An 84-year-old man with dementia presented with 4 months of fevers, night sweats, and dark urine. He lived in Central Pennsylvania and previously underwent splenectomy following a motor vehicle accident. Physical exam showed scleral icterus, palmar crease pallor, and jaundice. Laboratory studies showed hemolytic anemia and a positive direct antiglobulin test for warm autoantibodies. Serum parasitemia levels were 5% with elevated Babesia microti IgG and IgM titers. Peripheral-blood smear was consistent with asplenia and warm autoimmune hemolytic anemia. Babesia extracellular (Fig. 1, red arrowhead) and intracellular ring forms were present (Fig. 2, thin arrows). He was diagnosed with warm autoimmune hemolytic anemia (WAHA) triggered by B. microti in the setting of asplenia and chronic infection.

Figure 1
figure 1

Peripheral-blood smear showing a Howell-Jolly body (thin arrow) indicating asplenia, Babesia microti extracellular ring form (red arrowhead), spherocytes (blue arrowhead), and a nucleated red blood cell (thick arrow).

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Figure 2
figure 2

Peripheral-blood smear demonstrating both Babesia microti intracellular (thin arrows) and extracellular (thick blue arrow) ring forms.

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Babesiosis is associated with two mechanisms of hemolytic anemia. Non-immune-mediated hemolytic anemia occurs from merozoite egress and resolves with antibiotic treatment. WAHA, however, is a late complication that can develop 2 to 4 weeks following treatment, especially in asplenic patients.1,2 The peripheral-blood smear provided valuable insight into multiple processes: Howell-Jolly bodies indicated asplenia, nucleated red blood cells signaled hemolysis, and spherocytes pointed to WAHA. He was treated with prednisone, azithromycin, and atovaquone. After 4 months, his hemoglobin normalized and parasite levels were undetectable.