<p>  </p> <p>Predators and parasites are critical, interconnected members of the community and have the potential to influence host populations. Predators, in particular, can have direct and indirect impacts on disease dynamics. By removing hosts and their parasites, predators alter both host and parasite populations and ultimately shape disease transmission. Our ability to accurately predict disease dynamics requires understanding the ecological effects of predation on prey and host densities and its role in the coevolution of host resistance and parasite virulence. While the impact of predators on disease dynamics has received considerable attention, research has focused on selective predation on infected prey. There is, however, substantial evidence that some predators avoid infected prey, preferentially attacking uninfected individuals. Such different strategies of prey selectivity by predators modulate host-parasite interactions, changing the fitness payoffs both for hosts and their parasites. I use empirical results and theoretical predictions as a framework to discuss the mechanisms by which predation for infected versus uninfected individuals can affect disease dynamics. First, by integrating hypotheses from behavioral ecology and disease ecology, I outlined novel perspectives that complement the prevailing view of selective predation of infected individuals (Chapter 1). Then, exploring short-term ecological outcomes and long-term host-parasite coevolution, I investigated patterns of <em>Daphnia dentifera</em> host population densities and host susceptibility over several generations under different types of predation pressure, including selective predation on infected and uninfected individuals (Chapter 2). Finally, building on the results of this research, I developed a high school project-based lesson plan that facilitates the instruction of the nature of science, implementing on-going ecological research in activities to improve student learning based on a constructivist approach to learning (Chapter 3). Together this research highlights the differential ecological and evolutionary outcomes of host-parasite interactions under varying community contexts.</p>

Supplemental feeding of deer is a common management action. However, concentrating animals, as feeding does, is known to promote the transmission of disease. We examined how feeding alters three sources of disease: aflatoxins, gastrointestinal parasites, and ticks. To do this, we paired 79 feeder sites throughout Mississippi with ecologically-equivalent sites without feeders. Wildlife visitation increased at feeders compared to sites without feeders. For aflatoxins, we sampled during the summer and hunting season and found low prevalence and levels in feeders and bagged/bulk feed. The greater concern was environmental exposure to aflatoxins. All corn piles exposed to environmental contamination in July contained toxic levels of aflatoxins after eight days. The environmental load of gastrointestinal parasites was elevated for coccidia (4x) and strongylids (3x). Finally, feeding reduced the number of ticks at feeder sites, but did not alter the prevalence of tick-borne diseases within captured ticks compared to sites without feeders.

No description available.

