Toxoplasma gondii is an obligate intracellular parasite with the capacity to infect all nucleated cells. Different strategies have evolved to optimize growth and quiescence, between acute and chronic stages of infection. The work presented in this thesis addressed the metabolic needs and capabilities of the T. gondii stages responsible for acute and chronic infection. Specifically, I investigated the synthesis and salvage strategies for acquisition of vitamins (B5 and B6) and a cofactor (Coenzyme A), essential for the growth of the parasite. Individual metabolic pathways were dissected by reverse genetics, metabolomic and in vivo studies. Genome mining approaches, as well as genome-wide CRISPR-Cas9 loss of function screens were employed for the identification of essential metabolite transporters. This work was aimed at understanding the basis of parasitism, and at the identification of novel drug targets to treat toxoplasmosis, malaria and apicomplexan diseases.