Abstract
Toxoplasma gondii (T. gondii) is a prevalent protozoan parasite of medical and veterinary significance. It is the etiologic agent of toxoplasmosis, a neglected disease in which incidence and symptoms differ between patients and regions. In immunocompetent patients, toxoplasmosis manifests as acute and chronic forms. Acute toxoplasmosis presents as mild or asymptomatic disease that evolves, under the host immune response, into a persistent chronic disease in healthy individuals. Chronic toxoplasmosis establishes as latent tissue cysts in the brain and skeletal muscles. In immunocompromised patients, chronic toxoplasmosis may reactivate, leading to a potentially life-threatening condition. Recently, the association between toxoplasmosis and various diseases has been shown. These span primary neuropathies, behavioral and psychiatric disorders, and different types of cancer. Currently, a direct pre-clinical or clinical molecular connotation between toxoplasmosis and most of its associated diseases remains poorly understood. In this review, we provide a comprehensive overview on Toxoplasma-induced and associated diseases with a focus on available knowledge of the molecular players dictating these associations. We will also abridge the existing therapeutic options of toxoplasmosis and highlight the current gaps to explore the implications of toxoplasmosis on its associated diseases to advance treatment modalities.
Highlights
Toxoplasma gondii (T. gondii) is an obligate intracellular parasite that infects a broad range of animals including approximately one third of the world’s human population [1]
It is worth noting that the percentage of acquiring toxoplasmosis during pregnancy varies according to regions and prevalence [19,20], and re-infection with atypical T. gondii genotypes was reported even in sero-positive pregnant women [21], and resulted in a more severe congenital toxoplasmosis [22]
ELISA performed on 22 cryptogenic epilepsy patients revealed that 75% of these patients had greater T. gondii antibody titers than those recorded among the controls [71]
Summary
Toxoplasma gondii (T. gondii) is an obligate intracellular parasite that infects a broad range of animals including approximately one third of the world’s human population [1]. In French Guiana and Latin America, atypical strains showed high genetic diversity and represented a severe acquired toxoplasmosis among immunocompetent individuals. These subjects developed fatal pneumonitis, myocarditis, meningo-encephalitis, and polymyositis [2]. To enter the CNS, three mechanisms have been proposed: the “Trojan horse” mechanism, through which the parasite highjacks an immune cell to enter, the paracellular crossing mechanism, and the transcellular crossing mechanism [7]. The “Trojan horse” mechanism was based on several in vitro studies showing that infected immune cells exhibit increased motility and are capable of crossing endothelial barriers [8,9,10]. In the paracellular mechanism of entry, it has been proposed that T. gondii uses its actin-myosin motors, gliding motility, to cross the BBB [12]
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