Abstract
Humans infected with Plasmodium falciparum and bovines infected with Babesia bovis display severe haemolysis, alterations in red cell deformability and rigidity, and endothelial cell damage leading to pulmonary oedema and cerebral dysfunction. Much of the pathology associated with these infections is not easily attributable to the relatively small numbers of parasites present. This paper considers the possible roles of soluble mediators released from macrophages, and chemical and physical changes in die infected red cell membrane, in the pathogenesis of babesial infections, and also discusses the effects of prior immunization with various immunogens.
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