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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...

We analyzed retrospective data on harvest management practices and corresponding chronic wasting disease (CWD) prevalence trends in 36 western US and Canadian mule deer (Odocoileus hemionus) management units (units). Our analyses employed logistic regression and model selection, exploiting variation in practices within and among jurisdictions to examine relationships between harvest management and apparent prevalence (the proportion of positive animals among those sampled). Despite notable differences in hunting practices among jurisdictions, our meta-analysis of combined data revealed strong evidence that the amount of harvest was related to CWD prevalence trends among adult male mule deer in the 32 units where prevalence at the start of the analysis period was ≤5%. All competitive models included the number of male deer harvested or number of hunters 1-2 yr prior as an explanatory variable, with increasing harvest leading to lower prevalence among males harvested in the following year. Competitive models also included harvest timing. Although less definitive than the number harvested, median harvest dates falling closer to breeding seasons were associated with lower prevalence in the following year. Our findings suggest harvest-when sufficient and sustained-can be an effective tool for attenuating CWD prevalence in adult male mule deer across western ranges, especially early in the course of an epidemic. Evidence of a broad relationship between the amount of harvest and subsequent changes in CWD prevalence among adult male mule deer provides an empirical basis for undertaking adaptive disease management experimentation aimed at suppressing or curtailing CWD epidemics.

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.

Disease risk modeling is a key first step to understand the spatio-temporal dynamics of wildlife disease and to direct cost-effective surveillance and management. In Alberta, active surveillance for chronic wasting disease (CWD) in wild cervids began in 1998 with the first case detected in free-ranging cervids in 2005. Following the detection, a herd reduction program was implemented during 2005-2008 and in 2006 the ongoing hunter-based CWD Surveillance Program became mandatory in high-risk Wildlife Management Units (WMU). We used data collected during the CWD surveillance program to 1) document growth in sex-specific CWD prevalence (proportion of deer in sample that is CWD-positive) in hunter-harvest deer in 6 WMUs consistently monitored from 2006 to 2018, 2) document landscape features associated with where CWD-positive compared to CWD-negative deer were removed during hunter harvest and herd reduction in an early (2005-2012) and in a late period (2013-2017), and 3) to map the spatial risk of harvesting a deer infected with CWD in the prairie parklands of Alberta. In the 6 continuously monitored WMUs, risk of a harvested deer being CWD positive increased from 2006 to 2018 with CWD prevalence remaining highest in male mule deer whereas overall growth rate in CWD prevalence was greater in female mule deer, but similar to male white-tailed deer. We found no evidence that the 3-year herd reduction program conducted immediately after CWD was first detected affected the rate at which CWD grew over the course of the invasion. Risk of deer being CWD-positive was the highest in animals taken near small stream drainages and on soils with low organic carbon content in the early period, whereas risk became highest in areas of agriculture especially when far from large river drainages where deer often concentrate in isolated woody patches. The change in the influence of proximity to known CWD-positive cases suggested the disease was initially patchy but became more spatially homogeneous over time. Our results indicate that a targeted-removal program will remove more CWD positive animals compared to hunter harvest. However, the discontinuation of targeted removals during our research program, restricted our ability to assess its long term impact on CWD prevalence.

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.

Summary Predicting the spatial pattern of disease risk in wild animal populations is important for implementing effective control programmes. We developed a risk model predicting the probability that a deer harvested in a wild population was chronic wasting disease positive (CWD+) and evaluated the importance of landscape connectivity based on deer movements. We quantified landscape connectivity from deer ‘resistance’ to move across the landscape similar to the flow of electrical current across a hypothetical electronic circuit. Resistance values to deer movement were derived as the inverse of step selection function values constructed using movement data from GPS-collared deer. The top CWD risk model indicated risk increased over time was higher among mule deer Odocoileus hemionus than white-tailed deer Odocoileus virginianus, males than females, and was greater in areas with high stream density and abundant agriculture. A metric of connectivity derived from mule deer movements outperformed models including Euclidean distance, with high connectivity being associated with high CWD risk. The CWD risk model was a good predictor of CWD occurrence among an independent set of surveillance data collected in subsequent years. Synthesis and applications. We found that landscape connectivity was a major contributor to the spatial pattern of chronic wasting disease (CWD) risk on a heterogeneous landscape. For this reason, future disease surveillance programmes and models of disease spread should consider landscape connectivity. In the aspen parkland ecosystem, we recommend managers focus surveillance and control efforts along river valleys surrounded by agriculture where mule deer abound, because of the high risk of CWD infection.

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 transmissible spongiform encephalopathy affecting North American cervids. We assessed the feasibility of association mapping CWD genetic risk factors in wild white-tailed deer (Odocoileus virginianus) and mule deer (Odocoileus hemionus) using a panel of bovine microsatellite markers from three homologous deer linkage groups predicted to contain candidate genes. These markers had a low cross-species amplification rate (27.9%) and showed weak linkage disequilibrium (

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.

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 is a transmissible spongiform encephalopathy of cervids, similar to sheep scrapie that has only recently been detected in wild populations of white-tailed deer (Odocoileus virginianus) and mule deer (Odocoileus hemionus hemionus) in western Canada. Relatively little is known about local transmission dynamics of the disease or the potential for long-distance spread. We analysed the population genetic structure of over 2000 white-tailed deer sampled from Alberta, British Columbia, and Saskatchewan using microsatellite profiles and mtDNA sequencing to assess the relative risk of disease spread. There was very little differentiation among subpopulations and a weak trend of increasing differentiation with geographic distance. This suggests that the potential for long-distance disease spread through the dispersal of infected individuals is possible, yet the risk of spread should gradually diminish with distance from infection foci. Within subpopulations, females were more related than expected by chance (R > 0) within a radius of approximately 500 m. Sex-biased philopatry and social interactions among related females may facilitate local disease transmission within social groups. Local herd reduction may therefore be an effective tool for reducing the disease prevalence when implemented at the appropriate spatial scale.

