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Abstract
Multi-host parasites, such as Plasmodium, face a variety of host environments, and successful reproduction requires the parasites to circulate between the vertebrate and the invertebrate hosts. Plasmodium is the causative agent of malaria, responsible for over 240 million cases and 600 thousand deaths, in 2021. Therefore, understanding parasite fitness may have provided additional insights into disease transmission. In this dissertation, I examined parasite fitness in response to its vertebrate host, and invertebrate host environments. With the vertebrate host, I used an in vitro primary hepatocyte culture model to assess how host heterogeneity drives P. falciparum liver-stage susceptibility and how environmental oxygen level impacts P. falciparum liver-stage development. With the invertebrate host (mosquitoes), I assessed how nutrient availability in the context of oviposition status affects infection prevalence and parasite densities using P. berghei and An. stephensi mosquitoes. Lastly, I assessed how additional bloodmeals from non-host vertebrates (cannot be infected by the studied Plasmodium) can change the parasite development dynamic inside the mosquitoes using P. falciparum and P. berghei with An. stephensi mosquitoes.