Investigating the Dynamics of Elk Population Size and Body Mass in a Seasonal Environment Using a Mechanistic Integral Projection Model

Environmentally mediated changes in body size often underlie population responses to environmental change, yet this is not a universal phenomenon. Understanding when phenotypic change underlies population responses to environmental change is important for obtaining insights and robust predictions of population dynamics in a changing world. We develop a dynamic integral projection model that mechanistically links environmental conditions to demographic rates and phenotypic traits (body size) via changes in resource availability and individual energetics. We apply the model to the northern Yellowstone elk population and explore population responses to changing patterns of seasonality, incorporating the interdependence of growth, demography, and density-dependent processes operating through population feedback on available resources. We found that small changes in body size distributions can have large impacts on population dynamics but need not cause population responses to environmental change. Environmental changes that altered demographic rates directly, via increasing or decreasing resource availability, led to large population impacts in the absence of substantial changes to body size distributions. In contrast, environmentally driven shifts in body size distributions could occur with little consequence for population dynamics when the effect of environmental change on resource availability was small and seasonally restricted and when strong density-dependent processes counteracted expected population responses. These findings highlight that a robust understanding of how associations between body size and demography influence population responses to environmental change will require knowledge of the shape of the relationship between phenotypic distributions and vital rates, the population status with regard to its carrying capacity, and importantly the nature of the environmentally driven change in body size and carrying capacity

Demographic profiles and environmental drivers of variation relate to individual breeding state in a long-lived trans-oceanic migratory seabird, the Manx shearwater.

Understanding the points in a species breeding cycle when they are most vulnerable to environmental fluctuations is key to understanding interannual demography and guiding effective conservation and management. Seabirds represent one of the most threatened groups of birds in the world, and climate change and severe weather is a prominent and increasing threat to this group. We used a multi-state capture-recapture model to examine how the demographic rates of a long-lived trans-oceanic migrant seabird, the Manx shearwater Puffinus puffinus, are influenced by environmental conditions experienced at different stages of the annual breeding cycle and whether these relationships vary with an individual's breeding state in the previous year (i.e., successful breeder, failed breeder and non-breeder). Our results imply that populations of Manx shearwaters are comprised of individuals with different demographic profiles, whereby more successful reproduction is associated with higher rates of survival and breeding propensity. However, we found that all birds experienced the same negative relationship between rates of survival and wind force during the breeding season, indicating a cost of reproduction (or central place constraint for non-breeders) during years with severe weather conditions. We also found that environmental effects differentially influence the breeding propensity of individuals in different breeding states. This suggests individual spatio-temporal variation in habitat use during the annual cycle, such that climate change could alter the frequency that individuals with different demographic profiles breed thereby driving a complex and less predictable population response. More broadly, our study highlights the importance of considering individual-level factors when examining population demography and predicting how species may respond to climate change

Emergence of a Novel Avian Pox Disease in British Tit Species

Avian pox is a viral disease with a wide host range. In Great Britain, avian pox in birds of the Paridae family was first diagnosed in a great tit (Parus major) from south-east England in 2006. An increasing number of avian pox incidents in Paridae have been reported each year since, indicative of an emergent infection. Here, we utilise a database of opportunistic reports of garden bird mortality and morbidity to analyse spatial and temporal patterns of suspected avian pox throughout Great Britain, 2006–2010. Reports of affected Paridae (211 incidents) outnumbered reports in non-Paridae (91 incidents). The majority (90%) of Paridae incidents involved great tits. Paridae pox incidents were more likely to involve multiple individuals (77.3%) than were incidents in non-Paridae hosts (31.9%). Unlike the small wart-like lesions usually seen in non-Paridae with avian pox in Great Britain, lesions in Paridae were frequently large, often with an ulcerated surface and caseous core. Spatial analyses revealed strong clustering of suspected avian pox incidents involving Paridae hosts, but only weak, inconsistent clustering of incidents involving non-Paridae hosts. There was no spatial association between Paridae and non-Paridae incidents. We documented significant spatial spread of Paridae pox from an origin in south-east England; no spatial spread was evident for non-Paridae pox. For both host clades, there was an annual peak of reports in August/September. Sequencing of the avian poxvirus 4b core protein produced an identical viral sequence from each of 20 great tits tested from Great Britain. This sequence was identical to that from great tits from central Europe and Scandinavia. In contrast, sequence variation was evident amongst virus tested from 17 non-Paridae hosts of 5 species. Our findings show Paridae pox to be an emerging infectious disease in wild birds in Great Britain, apparently originating from viral incursion from central Europe or Scandinavia

Understanding the impacts of Devil Facial Tumour Disease in wild Tasmanian devil (Sarcophilus harrisii) populations to inform management decisions

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

Data from: Evidence of a link between survival and pair fidelity across multiple tit populations

