A 28-year-old patient with sickle cell disease develops sudden severe aplastic crisis with Hb dropping to 4 g/dL and reticulocyte count near zero. The most likely causative agent and mechanism is:
- A Plasmodium falciparum infecting reticulocytes and suppressing marrow
- B Salmonella typhi causing marrow infiltration during bacteremia
- C Epstein-Barr virus suppressing erythropoiesis via type I interferon
- D Parvovirus B19 infecting erythroid progenitors expressing P antigen (globoside) causing lytic infection ✓
Explanation
Parvovirus B19 causes transient aplastic crisis in patients with hemolytic anemia (sickle cell, hereditary spherocytosis, thalassemia) by infecting erythroid progenitor cells (burst-forming unit-erythroid, BFU-E and colony-forming unit-erythroid, CFU-E) via the P antigen (globoside, also known as Pk antigen), causing lytic infection that halts RBC production. In normal individuals this results in brief reticulocytopenia easily compensated, but in hemolytic anemia with shortened RBC survival, the cessation of production precipitates life-threatening anemia. Reticulocyte count is characteristically zero or near zero. This is self-limited in immunocompetent individuals, lasting 7–10 days.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.