Emerging infectious diseases of wildlife have threatened host populations of diverse taxa in recent history, which is largely attributable to anthropogenic global change. In three data chapters, this dissertation examines the drivers of individual- to population-level variation in how host populations respond to novel and emerging pathogens. Each chapter explores these processes in bat populations of North America, predominantly the Northeast and Midwest regions of the United States, impacted by the emerging fungal pathogen that causes white-nose syndrome, Pseudogymnoascus destructans. In Chapter 2, I disentangle the effects of adaptive host traits and environmental influences in driving host population stabilization of the little brown bat (Myotis lucifugus), finding that host-pathogen coexistence in this system is the product of their complex interaction. In Chapter 3, I characterize the range-wide variation in white-nose syndrome impacts on a federally endangered and poorly studied species, the Indiana bat (Myotis sodalis), as well as environmental and demographic determinants of its declines over epidemic time. In Chapter 4, I explore the role of individual variation in roosting microclimate selection of little brown bats in driving their infection severity, yielding important insights into the pathophysiology and environmental dependence of white-nose syndrome. Ultimately, this dissertation characterizes complex drivers of variation in host responses to emerging and invading pathogens, yielding insights essential to the successful mitigation of their impacts. / Doctor of Philosophy / In the same way that Covid-19 swept through our global human population in the year 2020, novel infectious diseases have threatened wildlife populations, sometimes to the point of extinction. Often, however, the processes driving the impacts of novel infectious diseases in wildlife are unknown, despite being important information to protect susceptible populations. In this dissertation, I explore how North American bat populations have been impacted by a recently emerged disease, white-nose syndrome, and what processes cause variation in how individual bats and bat colonies have responded to the disease. In Chapter 2, I explore how the little brown bat (Myotis lucifugus) has evolved to co-exist with its new pathogen and how this coexistence is affected by environmental conditions like temperature and humidity. In Chapter 3, I characterize variation in how populations of the Indiana bat (Myotis sodalis) have responded to white-nose syndrome and how environmental and demographic conditions have affected declines since the disease first emerged. In Chapter 4, I explore how the temperatures used by little brown bats during hibernation affect the severity of their infection, giving us important information on how bats survive with white-nose syndrome and the role of temperature. Altogether, the research in this dissertation describes complex interactions between hosts, pathogens, and their environment in driving the patterns we observe after the emergence of novel infectious diseases.

Adaptive evolution of Toll-like receptors in birds Hana Velová, PhD thesis 6 Abstract Toll-like receptors (TLRs) are one of the key and presumably also evolutionary most original components of animal immune system. As Pattern recognition receptors they form the first line of innate immune defence against various pathogens. The proper receptor binding of pathogenic ligands is crucial for their correct recognition and for subsequent triggering of an appropriate immune response. Because there exists a direct interaction between the receptor surface and the pathogenic ligand, host-pathogen coevolution on molecular level can be predicted. Thus, through variability of their ligands, TLRs are exposed to extensive selective pressures that may be detected on both genetic and protein levels. Surprisingly, the variability we revealed in birds is even higher than previously expected based on the reports from other vertebrates, mainly mammals. In my doctoral thesis I summarise the results of my contribution to the avian TLR research. We were the first who experimentally verify the absence of functional TLR5 in several avian species and duplication of TLR7 in others. We finally resolved the origin of duplication in TLR1 and in TLR2 family. An important part of my research project focused on the prediction of potentially...