In recent decades many new diseases have emerged, often because a pathogen jumped to a novel host. The jump of the bacterium Mycoplasma gallisepticum from domestic poultry to House Finches is one such case that is amenable to facilitating the development of general models of disease dynamics. This project will explore the effects on disease dynamics of multiple hosts that differ in competence and transmissions routes that differ in disease expression. By combining experimental work, studies of free-living bird communities, and mathematical models, it is possible to determine under what conditions epidemics will arise, and hence how they can be halted.
A variety of broader impacts will result. Thousands of members of the general public participate in monitoring the disease among wild birds through a citizen science program. Because the Cornell Laboratory of Ornithology routinely communicates research results and their relevance to the general public through a newsletter that reaches over 40,000 households, members of the public are educated about the process and products of this research. By formally involving postdoctoral researchers, graduate students, and undergraduates in the research a large number of students are trained in interdisciplinary research that is the hallmark of studies in disease ecology. Many of these belong to minorities currently under-represented in biological research.
In 1994 a new wildlife disease emerged among wild house finches (a small songbird) that caused severe conjunctivitis (eye infections) in large numbers of birds. The disease rapidly spread causing a major epidemic throughout North America. House finch numbers were reduced by half in eastern North America, where house finches had been introduced, but no such effect was observed in western North America where house finches are native. Both our research and that of others showed that the house finch was not the only bird species that became infected with the pathogenic bacterium Mycoplasma gallisepticum (MG). So in this project the goal was to study MG in a community of wild passerine birds, to allow us to develop a model for studying the complex interactions among multiple hosts and a single pathogen (disease causing organism). In order to achieve the goal we brought a large team of scientists from different universities and different disciplines together. The team included bird ecologists, veterinarians, microbiologists, immunologists, the world’s leading Mycoplasma specialist, and mathematical modelers. Following hypotheses were tested: 1. Mode of initial infection influences disease expression and transmission probabilities both within and among host species. 2. The duration of acquired immunity varies with mode of exposure and infection. 3. Probabilities of disease transmission are not equal among hosts, but asymmetrically favor transmission from some key hosts to other species. In order to place the results from tests of the first three hypotheses into an ecological and evolutionary context, we also tested two additional hypotheses: 4. Variation in host genetic diversity affects disease expression, probability of transmission from the infected host, and immunity duration. This may affect disease dynamics both in local populations and at large geographic scales (e.g. eastern vs. western North America). 5. Over time the pathogen has evolved in ways that affect disease expression and transmission rates. Significant results - Sequencing MG isolates allowed us to show that although MG moved between poultry and house finches multiple times, a single successful host jump resulted in the continent-wide epidemic by single lineage. - Since the beginning of the epidemic in 1994 MG virulence (disease severity) increased rapidly. This happened independently in eastern (introduced) and western (native) parts of the house finch range. - MG can be successfully transmitted between house finches by direct and indirect (via fomites) contact, and through ingestion; - Severity of disease varies with mode of infection, with host species, and with isolate; - Although different bird species are not equally competent hosts, American goldfinches can maintain an MG epidemic, and the species composition of the bird community in which house finches live can have an effect on disease prevalence in house finches; - Canaries are a potential model for the study of MG infections as they respond similarly to experimental infections than house finches; - A large number of bird species show evidence of MG infection but not necessarily disease; MG may thus be more widespread among wild birds than originally thought. - MG causes multiple changes in host behavior such as activity, flocking, feeding, migration; - Response to infection and resulting disease varies with MG vlhA expression. - House finches passed through a genetic bottleneck when introduced to the eastern part of their current range around 1942; nevertheless differences in responses to the epidemic in east and west (more severe effect in east than in west) were not caused by host genetic variation but are the result of changes in MG; - House finches evolved after endemic MG infection becoming more genetically diverse at the MHC loci; - House finch immunological response varies between different geographical populations ; - Bird social behavior affects probability of and response to infection; - House finch roosting behavior is most likely not important in MG transmission, because house finches do not roost in large flocks; - The decline in house finch abundance resulting from the MG epidemic had an impact of house sparrow abundance; - Field study data enabled developed of various new methods to estimate disease prevalence using Capture-Mark-Recapture models; the probability of observing a bird depends on its disease state; hence this probability needs to be estimated in order to accurately estimate disease prevalence - Multiple more theoretical and more applied mathematical models were developed as part of this study. These can be extrapolated to other study systems. Key outcome: In this study we showed that an emerging wildlife disease, caused by a recent successful between-host jump, can spread rapidly, impact host abundance and indirectly the abundance of competitors, whereby pathogen and host can evolve rapidly. This study will become a textbook example because of the integrated collaboration between scientists from very different fields. The next question that we want to study is what causes evolutionary changes leading to an increase in virulence (severity of disease in the host).
