It is widely believed that cysts remain intracellular within neurons possibly minimizing their contact with host defense systems [15] . However it has been known for some time that cyst burden reaches a peak, declines and becomes stable over time pointing to some form of effector mechanism that can target this stage of the parasite [16] . Studies have implicated CD8+ T cell production of perforin in cyst clearance with perforin deficient mice exhibiting higher cyst burden and susceptibility at the chronic stage of infection [17, 18] . Nevertheless, histological analysis from these studies as well as recent live imaging of cell interactions in the CNS [19] demonstrates monocyte accumulation and contact with cysts.