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Hybridization of mule deer (Odocoileus hemionus) and white‐tailed deer (O. virginianus) appears to be a semi‐regular occurrence in western North America. Previous studies confirmed the presence of hybrids in a variety of sympatric habitats, but their developing molecular resources limited identification to the earliest, most admixed generations. For this reason, estimates of hybrid production in wild populations often rely on anecdotal reports. As well, white‐tailed deer populations’ continued encroachment into historically mule deer‐occupied habitats due to changes in land use, habitat homogenization, and a warming climate may increase opportunities for interspecific encounters. We sought to quantify the prevalence and extent of hybrid deer in the prairies of western Canada using a SNP assay with enhanced discriminating power. By updating the available molecular resources, we sought to identify and characterize previously cryptic introgression. We also investigated the influence of various parameters on hybridity by way of logistic regression. We observed overall hybridization rates of ~1.0%, slightly lower than that reported by previous studies, and found white‐tailed‐like hybrids to be more common than their mule deer‐like counterparts. Here, we build upon past studies of hybridization in North American deer by increasing hybrid detection power, expanding sample sizes, demonstrating a new molecular resource applicable to future research and observing asymmetrical directionality of introgression.

Chronic wasting disease (CWD) has impacted wildlife management in Canada. An integral partner in CWD management is the hunting community. This article empirically explored the response of Alberta m...

Thirty-seven adult female moose ( Alces alces) from 2 distinct but adjacent populations in Elk Island National Park (EINP), Alberta, Canada (19 in north EINP and 18 in south EINP), were fitted with mortality-sensing VHF radio-collars, and radio signals were acquired daily to ascertain mortality status. At capture, serum, whole blood, and feces were collected; pregnancy was determined; teeth were aged by visual inspection; and a portion of liver was assessed by ultrasound examination. Postmortem examination was conducted on 20 suitable carcasses. Clinical pathological abnormalities, including eosinophilia, polycythemia, elevated levels of liver enzymes in serum, hemoglobin, hematocrit, and red blood cell distribution, and liver damage as seen in ultrasound images occurred only in moose from north EINP. Infected moose had 4.7 ± 4.8 Fascioloides magna flukes per liver (mean ± SD). The proportion of moose pregnant at capture was similar in both populations (74% in north EINP, 61% in south EINP). Proportional mortality was significantly higher in moose from the north (68%) than the south (32%). Fascioloides magna was associated as a cause of death in 7 of 14 (50%) moose in the north where cause of death was determined, while predation ( n = 1), acute toxemic syndrome ( n = 3), dystocia ( n = 1), and roadkill and undetermined causes ( n = 3) were additional causes of mortality. F. magna was associated with poor body condition and was a major cause of mortality in north EINP but not south EINP, despite very similar habitat and proximity, suggesting a significant role for these flukes in affecting health and viability of naturally infected moose populations.

Reintroductions are a common tool for restoring lost biodiversity around the globe and across taxa. The decision to pursue a reintroduction is often based upon the success of past efforts, yet in most cases the assumption that resulting populations are the products of recolonization, is not tested. By collecting data from source populations, reintroduced populations, and natural populations adjacent to reintroductions, it is possible to evaluate the success of past reintroduction events and these data may be used to guide future conservation initiatives. We used the fisher (Pekania pennanti), one of North America's most commonly reintroduced species, as a model to conduct an evaluation of reintroduction success. We genotyped 147 individuals at 15 microsatellite loci to determine the genetic contribution of reintroduced individuals to an ostensibly successfully reintroduced population in central Alberta, Canada. Principle component analysis and Bayesian statistical methods converged with confidence on one result: assayed individuals were descended from adjacent native Albertan populations, not putative founders from eastern Canada. A review of fisher reintroduction literature reveals similar patterns: a large proportion of contemporary individuals appear to be the result of recolonization events. Our study has broad implications for conservation as it may imply a 1) over-confidence in past reintroductions, which might lead to significant expenditure of financial and human capital on future initiatives of modest, if any, benefit, and 2) underestimation of some species' ability to disperse and (re-)colonize, highlighting limits to our understanding of functional connectivity. Obtaining appropriate genetic samples in relation to reintroductions will help determine when future reintroduction is likely to be the best conservation initiative.

