Cerebral toxoplasmosis – Toxoplasma gondii & Human Phenotype

Presence of Toxoplasma gondii infection in brain as a potential cause of risky behavior: a report of 102 autopsy cases

February 1, 2020
Samojlowicz, D. Twarowska-Malczynska, J. Borowska-Solonynko, A. Poniatowski, L. A. Sharma, N. Olczak, M.
European Journal of Clinical Microbiology and Infectious Diseases 2019, 38: 305 - 317 Toxoplasma gondii Toxoplasmosis Brain Risky behavior Alcohol Mental health Drivers cerebral toxoplasmosis decreased level novelty seeking dopamine parasite host schizophrenia personality depression strategies

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Anti-Toxoplasma antibodies in Egyptian rheumatoid arthritis patients

December 8, 2017
El-Henawy, A. A., Hafez, E. A. R., Nabih,N., Shalaby, N. M., Mashaly, M.
Rheumatology International 2017;37:785-790

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A man in his 40s with altered mental status, ataxia and unilateral weakness

January 3, 2017
Malhotra, K., Khunger, M., Pu, C. F., Scott, T. F.
Neuropathology 2017; 37: 286-290

Possible link between Toxoplasma gondii and the anosmia associated with neurodegenerative diseases

October 10, 2014
Prandota J.
American Journal of Alzheimers Disease and Other Dementias 2014; 29: 205-214

Recurrent headaches may be caused by cerebral toxoplasmosis

October 9, 2014
Prandota, J., Gryglas, A., Fuglewicz, A., Zeslawska-Falenczyk, A., Ujma-Czapska, B., Szenborn, L., Mierzwa, J.
World Journal of Clinical Pediatrics 2014; 3: 59-68

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AIM: To establish seroprevalence and provide characteristics of Toxoplasma gondii (TG) infection in children with recurrent headaches. METHODS: The study was performed in 178 children aged 7-17 years admitted consecutively to the Department of Pediatric Neurology from November 2009 to July 2011. The children were surveyed with a questionnaire with the help and assistance of their parents and blood samples taken on admission were studied for the presence of specific anti-TG IgM, IgG antibodies and IgG avidity using enzyme immunoassay Platelia Toxo IgM, IgG. RESULTS: The study showed that 19 children (8 boys, 11 girls; 8-17 years old, mean age 14.36 years) had high serum anti-TG IgG antibody levels (range: 32.2 > 240 UI/mL, mean 120.18 UI/mL; positive value for IgG was >/= 9 UI/mL). The avidity index (AI) ranged from 0.202 to 0.925 (scale: >/= 0.5 high AI). The results for IgM antibodies were all negative and the obtained results ranged from 0.113 to 0.25 U/mL (mean = 0.191 IU/mL) and all values below 0.8 IU/mL were considered negative. The most frequent complaints found in the seropositive patients were headaches that affected the frontal (13 children), occipital (4) and parietal areas (5). Headaches usually had a pulsating (in 7 patients) and squeezing (6) character and rarely were piercing, dull or expanding. Interestingly, 8 children did not feel discomfort during the headaches, probably because they did not have sufficiently increased intracranial pressure yet. The headaches usually appeared 1-2 times/mo, lasted for 2-6 h, and had a mean intensity of 5.5 points in a 10 point subjective scale. The comorbidities included epilepsy (5 patients), various infections in 3 children (chronic eustachitis, chronic rhinitis, chronic purulent tonsillitis, streptococcal pharyngitis, meningitis, allergic diseases), disturbances of behavior, deficits of attention, and ocular and motor concentration disorders in 1 child. The electroencephalographic and neuroimaging studies performed in our patients had a very limited value in establishing cerebral toxoplasmosis. CONCLUSION: Ten point six seven percent of the studied children had markedly increased serum anti-TG IgG antibodies and high AI indicated chronic infestation. It is suggested that tests for TG infection should be introduced to routine diagnostics in patients with recurrent headaches.

Toxoplasmosis and neuropsychiatric diseases: can serological studies establish a clear relationship?

