Epidemiological studies indicate that infectious agents may be involved in the pathogenesis of schizophrenia, a debilitating psychiatric disease. Toxoplasma gondii is a unique Apicomplexan parasite that has the ability to infect and persist within the nervous system of its intermediate hosts, including rodents and humans. Although research has shown that this organism has the ability to alter host behavior, the mechanism through which this phenomenon occurs is unknown. It is likely that T. gondii directly manipulates the behavior of intermediate rodent hosts by disrupting the levels or receptors of host neurochemicals to enhance their vulnerability to definitive host predation. In contrast, humans are accidental hosts of T. gondii who may develop schizophrenia as a by-product of parasitic infection. The mechanism by which T. gondii is able to cause these severe psychological symptoms is unknown. However, data from clinical research and animal studies indicate that T. gondii may alter the levels of neurochemicals (e.g. reelin and/or dopamine) or disrupt the expression/function of N-methyl-D-aspartate (NMDA) receptors in the brain. These changes could disrupt fetal brain development and thus contribute to the emergence of psychiatric symptoms in some individuals. Furthermore, the application of the Bradford Hill Criteria to the T. gondii-schizophrenia association provides sufficient evidence to support the hypothesis that T. gondii is a causative agent of schizophrenia. In light of the negative behavioral consequences of T. gondii infection, the immediate treatment of patients diagnosed with toxoplasmosis may prevent the emergence of psychiatric symptoms in some individuals.