Toxoplasma gondii: determinants of tachyzoite to bradyzoite conversion

Abstract

Apicomplexa are primarily obligate intracellular protozoa that have evolved complex developmental stages important for pathogenesis and transmission. Toxoplasma gondii, responsible for the disease toxoplasmosis, has the broadest host range of the Apicomplexa as it infects virtually any warm-blooded vertebrate host. Key to T. gondii’s pathogenesis is its ability to differentiate from a rapidly replicating tachyzoite stage during acute infection to a relatively non-immunogenic, dormant bradyzoite stage contained in tissue cysts. These bradyzoite cysts can reconvert back to tachyzoites years later causing serious pathology and death if a person becomes immune-compromised. Like the sexual stage sporozoites, bradyzoites are also orally infectious and a major contributor to transmission. Because of the critical role of stage conversion to pathogenesis and transmission a major research focus is aimed at identifying molecular mediators and pathways that regulate differentiation. Tachyzoite to bradyzoite development can occur spontaneously in vitro and be induced in response to exogenous stress including but not limited to host immunity. The purpose of this review is to explore the potential contributors to stage differentiation in infection and how a determination is made by the parasite to differentiate from tachyzoites to bradyzoites.

Estimation of Toxoplasma gondii infection by Serological and Immunohistochemical methods in Baghdad City-Iraq

“…The protozoan T. gondii is an obligate intracellular parasite that infects human and a broad spectrum of vertebrate hosts (Skariah, 2010). The transmission of T. gondii occurs by; ingestion of oocysts shed in feline feces, ingestion of T. gondii cysts from chronically infected tissues, or by vertical transmission.…”

Inhibitors of eIF2α Dephosphorylation Slow Replication and Stabilize Latency in Toxoplasma gondii

“…However, bradyzoites can reconvert to actively replicating tachyzoites when host immunity is attenuated, causing lifelong chronic infection. The recurrent reactivation of acute infection can lead to serious damage of the central nervous system (CNS) and heart, where bradyzoite cysts have a tendency to reside (1)(2)(3). While antifolates and other antibiotics are used to treat acute infection, the frontline drugs cause severe adverse effects and do not appear to exert activity against encysted parasites (1,3,4).…”

Significant Reduction of Brain Cysts Caused by Toxoplasma gondii after Treatment with Spiramycin Coadministered with Metronidazole in a Mouse Model of Chronic Toxoplasmosis

“…T. gondii is able to cross the intestinal membrane, disseminate in body tissues, cross the blood-brain barrier (BBB), and migrate to the central nervous system (23). It is an obligate intracellular replication parasite (12), releasing more tachyzoites, which may form cysts containing bradyzoites that evade the immune system and remain in tissues (33).…”