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Toxoplasma gondii & Human Phenotype

Compendium of Known Effects and Ongoing Research

nervous system

Association between prenatal exposure to maternal infection and offspring mood disorders: A review of the literature

May 25, 2015
Simanek, A. M., Meier, H. C. S.
Current Problems in Pediatric and Adolescent Health Care 2015; 45: 325-364
Click for abstract
The purpose of this article is to provide a systematic review of studies that have examined the association between prenatal exposure to maternal infection and development of mood disorders across the life course. Drawing from both human- and animal-based studies, we give an overview of hypothesized biological mechanisms by which exposure to maternal infection during critical periods of gestation may contribute to fetal programming of mood disorders in offspring. We discuss studies examining the association between prenatal exposure to maternal infection with pathogens including influenza as well as other respiratory viruses, herpesviruses, hepatitis viruses, and Toxoplasma gondii and mood disorders in human populations. Moreover, we outline strengths and limitations of the current body of evidence and make recommendations for future research. We also discuss findings in the context of well-documented gender and socioeconomic disparities in the prevalence and severity of mood disorders, particularly major depression, and the role that early exposure to infection may play in explaining the perpetuation of such disparities across generations. Overall, this review of the current knowledge on this topic has important implications for determining future research directions, designing interventions as well as prenatal care guidelines targeted at prevention or treatment of infection during pregnancy, and clinical practice for the identification of individuals that may be at increased risk for mood disorders beginning early in life. Importantly, such efforts may not only lower the overall burden of mood disorders but also serve to address social disparities in these adverse mental health conditions in the U.S.

Tagged: bipolar disorder, comorbidity survey replication, depression-related behaviors, gray-matter volume, herpes-simplex-virus, immune activation, major affective-disorder, nervous system, toxoplasma gondii infection, united-states

Mental healthReproductionReviews

Brain cancer mortality rates increase with Toxoplasma gondii seroprevalence in France

October 11, 2012
Vittecoq, M., Elguero, E., Lafferty, K. D., Roche, B., Brodeur, J., Gauthier-Clerc, M., Misse, D., Thomas, F.
Infection Genetics and Evolution 2012; 12: 496-498
Click for abstract
The incidence of adult brain cancer was previously shown to be higher in countries where the parasite Toxoplasma gondii is common, suggesting that this brain protozoan could potentially increase the risk of tumor formation. Using countries as replicates has, however, several potential confounding factors, particularly because detection rates vary with country wealth. Using an independent dataset entirely within France, we further establish the significance of the association between T. gondii and brain cancer and find additional demographic resolution. In adult age classes 55 years and older, regional mortality rates due to brain cancer correlated positively with the local seroprevalence of T. gondii. This effect was particularly strong for men. While this novel evidence of a significant statistical association between T. gondii infection and brain cancer does not demonstrate causation, these results suggest that investigations at the scale of the individual are merited. (C) 2012 Elsevier B.V. All rights reserved.

Tagged: encephalon tumors, Epidemiology, latent toxoplasmosis, malignancy, medical geography, nervous system, tumors

Physical health

Autism spectrum disorders may be due to cerebral toxoplasmosis associated with chronic neuroinflammation causing persistent hypercytokinemia that resulted in an increased lipid peroxidation, oxidative stress, and depressed metabolism of endogenous and exogenous substances

October 19, 2010
Prandota J.
Research in Autism Spectrum Disorders 2010; 4: 119-155
Click for abstract
Worldwide, approximately 2 billion people are chronically infected with Toxoplasma gondii with largely yet unknown consequences. Patients with autism spectrum disorders (ASD) similarly as mice with chronic toxoplasmosis have persistent neuroinflammation, hypercytokinemia with hypermetabolism associated with enhanced lipid peroxidation, and extreme changes in the weight resulting in obesity or wasting. Data presented in this review suggest that environmental triggering factors such as pregnancy, viral/bacterial infections, vaccinations, medications, and other substances caused reactivation of latent cerebral toxoplasmosis because of changes in intensity of latent central nervous system T. gondii infection/inflammation and finally resulted in development of ASD. Examples of such environmental factors together with their respective biomarker abnormalities are: pregnancy (increased NO, IL-1 beta, TNF-alpha, IL-6, IL-10, prolactin: decreased IFN-gamma, IL-12), neuroborreliosis (increased IL-1 beta, sIL-1R2, TNF-alpha, IFN-gamma, IL-6, IL-10, IL-12, IL-18, transforming growth factor-beta 1 (TGF-beta 1)), vital infections (increased IL-1 beta, IL-6, IL-8, TNF-alpha, IFN-gamma/alpha/beta,TGF-beta 1), thimerosal (increased IL-5, IL-13; decreased IFN-gamma,TNF-alpha,IL-6, IL-12p70, NOS), and valproic acid (increased NO, reactive oxygen species; decreased TNF-alpha, IL-6, IFN-gamma). The imbalances in pro- and antiinflammatory processes could markedly hinder [lost defense mechanisms important for immune control of the parasite, such as the production of NO, cytokines, and reactive oxygen/nitrogen species, tryptophan degradation by indoleamine 2,3-dioxygenase and/or tryptophan 2,3-dioxygenase, limitation of the availability of intracellular iron to T gondii, and the mechanisms mediated by an IFN-gamma responsive gene family. These fluctuations could result in a recurrent profuse multiplication of T. gondii in the brain associated with persistent neuroinflammation, chronic overproduction of pro- and antiinflammatory cytokines, and NO causing increased oxidative stress, and significantly depressed activity of several enzymes including cytochrome P450 monooxygenase family responsible for metabolism of physiological substrates and xenobiotics, such as steroids, fatty acids, prostaglandins, drugs, pollutants, and carcinogens, finally leading to development of ASD. This reasoning may be supported by such abnormal metabolic events as: (1) patients with ASD have significantly decreased melatonin levels caused by marked deficit in acetylserotonin methyltransferase activity, possibly resulting from maternal and/or fetal/postnatal overproduction of NO, characteristic for this clinical entity; (2) thimerosal inhibited both insulin-like growth factor-1- and dopamine-stimulated methylation reactions, and depressed methionine synthase activity, the metabolic events important for promoting normal neurodevelopment; (3) valproic acid, a strong histone deacetylase inhibitor, have potent anti-T. gondii activity. Thus, patients with ASD should be tested for T. gondii infection. (C) 2009 Elsevier Ltd. All rights reserved

