In vitro experiments and studies on B. microti using animal models (mice and cattle) provide information on the pathogenesis of human babesiosis. It is shown from such studies that cellular immunity has an upper hand over humoral immunity in containing babesiosis (Hunfeld et al. 1227). This is evident in mice experiments where T helper cells play a significant role in keeping parasitemia under control. These findings are consistent with the inability of immunocompromised patients to control unrelenting parasitemia. In the same way, a reduction of natural killer cells and macrophages makes individuals more vulnerable to babesiosis infection. All these findings lead to the conclusion that the pathobiology of babesiosis is not a consequence of the parasite, but the host immune response.
Splenectomy, which is the surgical removal of the spleen, increases the risk of babesiosis. This is because the spleen performs a crucial function in host protection by eliminating infected red blood cells from the bloodstream. In addition, the spleen is a secondary lymphoid organ and participates in intensifying a protective immune rejoinder.