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Babesia microti (Franca, 1909), an intraerythrocytic, ticktransmitted haemoprotozoan parasite is a common pathogen of free-living small mammals, particularly rodents. Babesiosis caused by this species of Babesia is gaining increasing interest as emerging zoonosis in humans (Parry M.F., Fox M., Burka S.A., Richar W.J. 1977: J. Am. Vet. Med. Assoc. 238: 1282– 1283; Homer M.J., Aguilar-Delfini, Telford III, S.R., Krause P.J., Persing D.H. 2000: Clin. Microbiol. Rev. 13: 451–469). This is especially the case in North America, where human babesiosis is caused predominantly by B. microti and occasionally by a newly recognized species called WA1 piroplasm (Dammin G.J., Spielman A., Benach J.L., Piesman J. 1981: Hum. Pathol. 12: 398–400; Persing D.H., Herwaldt B.L., Glaser C., Lane R.S., Thomford J.W., Mathiesen D., Krause P.J., Phillip D.F., Conrad P.A. 1995: New Engl. J. Med. 332: 298–303). However, in Europe, human babesiosis is rather unique but more lethal, and mostly caused by Babesia divergens (Mac Fadyean et Stockman, 1911). Human infections occur always or nearly always in persons who lack a spleen (Brasseur P., Gorenflot A. 1992: Mem. Inst. Oswaldo Cruz 87, Suppl. 3: 131–132). Also, quite recently a new pathogenic B. microti-like species from dogs was described in Germany (Zahler M., Rinder H., Schein E., Gothe R. 2000: Vet. Parasitol. 89: 241–248). In natural conditions, B. microti is transmitted by Ixodes ricinus complex ticks, in Europe, predominantly by nymphs of I. ricinus. Free-living small rodents (Clethrionomys glareolus, Apodemus flavicollis, Microtus arvalis) are important reservoir hosts. Although in enzootic regions these animals generally are parasitaemic, chronic infection (less than 0.5% infected erythrocytes) evidently persists for few weeks (Karbowiak G., Sinski E. 1996: Acta Parasitol. 41: 50–51; Bajer A., Pawelczyk A., Behnke J.M., Gilbert F.S., Sinski E. 2001: Parasitology 122: 43–54). Babesia microti is widely used as an experimental model for the study of mechanisms of protective immunity induced by both natural and controlled infections (Cox F.E.G., Young A.S. 1969: Parasitology 59: 257–268; Hu R., Yeh M.T., Hyland K.E., Mather T.N. 1996: J. Parasitol. 82: 728–732). Protection to subsequent infection is afforded partly by antibodies against surface and E/S antigens of free merozoites or infected erythrocytes (Winger C.M., Canning E.U., Culverhouse J.D. 1989: Parasitology 3: 341–348). In the acute phase of infection IgM antibodies are produced as a first response against the parasite (Chen D., Copeman D.B., Burnell J., Hutchinson G.W. 2000: Parasite Immunol. 22: 81–88). Also, specific IgG antibodies are responsible for reducing the number of parasites in the blood (Hu et al. 1996, op. cit.). However, the role of humoral immunity to B. microti infection in rodents is not fully clarified (Clawson M.L., Paciorkowski N., Rajan T.V., La Vake C., Pope C., La Vake M., Wikel S.K., Krause P.J., Radolf J.D. 2002: Infect. Immun. 70: 5304– 5306). The present study was designed to test the protective effect of a B. microti strain maintained by syringe passage under laboratory conditions since 1991 to challenge the infection of BALB/c mice. We have measured and compared the parasitaemia of primary and challenge infections as well as IgM, IgG1 and IgG2a antibody response, against specific B. microti antigens. Babesia microti strain (King’s 67 strain), originally obtained in 1991 from Dr. S. Randolph (Oxford University) has been maintained by weekly syringe passage using both sexes of BALB/c mice. Fifty two male BALB/c mice aged 8– 12 weeks, used in this study, were divided in two groups (26 animals each). Animals were kept in clean labelled plastic cages and provided with food and water ad libitum. The first group was injected once with 5 × 10 parasitized mouse erythrocytes by the intraperitoneal route. The second group was infected twice; the first infection on day 0 (as in group 1) and the second infection on day 38 after the first injection. Parasitaemia was examined on days 2, 4, 6, 7, 8, 9, 10, 11, 13, 14, 18 and 24 post primary infection (DPPI) and on 4, 8, 14, 18 and 24 days post challenge infection (DPCHI). The presence of B. microti was detected by microscopic examination of blood smears stained with Giemsa. Two smears were obtained from the tail tip of each mouse on these days. One hundred erythrocytes were examined and the level of parasitaemia was expressed as the percentage of parasitized erythrocytes. Heparinized blood was collected from the mice when the level of parasitaemia was about 75% of infected erythrocytes. The blood samples were centrifuged at 1000 g for 5 min and the parasites were isolated according to Machado et al. (Machado R.Z., Valadao C.A.A., Melo W.R., Alessi A.C. 1994: Braz. J. Med. Biol. Res. 27: 2591–2598). Purified piroplasms were homogenized in 0.1 M PBS, pH 7.4, containing protease inhibitors (PMSF, TPCC), sonicated FOLIA PARASITOLOGICA 50: 237–239, 2003

Babesia microti: parasitaemia and antibody responses to primary and challenge infections in BALB/c mice