Toxoplasmosis is the disease caused by infection with the obligate intracellular parasite, Toxoplasma gondii. Both acute and chronic toxoplasmosis are conditions in which the parasite is responsible for the development of clinically evident disease.

Keywords: intracellular parasitism; host immunity; host–pathogen interaction; congenital infection; opportunistic infection; AIDS

Figure 1.

Structure of a tachyzoite of Toxoplasma gondii (a) Freeze–fracture electron micrograph of a tachyzoite. (b) Diagram of organelles that are not demonstrated in (a). The surface antigens are involved in attachment and are the primary antigens identified by the infected host. Microneme proteins are released at the onset of the invasion process. The contents of the rhoptries are secreted during the process of invasion. Dense granule proteins are secreted from the parasite after invasion, during replication, and before egress from the infected host cell.

Figure 2.

The process of attachment, penetration and invasion of Toxoplasma gondii. (1) The parasite attaches to the host cell and rolls up on to its anterior pole. (2) The conoid extends and releases penetration‐enhancing factor from the rhoptries. This perturbs the membrane and increases infectivity of the parasite. (3–5) The parasite releases microneme proteins, which form a tight junction between the pellicle of the parasite and the plasma membrane of the cells. This junction translocates to the posterior end of the parasite and (6) seals off the host cell membrane to form the parasitophorous vacuole.

Figure 3.

Host immune response to Toxoplasma gondii. Interaction of the parasite with the host elicits a complex series of immunological events. The parasite is acquired by oral ingestion and following release from the tissue cyst comes into contact with the gut mucosa. The parasite infects enterocytes and stimulates the production of proinflammatory cytokines, in particular interleukin (IL)‐12, by various cells within the Peyer patch. This innate immune response mediates antigen‐specific CD8+ T‐cell immunity at both the mucosal and systemic level. The responding T cells exhibit cytolytic activity against parasite‐infected targets and release interferon (IFN)γ, which is microbicidal to the replicating parasite via the induction of nitric oxide (NO). The activated T cells also downregulate the proinflammatory response by the production of both IL‐10 and transforming growth factor (TGF) β. This counterinflammatory response allows for homeostasis and prevents tissue damage due to hyperinflammation secondary to the production of IFNγ and TNFα.



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Further Reading

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Dubey JP, Lindsay DS and Speer CA (1998) Structures of Toxoplasma gondii tachyzoites, bradyzoites, and sporozoites and biology and development of tissue cysts. Clinical Microbiology Reviews 11: 267–299.

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Soete M and Dubremetz JF (1996) Toxoplasma gondii: kinetics of stage‐specific protein expression during tachyzoite–bradyzoite conversion in vitro. Current Topics in Microbiology and Immunology 219: 76–80.

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Kasper, Lloyd H(Apr 2001) Toxoplasmosis. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1038/npg.els.0001939]