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Does Parasite Play Role in Schizophrenia Etiology?

Updated on September 29, 2014

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 T. gondii can infect the eyes and brain, often resulting in blindness and severe neurological disease. Neurological damage (encephalitis) occurs in children who contract the infection congenitally and in compromised individuals.
T. gondii can infect the eyes and brain, often resulting in blindness and severe neurological disease. Neurological damage (encephalitis) occurs in children who contract the infection congenitally and in compromised individuals.

Does Parasite Play Role in Schizophrenia Etiology?

There is growing evidence that the parasite Toxoplasma gondii is implicated in certain cases of schizophrenia. First the evidence came from prenatal blood samples. Now it comes from young people developing symptoms of schizophrenia.

Toxoplasma gondii

T gondii is a protozoan parasite whose definitive host is the cat family. Humans become infected by ingesting oocysts (eggs) shed in the feces of infected cats or by eating undercooked meat from an animal that came into contact with infected cat feces. T gondii is one of the most widespread human parasites; 10% to 20% of Americans test seropositive by adulthood. Exposure to T gondii during early pregnancy can cause severe fetal CNS abnormalities. Exposure during late pregnancy was never considered a problem until recently, when animal data showed that late exposure to the organism causes behavioral changes, neurologic symptoms, and stillbirths.

Since 1956, more than 20 studies have compared antibodies to T gondii in adults with and without schizophrenia. An overall analysis of the studies indicates that serologic evidence of Toxoplasma infection is almost 3 times more common in persons with schizophrenia than in controls living in the same geographic region. Two additional studies reported an increased level of T gondii antibodies in the late-pregnancy serum of women giving birth to infants in whom schizophrenia later developed. Other studies have reported greater childhood exposure to cats among persons with schizophrenia than among controls. Research is focusing on the timing of Toxoplasma infections in relation to development, as well as on possible differences in T gondii strains and human genetic susceptibility.

Numerous studies indicate that, although the symptoms of schizophrenia generally do not manifest until late adolescence or early adulthood, the disease process has its origins in earlier stages of brain development. The ability of Toxoplasma organisms to infect the perinatal brain is thus consistent with this aspect of schizophrenia pathogenesis. However, prospective studies also support a possible role of postnatal infections in some cases of schizophrenia. The potential effects of the transmission of Toxoplasma in early childhood or later in life should be considered.

Epidemiologically, two studies have reported that adults who have schizophrenia or bipolar disorder had a greater exposure to cats in childhood.


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