Emerging infectious diseases represent a threat to biodiversity, posing significant challenges to wildlife conservation globally. Infectious diseases can cause population declines, local extirpations and, in rare cases, complete species extinction. Among emerging pathogens, pathogenic fungi have been responsible for drastic declines in several high-profile vertebrate taxa, such as Batrachochytrium dendrobatidis causing chytridiomycosis in many species of amphibians worldwide. Recently, an emerging infectious disease, 'snake fungal disease' (SFD), caused by the fungal pathogen Ophidiomyces ophidiicola, is affecting the health of snake populations in North America by causing skin infections which can be fatal. Given the potential impact of this disease on snake biodiversity worldwide, compounded by the pressure of anthropogenic stressors that already jeopardize the viability of many snake populations, there is a clear need for ecological research in this understudied system. This dissertation is comprised of 4 data chapters focusing on the disease dynamics of snake fungal disease in Europe, and the factors resulting in differential infection. In chapter 2, I develop a large field-based data collection in 10 countries in Europe to investigate the presence of disease hotspots and the variation of disease prevalence across host species, and to examine the pathogen genotypes that are present on the landscape. I found isolated areas of disease hotspots, and models including an interactive effect of host species and which pathogen clade are present on the landscape were best at explaining disease prevalence. In chapter 3, I perform a virulence challenge assay using 120 corn snakes (Pantherophis guttatus) and 7 strains of O. ophidiicola (3 collected from Europe, 4 from the USA). This experiment reveals that pathogen genotypes associated with higher disease prevalence in Europe also have higher pathogen virulence, and that different strains from the USA show variation in virulence. These results also match both physiological host responses measured in the lab and landscape patterns of disease. In chapter 4, I explore two mitigation-driven snake translocation projects in Europe that were complicated due to O. ophidiicola outbreaks. One snake species, N. tessellata, appears highly susceptible to SFD, indicating that under stressful conditions, O. ophidiicola can cause mortality regardless of pathogen genotype, and that this snake species may be important in pathogen maintenance. Finally in chapter 5, I report the presence of a different fungal pathogen in Spain, Parannannizziopsis sp., never reported in wild snakes in Europe before. Broadly, my dissertation demonstrates coevolutionary relationships between hosts and pathogens and has important implications to snake conservation over large scales. / Doctor of Philosophy / Biodiversity conservation is under significant threat globally due to the ever-growing human population. Threats such as habitat loss, climate change, pollution and infectious diseases are all important factors that are affecting wildlife populations. Snakes, and specifically infectious diseases of snakes, have been understudied compared to that of other types of wildlife in Europe. My dissertation focuses on understanding the disease ecology and conservation implications of snake fungal disease, an infectious disease that can be life-threatening to snakes. I first developed a study of this disease in multiple countries over three years to understand how common the disease is across the landscape, which species of snakes are most infected, and how severe skin infections are. I found specific areas in Europe where disease prevalence is high and attributed these higher disease areas to specific snake species and fungal strains that interact together to cause higher infection rates (chapter 2). Secondly, I designed a controlled experimental study in the laboratory to test the capacity of different pathogenic strains, collected in Europe and the USA, to harm its host. I chose a single host species, the corn snake (Pantherophis guttatus) to test this question. I found that different pathogen strains vary in their ability to cause severe disease, and these results were confirmed with field observations. I also found that one strain collected from coastal Virginia is able to cause more severe disease when compared to all other strains (chapter 3). Finally, I found that under captive stress, strains that might not be able to cause severe disease in the wild can lead to snake mortality, specifically in one snake species that might be more susceptible than others (chapter 4). Broadly, this dissertation describes complex interactions between snakes and fungal pathogens and has relevance to reptile conservation.

Emerging infectious diseases (EID) pose significant threats to biodiversity. Human influence over the environment has increased opportunities for the introduction of novel pathogens to naïve hosts, potentially leading to host extinction. Understanding mechanisms of host persistence is critical for effectively conserving species affected by EIDs. Our study investigated the disease dynamics of white-nose syndrome (WNS), caused by the fungal pathogen Pseudogymnoascus destructans (Pd), in little brown bats (Myotis lucifugus) across a spatiotemporal gradient. We explored the relationship between bat roosting temperatures and Pd growth rates across three phases of pathogen invasion comprising years since WNS has been present at sites: invasion (0-3), established (4-8), and endemic (9+ years). Data used by this study comes from a combination of field-based data collection in New York where WNS has been present the longest and data from a long-running project which includes from other locations in the Northeast and Midwest regions of the United States. Our results reveal a weakening interaction between temperature and fungal growth rates time with WNS progresses. We additionally observed a decrease in early hibernation fungal loads and variation in infection prevalence over time, suggesting the onset of a coevolutionary relationship between bats and Pd. This study highlights the importance of investigating changing disease dynamics when understanding the reasonings for host persistence. / Master of Science / Emerging infectious diseases threaten species with the risk of extinction. Human activities have altered habitats which has increased the spread of new pathogens to vulnerable host populations. This research focuses on white-nose syndrome (WNS), an emerging disease caused by the fungal pathogen Pseudogymnoascus destructans (Pd). The arrival of Pd to North America resulted in widespread declines in little brown bat (Myotis lucifugus) populations, however, some populations persist at stable or growing rates. This study aims to investigate how the relationship between the growth rate of Pd and bat hibernation temperature may have changed over time. We used a combination of contemporary data collected in New York and a long-running dataset that documents the invasion and establishment of Pd across the Northeast and Midwestern regions of the United States to investigate fungal growth rates during different phases of Pd invasion: invasion, established, and endemic phases. Our results indicate the relationship between temperature and pathogen growth rate has weakened over time, suggesting potential changes in the host-pathogen relationship. Additionally, we found changes in fungal loads and infection prevalence throughout hibernation, suggesting the foundation of a coevolutionary relationship between bats and Pd. This research highlights the importance of understanding changes in disease dynamics to help understand how other species at risk of emerging infectious diseases may be able to persist.

