U01.03.021 Staphylococcus aureus

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Learning Objective: Be able to identify Staphylococcus aureus based on lab features (Gram+, β-hemolysis, catalase+, coagulase+), virulence factors (Protein A, toxins), and its spectrum of inflammatory vs. toxin-mediated diseases, as well as understand the mechanism of MRSA resistance.

Basic Characteristics

Feature	Key Point
Gram stain	Gram-positive cocci in clusters
Hemolysis	β-hemolytic on blood agar
Catalase test	Positive
Coagulase test	Positive
Colonization sites	Skin, nares, ears, axilla, groin

Virulence Factors

Virulence Factor	Mechanism / Role
Protein A	Binds the Fc region of IgG → prevents complement activation and phagocytosis
Coagulase	Promotes fibrin clot formation → walling-off of infection (abscess)
Toxins	TSST-1 (superantigen → cytokine storm), exfoliative toxin (scalded skin syndrome), enterotoxins (rapid food poisoning)
PVL (Panton-Valentine leukocidin)	Kills leukocytes, causes tissue necrosis (some strains)

Clinical Manifestations

A. Inflammatory Diseases

Skin infections (impetigo, cellulitis, abscesses)
Organ abscesses
Pneumonia (often post-influenza)
Infective endocarditis
Septic arthritis
Osteomyelitis

B. Toxin-Mediated Diseases

Disease	Toxin	Clinical Features
Toxic Shock Syndrome (TSS)	TSST-1 (superantigen)	Fever, vomiting, diarrhea, rash → desquamation, shock, multi-organ failure; ↑ AST/ALT/bilirubin; linked to tampons/nasal packing
Scalded Skin Syndrome	Exfoliative toxin	Widespread epidermal sloughing
Food Poisoning	Preformed enterotoxin (heat-stable)	Rapid onset (2–6 hr), non-bloody diarrhea + emesis; not destroyed by cooking

Antibiotic Resistance

MRSA (Methicillin-Resistant S. aureus)
- Resistance due to the mecA gene → altered penicillin-binding proteins
- The major cause of healthcare-associated and community-acquired infections

Key Comparison

S. aureus TSS: Mediated by superantigen TSST-1
S. pyogenes TSS: “Toxic shock–like syndrome,” usually associated with painful skin infection