October 11, 2013
Fabiani, S., Pinto, B., Bruschi, F.
Neurological Sciences 2013; 34: 417-425

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Latent Toxoplasmosis gondii: Emerging Evidence for Influences on Neuropsychiatric Disorders

October 16, 2012
Hurley, R. A., Taber, K. H.
Journal of Neuropsychiatry and Clinical Neurosciences 2012; 24: 376-383

Toxoplasma gondii immunoglobulin G antibodies and nonfatal suicidal self-directed violence

October 11, 2012
Zhang, Y. F., Traskman-Bendz, L., Janelidze, S., Langenberg, P., Saleh, A., Constantine, N., Okusaga, O., Bay-Richter, C., Brundin, L., Postolache, T. T.
Journal of Clinical Psychiatry 2012; 73: 1069-1076

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Objective: The primary aim was to relate Toxoplasma gondii seropositivity and serointensity to scores on the self-rated Suicide Assessment Scale (SUAS-S). Another aim was to reevaluate the previously reported positive association between T gondii serointensity and a history of nonfatal suicidal self-directed violence. Method: This cross-sectional, observational study compared T gondii serointensity and seropositivity in plasma from 54 adult suicide attempters (inpatients at Lund University Hospital, Lund, Sweden) and 30 adult control subjects (randomly selected from the municipal population register in Lund, Sweden) recruited between 2006 and 2010.The potential of patients and controls for self-directed violence was evaluated with the SUAS-S. Psychiatric diagnoses were made according to DSM-IV criteria. Plasma samples were tested for immunoglobulin G antibodies to T gondii, cytomegalovirus, and herpes simplex virus type 1. Data were analyzed using multivariable logistic regression to investigate the association between T gondii serointensity or seropositivity and a history of nonfatal suicidal self-directed violence; multivariable linear regression was used to explore the relationship between T gondii serointensify or seropositivity and the SUAS-S. Both regression models included sex, age, and body mass index as covariates. Results: Seropositivity of T gondii (adjusted odds ratio [OR]=7.12; 95% CI, 1.66-30.6; P=.008) and serointensity of T gondii (adjusted OR=2.01; 95% CI, 1.09-3.71; P=.03) were positively associated with a history of nonfatal suicidal self-directed violence. Seropositivity of T gondii was associated with higher SUAS-S scores, a relationship significant for the whole sample (P=.026), but not for suicide attempters only. No significant associations with other pathogens were identified. Conclusions: These results are consistent with previous reports on the association between T gondii infection and nonfatal suicidal self-directed violence. Confirming these results in future large longitudinal studies and including suicide as an outcome may lead to novel individualized approaches in suicide prevention. J Clin Psychiatry 2012;73 (8):1069-1076 (c) Copyright 2012 Physicians Postgraduate Press, Inc.

Toxoplasma gondii antibody titers and history of suicide attempts in patients with schizophrenia

October 16, 2011
Okusaga, O,. Langenberg, P., Sleemi, A., Vaswani, D., Giegling, I., Hartmann, A. M., Konte, B., Friedl, M., Groer, M. W., Yolken, R. H., Rujescu, D., Postolache, T. T.
Schizophrenia Research 2011; 133: 150-155

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Neuropathological changes and clinical features of autism spectrum disorder participants are similar to that reported in congenital and chronic cerebral toxoplasmosis in humans and mice

October 19, 2010
Prandota J.
Research in Autism Spectrum Disorders 2010; 4: 103-118.