The aim of this study is to improve our understanding of the ecology, spatiotemporal patterns, and risk of infectious pathogens of migratory waterfowl, using the blue-winged teal (Anas discors, BWTE), as a model. From 2007-2010, 1,869 BWTE were sampled in the prairie provinces (Alberta, Saskatchewan and Manitoba, Canada) to examine infection status and/or evidence of previous exposure to avian influenza virus (AIV), West Nile virus (WNV), and avian paramyxovirus-1 (APMV-1), in relation to host demographic variables (age, sex, body condition, exposure to other pathogens), other ecological variables such as local waterfowl breeding population density and local pond density, and year. The probability of AIV infection depended on an interaction between age and AIV antibody status. Hatch year birds with antibodies to AIV were more likely to be infected, suggesting an antibody response to an active infection. After hatch year birds with antibodies to AIV were less likely to be infected, suggesting immunity resulting from previous exposure. AIV infection was positively associated with local BWTE density, supporting the hypothesis of density dependent transmission. Exposure to WNV and APMV-1 were also associated with age and year. Furthermore, the probability of WNV exposure was positively associated with local pond density rather than host population density, likely because ponds provide suitable breeding habitat for mosquitoes, the primary vectors for transmission. We also investigated large-scale spatiotemporal trends in apparent prevalence of AIV across Canada and the United States throughout the year, using data from national avian influenza surveillance programs in Canada and the US in 2007-2010. Our analyses revealed that age, sex, year of sampling, flyway, latitude, and season (categorized by stages of the BWTE annual life cycle) were all important variables in predicting probability of AIV infection. There was an interaction between age and season. During late summer staging (August) and fall migration (September-October), hatch year birds were more likely to be infected than after hatch year birds, however there was no difference between age categories for the remainder of the year (winter, spring migration, and breeding season). Probability of infection increased non-linearly with latitude, and was highest in summer, corresponding to the beginning of fall migration when densities of birds and the proportion of susceptible hatch year birds in the population are highest. Birds in the Pacific, Central and Mississippi flyways were significantly more likely to be infected compared to those in the Atlantic flyway. Observed trends in seasonal, annual, and geographic patterns of AIV infection in BWTE across Canada and the US were primarily driven by the dynamics of AIV infection in hatch year birds. Our results demonstrate demographic as well as seasonal, latitudinal and flyway trends across Canada and the US. This research provided further evidence for the role of wild dabbling ducks, particularly BWTE, in the maintenance and ecology of AIV. This improved understanding of the role of BWTE as natural hosts, and the geographic, demographic and temporal variables that affect infection and transmission parameters, moves us closer to deciphering the overall ecology of the virus and its transmission and transportation pathways at the individual, population and continental levels. This knowledge, in turn, will permit development of better tools to predict and perhaps to prevent possible outbreaks in domestic animals as well as in humans.

No description available.

