A 55-year-old hypertensive man has a descending thoracic aortic aneurysm. Histology shows loss of medial smooth muscle cells, elastin fragmentation, and an inflammatory infiltrate. The most common causative treatable organism in luetic (syphilitic) aortitis — the classic cause of thoracic aortic aneurysm — acts by:
- A Direct proteolysis of elastin by Treponema pallidum outer membrane proteins
- B Complement-mediated endothelial lysis causing transmural necrosis
- C Obliterative endarteritis of the vasa vasorum causing ischemic medial destruction ✓
- D Autoimmune anti-elastin antibody formation cross-reacting with spirochetal proteins
Explanation
Syphilitic (luetic) aortitis affects the thoracic aorta (ascending and arch), where the vasa vasorum are most prominent. Treponema pallidum invades the adventitial vasa vasorum, triggering obliterative endarteritis that reduces medial blood supply, causing ischemic necrosis of smooth muscle cells and elastin. Grossly, the intima shows 'tree-bark' wrinkling. The resulting medial destruction leads to aneurysm formation, aortic regurgitation (root involvement), and coronary ostial stenosis. This is the classic cause of saccular thoracic aneurysm in pre-antibiotic era.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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Written and medically reviewed by the StethoPrep medical team.