Although they have the potential to strongly influence individual fitness and the dynamics and productivity of populations, the survival consequences of pairing outcomes and the influence of current pairing outcomes on those in the future have rarely been addressed. Previously, we have shown that pair fidelity increases both survival and future pair fidelity in a population of great tits (Parus major). The aim of this study was to explore the generality of our previous findings by evaluating the influence of current paring outcomes on survival and on future pairing outcomes in two different species and in different populations. We addressed our aims within a multievent capture-mark-recapture (MECMR) statistical framework, which accounts for differences in recapture rates and uncertainty in the assignment of pair status (i.e. whether an individual is breeding with the same partner or not). We applied the framework to breeding records of two great tit populations and one blue tit (Cyanistes caeruleus) population. We detected survival benefits (i.e. increased survival) of pair fidelity in all three populations. These were similar in both great tit populations, but higher for male great tits than for male blue tits. We found that age-dependence in the rate of pair fidelity was shared between different populations and species, but did not detect any influence of current pair status on future pair status. Our study highlights the importance of considering survival when studying the fitness benefits of pair fidelity. Some of the differences in pair fidelity rates and survival benefits of pair fidelity are likely the result of long-term and short-term demographic and environmental factors in the population. We advocate the use of the MECMR framework used here for further exploration of these differences

Data from: Mhc-linked survival and lifetime reproductive success in a wild population of great tits

Major histocompatibility complex (Mhc) genes are frequently used as a model for adaptive genetic diversity. Although associations between Mhc and disease resistance are frequently documented, little is known about the fitness consequences of Mhc variation in wild populations. Further, most work to date has involved testing associations between Mhc genotypes and fitness components. However, the functional diversity of the Mhc, and hence the mechanism by which selection on Mhc acts, depends on how genotypes map to the functional properties of Mhc molecules. Here, we test three hypotheses that relate Mhc diversity to fitness: (1) the maximal diversity hypothesis; (2) the optimal diversity hypothesis, and (3) effect of specific Mhc types. We combine mark-recapture methods with analysis of long-term breeding data to investigate the effects of Mhc class I functional diversity (Mhc supertypes) on individual fitness in a wild great tit (Parus major) population. We found that the presence of three different Mhc supertypes was associated with three different components of individual fitness: survival, annual recruitment and lifetime reproductive success (LRS). Great tits possessing Mhc supertype 3 experienced higher survival rates than those that did not, whereas individuals with Mhc supertype 6 experienced higher LRS and were more likely to recruit offspring each year. Conversely, great tits that possessed Mhc supertype 5 had reduced LRS. We found no evidence for a selective advantage of Mhc diversity, either in terms of maximal or optimal supertype diversity. Our results support the suggestion that specific Mhc types are an important determinant of individual fitness

DataSheet1_The Certainty of Uncertainty: Potential Sources of Bias and Imprecision in Disease Ecology Studies.docx

<p>Wildlife diseases have important implications for wildlife and human health, the preservation of biodiversity and the resilience of ecosystems. However, understanding disease dynamics and the impacts of pathogens in wild populations is challenging because these complex systems can rarely, if ever, be observed without error. Uncertainty in disease ecology studies is commonly defined in terms of either heterogeneity in detectability (due to variation in the probability of encountering, capturing, or detecting individuals in their natural habitat) or uncertainty in disease state assignment (due to misclassification errors or incomplete information). In reality, however, uncertainty in disease ecology studies extends beyond these components of observation error and can arise from multiple varied processes, each of which can lead to bias and a lack of precision in parameter estimates. Here, we present an inventory of the sources of potential uncertainty in studies that attempt to quantify disease-relevant parameters from wild populations (e.g., prevalence, incidence, transmission rates, force of infection, risk of infection, persistence times, and disease-induced impacts). We show that uncertainty can arise via processes pertaining to aspects of the disease system, the study design, the methods used to study the system, and the state of knowledge of the system, and that uncertainties generated via one process can propagate through to others because of interactions between the numerous biological, methodological and environmental factors at play. We show that many of these sources of uncertainty may not be immediately apparent to researchers (for example, unidentified crypticity among vectors, hosts or pathogens, a mismatch between the temporal scale of sampling and disease dynamics, demographic or social misclassification), and thus have received comparatively little consideration in the literature to date. Finally, we discuss the type of bias or imprecision introduced by these varied sources of uncertainty and briefly present appropriate sampling and analytical methods to account for, or minimise, their influence on estimates of disease-relevant parameters. This review should assist researchers and practitioners to navigate the pitfalls of uncertainty in wildlife disease ecology studies.</p

Capture histories used to model pair fidelity and survival in E_surge

Data include capture histories (column 'H:') for a) female blue and great tits of Wytham woods; b) male blue and great tits of Wytham woods; c) female great tits of Wytham and Bagley woods; d) male great tits of Wytham and Bagley woods. For each dataset, the capture history is followed by the column 'S:' (denotes number of individuals with the capture history), the column '$COV:Mgp' (covariate coding for age, either Juvenile or Adult), and the column '$COV:Sp; or ;$COV:Pop; (coding for Species: G - great tit, B -Blue tit; or population Bag - Bagley wood, Wyth = Wytham woods). These capture histories were used to model pair fidelity and survival in program E_Surge as described in the Supplementary material of the Culina et al. 2015. Capture histories consist of 6 different codes that describe the 'event' that happen for a particular bird in a particular season. The original data on breeding pairs come from the long-term monitored populations in these woods

individual sequence dataset

Mhc class I allele data of 618 great tits. Alleles are identified with their Genbank accession number

Additional file 2: Figure S1. of Associations between perceived institutional support, job enjoyment, and intentions to work in the United Kingdom: national questionnaire survey of first year doctors

Percentage of doctors responding to each of the 12 attitude statements on a 5-point scale: Strongly Agree (SA), Agree (A), Neither agree nor disagree (N), Disagree (D), Strongly Disagree (SD). See Methods/Table 1 for full wording of the attitude statements. (TIFF 2294 kb