Observations on bradyzoite biology

Abstract

Tachyzoites of the Apicomplexan Toxoplasma gondii cause acute infection, disseminate widely in their host, and eventually differentiate into a latent encysted form called bradyzoites that are found within tissue cysts. During latent infection, whenever transformation to tachyzoites occurs, any tachyzoites that develop are removed by the immune system. In contrast, cysts containing bradyzoites are sequestered from the immune system. In the absence of an effective immune response released organisms that differentiate into tachyzoites cause acute infection. Tissue cysts, therefore, serve as a reservoir for the reactivation of toxoplasmosis when the host becomes immunocompromised by conditions such as HIV infection, organ transplantation, or due to the impaired immune response that occurs when pathogens are acquired in utero. While tachyzoites and bradyzoites are well defined morphologically, there is no clear consensus on how interconversion occurs or what exact signal(s) mediate this transformation. Advances in research methods have facilitated studies on T. gondii bradyzoites providing important new insights into the biology of latent infection.

Keywords: Bradyzoite; Cyst wall; Differentiation; Latent infection; Metabolism; Toxoplasma.

Figure 1

Localization of various tachyzoite and bradyzoite markers

Figure 2. Leaky cyst phenotype

CST1-knockout (Δcst) strain of T. gondii stained with mAb 4B8 that recognizes an unknown cyst wall/cyst matrix protein (A); co-localized with DAPI (B). Parental strain of T. gondii (PruΔKu80) stained with mAb 4B8 8 (C); co-localized with DAPI (D). T. gondii strains were cultured in bradyzoite conditions (pH 8.0, 0.5% CO2).