In complement cascade, C3b deposition on bacteria promotes opsonisation. In which primary immunodeficiency disease is there a specific defect in C3b opsonisation leading to recurrent pyogenic infections?
- A C3 deficiency — leads to complete failure of all complement pathways and opsonisation ✓
- B C5–C9 (terminal complement) deficiency — leads to recurrent Neisseria infections
- C C1q deficiency — most commonly presents with SLE-like autoimmune disease
- D Mannose-binding lectin (MBL) deficiency — leads to recurrent viral respiratory infections only
Correct answer: A. C3 deficiency — leads to complete failure of all complement pathways and opsonisation
Explanation
C3 is the central molecule where all three complement activation pathways (classical, lectin, alternative) converge; C3b is the critical opsonin. C3 deficiency results in absent opsonisation, absent C3a/C5a anaphylatoxin generation, and absent MAC formation — leading to recurrent severe pyogenic infections (S. pneumoniae, H. influenzae). Terminal complement deficiencies (C5–C9) specifically predispose to Neisseria infections (N. meningitidis, N. gonorrhoeae) due to absence of MAC. C1q deficiency predisposes to SLE (impaired apoptotic debris clearance).
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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