A veterinarian previously sensitized to tetanus toxoid receives an intradermal booster and develops marked edema and hemorrhagic necrosis at the injection site within 4 hours. Biopsy shows fibrinoid necrosis of vessel walls with abundant neutrophils and deposits of antigen, IgG, and complement. Which hypersensitivity mechanism is responsible?

• A IgG binding to fixed tissue antigen with direct complement-mediated lysis
• B Antigen cross-linking IgE on mast cells causing immediate mediator release
• C CD4+ Th1 cells secreting IFN-gamma and activating macrophages
• D Local deposition of preformed antigen-antibody complexes activating complement and recruiting neutrophils ✓

Explanation

The Arthus reaction is the experimental model of a localized type III hypersensitivity response. Circulating IgG against a previously injected antigen forms immune complexes in the vessel wall at the inoculation site, fixing complement, generating C5a, and attracting neutrophils that cause fibrinoid necrosis within 4 to 6 hours. Option C describes type IV delayed-type hypersensitivity, which peaks at 48 to 72 hours and is lymphocyte rich rather than neutrophil rich. Option B would produce wheal and flare within minutes, not hemorrhagic necrosis.

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.