Babesiosis is an emerging zoonotic disease caused by intraerythrocytic protozoa and transmitted by ticks. The first well-documented case of human Babesia infection was reported in 1957 in a splenectomized resident of Yugoslavia, who died after an acute illness marked by anemia, fever, hemoglobinuria, and renal failure. Intraerythrocytic parasites were noted and tentatively identified as Babesia bovis. Since then, other Babesia species have been found to cause disease in humans: Babesia microti, Babesia duncani, Babesia duncani-type, and Babesia divergens-like in North America; B. divergens, B. microti, and Babesia venatorum in Europe; and B. microti-like and KO-1 in Asia. The clustering of cases of human B. microti infection in the United States contrasts with the sporadic occurrence of the disease in Europe, Africa, and Asia. Rarely, babesiosis may be transmitted through blood transfusion or transplacentally.

Epidemiology

More than 90 species in the genus Babesia infect a wide variety of wild and domestic animals. Humans are an uncommon and terminal host for Babesia species, which depend on other species for their development and transmission. The most common cause for human babesiosis is B. imicroti, a babesia of rodents. The primary reservoir for B. microti in eastern North America is the white-footed mouse (Peromyscus leucopus). As many as two-thirds of P. leucopus have been found to be parasitemic in endemic areas. Babesia species are transmitted by hard-bodied (ixodid) ticks. The primary vector in eastern North America is Ixodes scapularis (also known as Ixodes dammini), which is the same tick that transmits Borrelia burgdorferi, the etiologic agent of Lyme disease, and Anaplasma phagocytophilum, the agent of human granulocytic anaplasmosis. Thus, simultaneous human infection with two or more of these pathogens may occur.