Mechanisms and Evolution of Disease Resistance in Birds

Abstract

Disease outbreaks in wildlife, agricultural animals, and humans have increased in both frequency and magnitude in recent decades, refocusing research efforts on understanding the factors that influence disease emergence. However, at least in wildlife, such research is constrained by a lack of knowledge regarding host immune responses to novel pathogens and how those responses may evolve in the face of pathogen driven selection. Consequently, the selective pressures encountered by the pathogen in the novel host, how such pressure may dictate pathogen evolution, and how adaptations to a particular host influence a pathogen’s host range are also poorly understood. Here I focus on one of the best-documented wildlife epizootics in history: the emergence of Mycoplasma gallisepticum (Mg) in wild North American house finches (Haemorhous mexicanus) following a host shift from poultry in the mid-1990s. To begin, I review the immune responses wild birds have been shown to mount against novel pathogens and how these responses relate to disease outcome. Subsequently, I examine the house finch-Mg system, emphasizing the evolution of house finch immune responses due to Mg-driven selection. Second, I expand upon the existing data set regarding the occurrence of Mg in house finches near the leading edge of pathogen spread in Arizona, USA. Then, using an experimental infection study with both poultry and early epizootic house finch Mg isolates, I show exposure to the novel house finch host was not the key limiting factor in the Mg host shift. Lastly, through an experimental infection study where I inoculated chickens with either a poultry or an early epizootic house finch Mg isolate, I show adaptation to house finches compromised the ability of Mg to re-infect poultry. Taken together, the chapters of this dissertation highlight that wild birds are capable of mounting immune responses to novel pathogens such as Mg and, in the face of strong-pathogen-driven selection, can undergo rapid evolution of immune responses. Furthermore, Mg host shifting was not limited by exposure to the novel host. Rather, genetic adaptation to the novel host environment was likely required at the cost of being able to re-infect poultry.