The multiplication of parasites frequently leads to massive loss of erythrocytes. Parasite infected erythrocytes expose parasite encoded proteins on their surface which make these erythrocytes stick to endothelial surface receptors. This phenomenon is responsible for cerebral Malaria, a deadly form of Malaria. Like Plasmodium it belongs to the phylum Apicomplexa. T. gondii is able to infect almost all warm-blooded animals.
Infection is initiated by a rapid multiplication of the parasites.
After the onset of the immunresponse of the host the parasite develops encysted dormant stages preferentially in mucles or the brain. The sexual development of the parasite takes place in Felidae, where the parasites multiply in the epithelium of the gut. The first infection with T. gondii can cause abortion or severe damage of the newborn. In immuncompromised persons reactivation of T. gondii can cause severe health problems or death. Expressing the major surface protein SAG1 of T. gondii using the baculovirus expression system showed that only marginal amounts of the protein are modified by a GPI-anchor.