Toxoplasmosis of the central nervous system in the adult. Electron microscopic observations

Hc, Powell; Cj, Gibbs; Am, Lorenzo; Pw, Lampert; Dc, Gajdusek

doi:10.1007/bf00690438

Cited by 37 publications

(12 citation statements)

References 21 publications

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“…They may gain access to the brain and form dormant cysts (Sims et al, 1989;Baragan & Sibley, 2002;Lambert et al, 2006). Proliferating T. gondii tachyzoites have been identified in glial cells and Purkinje cell in human patients who developed toxoplasmosis encephalitis (Powell et al, 1978;Palmer, 2007).…”

Section: Toxoplasma Gondii and Toxoplasmosismentioning

confidence: 99%

Epilepsy and tropical parasitic infections in Sub-Saharan Africa: a review

Mazigo

Morona

Kweka

et al. 2013

Tanzania J Hlth Res

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Several reports have suggested that the high prevalence of epilepsy in sub-Saharan Africa is associated with the high prevalence of parasitic infections affecting the central nervous system. Though epidemiological evidence suggests an association between parasitic infections and epilepsy, the biological causal relationship has not been fully demonstrated for many of these infections. The objective of this paper is to review the available epidemiological evidence on the links between parasitic infections and epilepsy, the pathogenesis and the current gap of knowledge indicating the areas requiring further research. Data for this review were identified and collected using manual and electronic search strategies of published and unpublished sources. In Sub-Saharan Africa, the epidemiology of epilepsy remains unclear and given the differing study designs, the results of available epidemiological studies are difficult to interpret and compare. Evidence from surveys reported a median prevalence of 1.5%. Co-infection of parasitic infections and epilepsy in sub-Saharan Africa are common, particularly in areas characterized by poor hygiene standards. There is an epidemiological link on the association between epilepsy and various parasitic infections. However, the biological causal relationship requires further investigation in adequately designed studies. In conclusion, although several epidemiological and case control studies indicate a relationship between parasitic agents and epilepsy in sub-Saharan Africa, there is a considerable gap of knowledge on the cause and magnitude of the association. Thus, there is an urgent need for systematic epidemiological studies to understand the burden of epilepsy in areas endemic due to preventable parasitic infections, to prove a causal relationship, and to understand the impact of controlling these parasitic diseases on reduction of the burden of epilepsy.___________________________________________________________________________________

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Section: Toxoplasma Gondii and Toxoplasmosismentioning

confidence: 99%

Epilepsy and tropical parasitic infections in Sub-Saharan Africa: a review

Mazigo

Morona

Kweka

et al. 2013

Tanzania J Hlth Res

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“…[53][54][55][56] Most studies are in animal models, but a case report of incidental findings at autopsy of an immunocompetent patient indicated a similar pattern in humans. 56 An early study of chronic latent infection in mice (examined at 3, 6, and 12 months post-infection) reported that infected brains appeared normal on gross inspection.…”

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confidence: 95%

Latent Toxoplasmosis gondii: Emerging Evidence for Influences on Neuropsychiatric Disorders

Hurley

Taber²

2012

JNP

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Cover and FIGURE 1. A coronal section from the Mouse Brain Library is shown on the cover. 1 Toxoplasmosis gondi cysts can be present in any part of a host neuron in the brains of mice with chronic latent infection. Shown on the left a are representative brain sections immune-stained for T. gondii antibody (brown, black scale bar: 50 um). 2 The upper set show a cyst within a dendrite of a striatal neuron; the lower set show a cyst within the soma of a cortical neuron (two levels of magnification). Note that T. gondii antigen is also present within the cytosol of the host neurons. Cysts can contain dopamine (or its immediate precursor), as illustrated on the right (yellow scale bar: 10 mm) for two different areas (upper and lower rows) immune-stained for anti-dopamine antibody (green) and TRITC-lectin (red, cyst wall). 3 Addition of immune-staining with DAPI (blue, right column) provides visualization of neural cells and individual bradyzoites.FIGURE 2. Studies quantifying T. gondii cyst burden in multiple brain areas in rodents with chronic infection found differences in relative burden across regions, but the patterns vary considerably. 2,4-7 Results for a few commonly reported regions are illustrated, with longer times post-infection indicated by lighter colors. Studies are separated into two histograms, based on method of quantification used. Note that every anatomic area had the heaviest burden of cysts in at least one study. FIGURE 3. A recent voxel-based morphometry study assessed T. gondii status as well as average graymatter volume in patients with schizophrenia [R] and matched healthy controls [L]. 8 As compared with controls, the group with schizophrenia had reduced gray-matter volume in multiple areas of cortex, hippocampus, and caudate (not illustrated). Both groups were split based on T. gondii status, and comparisons were repeated. Major areas of significantly reduced gray matter in the groups with schizophrenia are approximated on representative magnetic resonance images. Note the much greater number and extent of areas in the group of patients with schizophrenia that were positive (pink) than negative (blue) for T. gondii when compared with their respective healthy controls.a Reproduced under the terms of the Creative Commons Attribution License.

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“…In addition, in these keratinocyte host cells, tissue cysts are surrounded by thick keratin filament bundles which consistently obstruct attempts to purify the parasites (25). Close association of intermediate filaments with parasitophorous vacuoles and tissue cysts of T. gondii and N. caninum had also been observed in other host cells (19,44,56).…”

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confidence: 99%

In Vitro Induction of Neospora caninum Bradyzoites in Vero Cells Reveals Differential Antigen Expression, Localization, and Host-Cell Recognition of Tachyzoites and Bradyzoites

et al. 2004

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We report on an optimized method for the in vitro culture of tissue cyst-forming Neospora caninum bradyzoites in Vero cells and the separation of viable parasites from host cells. Treatment of tachyzoite-infected Vero cell cultures with 17 M sodium nitroprusside for 8 days severely scaled down parasite proliferation, led to reduced expression of tachyzoite surface antigens, and induced the expression of the bradyzoite marker NcBAG1 and the cyst wall antigen recognized by the monoclonal antibody MAbCC2. Transmission electron microscopy demonstrated that intracellular parasites were located within parasitophorous vacuoles that were surrounded by a cyst wall-like structure, and the dense granule antigens NcGRA1, NcGRA2, and NcGRA7 were incorporated into the cyst wall. Adhesion-invasion assays employing purified tachyzoites and bradyzoites showed that tachyzoites adhered to, and invaded, Vero cells with higher efficiency than bradyzoites. However, removal of terminal sialic acid residues from either the host cell or the parasite surface increased the invasion of Vero cells by bradyzoites, but not tachyzoites.

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Toxoplasmosis of the central nervous system in the adult. Electron microscopic observations

Cited by 37 publications

References 21 publications

Epilepsy and tropical parasitic infections in Sub-Saharan Africa: a review

Epilepsy and tropical parasitic infections in Sub-Saharan Africa: a review

Latent Toxoplasmosis gondii: Emerging Evidence for Influences on Neuropsychiatric Disorders

In Vitro Induction of Neospora caninum Bradyzoites in Vero Cells Reveals Differential Antigen Expression, Localization, and Host-Cell Recognition of Tachyzoites and Bradyzoites

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