Parvovirus B19 infects erythroblasts in bone marrow. In a patient with hereditary spherocytosis (chronic haemolytic anaemia), acute Parvovirus B19 infection leads to a dramatically low haematocrit within days. What is this clinical syndrome called, and why are patients with haemolytic anaemia at especially high risk?
- A Fifth disease (erythema infectiosum) — haemolysis accelerates because parvovirus induces RBC antibodies
- B Aplastic anaemia — parvovirus B19 destroys all bone marrow precursors including myeloid and megakaryocyte lines
- C Transient aplastic crisis (TAC) — parvovirus B19 destroys erythroid progenitors (binds globoside/P antigen on erythroblasts), causing cessation of erythropoiesis; patients with high RBC turnover (haemolytic anaemias) cannot survive even a brief pause in erythropoiesis ✓
- D Hydrops fetalis — occurs only in fetuses; adults with haemolysis develop only mild exacerbation
Explanation
Parvovirus B19 uses globoside (blood group P antigen) as its receptor on erythroblasts and megakaryocytes. It infects and lyses erythroid progenitors, causing complete cessation of erythropoiesis for ~7–10 days. In immunocompetent individuals with normal RBC lifespan (120 days), this brief pause is clinically inapparent. However, in patients with chronic haemolytic anaemias (spherocytosis, sickle cell, thalassaemia) where RBC survival is shortened to days and bone marrow compensates with high-output erythropoiesis, even a brief cessation causes profound anaemia — transient aplastic crisis (TAC), with haematocrit dropping precipitously. Treatment is supportive (transfusion, IVIG in immunocompromised). Hydrops fetalis occurs in pregnant women transmitting the virus to the fetus.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
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