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.

Heads of 64 white-tailed deer (Odocoileus virginianus) fawns, harvested in the vicinity of Magrath, Alberta, Canada, (49 degrees 24'782''N, 112 degrees 52'113''W) were examined for the presence of nasal bots and lice. The deer were collected between 8-30 January 2004 as part of a government-approved herd reduction protocol. The entire surface of each head was scanned visually for the presence of lice. Each head was split longitudinally, and the nasal passages, sinuses, and ethmoid region were washed for recovery of nasal bots. First instar Cephenemyia spp. were recovered from 17 heads (27%). Intensity of infestation ranged from 1-18 larvae (mean intensity 4.8). Among fawns, there were no significant differences in prevalence or mean intensity between the sexes. Two species of nasal bots were identified. Smaller larvae, tentatively identified as C. jellisoni, were present in 16 of 17 infested deer while larger specimens, tentatively identified as C. phobifera, were found in four deer; and in three of the four it co-occurred with C. jellisoni. The presence of C. phobifera in Alberta would represent a range extension for this species, which has not been known to occur west of North Dakota. Thirty-one fawns (48%) were infested with the sucking louse Solenopotes ferrisi. One infested fawn also had one specimen of the chewing louse, Tricholiopeurus lipeuroides.

We develop a model of CWD management by nonselective deer harvest, currently the most feasible approach available for managing CWD in wild populations. We use the model to explore the effects of 6 common harvest strategies on disease prevalence and to identify potential optimal harvest policies for reducing disease prevalence without population collapse. The model includes 4 deer categories (juveniles, adult females, younger adult males, older adult males) that may be harvested at different rates, a food-based carrying capacity, which influences juvenile survival but not adult reproduction or survival, and seasonal force of infection terms for each deer category under differing frequency-dependent transmission dynamics resulting from environmental and direct contact mechanisms. Numerical experiments show that the interval of transmission coefficients β where the disease can be controlled is generally narrow and efficiency of a harvest policy to reduce disease prevalence depends crucially on the details of the disease transmission mechanism, in particular on the intensity of disease transmission to juveniles and the potential differences in the behavior of older and younger males that influence contact rates. Optimal harvest policy to minimize disease prevalence for each of the assumed transmission mechanisms is shown to depend on harvest intensity. Across mechanisms, a harvest that focuses on antlered deer, without distinguishing between age classes reduces disease prevalence most consistently, whereas distinguishing between young and older antlered deer produces higher uncertainty in the harvest effects on disease prevalence. Our results show that, despite uncertainties, a modelling approach can determine classes of harvest strategy that are most likely to be effective in combatting CWD.

We consider the problem of estimating the basic reproduction number R 0 from data on prevalence dynamics at the beginning of a disease outbreak. We derive discrete and continuous time models, some coefficients of which are to be fitted from data. We show that prevalence of the disease is sufficient to determine R 0. We apply this method to chronic wasting disease spread in Alberta determining a range of possible R 0 and their sensitivity to the probability of deer annual survival.

Ectoparasites - lice biting Flies blot Flies and warble flies ticks sarcoptes scabiei and sarcoptic mange live flukes taeniasis/echinococcosis gastrointestinal strongyles elaphostrongylin lungworms of cervids lungworms of marine mammals baylisascaris procyonis and related nematodes diseases caused by filaroid nematodes dioctophymatosis hepatic capillariasis trichinella and trichinosis protozoa - enteric protozoan infections giardia and giardiasis cyclospora, eimeria, iospora and cryptosporidium opportunistically pathogenic free-living amoeba hepatozoon infection besnoitia spp toxoplasmosis and related infections.

Six fallow deer (Dama dama) fawns died after receiving 25 to 150 infective larvae of Parelaphostrongylus tenuis. Fawns given higher doses usually died sooner (6 to 23 days) than those given lower doses (54 to 67 days). Early deaths were associated with severe acute peritonitis resulting from perforation of the intestinal wall; later deaths were associated with paralysis and inability to rise. Numerous adult P. tenuis were found within neural tissues of the brain and spinal cord in the three fawns with paralysis. One white-tailed deer (Odocoileus virginianus) exposed to infective larvae from the same source survived infection without exhibiting clinical signs and began passing larvae in feces 88 days post-exposure. At the doses used in this study, meningeal worm caused fatal infections in fallow deer. Results are compared to published observations of fallow deer naturally-infected with P. tenuis.

Pathologic effects and host response were evaluated in seven white-tailed deer ( Odocoileus virginianus) and six mule deer ( O. hemionus hemionus) each exposed per os to 300 or 1000 third-stage larvae of Parelaphostrongylus odocoilei. Pathologic effects in mule deer consisted of hemorrhagic myositis throughout skeletal muscles, severe verminous pneumonia, and moderate lymphadenitis. The major host response was a granulomatous inflammation associated with nematode eggs and larvae. Granulomas obliterated the normal architecture of affected tissues. Pathologic effects and host response were minimal in white-tailed deer. P. odocoilei is considered a potential direct or indirect pathogen in mule deer but an insignificant parasite in white-tailed deer.

Population reduction is being used currently to combat skunk rabies in Alberta. A total of 2,398 striped skunks (Mephitis mephitis) were removed from three counties of southern Alberta during 1980–1983 in an effort to combat rabies outbreaks in those areas. The methods employed included trapping, poisoning, and shooting. Skunks in Forty Mile County have been rabies-free for 4 yr and the outbreaks in Newell and Warner counties appear to be under control. The data suggest that population reduction has been effective in controlling rabies in those areas.