We develop a model for the spread of chronic wasting disease (CWD) in a mule deer (Odocoileus hemionus) population to assess possible mechanisms of disease transmission and parameterize it for the mule deer population in Alberta, Canada. We consider seven mechanisms of disease transmission corresponding to direct and indirect contacts that change with seasonal distribution and groupings of deer. We determine the minimum set of mechanisms from all possible combinations of mechanisms with different weights for duration of seasonal segregation of sexes that are able to reproduce the observed ratio of CWD prevalence in adult males and females of ∼2 and greater. Multiple mechanisms are likely to produce the ratio of male:female prevalence levels and include: (1) environmentally mediated transmission associated with higher food intake by males, (2) female to male transmission during mating of this polygamous species, (3) increased male susceptibility to CWD and (4) increased intensity of direct contacts within male social groups. All of these mechanisms belong to the class of frequency-dependent transmission. Also important is seasonality in deer social structure with an increasing ratio of prevalence in males:females under all mechanisms as the duration of sexual segregation increases throughout a year.

Chronic wasting disease (CWD) is a fatal disease of North American cervids that was first detected in a wild, hunter-shot deer in Saskatchewan along the border with Alberta in Canada in 2000. Spatially explicit models for assessing factors affecting disease detection are needed to guide surveillance and control programs. Spatio-temporal patterns in CWD prevalence can be complicated by variation in individual infection probability and sampling biases. We assessed hunter harvest data of mule deer (Odocoileus hemionus) and white-tailed deer (Odocoileus virginianus) during the early phases of an outbreak in Saskatchewan (i.e., 2002-2007) for targeting the detection of CWD by defining (1) where to look, and (2) how much effort to use. First, we accounted for known demographic heterogeneities in infection to model the probability, P(E), that a harvested deer was infected with CWD given characteristics of the harvest location. Second, in areas where infected deer were harvested we modelled the probability, P(D), of the hunter harvest re-detecting CWD within sample units of varying size (9-54 km(2)) given the demographics of harvested deer and time since first detection in the study area. Heterogeneities in host infection were consistent with those reported elsewhere: mule deer 3.7 timeswhite-tailed deer, males 1.8 timesfemales, and quadratically related to age in both sexes. P(E) increased with number of years since the first detection in our study area (2002) and proximity to known disease sources, and also varied with distance to the South Saskatchewan River and small creek drainages, terrain ruggedness, and extent of agriculture lands within a 3 km radius of the harvest. The majority (75%) of new CWD-positive deer from our sample were found within 20 km of infected deer harvested in the previous year, while approximately 10% were greater than 40 km. P(D) modelled at 18 km(2) was best supported, but for all scales, P(D) depended on the number of harvested deer and time since the first infected deer was harvested. Within an 18 km(2) sampling unit, there was an 80% probability of detecting a CWD-positive deer with 16 harvested deer five years after the initial infected harvest. Identifying where and how much to sample to detect CWD can improve targeted surveillance programs early in the outbreak of the disease when based on hunter harvest.

Managing wildlife diseases requires an understanding of disease transmission, which may be strongly affected by host population density and landscape features. Transmission models are typically fit from time-series disease prevalence data and modelled based on how the contact rate among hosts is affected by density, which is often assumed to be a linear (density-dependent transmission) or constant (frequency-dependent transmission) relationship. However, long-term time-series data is unavailable for emerging diseases, and this approach cannot account for independent effects of landscape. We developed a mechanistic model based on ecological data to empirically derive the contact rate–density relationship in white-tailed and mule deer in an enzootic region of chronic wasting disease (CWD) in Alberta, Canada and to determine whether it was affected by landscape. Using data collected from aerial surveys and GPS-telemetry, we developed empirical relationships predicting deer group size, home range size, and habitat selection to iteratively simulate deer distributions across a range of densities and landscapes. We calculated a relative measure of total per-capita contact rate, which is proportional to the number of other deer contacted per individual per unit time, for each distribution as the sum of pairwise contact rates between a target deer and all other individuals. Each pairwise contact rate was estimated from an empirical relationship developed from GPS-telemetry data predicting pairwise contact rates as a function of home range overlap and landscape structure. Total per-capita contact rates increased as a saturating function of density, supporting a transmission model intermediate between density- and frequency-dependent transmission. This pattern resulted from group sizes that reached an asymptote with increasing deer density, although this relationship was mediated by tree and shrub coverage in the landscape, such that in heavily wooded areas, the contact rate saturated at much lower densities. These results suggest that CWD management based on herd reductions, which require a density-dependent contact rate to be effective, may have variable effects on disease across a single management region. The novel mechanistic approach we employed for estimating effects of density and landscape on transmission is a powerful complement to typical data-fitting approaches for modelling disease transmission.

