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Toxoplasma gondii & Human Phenotype

Compendium of Known Effects and Ongoing Research

mechanism

The missing link in parasite manipulation of host behaviour

February 12, 2018
Herbison, R. , Lagrue, C. , Poulin, R.
Parasites Vectors 2018; 10.1186/s13071-018-2805-9
Click for abstract
The observation that certain species of parasite my adaptively manipulate its host behaviour is a fascinating phenomenon. As a result, the recently established field of 'host manipulation' has seen rapid expansion over the past few decades with public and scientific interest steadily increasing. However, progress appears to falter when researchers ask how parasites manipulate behaviour, rather than why. A vast majority of the published literature investigating the mechanistic basis underlying behavioural manipulation fails to connect the establishment of the parasite with the reported physiological changes in its host. This has left researchers unable to empirically distinguish/identify adaptive physiological changes enforced by the parasites from pathological side effects of infection, resulting in scientists relying on narratives to explain results, rather than empirical evidence. By contrasting correlative mechanistic evidence for host manipulation against rare cases of causative evidence and drawing from the advanced understanding of physiological systems from other disciplines it is clear we are often skipping over a crucial step in host-manipulation: the production, potential storage, and release of molecules (manipulation factors) that must create the observed physiological changes in hosts if they are adaptive. Identifying these manipulation factors, via associating gene expression shifts in the parasite with behavioural changes in the host and following their effects will provide researchers with a bottom-up approach to unraveling the mechanisms of behavioural manipulation and by extension behaviour itself.

Tagged: behaviour, manipulation factor, manipulation., mechanism, Parasite, toxoplasma gondii infection, us

Behavior

Association between latent toxoplasmosis and clinical course of schizophrenia – continuous course of the disease is characteristic for Toxoplasma gondii-infected patients

October 9, 2015
Celik, T., Kartalci, S., Aytas, O., Akarsu, G. A., Gozukara, H., Unal, S.
Folia Parasitologica 2015; 62
Click for abstract
The aim of the present study was to investigate the association between various clinical aspects of schizophrenia and seropositivity against Toxoplasma gondii (Nicolle et Manceaux, 1908). We selected 94 patients with schizophrenia and investigated the seropositivity rate for anti-T. gondii IgG antibodies by ELISA. Clinical parameters of schizophrenic patients such as illness type and status, clinical course, awareness of the illness and need for electroconvulsive therapy (ECT) were compared with their serological status. Anti-T. gondii IgG antibodies were detected in 43 (46%) of schizophrenic patients. Chronic patients had a rate of 34 (72%) seropositivity, whereas 9 (22%) of the patients with partial remission showed evidence of latent toxoplasmosis. Of continuous patients, 35 (81%) were found to be seropositive and this rate was significantly more than in the other groups. The rate of latent toxoplasmosis was detected significantly higher in patients who lack awareness of schizophrenia (36, i.e. 72%) than the patients who were aware of their illnesses (7, i.e. 16%). Anti-T. gondii IgG antibodies were detected in 38 (70%) of ECT performed patients while this percentage was 13% in the ones who had never been treated with ECT. This difference was also statistically significant. We showed that Toxoplasma-infected subjects had 15x higher probability of having continuous course of disease than Toxoplasma-free subjects. Our results put forth the possibility of latent toxoplasmosis to have a negative impact on the course of schizophrenia and treatment response of schizophrenic patients.

Tagged: agents, antibodies, cell-cultures, CMV, Dopamine, individuals, mechanism, mice, prognosis, risk factors, schizophrenia patients, serology, toxoplasmosis

Mental health

Toxoplasma gondii associated behavioural changes in mice, rats and humans: Evidence from current research

January 10, 2012
Bech-Nielsen, S.
Preventive Veterinary Medicine 2012; 103: 78-79
Tagged: host behavior, mechanism, traffic accidents

BehaviorPersonalityReviews

Could Toxoplasma gondii have any role in Alzheimer disease?

October 19, 2011
Kusbeci, O. Y., Miman, O., Yaman, M., Aktepe, O. C., Yazar, S.
Alzheimer Disease and Associated Disorders 2011; 25: 1-3
Tagged: activated microglia, alzheimer disease, antibodies, brain, infection, inflammation, interferon-gamma, mechanism, neurodegeneration, neuroinflammation, parkinson's disease, pathogenesis, Schizophrenia, Toxoplasma gondii, toxoplasmosis

Mental 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

Topics

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

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Recent articles

  • Mortality Patterns of Toxoplasmosis and Its Comorbidities in Tanzania: A 10-Year Retrospective Hospital-Based Survey February 6, 2020
  • 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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