Toxoplasma gondii is a zoonotic protozoan parasite that can cause morbidity and mortality in humans, domestic animals, and terrestrial and aquatic wildlife. The environmentally robust oocyst stage of T. gondii is fundamentally critical to the parasite's success, both in terms of its worldwide distribution as well as the extensive range of infected intermediate hosts. Despite the limited definitive host species (domestic and wild felids), infections have been reported on every continent, and in terrestrial as well as aquatic environments. The remarkable resistance of the oocyst wall enables dissemination of T. gondii through watersheds and ecosystems, and long-term persistence in diverse foods such as shellfish and fresh produce. Here, we review the key attributes of oocyst biophysical properties that confer their ability to disseminate and survive in the environment, as well as the epidemiological dynamics of oocyst sources including domestic and wild felids. This manuscript further provides a comprehensive review of the pathways by which T. gondii oocysts can infect animals and people through the environment, including in contaminated foods, water or soil. We conclude by identifying critical control points for reducing risk of exposure to oocysts as well as opportunities for future synergies and new directions for research aimed at reducing the burden of oocyst-borne toxoplasmosis in humans, domestic animals, and wildlife.

Food- and water-borne pathogens exhibit spatial heterogeneity, but attribution to specific environmental processes is lacking while anthropogenic climate change alters these processes. The goal of this study was to investigate ecology, land-use and health associations of these pathogens and to make future disease projections.The rates of five acute gastrointestinal illnesses (AGIs) (campylobacteriosis, Verotoxin- producing Escherichia coli, salmonellosis, giardiasis and cryptosporidiosis) from 2000 to 2013 in British Columbia, Canada, were calculated across three environmental variables: ecological zone, land use, and aquifer type. A correlation analysis investigated relationships between 19 climatic factors and AGI. Mean annual temperature at the ecological zone scale was used in a univariate regression model to calculate annual relative AGI risk per 1 °C increase. Future cases attributable to climate change were estimated into the 2080s.Each of the bacterial AGI rates was correlated with several annual temperature-related factors while the protozoan AGIs were not. In the regression model, combined relative risk for the three bacterial AGIs was 1.1 [95% CI: 1.02–1.21] for every 1 °C in mean annual temperature. Campylobacteriosis, salmonellosis and giardiasis rates were significantly higher (p < 0.05) in the urban land use class than in the rural one. In rural areas, bacteria and protozoan AGIs had significantly higher rates in the unconsolidated aquifers. Verotoxin-producing Escherichia coli rates were significantly higher in watersheds with more agricultural land, while rates of campylobacteriosis, salmonellosis and giardiasis were significantly lower in agricultural watersheds. Ecological zones with higher bacterial AGI rates were generally projected to expand in range by the 2080s.These findings suggest that risk of AGI can vary across ecosystem, land use and aquifer type, and that warming temperatures may be associated with an increased risk of food-borne AGI. In addition, spatial patterns of these diseases are projected to shift under climate change.