ABSTRACT
The pathogenesis of Babesia infections are highly complex, as evidenced by multisystemic involvement described in this review and elsewhere. The bulk of evidence indicates that the pathogenesis is immunologically mediated and the role of complement in invasion remains putative for most Babesia species. The major system involved in modulating the pathogenesis of babesiosis is the reticuloendothelial system, particularly the spleen. Another important parameter in the pathogenesis of babesiosis is the virulence of the etiologic agent. The nature of this variability in virulence is not clearly understood, with the exception of B. bovis which has been the subject of intensive study. Severe coagulation disturbances have been reported in both acute B. bovis and acute B. canis infections. Babesial antigen and C3 were detected within these complexes, suggesting that infection produced an immune complex disease with consumption of complement. The presence of fatty infiltration in liver parenchymal cells in B. bovis infection has been reported by I. G. Wright.
