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A critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients

While postnatal toxoplasmosis in immune-competent patients is generally considered a self-limiting and mild illness, it has been associated with a variety of more severe clinical manifestations. The causal relation with some manifestations, e.g. myocarditis, has been microbiologically proven, but th...

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Autores principales: Uzorka, J. W., Arend, S. M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5495839/
https://www.ncbi.nlm.nih.gov/pubmed/28083719
http://dx.doi.org/10.1007/s10096-016-2897-0
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author Uzorka, J. W.
Arend, S. M.
author_facet Uzorka, J. W.
Arend, S. M.
author_sort Uzorka, J. W.
collection PubMed
description While postnatal toxoplasmosis in immune-competent patients is generally considered a self-limiting and mild illness, it has been associated with a variety of more severe clinical manifestations. The causal relation with some manifestations, e.g. myocarditis, has been microbiologically proven, but this is not unequivocally so for other reported associations, such as with epilepsy. We aimed to systematically assess causality between postnatal toxoplasmosis and epilepsy in immune-competent patients. A literature search was performed. The Bradford Hill criteria for causality were used to score selected articles for each component of causality. Using an arbitrary but defined scoring system, the maximal score was 15 points (13 for case reports). Of 704 articles, five case reports or series and five case–control studies were selected. The strongest evidence for a causal relation was provided by two case reports and one case–control study, with a maximal causality score of, respectively, 9/13, 10/13 and 10/15. The remaining studies had a median causality score of 7 (range 5–9). No selection bias was identified, but 6/10 studies contained potential confounders (it was unsure whether the infection was pre- or postnatal acquired, or immunodeficiency was not specifically excluded). Based on the evaluation of the available literature, although scanty and of limited quality, a causal relationship between postnatal toxoplasmosis and epilepsy seems possible. More definite proof requires further research, e.g. by performing Toxoplasma serology in all de novo epilepsy cases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10096-016-2897-0) contains supplementary material, which is available to authorized users.
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spelling pubmed-54958392017-07-18 A critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients Uzorka, J. W. Arend, S. M. Eur J Clin Microbiol Infect Dis Original Article While postnatal toxoplasmosis in immune-competent patients is generally considered a self-limiting and mild illness, it has been associated with a variety of more severe clinical manifestations. The causal relation with some manifestations, e.g. myocarditis, has been microbiologically proven, but this is not unequivocally so for other reported associations, such as with epilepsy. We aimed to systematically assess causality between postnatal toxoplasmosis and epilepsy in immune-competent patients. A literature search was performed. The Bradford Hill criteria for causality were used to score selected articles for each component of causality. Using an arbitrary but defined scoring system, the maximal score was 15 points (13 for case reports). Of 704 articles, five case reports or series and five case–control studies were selected. The strongest evidence for a causal relation was provided by two case reports and one case–control study, with a maximal causality score of, respectively, 9/13, 10/13 and 10/15. The remaining studies had a median causality score of 7 (range 5–9). No selection bias was identified, but 6/10 studies contained potential confounders (it was unsure whether the infection was pre- or postnatal acquired, or immunodeficiency was not specifically excluded). Based on the evaluation of the available literature, although scanty and of limited quality, a causal relationship between postnatal toxoplasmosis and epilepsy seems possible. More definite proof requires further research, e.g. by performing Toxoplasma serology in all de novo epilepsy cases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10096-016-2897-0) contains supplementary material, which is available to authorized users. Springer Berlin Heidelberg 2017-01-12 2017 /pmc/articles/PMC5495839/ /pubmed/28083719 http://dx.doi.org/10.1007/s10096-016-2897-0 Text en © The Author(s) 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Original Article
Uzorka, J. W.
Arend, S. M.
A critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients
title A critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients
title_full A critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients
title_fullStr A critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients
title_full_unstemmed A critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients
title_short A critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients
title_sort critical assessment of the association between postnatal toxoplasmosis and epilepsy in immune-competent patients
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5495839/
https://www.ncbi.nlm.nih.gov/pubmed/28083719
http://dx.doi.org/10.1007/s10096-016-2897-0
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