TrendsinParasitology TrendsinParasitology Trends in Parasitology | Parasite of the Month Toxoplasma gondii Sebastian Lourido1,2, * 1 Whitehead Institute for Biomedical Research, Cambridge, MA, USA 2 Biology Department, Massachusetts Institute of Technology, Cambridge, MA, USA TrendsinParasitology KEY FACTS: Broad host range, infecting warm-blooded animals from birds to humans, with sexual recombination restricted to felines. Following infection of the intestine from consumption of oocysts or tissue cysts, parasites disseminate systemically to replicate in a variety of nucleated cell types. Slow-replicating chronic stages may persist life-long as tissue cysts within neurons and muscle cells. Three genomes in the nucleus (66 Mb encoding ~8320 genes), mitochondrion, and apicoplast. Continuous asexual culture and extensive genetic approaches enable the study of physiology, cell biology, and host–parasite interactions. DISEASE FACTS: Most infections are asymptomatic, although ocular lesions can occur in immunocompetent individuals and are frequently associated with recrudescence. Parasites can enter immunologically privileged sites by crossing biologically restrictive barriers like the blood–brain and placental barriers. Reactivation of chronic infection in immunocompromised individuals can cause life-threatening infections of the central nervous system. Congenital transmission can occur during an untreated primary infection of the mother, commonly resulting in chorioretinitis and hydrocephalus in the newborn. Chemotherapy is effective against the acute disease but fails to clear chronic stages. TAXONOMY AND CLASSIFICATION: PHYLUM: Apicomplexa CLASS: Conoidasida ORDER: Eucoccidiorida FAMILY: Sarcocystidae GENUS: Toxoplasma SPECIES: T. gondii *Correspondence: lourido@wi.mit.edu Toxoplasma gondii is an obligate intracellular eukaryotic parasite from the phylum Apicomplexa that infects up to one-third of the global population. Although most infections are asymptomatic, some cause retinal lesions and, in immunocompromised individuals or when contracted congenitally, can lead to life-threatening disseminated infections involving the central nervous system. Parasites can enter a chronic state, resistant to current therapies, which can be a reservoir for recrudescence. Felines are the strict definitive hosts for T. gondii, in which the parasite can sexually develop, forming highly infectious, environmentally resistant oocysts. Virtually all warm-blooded animals can act as intermediate hosts, acquiring the infection from consuming oocysts or tissues of chronically infected animals. A variety of specialized organelles release proteins that mediate motility and invasion and modulate host pathways. Extensive genetic tools make T. gondii a tractable model to dissect the biology of the phylum. 944 Trends in Parasitology, November 2019, Vol. 35, No. 11    © 2019 Elsevier Ltd. All rights reserved.       https://doi.org/10.1016/j.pt.2019.07.001 Trends in Parasitology | Parasite of the Month Acknowledgments Jeroen Saeij, Vern Carruthers, and members of the Lourido laboratory provided helpful discussions and comments. Wandy Beatty at the Washington University Molecular Microbiology Imaging Facility performed the electron microscopy. This work was supported by the National Institutes of Health (NIH) Director’s Early Independence Award (1DP5OD017892) and a grant from the Mathers Foundation (1706-00164) to S.L. Resources www.toxodb.org www.cdc.gov/parasites/toxoplasmosis/ www.llamp.net Literature 1. Frenkel, J.K. et al. (1970) Toxoplasma gondii in cats: fecal stages identified as coccidian oocysts. Science 167, 893–896 2. Schwartzman, J.D. and Pfefferkorn, E.R. (1981) Pyrimidine synthesis by intracellular Toxoplasma gondii. J. Parasitol. 67, 150–158 3. Montoya, J.G. and Liesenfeld, O. (2004) Toxoplasmosis. Lancet 363, 1965–1976 4. Sibley, L.D. and Ajioka, J.W. (2008) Population structure of Toxoplasma gondii: clonal expansion driven by infrequent recombination and selective sweeps. Annu. Rev. Microbiol. 62, 329–351 5. Hunter, C.A. and Sibley, L.D. (2012) Modulation of innate immunity by Toxoplasma gondii virulence effectors. Nat. Rev. Microbiol. 10, 766–778 6. Yarovinsky, F. (2014) Innate immunity to Toxoplasma gondii infection. Nat. Rev. Immunol. 14, 109–121 7. Wang, J.-L. et al. (2016) The past, present, and future of genetic manipulation in Toxoplasma gondii. Trends Parasitol. 32, 542–553 8. Tardieux, I. and Baum, J. (2016) Reassessing the mechanics of parasite motility and host-cell invasion. J. Cell Biol. 214, 507–515 9. Frénal, K. et al. (2017) Gliding motility powers invasion and egress in Apicomplexa. Nat. Rev. Microbiol. 15, 645–660 10. Jeffers, V. et al. (2018) A latent ability to persist: differentiation in Toxoplasma gondii. Cell. Mol. Life Sci. 75, 2355–2373 Trends in Parasitology, November 2019, Vol. 35, No. 11    © 2019 Elsevier Ltd. All rights reserved.       https://doi.org/10.1016/j.pt.2019.07.001       945