A 28-year-old intravenous drug user is found to have Staphylococcus aureus bacteremia and right-sided endocarditis affecting the tricuspid valve. Vegetation pathology shows abundant neutrophils, fibrin, and gram-positive cocci. Which virulence factor of S. aureus is most critical for initiating valvular colonization?
- A Protein A — binds Fc region of IgG to evade opsonization
- B Clumping factor A (ClfA) — fibrinogen-binding surface protein mediating adherence to damaged endothelium ✓
- C Alpha-toxin (alpha-hemolysin) — pore-forming toxin causing direct valvular endothelial necrosis
- D Toxic shock syndrome toxin-1 (TSST-1) — superantigen activating T cells non-specifically
Explanation
S. aureus endocarditis can occur on previously normal valves (unlike viridans streptococci, which require pre-existing damage). The key virulence factor initiating valvular infection is Clumping Factor A (ClfA), a surface-anchored MSCRAMM (microbial surface component recognizing adhesive matrix molecules) that binds fibrinogen deposited on traumatized endothelium (from turbulent flow or IV catheter injury). ClfA-fibrinogen interaction enables initial colonization. Protein A aids immune evasion after colonization. Alpha-toxin causes endothelial damage, amplifying the process but is not the initiating step. TSST-1 mediates toxic shock syndrome rather than endocarditis.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.