Tagged: abnormalities, abnormality, acid, acids, aktivity, autism, autistic spectrum disorders, availability, beta, biomarker, brain, cell-mediated-immunity, central-nervous-system, cerebral, Cerebral toxoplasmosis, change, changes, chronic, chronic neuroinflammation, chronic toxoplasmosis, clinical, congenital cytomegalovirus-infection, consequence, consequences, control, could, cytochrome, cytochrome p450, cytokine, cytokines, data, defense, defense-mechanisms, deficit, degradation, depressed enzyme activities, development, disorder, disorders, drug, drugs, environmental, environmental factors, enzyme, enzymes, event, events, example, families, family, fluctuation, fluctuations, gene, gene families, gene family, gondii, gondii infection, growth, growth-factor-beta, hepatic drug-metabolism, herpes-simplex-virus, histone, histone deacetylase, hypercytokinemia, hypermetabolic state, il-1, il-10, il-12, il-13, il-6, immune, immune irregularities, important, infection, infections, inhibitor, insulin-like, intensity, interferon-inducing agents, intracellular, iron, latent, level, limitation, lipid, lipid-peroxidation, maternal, mechanism, mechanisms, medication, melatonin, metabolism, methionine, methylation, methyltransferase, methyltransferase aktivity, mice, multiplication, nervous, nervous system, neurodevelopment, nf-kappa-b, nitric oxide, nitric-oxide synthase, obesity, or, overproduction, oxidative stress, oxygen, p-450-dependent monooxygenase systems, Parasite, patient, patients, people, persistent, pregnancies, pregnancy, proces, prolactin, prostaglandins, reaction, reactivation, review, species, spectrum, spectrum disorders, spektra, steroids, stress, substrate, systém, t, tgf-beta, tnf-alpha, Toxoplasma, Toxoplasma gondii, toxoplasmosis, tryptophan, tumor-necrosis-factor, vaccination, vital, weight, xenobiotics

Mental health

Tumours of the brain and presence of antibodies to Toxoplasma gondii

November 7, 1993
Ryan, P., Hurley, S. F., Johnson, A. M., Salzberg, M., Lee, M. W., North, J. B., Mcneil, J. J., Mcmichael, A. J.
International Journal of Epidemiology 1993; 22: 412-419
Click for abstract
The possible association between prior infection with the protozoan Toxoplasma gondii and development of brain tumours was investigated as part of two Australian population-based case-control studies of adult brain tumours. One study, based in Adelaide, South Australia, collected blood from 73 subjects with glioma, 53 subjects with meningioma and 348 controls. The other study, based in Melbourne, Victoria, collected blood from 44 subjects with glioma and 67 controls. All tumours had been verified histologically. IgG antibodies to T. gondii were measured using Enzyme Linked Immunosorbent Assay (ELISA) techniques. In both the centre-specific and combined analyses, there was no difference between subjects with glioma and controls in the prevalence of antibody test-positivity (35% test-positive in glioma versus 33% in controls, age-, sex- and centre-adjusted odds ratio (OR) = 1.00, 95% confidence interval (CI): 0.64-1.56). In the Adelaide study, there was a statistically significant increased risk of meningioma associated with antibody test-positivity (47% test-positive in meningioma versus 31% in controls, P = 0.02, adjusted OR = 2.09, 95% CI: 1.14-3.83). Our results do not support the hypothesis that antibody positivity to T. gondii is a risk factor for glioma, but suggest that it might be associated with meningioma.

Tagged: childhood, diagnosis, immunosorbent-assay elisa, los-angeles county, meningiomas, nervous system, risk factors, tests, tumors

Physical health

Topics

  • Behavior 105
  • Cognitive functions 64
  • Mental health 439
  • Morphology 6
  • Motor functions 10
  • Personality 36
  • Physical health 134
  • Reproduction 36
  • Reviews 40
  • Sensory functions 3
  • Uncategorized 2

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Recent articles

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  • The role of latent toxoplasmosis in the aetiopathogenesis of schizophrenia–the risk factor or an indication of a contact with cat? February 6, 2020
  • The Association between Toxoplasma gondii Infection and Risk of Parkinson’s Disease: A Systematic Review and Meta-Analysis February 6, 2020

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