Treatment regimens for toxoplasmosis patients have essentially remained the same since the 1950s (Eyles & Coleman, 1953). They largely depend on the repurposing of antibacterials (sulfadiazine, spiramycin and clindamycin) and antimalarials (pyrimethamine and atovaquone) (Opremcak et al. 1992; Andrews et al. 2014; Antczak et al. 2016) in combination, therapies that target parasite folic acid synthesis, protein synthesis or oxidative phosphorylation (Greif et al. 2001; Antczak et al. 2016). Most of these chemotherapeutics are not readily bioavailable at the site of infection (e.g. unable to cross the blood-brain barrier); cannot be administered by patients with hypersensitivity to sulphonamides; have suspected teratogenic properties (Montoya & Remington, 2008; Paquet & Yudin, 2013); are threatened by the emergence of resistance (Sims, 2009); or require adjuvant therapies (folinic acid supplement) to minimize toxic side effects (for a detailed review see Antczak et al. 2016).