Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Babesiosis is a tick-borne zoonosis caused by protozoans of the genus Babesia, apicomplexan parasites that replicate within erythrocytes. However, unlike related Plasmodium species, the pathogenesis of Babesia infection remains poorly understood. The primary etiological agent of babesiosis in the United States is B. microti. In healthy individuals, tick-transmitted infection with Babesia causes no specific clinical manifestations, with many having no symptoms at all. However, even in asymptomatic people, a Babesia carriage state can be established that can last up to a year or more. Current blood bank screening methods do not identify infected donors, and Babesia parasites survive blood-banking procedures and storage. Thus, Babesia can also be transmitted by infected blood, and it is currently the number one cause of reportable transfusion-transmitted infection in the United States. Despite a significant impact on human health, B. microti remains understudied. In this study, we evaluated the course of Babesia infection in three strains of mice, C57BL/6J, BALB/cJ, and C3H-HeJ, and examined the contribution of multiple immune parameters, including TLRs, B cells, CD4(+) cells, IFN-gamma, and NO, on the level of parasitemia and parasite clearance during acute babesiosis. We found that B. microti reaches high parasitemia levels during the first week of infection in all three mice strains before resolving spontaneously. Our results indicate that resolution of babesiosis requires CD4 T cells and a novel mechanism of parasite killing within infected erythrocytes.