The giant liver fluke, Fascioloides magna, a liver parasite of free-living and domestic ruminants of Europe and North America, was analysed in order to determine the origin of European populations and to reveal the biogeography of this originally North American parasite on the European continent. The variable fragments of the mitochondrial cytochrome c oxidase subunit I (cox1; 384bp) and nicotinamide dehydrogenase subunit I (nad1; 405bp) were used. Phylogenetic trees and haplotype networks were constructed and the level of genetic structuring was evaluated using population genetic tools. In F. magna individuals originating from all European foci of infection (Italy, Czech Republic and Danube floodplain forests involving the territories of Slovakia, Hungary and Croatia) and from four of five major North American enzootic areas, 16 cox1 and 18 nad1 haplotypes were determined. The concatenated sequence set produced 22 distinct haplotypes. The European fluke populations were less diverse than those from North America in that they contained proportionately fewer haplotypes (eight), while a more substantial level of genetic diversity and a greater number of haplotypes (15) were recorded in North America. Only one haplotype was shared between the European (Italy) and North American (USA/Oregon and Canada/Alberta) flukes, supporting a western North American origin of the Italian F. magna population. Haplotypes found in Italy were distinct from those determined in the remaining European localities which indicates that introduction of F. magna to the European continent occurred more than once. In the Czech focus of infection, a south-eastern USA origin was revealed. Identical haplotypes, common to parasites from the Czech Republic and from an expanding focus in Danube floodplain forests, implies that the introduction of F. magna to the Danube region came from an already established Czech focus of infection.

To successfully manage wildlife diseases, it is necessary to understand factors that influence spread. One approach is to analyze host movement and social structure, as these behaviors can be associated with the probability of transmission. Some populations of mule deer ( Odocoileus hemionus hemionus (Rafinesque, 1817)) in western Canada are infected with chronic wasting disease (CWD), a transmissible and fatal neurodegenerative disease. We used population analysis of spatial genetic structure of mule deer at broad and local scales to understand factors that influence spread. We genotyped 2535 mule deer sampled from Alberta, Saskatchewan, and portions of British Columbia using 16 microsatellite loci. We found weak genetic structure at broad spatial scales (overall FST = 0.008) that was well defined by geographic distance, indicating the risk of CWD spread from the focus of infection will decline gradually with increasing distance, but there are no barriers to the spread over time. At the local scale of approximately 2 km, elevated relatedness among CWD-infected individuals suggests transmission rates within social groups. Sex-biased spatial autocorrelation in genetic relatedness also indicates that female philopatry underlies the social structure, and therefore transmission among relatives is potentially driving local disease persistence.

Chronic wasting disease (CWD) is increasingly prevalent in multiple wild mule (Odocoileus hemionus) and white-tailed deer (O. virginianus) herds in North America. CWD was first found in Canadian wild mule deer in Saskatchewan in 2000 and has since spread into the neighboring province of Alberta. The infectious agent for CWD is a misfolded prion protein encoded by the PRNP gene. Previous studies revealed association between PRNP genotype and susceptibility to CWD in both mule and white-tailed deer in other regions. To investigate this link in Canadian populations, PRNP gene sequence was examined in 166 CWD- and 83 CWD+ mule deer, and 197 CWD- and 30 CWD+ white-tailed deer from Saskatchewan and Alberta. Two variable sites were found in mule deer, and 15 in white-tailed deer. In both species PRNP genotype was associated with CWD status. Mule deer possessing at least one copy of the common allele at codon 20 were less likely to test positive for CWD than expected, given the frequency of this allele in the population. A variant at codon 96 in white-tailed deer was also linked with reduced incidence of CWD. A greater knowledge of the genetic sources of heterogeneity in CWD susceptibility may improve our understanding of the mechanisms underlying the CWD epidemic in western Canada.

Translocation of wild ungulates is a common wildlife management tool and an integral component of game farming activities throughout the world. Elk (Cervus elaphus) are a primary species being moved, and the possibility of translocating a hazardous parasite led us to examine the potential for elk to survive infections of meningeal worm (Parelaphostrongylus tenuis), to shed larvae in feces, and thus, to translocate the parasite. Twenty-six elk calves were exposed to 15-300 infective larvae of meningeal worm. All 13 elk exposed to >125 larvae developed neurologic disease and died; 2 shed larvae in feces prior to death