Congenital Anomalies Induced by Toxoplasma Infection

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Abstract

Abstract A comprehensive review regarding congenital toxoplasmosis, which is caused by transmission of Toxoplasma gondii from an infected mother to her fetus during pregnancy, is presented. In most cases in humans the route of infection is oral and by either of the two forms of Toxoplasma; cysts in the raw flesh of an infected animal and oocysts in the feces of an infected cat. The clinical manifestations in 9 cases of congenital toxoplasmosis encountered by the author are preserted. The findings of computed tomography (CT) and magnetic resonance imaging (MRI) in 3 of these cases are presented. Delayed migration and myelination are suggested to have occurred in 2 cases in which abnormal MRI findings were noted. These MRI findings reflected the clinical manifestations and may also have reflected the pathologic findings. Experimental studies of transplacental infection following oral inoculation of Toxoplasma oocyst were performed in 3 groups of mice, in which infection of the dams was acute, subchronic, or chronic. The incidence of congenital infection was markedly higher in the acute infection group than in the subchronic or chronic infection groups. The incidence of 19S‐Toxoplasma (T)‐IgM positivity was also higher in the acute infection group than in either of the other two groups. Women should avoid contact with materials that have potentially been contaminated with cat feces, because Toxoplasma in the form of oocyst evacuated in cat feces is very highly infectious. Congenital toxoplasmosis is often accompanied by severe sequelae involving the central nervous system, but treatment is not effective once the symptoms are manifested. Early diagnosis and early treatment, before symptoms are manifest, are therefore important for the prevention of congenital toxoplasmosis. Copyright © 1995, Wiley Blackwell. All rights reserved

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YOKOTA, K. (1995). Congenital Anomalies Induced by Toxoplasma Infection. Congenital Anomalies. https://doi.org/10.1111/j.1741-4520.1995.tb00607.x

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