A 21-year-old man has suffered two separate episodes of fulminant meningococcal septicemia. Complement studies show normal activity of C1q, C4, and C3. Which additional deficiency best explains his susceptibility?

• A Deficiency of C2
• B Deficiency of properdin alone, with normal C5 through C9
• C Deficiency of a terminal complement component (C5, C6, C7, C8, or C9) ✓
• D Deficiency of C1 inhibitor

Explanation

Terminal complement component deficiencies impair formation of the membrane attack complex (MAC, C5b-9), the only mechanism by which complement directly kills Neisseria. Recurrent meningococcemia or gonococcemia is the classic presentation, while early components remain intact. C1 inhibitor deficiency causes hereditary angioedema, C2 deficiency predisposes to immune complex disease such as SLE, and isolated properdin deficiency also increases neisserial risk but does not match the stem's emphasis on a single definable late-component block.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.