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Anatomic, histopathologic, and MRI/SPET studies of autistic spectrum disorders (ASD) patients' brains confirm existence of very early developmental deficits. In congenital and chronic murine toxoplasmosis several cerebral anomalies also have been reported, and worldwide, approximately two billion people are chronically infected with T. gondii with largely yet unknown consequences. The aim of the study was therefore to compare brain abnormalities in ASD patients with those found in mice with cerebral toxoplasmosis (CT) because this may help in understanding pathophysiology of ASD. Data from available published studies were analyzed to compare postmortem pathologic changes found in the brains of ASD patients with those of mice developed after intraperitoneal T.gondii infection. Patients with ASD had the following brain abnormalities: active neuroinflammatory process notably in cerebellum, microglial nodules, accumulation of perivascular macrophages, decreased number and size of Purkinje cells in cerebellar nuclei and inferior olive, hypoperfusion of brain. Mice with congenital toxoplasmosis also had persistent neuroinflammation and ventricular enlargement, periventricular edema, meningeal and perivascular inflammation, and focal loss of Purkinje and granule cells. In murine acquired CT, the brain anomalies included: ventricular dilatation probably reflecting loss of brain parenchyma; perivascular inflammation particularly in hippocampus, and periaqueductal/periventricular areas, Purkinje cell layer markedly disfigured with focal loss of cells: perivascular cuffing by mononuclear cells and localized microglial/inflammatory nodules. Infection of mice with different strains of T. gondii resulted in distinctive neuropathological changes and various stadium of maturity of cysts and the parasite itself, which is in line with the diversity of the autistic phenotypes. Also, the abnormalities in behavior and clinical features associated with autism resembled that reported in chronic latent toxoplasmosis in humans and rodents. All these similarities suggest that T gondii should be regarded as an important infectious factor that may trigger development of ASD and some other neurodegenerative diseases, such as obsessive-compulsive and attention-deficit/hyperactivity disorders, and cryptogenic epilepsy. Thus, all these patients should be tested for T. gondii infection. (C) 2009 Elsevier Ltd. All rights reserved.

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

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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

Toxoplasma gondii: host-parasite interaction and behavior manipulation

October 26, 2009
da Silva, R.C., Langoni, H.
Parasitology Research 2009; 105: 893-898

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The importance of Toxoplasma gondii infection in diseases presenting with headaches. Headaches and aseptic meningitis may be manifestations of the Jarisch-Herxheimer reaction

October 26, 2009
Prandota J.
International Journal of Neuroscience 2009; 119: 2144-2182.

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Alzheimer’s dementia or cerebral toxoplasmosis? Case study of dementia following toxoplasmosis infection

November 7, 2002
Freidel S, Martin-Solch C, Schreiter-Gasser U.
Nervenarzt 2002; 73: 874-878

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Parkinsonian symptoms as an initial manifestation in a Japanese patient with acquired immunodeficiency syndrome and Toxoplasma infection

November 7, 2000
Murakami, T., Nakajima, M., Nakamura, T., Hara, A., Uyama, E., Mita, S., Matsushita, S., Uchino, M.
Internal Medicine 2000; 39: 1111-1114

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Seroprevalence of Toxoplasma gondii infection in arthritis patients in eastern China

December 8, 1970
Tian, A. L., Gu, Y. L., Zhou, N., Cong, W., Li, G. X., Elsheikha, H. M., Zhu, X. Q.
Infectious Diseases of Poverty 1970; 6

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Background: There is accumulating evidence for an increased susceptibility to infection in patients with arthritis. We sought to understand the epidemiology of Toxoplasma gondii infection in arthritis patients in eastern China, given the paucity of data on the magnitude of T. gondii infection in these patients. Methods: Seroprevalence of T. gondii infection was assessed by enzyme-linked immunosorbent assay using a crude antigen of the parasite in 820 arthritic patients, and an equal number of healthy controls, from Qingdao and Weihai cities, eastern China. Sociodemographic, clinical and lifestyle information on the study participants were also obtained. Results: The prevalence of anti-T. gondii IgG was significantly higher in arthritic patients (18.8%) compared with 12% in healthy controls (P < 0.001). Twelve patients with arthritis had anti-T. gondii IgM antibodies - comparable with 10 control patients (1.5% vs 1.2%). Demographic factors did not significantly influence these seroprevalence frequencies. The highest T. gondii infection seropositivity rate was detected in patients with rheumatoid arthritis (24.8%), followed by reactive arthritis (23.8%), osteoarthritis (19%), infectious arthritis (18.4%) and gouty arthritis (14.8%). Seroprevalence rates of rheumatoid arthritis and reactive arthritis were significantly higher when compared with controls (P < 0.001 and P = 0.002, respectively). A significant association was detected between T. gondii infection and cats being present in the home in arthritic patients (odds ratio [OR], 1.68; 95% confidence interval [CI]: 1.24 - 2.28; P = 0.001). Conclusions: These findings are consistent with and extend previous results, providing further evidence to support a link between contact with cats and an increased risk of T. gondii infection. Our study is also the first to confirm an association between T. gondii infection and arthritis patients in China. Implications for better prevention and control of T. gondii infection in arthritis patients are discussed.