Toxoplasma gondii and Schizophrenia: A Relationship That Is Not Ruled Out

Abstract

Over recent years, it has been proposed that some diseases of unknown origin, such as schizophrenia, may be caused by persistent chronic infections coupled with a genetic component and may be perpetuated by the immune system. This hypothesis is supported by epidemiological and biological evidence on the exposure of schizophrenics to infectious diseases during prenatal or postnatal periods, including Toxoplasma gondii, chlamydia, human herpes virus, human endogenous retroviruses, parvovirus B19, mumps, and flu viruses. This growing list of microbes will undoubtedly continue to increase in the future. Linking infection to schizophrenia is a complex challenge that requires further experimental and epidemiological research. T. gondii is the infectious agent that has most frequently been related to neuropsychiatric disorders, including schizophrenia, and it is considered to represent a highly useful model to analyze the influence of a microorganism on human behavior and the development of psychiatric disease. It may also help to detect patient subpopulations susceptible to treatment with specific antimicrobials by improving definition of the differential phenotype of the disease, and it offers the possibility of a preventive approach.

Associations between Toxoplasma gondii seropositivity and psychopathological manifestations in schizophrenic patients: A single-center study from Ecuador

“…For over fifty years, a possible relationship between schizophrenia and Toxoplasma gondii has been studied [9][10][11][12][13][14][15][16]. When Toxoplasma gondii stays dormant in tissue cysts in the brain it causes a compression damage to the neural tissue, reduces gray matter density and alters the brain physiology by altering the neurotransmitters activity leading to mood and behavior abnormalities as well as cognitive impairment [7,17,18].…”

The Effects of Two Antipsychotic Drugs and Prolactin on Toxoplasma Gondii Tachyzoites in Vivo

“…There were complex mechanisms including immune, humoral, neurotransmitter, epigenetic, genetic, and structural effects (Sorlozano-Puerto, 2016). Psychiatric disorders were mostly mediated by brain immune reaction to T. gondii infection affected glutamatergic systems, and T. gondii biochemical activity affected dopaminergic systems (Flegr, 2015).…”

Insights into the interplay of latent toxoplasmosis, testosterone, cortisol and oxidative stress in screened schizophrenic patients in Egypt

“…Toxoplasmosis has been linked to schizophrenia through epidemiological data, serological evidence, neuropathological and molecular studies [14] . The causal relationship was speculated to involve susceptibility genes targeting, pro-inflammatory cytokines, neurotransmitters and hormones [15] . It was explained that T. gondii encysted in the host tissues constitutes a source of chronic infection, which leads to the activation of hypothalamic pituitary adrenal axis and subsequently, an increase in glucocorticoid concentration.…”