A 35-year-old presents with fever for 5 days, severe thrombocytopenia (platelets 18,000/µL), petechiae, and a positive tourniquet test. NS1 antigen is positive on day 3. On day 6, the patient develops dengue hemorrhagic fever grade III. The primary pathophysiologic mechanism is:
- A Direct cytotoxic destruction of platelets by dengue virus
- B IgE-mediated hypersensitivity to dengue antigens
- C Cross-reactivity with P. falciparum antigens causing hemolysis
- D Antibody-dependent enhancement with increased viral replication and complement-mediated vascular leak ✓
Explanation
Dengue hemorrhagic fever is primarily due to antibody-dependent enhancement (ADE): during secondary infection with a different dengue serotype, preformed non-neutralizing IgG antibodies enhance viral uptake by Fc receptor-bearing monocytes, dramatically increasing viral load. Activated T-cells and monocytes release vasoactive cytokines (TNF-α, IL-6) that increase vascular permeability, causing plasma leak, thrombocytopenia, and hemorrhage. This is why DHF is more common in secondary dengue infections. Direct viral cytotoxicity plays a minor role; IgE and malaria cross-reactivity are not involved.
Reference: Park's Textbook of Preventive and Social Medicine, 27th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.