Complement does not play a role in promoting Babesia rodhaini infections in Balb/C mice.

A critical role of C3 and the C3b receptor for the erythrocyte invasion and the development of the parasitemia of B. rodhaini in rats has been described recently (Jack and Ward 1980a). In the present study the influence of the C system on B. rodhaini infection in Balb/C mice is documented. Depletion of serum C3 to less than 5% of the normal level by treatment of mice with CoF, the C3 inactivator isolated from cobra venom, did not affect the course of B. rodhaini parasitaemia. Treatment of mice with trypan blue, a reagent that inactivates the C3b receptor on human polymorphonuclear leukocytes, inhibited the development of parasitemia. However, when B. rodhaini parasitized erythrocytes were incubated in vitro with trypan blue and subsequently tested for the in vivo and in vitro replication of the parasites, this old-fashioned therapy for babesiosis in cattle showed its babesiacidal activity. This indicates that the inhibition of parasite development by trypan blue is caused by its parasitotoxicity. These data suggest that the C system does not play an essential role in the development of B. rodhaini infection of the Balb/C mouse.