The ubiquitous zoonotic pathogen Toxoplasma gondii has a unique life cycle involving domestic and wild animal hosts in diverse ecosystems. While historically T. gondii was primarily considered a terrestrial pathogen, this parasite has gained prominence in recent years for causing morbidity and mortality in marine wildlife and via waterborne transmission to people. Domestic and wild felids are the only definitive hosts of T. gondii that shed the environmentally resistant stage of the parasite, oocysts, in their feces. Many questions remain on the broader host and environmental factors that influence oocyst shedding in naturally infected domestic and wild felids, which are increasingly important in light of current and future environmental changes that may alter T. gondii transmission. The overall goal of this dissertation was to advance knowledge regarding the epidemiology, transmission, and disease ecology of T. gondii oocysts in wildlife and human hosts.In Chapter 1, I reviewed the current dynamics of oocyst shedding in domestic and wild felids and discussed key risk factors such as route of exposure, diet, and genotype. The difficulties of interpreting tests for detection of oocysts and T. gondii DNA, confirming parasite identity, repeat shedding, and the potential role of environmental contamination were also discussed. In Chapter 2, I utilized a longitudinal field study of T. gondii in feces from free-ranging feral cat colonies near sea otter habitats in Monterey Bay to evaluate temporal trends in oocyst shedding and the presence of virulent T. gondii strains previously associated with sea otter mortality. T. gondii DNA prevalence in feces was high (25.9%) and was more likely to be detected in the wet season and in colonies with kittens. Strains previously implicated in sea otter mortalities from toxoplasmosis (Type X and X-variants) represented 14.8% of strains present in feral cat feces; other genotypes detected included Type I (59%), Type II/III (18.5%), and two atypical genotypes (7.4%) based on characterization at the B1 locus. In Chapter 3, I evaluated climatic and anthropogenic risk factors for oocyst shedding in free-ranging domestic and wild felids using generalized linear mixed models. Human population density was associated with higher confirmed T. gondii shedding in free-ranging domestic cats and wild felids. Climate variables that reflected annual averages were not significant, however variables that reflected smaller temporal changes such as mean temperature in the driest quarter and mean diurnal range were associated with oocyst shedding in wild and domestic felids respectively. Finally, I developed a Bayesian quantitative risk analysis (QRA) model of oocyst vs. non-oocyst foodborne toxoplasmosis in Brazil in Chapter 4. Predicted likelihood of infections from oocysts on contaminated produce were significantly higher than infections from consumption of bradyzoites in contaminated meat. The importance of parameters such as oocyst removal efficiency and oocyst viability were identified in sensitivity analyses. The results of this dissertation provide novel insight on the shedding behavior of T. gondii in definitive hosts, identification of anthropogenic predictors of oocyst shedding, and quantitative methods for evaluating foodborne risk of exposure to T. gondii. These insights will inform host and ecosystem level management strategies and areas of focus for future approaches to prevent T. gondii oocyst transmission and infection in animal populations and humans.