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      Association of T. gondii infection with suicide: a systematic review and meta-analysis

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          Abstract

          Background

          Findings on the association between Toxoplasma gondii ( T. gondii) infection and suicide are contradictory. This paper aimed to resolve this uncertainty by conducting a meta-analysis.

          Methods

          We found the relevant studies using keywords include “Toxoplasmosis” and “Suicide” and the related synonyms in international databases such as ISI, Medline, and Scopus. The eligible studies were included in the meta-analysis phase. The random effect approach was applied to combine the results.

          Results

          Out Of 150 initial studies, 15 were included in the meta-analysis. Odds of suicide in people with T. gondii infection was 43% (OR: 1.43, 95%CI; 1.15 to 1.78) higher than those without this infection. The test for publication bias was not statistically significant, which indicates the absence of likely publication bias.

          Conclusion

          This study confirms that T. gondii infection is a potential risk factor for suicide. To reduce cases of suicide attributable to T. gondii infection, it is recommended to implement some measures to prevent and control the transmission of the disease.

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          Most cited references30

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          Suicide, Suicide Attempts, and Suicidal Ideation

          E Klonsky, Alexis May, Boaz Y. Saffer (2016)
          Suicidal behavior is a leading cause of death and disability worldwide. Fortunately, recent developments in suicide theory and research promise to meaningfully advance knowledge and prevention. One key development is the ideation-to-action framework, which stipulates that (a) the development of suicidal ideation and (b) the progression from ideation to suicide attempts are distinct phenomena with distinct explanations and predictors. A second key development is a growing body of research distinguishing factors that predict ideation from those that predict suicide attempts. For example, it is becoming clear that depression, hopelessness, most mental disorders, and even impulsivity predict ideation, but these factors struggle to distinguish those who have attempted suicide from those who have only considered suicide. Means restriction is also emerging as a highly effective way to block progression from ideation to attempt. A third key development is the proliferation of theories of suicide that are positioned within the ideation-to-action framework. These include the interpersonal theory, the integrated motivational-volitional model, and the three-step theory. These perspectives can and should inform the next generation of suicide research and prevention.
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            The Neurotropic Parasite Toxoplasma Gondii Increases Dopamine Metabolism

            Emese Prandovszky, Elizabeth Gaskell, Heather Martin … (2011)
            The highly prevalent parasite Toxoplasma gondii manipulates its host's behavior. In infected rodents, the behavioral changes increase the likelihood that the parasite will be transmitted back to its definitive cat host, an essential step in completion of the parasite's life cycle. The mechanism(s) responsible for behavioral changes in the host is unknown but two lines of published evidence suggest that the parasite alters neurotransmitter signal transduction: the disruption of the parasite-induced behavioral changes with medications used to treat psychiatric disease (specifically dopamine antagonists) and identification of a tyrosine hydroxylase encoded in the parasite genome. In this study, infection of mammalian dopaminergic cells with T. gondii enhanced the levels of K+-induced release of dopamine several-fold, with a direct correlation between the number of infected cells and the quantity of dopamine released. Immunostaining brain sections of infected mice with dopamine antibody showed intense staining of encysted parasites. Based on these analyses, T. gondii orchestrates a significant increase in dopamine metabolism in neural cells. Tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, was also found in intracellular tissue cysts in brain tissue with antibodies specific for the parasite-encoded tyrosine hydroxylase. These observations provide a mechanism for parasite-induced behavioral changes. The observed effects on dopamine metabolism could also be relevant in interpreting reports of psychobehavioral changes in toxoplasmosis-infected humans.
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              Regulation and function of T-cell-mediated immunity during Toxoplasma gondii infection.

              Eric Y. Denkers, Ricardo T. Gazzinelli (1998)
              The intracellular protozoan Toxoplasma gondii is a widespread opportunistic parasite of humans and animals. Normally, T. gondii establishes itself within brain and skeletal muscle tissues, persisting for the life of the host. Initiating and sustaining strong T-cell-mediated immunity is crucial in preventing the emergence of T. gondii as a serious pathogen. The parasite induces high levels of gamma interferon (IFN-gamma) during initial infection as a result of early T-cell as well as natural killer (NK) cell activation. Induction of interleukin-12 by macrophages is a major mechanism driving early IFN-gamma synthesis. The latter cytokine, in addition to promoting the differentiation of Th1 effectors, is important in macrophage activation and acquisition of microbicidal functions, such as nitric oxide release. During chronic infection, parasite-specific T lymphocytes release high levels of IFN-gamma, which is required to prevent cyst reactivation. T-cell-mediated cytolytic activity against infected cells, while easily demonstrable, plays a secondary role to inflammatory cytokine production. While part of the clinical manifestations of toxoplasmosis results from direct tissue destruction by the parasite, inflammatory cytokine-mediated immunopathologic changes may also contribute to disease progression.
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                Author and article information

                Contributors
                Eissa Soleymani: Soleymanieissa@gmail.com
                Fariba Faizi: faizeif@yahoo.com
                Rashid Heidarimoghadam: r.heidari@umsha.ac.ir
                Lotfollah Davoodi: Lotfdavoodi@yahoo.com
                Younes Mohammadi:
                ORCID: http://orcid.org/0000-0001-7521-4909
                u.mohammadi@umsha.ac.ir
                Journal
                Journal ID (nlm-ta): BMC Public Health
                Journal ID (iso-abbrev): BMC Public Health
                Title: BMC Public Health
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-2458
                Publication date (Electronic): 24 May 2020
                Publication date PMC-release: 24 May 2020
                Publication date Collection: 2020
                Volume: 20
                Electronic Location Identifier: 766
                Affiliations
                [1 ]GRID grid.411950.8, ISNI 0000 0004 0611 9280, Students Research Committee, School of Medicine, , Hamadan University of Medical Sciences, ; Hamadan, Iran
                [2 ]GRID grid.411950.8, ISNI 0000 0004 0611 9280, Research Center for Health Sciences, School of Public Health, , Hamadan University of Medical Sciences, ; Hamadan, Iran
                [3 ]GRID grid.411623.3, ISNI 0000 0001 2227 0923, Antimicrobial Resistance Research Center, , Mazandaran university of Medical science, ; Sari, Iran
                [4 ]GRID grid.411950.8, ISNI 0000 0004 0611 9280, Modeling of Noncommunicable Diseases Research Center, School of Public Health, , Hamadan University of Medical Sciences, ; Hamadan, Iran
                [5 ]GRID grid.411950.8, ISNI 0000 0004 0611 9280, Department of Epidemiology, School of Public Health, , Hamadan University of Medical Sciences, ; Hamadan, Iran
                Author information
                http://orcid.org/0000-0001-7521-4909
                Article
                Publisher ID: 8898
                DOI: 10.1186/s12889-020-08898-w
                PMC ID: 7245947
                PubMed ID: 32448258
                SO-VID: 621f301a-cffb-41aa-af97-42b90d0fb23c
                Copyright © © The Author(s) 2020
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 12 June 2019
                Date accepted : 11 May 2020
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2020

                ScienceOpen disciplines: Public health
                Keywords: t. gondii,suicide,systematic review,meta-analysis
                Data availability:
                ScienceOpen disciplines: Public health
                Keywords: t. gondii, suicide, systematic review, meta-analysis

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