A 35-year-old IV drug user develops fever and a new pansystolic murmur. Blood cultures grow Staphylococcus aureus. Echocardiography shows bulky, friable vegetations on the tricuspid valve. The mechanism by which infective endocarditis vegetations form on cardiac valves is:
- A Prior sterile thrombus (NBTE) on damaged endothelium colonised by bacteraemic organisms ✓
- B Haematogenous bacteria directly infecting intact valvular endothelium
- C Immune complex deposition activating complement and recruiting bacteria
- D Direct cytotoxic T-cell attack on valvular endothelium followed by bacterial colonisation
Explanation
Infective endocarditis develops when haematogenous bacteraemia seeds pre-existing sterile vegetations (non-bacterial thrombotic endocarditis/NBTE) formed at sites of endothelial damage or turbulent flow. Damaged endothelium exposes subendothelial collagen, which captures platelets and fibrin; the resulting sterile thrombus provides a nidus for bacteraemic organisms (especially S. aureus, viridans streptococci) to adhere via surface adhesins (fibronectin-binding proteins, MSCRAMM). In IV drug users, right-sided (tricuspid) IE from skin flora injected directly is common.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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