A patient develops crusted, bloody lips and oral ulcerations approximately one week after starting a course of amoxicillin. Which immune mechanism is responsible?

Correct answer: D. Type IV, cell-mediated (T-lymphocyte) hypersensitivity

• A. Type II involves antibodies directed against cell surface antigens (e.g., autoimmune hemolytic anemia, pemphigus).
• B. Type III involves circulating immune complex deposition (serum sickness, lupus nephritis).
• C. Type I reactions occur within minutes to an hour (urticaria, angioedema, anaphylaxis) and involve mast cell degranulation — the timeline here is far too long.
• D. CORRECT. Hemorrhagic crusting of the vermilion with 'target' skin lesions one to two weeks after a drug exposure is ERYTHEMA MULTIFORME. It is a T-CELL MEDIATED (Type IV, delayed) reaction in which cytotoxic CD8+ lymphocytes attack keratinocytes. The delayed onset — days to weeks, not minutes — is the giveaway that this is not IgE-mediated. Common triggers: HSV (most common overall), sulfonamides, penicillins, NSAIDs, anticonvulsants.

Note: Timing is your diagnostic tool: minutes = Type I; 24–72 hours or longer = Type IV.