Comprendre l'émergence et la propagation des maladies infectieuses chez les animaux sauvages est devenue une priorité en santé publique et en conservation. En combinant la collecte de données et le développement de modèles épidémiologiques, cette thèse s'est focalisée sur la compréhension de deux phénomènes clés: (i) étudier comment l'hétérogénéité au niveau des individus, des groupes, de la population et de l'environnement influence la propagation de parasites et (ii) quantifier la transmission de bactéries résistantes aux antibiotiques depuis l'homme vers les animaux sauvages dans trois aires protégées d'Afrique (Tsaobis NP- Namibie, Lopé NP-Gabon et Dzanga-Ndoki NP- République Centrafricaine). Les principaux résultats de ce travail montrent que : (1) De multiples facteurs incluant la température, la pluie, l'utilisation du territoire, le genre, l'âge et la condition physique influencent la richesse spécifique de parasites gastro-intestinaux chez le babouin chacma, (2) Les contacts entre animaux autour des points d'attractions de l'habitat peuvent influencer de manière importante la propagation spatio-temporelle d'une maladie, (3) La transmission d'entérobactéries résistantes semble avoir lieu depuis les humains ou le bétail vers les animaux sauvages dans des zones où le contact entre ces populations est élevé, (4) Le gradient de densité de gorilles produit par la chasse peut générer une augmentation de prévalence d'un parasite avec la distance au point d'introduction. Les conclusions de ce travail ouvrent de nouvelles possibilités pour l'étude des maladies émergentes chez les animaux sauvages. / Understanding the emergence and spread of infectious disease in wild animal populations has become an important priority for both public health and animal conservation. Combining the collection of empirical data with the development of epidemiological models, this thesis focuses on understanding two key issues of wildlife epidemiology: (i) how heterogeneity at the individual, group, population and landscape level affects parasite spread (ii) investigating whether transmission of antibiotic resistant bacteria from humans to wildlife is occurring within three protected areas of Africa (Tsaobis NP-Namibia, Lope NP-Gabon and Dzanga-Ndoki NP-Central African Republic). The main findings of this work indicated that: (1) multiple-scale factors including temperature, rainfall, home range use, sex, age and body condition influence gastro-intestinal parasite richness among wild baboons; (2) animal contacts around ‘habitat hotspots' can substantially influence the spatio-temporal dynamics of a disease; (3) antibiotic resistant enterobacteria seem to be spreading from humans/livestock to wildlife when the territory overlap between these two populations is expected to be high; (4) gradients in gorilla density created by bushmeat hunting can reverse the expected pattern of decreasing parasite prevalence with distance to human-spillover. The conclusions of this work open new possibilities for studying the mechanisms explaining the spread of emerging infectious diseases among wild animals.

<p><a>Natural enemy ecology strives to integrate the fields of disease ecology and community ecology to forge a broader understanding of how pathogens and predators structure communities. To advance this field, we need a greater emphasis on: 1) quantifying pathogen-mediated effects on community structure and comparing these effects to those observed with predators and 2) determining the interactive effects of combined natural enemies on communities. I conducted a mesocosm experiment designed to assess the individual and combined effects of predators (dragonfly larvae and adult water bugs) and a pathogen (ranavirus) on a larval amphibian community. Additionally, I conducted laboratory experiments to assess whether ranavirus exposure increases the vulnerability of tadpoles to predation. In my laboratory experiments, I found that virus exposure increased predation rates with dragonflies, but not water bugs. For tadpoles in the dragonfly treatments, the probability of survival for virus-exposed tadpoles was 66-77% lower compared to unexposed tadpoles. This data suggests that predators may selectively remove infected individuals from the population, which can enhance the magnitude of the healthy herds effect. I found that the risk level of the predators largely explained effects on the community. For instance, high-risk dragonflies reduce overall survival to 30% whereas low-risk water bugs only reduced survival to 67%. Additionally, I found that virus reduce survival to 62%, which was comparable to effect of the low-risk predator. Interestingly, all three natural enemies influenced community structure (i.e. species relative abundance) in unique ways. These results demonstrate that pathogens can have effects similar to predators on communities, and that natural enemy identity is important when considering impacts on community structure. When predators were combined with the virus, I found that mortality was relatively unchanged from the predator-only treatments suggesting less than additive effects of combined natural enemies. This result was driven by the healthy herds effect; the presence of dragonflies reduced overall infection prevalence in the community to 7% compared to 30% in the virus-only treatment. This effect was observed in the water bug treatments, to a lesser degree, suggesting that predator risk or efficiency contributes the magnitude of the effect. Collectively, my work demonstrates the importance of examining the individual and combined effects of natural enemies on ecological communities.</a></p>

