“…This suggestion may be supported by the fact that in congenital murine toxoplasmosis, coronal sections of the cerebrum revealed marked periventricular edema, subependymal nodules bulging into the ventricles, and loss of subependymal germinal cells (Stahl & Kaneda, 1998). One may therefore speculate that other forms of brain neoplasia, such as recurrent intracranial ependymoma and myxopapillary ependymoma presenting with or without intracranial hypertension (Drozdowski & Pogorzelski, 2005;Good et al, 2001;Labauge, Gros, Pages, Benezech, & Salvaing, 1984;Philippon, Poisson, & Bleibel, 1980;Tseng, Hsu, Jung, & Chen, 2004;Warnick et al, 1993), glioblastoma multiforme masquerading as PTC (Aroichane, Miller, & Eggenberger, 1993), gliomatosis (Weston & Lear, 1995), and gliomas associated with epilepsy (Schlehofer et al, 1999;Schwartzbaum et al, 2005), food production or processing (Schlehofer et al, 2005), or occupations of women in agricultural services and farming (Zheng, Cantor, Zhang, Keim, & Lynch, 2001), have been caused by chronic untreated inflammation process due to recurrent reactivation of latent CT. This is consistent with the finding that patients with neoplasia had a significantly higher prevalence of anti-Toxoplasma gondii antibodies compared with healthy controls (Yazar et al, 2004).…”