Babesia bovis: adhesion of parasitized red blood cells to bovine umbilical vein endothelial cells in vitro does not select for virulence

Abstract

Babesia bovis is an economically important tick-borne pathogen of cattle in tropical and sub-tropical regions of the world. B. bovis infections in cattle bear many similarities to human Plasmodium falciparum infections. Both parasites invade RBC, and a common feature of both infections is the tendency for PRBC to sequester by adhesion to endothelial cells lining the microvasculature. It has been theorised that adhesion and sequestration are important in immune evasion and in parasite virulence, causing physical blocking of the microcirculation or localized inflammatory responses (reviewed by [Allred, 2001]; [Wright et al]).

The virulence of B. bovis isolates is reduced by rapid syringe passage in splenectomised calves and the resulting attenuated lines can be used to vaccinate cattle against the severe disease caused by infection with a virulent strain ([Callow and Mellors, 1966]). However, attenuated lines revert to virulence after a single syringe passage in a spleen-intact animal or transmission through Boophilus microplus ticks ([Timms et al]). It is unclear whether reversion to virulence is due to selection of a virulent sub-population of parasites present in the attenuated line or up-regulation of a virulence gene or genes similar to that reported for P. falciparum ([Cooke et al]). [Lew et al] demonstrated the existence of multiple populations in the Australian T and Dixie vaccine strains and [Timms et al] demonstrated that cloned parasite lines derived from the Australian K vaccine strain varied greatly in virulence. Similarly, [Nevils et al] showed that cloned lines derived from the same virulent isolate differed in their ability to induce cerebral babesiosis, a severe and often fatal manifestation of the disease.