The “behavioral manipulation” hypothesis proposes that a parasite can alter the behavior of a host in a way that will improve its chances of being retransmitted, without changing other innate behaviors. It has been hypothesized that T. gondii has evolved to specifically manipulate the behavior of rodents, its ideal secondary host, in order to improve its chances of being acquired by its definitive host, felines. Indeed, infection in mice and rats specifically abolishes innate fear of cat urine odor, replacing it with an actual attraction to the odor without removing other innate non-feline fears, or induction of deficits in other conditioned or fear-based learning behaviors 78-80. Examination of infected rodent brains found that twice as many
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On a more serious note, the relationship between T. gondii infection and schizophrenia onset dominates human behavior studies. A meta-analysis of 50 studies concluded that T. gondii confers an intermediate risk, with schizophrenics 2.7 times more likely to have anti-T. gondii antibodies than the general population 85. Studies of infected schizophrenics have identified reductions in grey matter volume and white-matter relative to non-infected 86, and schizophrenics show elevated levels IL-12, IL-1, IFN-γ, and TNF-α chronically, and IL-6 and IL-1β acutely 87 - the same cytokines seen during T. gondii activation of the immune system. Other epidemiological correlations include the fact that up-regulation and morphological changes in microglia are seen in both T. gondii infection and schizophrenia 88; that both schizophrenia and T. gondii infection are marked by increased levels of dopamine 75, 89; and that high levels of kynurenic acid (a metabolite of tryptophan catabolism by the parasite) have been found in CSF serum samples of schizophrenics 90. There is some speculation that the onset of schizophrenia may be induced by reactivation, rather than acute infection due to the fact that elevated levels of anti-T. gondii IgM are not seen in first onset
On a more serious note, the relationship between T. gondii infection and schizophrenia onset dominates human behavior studies. A meta-analysis of 50 studies concluded that T. gondii confers an intermediate risk, with schizophrenics 2.7 times more likely to have anti-T. gondii antibodies than the general population 85. Studies of infected schizophrenics have identified reductions in grey matter volume and white-matter relative to non-infected 86, and schizophrenics show elevated levels IL-12, IL-1, IFN-γ, and TNF-α chronically, and IL-6 and IL-1β acutely 87 - the same cytokines seen during T. gondii activation of the immune system. Other epidemiological correlations include the fact that up-regulation and morphological changes in microglia are seen in both T. gondii infection and schizophrenia 88; that both schizophrenia and T. gondii infection are marked by increased levels of dopamine 75, 89; and that high levels of kynurenic acid (a metabolite of tryptophan catabolism by the parasite) have been found in CSF serum samples of schizophrenics 90. There is some speculation that the onset of schizophrenia may be induced by reactivation, rather than acute infection due to the fact that elevated levels of anti-T. gondii IgM are not seen in first onset