multiorgan failure; a/w tampons or nasal packing [4]
  • Post-influenza pneumonia: classically S. aureus; CA-MRSA → necrotising pneumonia [5]
  • Infective endocarditis: most common cause of IE; attacks normal valves; acute onset, large vegetations, fulminant valvular destruction [7]
  • Osteomyelitis: most common pathogen in children > 2 y and adults; metaphysis in children [8]
  • Septic arthritis: most common pathogen (> 2 y); monoarthritis of knee [9]
  • Infective spondylitis: blood culture growing S. aureus + back pain + fever [10]
  • Bacteraemia, pyogenic liver abscess (external inoculation route), orbital cellulitis [11][12]
  • Food poisoning: preformed heat-stable enterotoxin; vomiting within 1–6 h, short illness, NO fever [6]
Diagnosis
  • Blood cultures (≥ 2 sets from different sites before antibiotics) [7]
  • Gram stain: G+ve cocci in clusters
  • Culture: blood agar (β-haemolytic), mannitol salt agar
  • Coagulase test (tube or slide) confirms S. aureus
  • For IE: ≥ 3 blood cultures, echocardiogram (TTE → TEE if negative), Modified Duke criteria [7]
  • Joint aspirate for septic arthritis; bone biopsy/MRI for osteomyelitis
  • SSSS: skin snip biopsy → split beneath stratum corneum (vs SJS/TEN full-thickness necrosis) [4]
  • Food poisoning: clinical diagnosis; culture of implicated food
Treatment
  • MSSA: IV cloxacillin (or flucloxacillin/nafcillin) or 1st-gen cephalosporin (cefazolin) [7][8]
  • MRSA: vancomycin is first-line [7]; alternatives include linezolid, daptomycin
  • IE principles: IV bactericidal agents, high dose, prolonged course (4–6 weeks); eradicate source (e.g. dental consult) [7]
  • Osteomyelitis / septic arthritis: IV cloxacillin × 4–6 weeks + surgical debridement [8]
  • SSSS: IV antistaphylococcal antibiotics (flucloxacillin/oxacillin) + supportive care [3][4]
  • Food poisoning: supportive only (self-limiting)
  • Key resistance: MRSA carries mecA gene → altered PBP2a → resistant to all β-lactams except 5th-gen cephalosporins (ceftaroline) [2]
Prevention
  • Contact precautions + hand hygiene for MRSA; active screening on admission in high-risk settings [2]
  • Decolonisation: intranasal mupirocin ± chlorhexidine body wash for carriers
  • IE prophylaxis now conservative; single-dose amoxicillin before high-risk dental procedures in susceptible patients [7]
  • MRSA is a notifiable multidrug-resistant organism under HK hospital surveillance [2]
  • No vaccine currently available
Classic traps
  • S. aureus food poisoning: vomiting-predominant, onset 1–6 h, NO fever → vs Norovirus (fever, vomiting + diarrhoea, person-to-person spread, onset 24–48 h) [6]
  • S. aureus IE: acute, normal valves, IVDU → vs viridans strep IE: subacute, damaged valves, dental source [7]
  • SSSS (intra-epidermal split, Nikolsky +ve, children) → vs TEN (full-thickness necrosis, drug-induced, adults) [4]
  • CoNS single +ve blood culture = likely contaminant; S. aureus single +ve = always significant → never dismiss [1]
  • Osteomyelitis in sickle cell disease: Salmonella (not S. aureus) is the classic pathogen [8]
  • Septic arthritis vs gout: both present as hot swollen joint; joint aspirate for crystals + Gram stain/C/ST is decisive [9]

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