Infectious diseases are increasingly being recognised as significant threatening processes in conservation biology. Developing strategies to effectively manage infectious diseases in wildlife is, therefore, of the utmost importance to the maintenance of global biodiversity. The effective management of infectious diseases relies on understanding the ecology of the host, the epidemiological characteristics of the pathogen and the impacts of the pathogen on the host population. However, for most wildlife-disease systems this information remains poorly understood. This is particularly true for endangered species threatened by novel infectious agents as opportunities to observe and assess disease impacts and host-pathogen dynamics in the wild are limited. The Tasmanian devil (Sarcophilus harrisii), the world’s largest carnivorous marsupial, is threatened with extinction as a result of an epidemic of an emerging disease, a fatal infectious cancer known as Devil Facial Tumour Disease (DFTD). In this thesis I capitalised on a unique dataset from a population of Tasmanian devils where disease arrived part-way through an intensive longitudinal study, and utilised existing genetic samples collected prior to DFTD outbreak, to determine the impact of DFTD on the demography, population dynamics, genetic diversity and population genetic structure of wild Tasmanian devils. I then used this knowledge of the impacts of DFTD impacts in an unmanaged population to evaluate the effectiveness of a disease management trial involving the selective culling of infected individuals. I employed mark-recapture models to investigate the impact of DFTD on age-specific and sex-specific apparent survival rates, to examine the pattern of variation in infection rates (force of infection), and to investigate the impact of DFTD on population growth rate. I investigated demography, life-history traits and morphometric parameters of infected and uninfected individuals to determine the impacts of DFTD on age-structure and sex-structure, female fecundity and individual growth rates. I used this information to assess the population’s ability to respond to low population densities and to compensate for the detrimental impacts of DFTD. To determine the genetic consequences of disease-induced population decline I used microsatellite DNA to compare genetic diversity, population genetic structure and dispersal patterns in three Tasmanian devil populations prior to and following DFTD outbreaks. Capture-mark-recapture analyses revealed that the arrival of DFTD triggered an immediate decline in apparent survival rates of devils, the rate of which was predicted well by the increase in disease prevalence in the population over time. Transition rates of healthy individuals to the diseased class (the force of infection) increased in relation to disease prevalence, while the arrival of DFTD coincided with a marked and ongoing decline in the population growth rate. There was a significant change to the age structure following the arrival of DFTD. This shift to a younger population was caused by the loss of older individuals as a direct consequence of DFTD-driven declines in adult survival rates. Evidence of reproductive compensation in response to these disease impacts was observed via a reduction in the age of sexual maturity of females over time. However, widespread precocial breeding in devils was precluded by physiological and ecological constraints that limited the ability of one year olds to breed. Using temporally-replicated spatial genetic data, I found evidence of increased inbreeding following DFTD arrival and greater population genetic differentiation in post-disease populations. These changes appeared to be driven by a combination of selection and altered dispersal patterns of females in DFTD-affected populations. Comparison of demographic and epidemiological parameters indicative of disease progression and impact between the managed and unmanaged populations revealed that selective culling of infected individuals neither slowed the rate of disease progression nor reduced the population level impacts of this debilitating disease; with culling mortality simply compensating for disease mortality. This thesis provides one of the few direct empirical evaluations of the impact of an emerging wildlife disease epidemic on a wild population. This thesis revealed that infectious diseases can result in major demographic and genetic changes in host populations over relatively few generations and short time-scales. Results showing dramatic and ongoing population declines and very limited population compensation in DFTD-affected populations indicate that DFTD poses a significant extinction risk for wild devil populations. Hence, this study confirms that host-specific pathogens can pose a significant extinction risk for wild species, even in the absence of alternate reservoir hosts, a finding critical to our understanding of host-pathogen dynamics. My thesis also highlights the potential negative interplay between disease susceptibility and host genetic variability, which is of utmost importance to the management of novel wildlife epizootics and the conservation of threatened wildlife in general. The thorough understanding of the ecology and impacts of DFTD in the wild obtained in this study has provided a solid base from which to both rigorously assess the outcome of management strategies and also formulate recommendations for the management of this disease in the wild. The lack of evidence for successful control of the DFTD epidemic in a wild population during the first phase of a selective culling experimental adaptive management approach, points to the need to implement a multi-faceted disease management program when attempting to control a novel infectious disease in the wild. By drawing on the lessons learnt in this case study I show that it is possible to establish a set of general guidelines for the future management of infectious diseases in threatened wildlife.