Persistent toxoplasma bradyzoite cysts in the brain: incidental finding in an immunocompetent patient without evidence of a toxoplasmosis

Pusch, Larissa; Romeike, Bernd; Deckert, Martina; Mawrin, Christian

doi:10.5414/npp28210

Cited by 22 publications

(14 citation statements)

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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. 57 Parasitecontaining cysts were found primarily in gray matter (90%).…”

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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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confidence: 95%

Latent Toxoplasmosis gondii: Emerging Evidence for Influences on Neuropsychiatric Disorders

Hurley

Taber²

2012

JNP

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“…However, in immune suppressed hosts, such as patients with AIDS, infections can be reactivated from these cysts with transformation of bradyzoites to tachyzoites resulting in severe and potentially fatal encephalitis [25, 26]. Additionally, recent studies suggest that chronic infections can be a cause of cryptogenic epilepsy and that these chronic infections are associated with an increased incidence of schizophrenia and/or psychosis [21,30,33–36]. This suggests that chronic infection has a neuropathological and neurophysiological effect on immune competent hosts.…”

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confidence: 99%

Host Cell Preference of Toxoplasma gondii Cysts in Murine Brain: A Confocal Study

Melzer¹,

Cranston²,

Weiss³

et al. 2010

J. Neuroparasitolog.

100

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Toxoplasma gondii is a protozoan parasite that is widely prevalent in humans and typically results in a chronic infection characterized by cysts located predominantly in the central nervous system. In immunosuppressed hosts, such as patients with HIV infection, the infection can be reactivated from the cysts in the brain resulting in a severe and potentially fatal encephalitis. Studies suggest that the chronic infection may also have neuropathological and behavioral effects in immune competent hosts. An improved understanding of tissue cyst behavior is of importance for understanding both the reactivation as well as the neurophysiological consequences of chronic infection. In vivo studies have identified neurons as host cells for cysts but in vitro studies have found that astrocytes can also foster development of the cysts. In this study we have addressed the question of which neural cell tissue cysts of T. gondii reside during chronic infection using a mouse model. Mice were infected with Me49 Strain T. gondii and the intracellular localization of the cysts analyzed during the development and establishment of a chronic infection at 1, 2, and 6 months post infection. Brains were fixed, cryosectioned, and stained with FITC-Dolichos biflorans to identify the Toxoplasma cysts and they were labeled with cell specific antibodies to neurons or astrocytes and then analyzed using confocal fluorescence microscopy. Cysts were found to occur almost exclusively in neurons throughout chronic infection. No cysts were identified in astrocytes, using the astrocyte marker, GFAP. Astrocyte interactions with neuronal-cysts, however, were frequently observed.

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“…It is estimated that 500 million to 2 billion people worldwide are chronically infected with this parasite (5,10). Despite the fact that such a large number of people are infected and most likely harbor T. gondii cysts in their brains (29), the clinical importance of this chronic infection remains largely unexplored and therefore unappreciated.…”

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Toxoplasma gondii Antigens Recognized by IgG Antibodies Differ between Mice with and without Active Proliferation of Tachyzoites in the Brain during the Chronic Stage of Infection

Hester

Mullins

et al. 2012

Infect Immun

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We examined whether tachyzoite proliferation in the brains of immunocompetent hosts during the chronic stage of infection with Toxoplasma gondii induces production of IgG antibodies that recognize parasite antigens different from those recognized by the antibodies of infected hosts that do not have tachyzoite growth. For this purpose, two groups of CBA/J mice, which display continuous tachyzoite growth in their brains during the later stage of infection, were infected, and one group received treatment with sulfadiazine to prevent tachyzoite proliferation during the chronic stage of infection. T. gondii antigens recognized by the IgG antibodies from these two groups of mice were compared using immunoblotting following separation of tachyzoite antigens by two-dimensional gel electrophoresis. Several antigens, including the microneme protein MIC2, the cyst matrix protein MAG1, and the dense granule proteins GRA4 and GRA7, were commonly recognized by IgG antibodies from both groups of mice. There were multiple antigens recognized mostly by IgG antibodies of only one group of mice, either with or without cerebral tachyzoite growth. The antigens recognized only by or mostly by the antibodies of mice with cerebral tachyzoite growth include MIC6, the rhoptry protein ROP1, GRA2, one heat shock protein HSP90, one (putative) HSP70, and the myosin heavy chain. These results indicate that levels of IgG antibody to only selected T. gondii antigens increase in association with cerebral tachyzoite proliferation (reactivation of infection) in immunocompetent hosts with chronic infection.

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Persistent toxoplasma bradyzoite cysts in the brain: incidental finding in an immunocompetent patient without evidence of a toxoplasmosis

Cited by 22 publications

References 0 publications

Latent Toxoplasmosis gondii: Emerging Evidence for Influences on Neuropsychiatric Disorders

Latent Toxoplasmosis gondii: Emerging Evidence for Influences on Neuropsychiatric Disorders

Host Cell Preference of Toxoplasma gondii Cysts in Murine Brain: A Confocal Study

Toxoplasma gondii Antigens Recognized by IgG Antibodies Differ between Mice with and without Active Proliferation of Tachyzoites in the Brain during the Chronic Stage of Infection

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