Abstract
The protozoan parasite Toxoplasma gondii infects a wide range of intermediate hosts. The parasite produces brain cysts during the latent phase of its infection, in parallel to causing a loss of innate aversion in the rat host towards cat odors. Host behavioral change presumably reflects a parasitic manipulation to increase predation by definitive felid hosts, although evidence for increased predation is not yet available. In this opinion piece, we propose a neuroendocrine loop to explain the role of gonadal steroids in the parasitized hosts in mediating the behavioral manipulation. We argue that the presence of tissue cysts within the host brain is merely incidental to the behavioral change, without a necessary or sufficient role.
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