What is the pathophysiology of babesiosis?

Updated: Apr 01, 2021
  • Author: Rachel E Strength, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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Fever, hemolytic anemia, and hemoglobinuria may result from Babesia infection. As with malaria, RBC fragments may cause capillary blockage or microvascular stasis, which could explain liver, splenic, renal, and central nervous system (CNS) involvement. Animal studies have shown that increased cytoadherence of infected RBCs could cause these vascular blockages, though further research is needed. [9]  As in malaria, cells of the reticuloendothelial system (RES) in the spleen remove damaged RBC fragments from the circulation. RBC destruction results in hemolytic anemia. The amount of hemolysis does not seem to be directly related to the degree of parasitemia, though the cause is unclear. [11]

The spleen offers a critical host defense against babesiosis, as suggested by the higher incidence and greater severity of babesiosis in asplenic patients. The spleen traps the infected erythrocytes, and their ingestion by macrophages follows. Additionally, hypersplenism can lead to platelet sequestration which causes thrombocytopenia. [11]

Complement activation by Babesia may lead to the generation of tumor necrosis factor (TNF) and interleukin-1 (IL-1). Decreased complement levels, increased circulating C1q-binding activity, and decreased C4, C3, and CH50 levels are observed in patients with babesiosis. The generation of these primarily macrophage-produced mediators may explain many of the clinical features, including fever, anorexia, arthralgias, myalgias, and the fulminant shock syndrome of bovine babesiosis.

Babesiosis elicits a B-cell response and a T-cell response. Patients with acute babesiosis may have an increase in T-suppressor lymphocytes and/or T-cytotoxic lymphocytes and a decreased response to lymphocyte mitogens with a polyclonal hypergammaglobulinemia.

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