Babesia and its hosts: adaptation to long-lasting interactions as a way to achieve efficient transmission

Abstract

Babesia, the causal agent of babesiosis, are tick-borne apicomplexan protozoa. True babesiae (Babesia genus sensu stricto) are biologically characterized by direct development in erythrocytes and by transovarial transmission in the tick. A large number of true Babesia species have been described in various vertebrate and tick hosts. This review presents the genus then discusses specific adaptations of Babesia spp. to their hosts to achieve efficient transmission. The main adaptations lead to long-lasting interactions which result in the induction of two reservoirs: in the vertebrate host during low long-term parasitemia and throughout the life cycle of the tick host as a result of transovarial and transstadial transmission. The molecular bases of these adaptations in vertebrate hosts are partially known but few of the tick-host interaction mechanisms have been elucidated.

Figure 1.

Babesia spp. life cycle. Merogonies in the vertebrate host are asynchronous and various divisional stages can be seen at the same time in the bloodstream: anaplasmoid forms (appearing just after penetrating the erythrocytes), rounded or ovoid forms (trophozoites), dividing forms, and merozoites, resulting from the binary fission, which are typically piriform and joined by their pointed extremities. Gamogony (gamete differentiation and zygote formation) occurs in tick intestinal cells. Ookinete and kinetes formed by asexual division of ookinete (sporogonies) occur in various tick organs. Final differentiation of sporozoites occurs in salivary glands. Graphic representation of kinetes and ray-bodies are line drawings reproduced from Sabine Wattendorff “dissertation zur Erlangang des Grades eines Doctor Medicinae Veterinariae”, Hanover, 1980.

Figure 2.

Effector immune mechanisms and their regulation developed by the vertebrate during B. bovis infection. NO secreted by IFNγ-activated macrophages is the major effector mechanism against iRBC. During the acute phase, the innate response regulated by inflammatory and type-1 cytokines leads to partial elimination of the parasites injected by the tick. During the chronic phases, Th-1 cells and antibodies control parasitemia at a low level. IL4 and IL10 secreted by Th-2 or regulatory cells inhibit the activation of macrophages.