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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]

Exam Intelligence

  1. GC 105 / Gen Clerk Microbiology: S. aureus is THE coagulase +ve staphylococcus; coagulase −ve staphylococci (S. epidermidis, S. saprophyticus, S. lugdunensis) are differentiated by coagulase test. A single +ve blood culture for CoNS is usually a contaminant, but S. aureus bacteraemia is always clinically significant [1].

  2. GC 099 (Antimicrobial Resistance): MRSA carries mecA gene encoding altered PBP2a → confers resistance to virtually all β-lactam antibiotics. Antibiotics active against MRSA include vancomycin, linezolid, daptomycin, TMP-SMX, and tigecycline. Hospital antibiogram is used to monitor MRSA susceptibility patterns [2].

  3. GC 071 / Adrian Lui Pediatrics: Staphylococcal toxins act as superantigens → bind to conserved region of TCR → non-specific massive T-cell activation → cytokine storm. This mechanism underlies both TSS and SSSS [3].

  4. GC 052 / Felix Lai Pediatrics: S. aureus is a classic cause of post-influenza secondary bacterial pneumonia. CA-MRSA is specifically associated with necrotising pneumonia (PVL-producing strains) [5].

  5. Infective endocarditis (GC lectures + Block A): S. aureus has now superseded viridans streptococci as the most common cause of IE overall. It attacks normal valves, causes acute IE with large vegetations and fulminant valvular destruction. IVDU patients classically develop right-sided (tricuspid) IE. Treatment: MSSA → IV cloxacillin; MRSA → IV vancomycin. Always consult dental to rule out dental source [7].

  6. Food poisoning (GC 105 / AOS): S. aureus enterotoxin is preformed and heat-stable → cooking does not destroy the toxin. Presents with explosive vomiting 1–6 hours after ingestion, self-limiting, NO fever. This distinguishes it from Norovirus (which causes fever and person-to-person spread) [6].

  • S. aureus vs CoNS in blood cultures: S. aureus bacteraemia is NEVER dismissed as a contaminant. CoNS in a single bottle is usually contaminant unless the patient has prosthetic material or an indwelling catheter [1].
  • S. aureus food poisoning vs Norovirus: The 2018 and 2019 Fourth Summative MCQ EMQs test this exact discrimination. Key clues: S. aureus = vomiting-predominant, no fever, onset < 6 h, food handler with skin lesion, take-away food. Norovirus = vomiting + diarrhoea, fever, person-to-person spread, projectile vomiting in a closed setting (school/care centre), onset 24–48 h [6].
  • SSSS vs TEN: Both have widespread epidermal loss and Nikolsky sign, but SSSS = intra-epidermal cleavage beneath stratum corneum (no scarring); TEN = full-thickness epidermal necrosis (drug-induced, high mortality). SSSS occurs in children; TEN in adults [4].
  • Osteomyelitis pathogen trap: S. aureus is the most common cause overall, but in sickle cell disease, Salmonella is the classic organism [8].
  • Infective spondylitis: S. aureus is the most common pathogen. Past papers have tested the scenario of persistent fever + back pain + blood culture growing S. aureus → think infective spondylitis, and examine for lower limb neurology (cord compression) [10].
  • IE organism matching: G+ve cocci in clusters on blood culture = S. aureus. G+ve cocci in chains = streptococci. G+ve cocci in clusters in a patient with persistent fever + Janeway lesions on palms + eczema = IE due to S. aureus [13].

2018 Fourth Summative MCQ Q26 [6]:

"Thirty students from a secondary school but in different classes presented with vomiting with no fever approximately one hour after consuming a take-away egg and ham sandwich bought from a street vendor."

  • Correct answer: I. Staphylococcus aureus
  • Rationale: Preformed heat-stable enterotoxin; vomiting-predominant; very short incubation (1 h); no fever; food handler-associated. Discriminator vs Norovirus (Q27 in same paper): Norovirus has fever, person-to-person spread, longer incubation.

