A 28-year-old intravenous drug user has fever, regurgitant murmur, and septic pulmonary emboli. Blood cultures grow Staphylococcus aureus. Echocardiography reveals a vegetation on the tricuspid valve. In infective endocarditis caused by S. aureus, the virulence mechanism allowing initial valve colonization without pre-existing valve damage involves which surface protein?

• A Protein A (spa gene), blocking IgG Fc opsonization
• B FnBP (fibronectin-binding proteins A and B), enabling adherence to intact endothelium ✓
• C Coagulase, converting fibrinogen to fibrin as a scaffold for colonization
• D Alpha-hemolysin (Hla), lysing endothelial cells to expose subendothelial matrix

Explanation

S. aureus can cause endocarditis on previously normal valves, a feature distinguishing it from most other causative organisms that require pre-existing damage. FnBP-A and FnBP-B (encoded by fnbA and fnbB) are MSCRAMM (microbial surface components recognizing adhesive matrix molecules) proteins that bind fibronectin on intact endothelial cells, enabling S. aureus to adhere to and invade intact endothelium without requiring pre-existing valve injury. This explains right-sided endocarditis in IVDU where venous valves are structurally normal. Coagulase is important for fibrin clot formation around the bacteria after colonization.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.