Microbiology · Immunology (Hypersensitivity, Transplant, Immunodeficiency, Antibody-Antigen)

A 40-year-old man develops fever, arthralgia, urticarial rash, and palpable purpura eight days after starting a sulfonamide antibiotic. Serum C3 and C4 levels are low. Which hypersensitivity mechanism explains this presentation?

  • A IgE-mediated mast cell degranulation
  • B IgG antibody binding to fixed tissue antigens
  • C Circulating immune complex deposition activating complement
  • D CD8+ T cell killing of drug-modified keratinocytes
Correct answer: C. Circulating immune complex deposition activating complement

Explanation

Serum sickness is a systemic Type III hypersensitivity reaction. Antibodies formed against the drug after about a week form circulating immune complexes that deposit in vessel walls, glomeruli, and joints, activate complement (hence low C3 and C4), and attract neutrophils. The 7 to 10 day latency reflects the time needed for antibody production, distinguishing it from IgE-mediated anaphylaxis which occurs within minutes. Fixed-tissue antigen binding describes Type II reactions such as penicillin-induced hemolytic anemia.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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