2023 Fourth Summative Minicase – Case Three, Section 3 [10]:

"Blood culture on admission grew Staphylococcus aureus. He had persistent fever and developed lower limb weakness after admission."

  • Q8: "Name three MOST RELEVANT components of neurological examination to be done at this stage." (6 marks)
  • Q9: "Name three microorganisms that can commonly cause infective spondylitis." (3 marks)
  • Q10: "List three principles of management of infective spondylitis." (6 marks)
  • Expected answers: Q8: Lower limb power, sensation, reflexes (including plantar response), rectal tone/perianal sensation. Q9: S. aureus, Mycobacterium tuberculosis, Streptococcus spp (or Gram-negative bacilli). Q10: IV antibiotics (prolonged course), immobilisation/spinal bracing, surgical decompression/debridement if cord compression or failure of medical therapy.

2023 Fourth Summative Minicase – Case Three, Section 4 [10]:

"Despite intravenous antimicrobial therapy, Mr. Chan's condition deteriorated…temperature 41°C, warm extremities, SpO2 85%, HR 125, BP 85/45."

  • Q13: "What is the MOST LIKELY clinical diagnosis causing his haemodynamic condition?" (3 marks)
  • Q14: "What would be your acute management? List five points." (15 marks)
  • Expected answers: Q13: Septic shock (secondary to S. aureus bacteraemia/spondylitis). Q14: Airway management, high-flow O₂, IV fluid resuscitation, IV vasopressors (e.g. noradrenaline), IV broad-spectrum antibiotics (escalate), blood cultures, consider source control (surgical drainage), lactate monitoring, catheterise for urine output.

2025 Fourth Summative MCQ Q39 [13]:

"A 36-year-old man presented to the hospital for fever which persisted for 2 weeks…small non-tender erythematous macular lesions over both palms…history of eczema…Two sets of blood culture grew Gram-positive cocci in cluster."

  • "What is the MOST LIKELY clinical diagnosis?"
  • Correct answer: D. Infective endocarditis
  • Rationale: Persistent fever + Janeway lesions (non-tender macular lesions on palms) + G+ve cocci in clusters (= S. aureus) in 2 blood culture sets = IE. Eczema provides portal of entry. Discriminators: Brucellosis = G−ve coccobacilli; TB = AFB; infectious mononucleosis = atypical lymphocytes/heterophile antibody, not G+ve cocci in clusters.

2018 Fourth Summative MCQ Q26–27 (EMQ stem XII) [6]:

The EMQ option list includes S. aureus (option I) alongside Norovirus (option G), Salmonella Enteritidis (H), Clostridium perfringens (C), etc. Q26 answer = S. aureus; Q27 answer = Norovirus. This pairing is a repeatedly tested discrimination.

[1] Senior notes: Gen Clerk Anaes + Microbiology Summary.pdf [2] Lecture slides: GC 099. Antimicrobial resistance.pdf [3] Senior notes: Adrian Lui Pediatrics Notes.pdf (p. 474–475) [4] Senior notes: Ryan Ho Rheumatology.pdf (p. 133) [5] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p. 160) [6] Past papers: 2018 Fourth Summative MCQ.pdf (Q26–27) [7] Senior notes: Ryan Ho Cardiology.pdf (p. 147–150); Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf (p. 35, 37) [8] Senior notes: Maksim Surgery Notes.pdf (p. 275) [9] Senior notes: Ryan Ho Rheumatology.pdf (p. 67) [10] Past papers: 2023 Fourth Summative Minicase.pdf (p. 21, 23) [11] Senior notes: Ryan Ho GI.pdf (p. 237) [12] Senior notes: Ryan Ho Opthalmology.pdf (p. 37) [13] Past papers: 2025 Fourth Summative MCQ.pdf (Q39)

Staphylococcus epidermidis

Coagulase-negative, Gram-positive coccus that is a normal skin commensal and a leading cause of biofilm-associated infections on indwelling medical devices and prosthetic implants.

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