Calves infected with the tick-borne parasites Babesia spp. do not develop severe clinical babesiosis. Instead they display persistent low parasitaemias without any apparent ill-effects. This age-related resistance not only benefits the host, but also furthers parasite transmission. Both calves and adult animals respond with a Th I immune response to primary infection. Here we hypothesize that the difference in the outcome of infection may at least partly be explained by the localization and timing of the inflammatory response: in calves NO production occurs early and appears to be concentrated in the spleen. On the other hand, there is evidence that a delayed and systemic inflammatory response occurs in adult animals that is ineffectual and probably contributes to the pathogenesis. An improved understanding of the possible mechanisms that underlie this phenomenon may lead to new approaches for the treatment and immune prophylaxis of the disease.