Aplastic Crisis Triggered by Parvovirus B19 in an Adult Man With Sickle Cell Disease

Patients with sickle cell disease (SCD) are vulnerable to acute hematologic complications due to chronic hemolysis and dependence on increased erythropoiesis. Parvovirus B19 infection can suppress erythroid progenitor cells, precipitating a transient aplastic crisis characterized by severe anemia and reticulocytopenia. Early recognition is critical to distinguish this condition from other causes of acute anemia in patients with SCD. A 22-year-old man with hemoglobin SS SCD and prior splenectomy presented with a three-day history of severe headache, non-bloody emesis, fevers, fatigue, and generalized myalgias distinct from his typical vaso-occlusive crises. On presentation, vital signs were stable, and physical examination was largely unremarkable. Laboratory evaluation demonstrated severe anemia with a hemoglobin of 4.5 g/dL (baseline: 7-10 g/dL), leukocytosis (19×10⁹/L), thrombocytopenia (94×10⁹/L), and a reticulocyte count of 2.8%. Hemolysis markers were elevated but consistent with his baseline chronic hemolysis. Peripheral smear revealed 1-3% sickled erythrocytes. Evaluation for alternative causes of acute anemia, including thrombotic microangiopathy, disseminated intravascular coagulation, autoimmune hemolytic anemia, and hemophagocytic lymphohistiocytosis, was unrevealing. Viral studies demonstrated elevated parvovirus B19 IgM and IgG antibodies, confirming acute infection. The patient received four units of packed red blood cells with improvement in hemoglobin to 6.6 g/dL. He was managed with supportive care, and hematologic parameters gradually returned toward baseline prior to discharge. This case highlights the importance of recognizing parvovirus B19-induced transient aplastic crisis as a potentially life-threatening but treatable complication in patients with SCD. Existing literature describes reticulocytopenia as a key distinguishing feature from other causes of acute anemia in SCD, yet diagnosis may be challenging when patients present with nonspecific viral symptoms or concurrent laboratory evidence of chronic hemolysis. Our case reinforces prior reports emphasizing that an inappropriately low reticulocyte response in the setting of profound anemia should prompt evaluation for parvovirus B19 infection, even in patients with baseline hemolysis and complex hematologic abnormalities. Additionally, the low percentage of sickled erythrocytes on peripheral smear despite severe anemia underscores the importance of considering aplastic crisis rather than vaso-occlusive or hyperhemolytic processes. Early recognition and supportive transfusion therapy remain essential to prevent morbidity and guide appropriate management.