Malaria is a vector-borne parasitic disease affecting tropical and subtropical regions. Regardless control efforts, malaria incidence is still incredible high with 219 million clinical cases and an estimated 660,000 related deaths (WHO, 2012). In this project, different population genetic approaches were explored to characterize parasite populations. The goal was to create a framework that considered temporal and spatial changes of Plasmodium populations in malaria surveillance. This is critical in a vector borne disease in areas of low transmission where there is not accurate information of when and where a patient was infected. In this study, fragment analysis data and single nucleotide polymorphism (SNPs) from South American samples were used to characterize Plasmodium population structure, patterns of migration and gene flow, and discuss approaches to differentiate reinfection vs. recrudescence cases in clinical trials. A Bayesian approach was also applied to analyze the Plasmodium population history by inferring genealogies using microsatellites data. Specifically, fluctuations in the parasite population and the age of different parasite lineages were evaluated through time in order to relate them with the malaria control plan in force. These studies are important to understand the turnover or persistence of "clones" circulating in a specific area through time and consider them in drug efficacy studies. Moreover, this methodology is useful for assessing changes in malaria transmission and for more efficiently manage resources to deploy control measures in locations that act as parasite "sources" for other regions. Overall, these results stress the importance of monitoring malaria demographic changes when assessing the success of elimination programs in areas of low transmission.

Epidemiological theory normally does not predict host extinction from infectious disease because of a host density threshold below which pathogens cannot persist. However, host extinction can occur when a biotic or abiotic pathogen reservoir allows for density-independent transmission. Amphibians are facing global population decline and extinction from the emerging infectious disease chytridiomycosis, caused by the fungus Batrachochytrium dentrobatidis (Bd). I use the model species Eleutherodactylus coqui to assess the impact of Bd on terrestrial direct-developing frog species, a common life history in the tropics. I tested the importance of two key factors that might influence this impact and then used laboratory experiments and published field data to model population-level impacts of Bd on E. coqui. First, I assessed the ontogenetic susceptibility of E. coqui by exposing juvenile and adult frogs to the same pathogen strain and dose. Juveniles exposed to Bd had significantly lower survival rates compared with control juveniles, while adult frogs often cleared infection. Second, I conducted experiments to determine whether E. coqui can become infected with Bd indirectly from contact with zoospores shed onto vegetation by an infected frog and from direct exposure to an infected frog. Both types of transmission were observed, making this the first demonstration that amphibians can become infected indirectly in non-aquatic habitats. Third, I tested the hypothesis that artificially-maintained cultures of Bd attenuate in pathogenicity, an effect known for other fungal pathogens. Comparing two cultures of the same Bd strain with different passage histories revealed reduced zoospore production and disease-induced mortality rates for a susceptible frog species (Atelopus zeteki) but not for the less-susceptible E. coqui. Finally, I used a mathematical model to project the population-level impacts of chytridiomycosis on E. coqui. Model analysis showed that indirect transmission, combined with either a high rate of zoospore production or low rate of zoospore mortality, is required for Bd to drive E. coqui populations below an extinction threshold. High rates of transmission plus frequent re-infection could lead to poor recruitment of infected juveniles and population decline. My research adds further insight into how emerging infectious disease is contributing to the loss of amphibian biodiversity.