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Microbiology · Immunology: hypersensitivity type III
Sample itemA 30-year-old man bitten by a snake receives equine antivenom. Nine days later he develops fever, a generalised urticarial rash, joint pains and proteinuria, and serum C3 is low. What is the underlying mechanism?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Deposition of circulating antigen-antibody complexes with complement activation
Serum sickness is a type III hypersensitivity in which antibodies to foreign serum proteins form soluble immune complexes that lodge in vessels, joints and glomeruli. Complement activation consumes C3 and C4, and symptoms begin 7 to 14 days after exposure, when antibody appears while antigen is still present.
Option by option
A. Deposition of circulating antigen-antibody complexes with complement activation (correct)
Correct. Soluble immune complexes with complement consumption explain the delayed onset and low C3.
B. IgE-mediated degranulation of tissue mast cells
IgE-mediated mast cell degranulation is type I and produces anaphylaxis within minutes, not after 9 days.
C. Sensitised CD4 T cells releasing cytokines at the site
Sensitised T cells cause type IV delayed hypersensitivity such as the tuberculin reaction, and do not lower C3.
D. Antibody binding to antigens on his own cell surfaces
Antibody against cell-surface antigens is type II, as in haemolytic anaemia or Goodpasture disease.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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