A 7-year-old child presents with prodromal fever, coryza, Koplik's spots on the buccal mucosa, and then a maculopapular rash descending from the face. Which immune effector mechanism is responsible for the rash?
- A Direct viral cytopathic destruction of epidermal keratinocytes
- B Type IV (delayed-type hypersensitivity) CD8+ T cell–mediated immune response to infected cells ✓
- C IgE-mediated mast cell degranulation
- D Neutrophil-mediated abscess formation in follicles
Explanation
The measles rash is immunopathological — paradoxically, severely immunocompromised children (e.g., agammaglobulinaemic or T-cell deficient) may not develop a rash. The rash represents CD8+ cytotoxic T-cell killing of MV-infected vascular endothelial cells in the skin (delayed-type hypersensitivity, Type IV), not direct viral destruction. This is why children with isolated agammaglobulinaemia get a normal rash (B cells not required), whereas those with SCID or advanced HIV have atypical measles without rash but with fatal pneumonia (Hecht's pneumonia). IgE-mediated reactions cause urticaria, not measles rash. Koplik's spots appear before the rash on buccal mucosa opposite the lower molars.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.