Key to understanding the epidemiology and pathogenesis of prion diseases, including chronic wasting disease (CWD) of cervids, is determining the mode of transmission from one individual to another. We have previously reported that saliva and blood from CWD-infected deer contain sufficient infectious prions to transmit disease upon passage into naïve deer. Here we again use bioassays in deer to show that blood and saliva of pre-symptomatic deer contain infectious prions capable of infecting naïve deer and that naïve deer exposed only to environmental fomites from the suites of CWD-infected deer acquired CWD infection after a period of 15 months post initial exposure. These results help to further explain the basis for the facile transmission of CWD, highlight the complexities associated with CWD transmission among cervids in their natural environment, emphasize the potential utility of blood-based testing to detect pre-clinical CWD infection, and could augur similar transmission dynamics in other prion infections.
Summary1. Social organization and interactions among individuals are suspected to play important roles in the transmission and potential management of wildlife diseases. However, few studies have been conducted to evaluate sociality in wildlife disease transmission. We evaluated the hypothesis of socially facilitated transmission of chronic wasting disease (CWD) among adult female white-tailed deer using spatial location and genetic relatedness for 1387 female deer, and spatial locations of 1321 adult male deer harvested during 2002-2004 CWD control efforts in Wisconsin, USA. 2. Genetically related female deer were significantly clustered at distances of <3AE2 km. However, spatial autocorrelation based on maternally inherited mitochondrial DNA was 50-fold higher than relatedness estimated from microsatellite loci, indicating spatial overlap of females from different social groups with high rates of male-mediated dispersal and gene flow among groups. 3. Probability of CWD infection in adult females was significantly increased by closely related (fullsibling, mother-offspring) infected females that were both spatially proximate (£3AE2 km) and farther distant. To a minor extent, the probability of infection was also influenced by the number of nearby infected females (£3AE2 km), but not by the number of infected males. 4. Direct deer-to-deer transmission of CWD between closely related female deer may be an important route of local CWD transmission. 5. Synthesis and applications. Random mixing and infectious contact may be inadequate models for CWD transmission and disease spread in female deer. Frequency-dependent CWD transmission may be important for females because infectious contacts are limited between members of different female social groups, even if ranges overlap. Given that our data demonstrate a strong relationship between infection probability and female relatedness, CWD management should consider female harvest to maintain smaller female social groups and reduce contact among female deer. However, evaluation of the effects of this strategy on deer social behaviour and contact is needed.
Chronic wasting disease (CWD) is a fatal disease of white‐tailed deer (Odocoileus virginianus) caused by transmissible protease‐resistant prions. Since the discovery of CWD in southern Wisconsin in 2001, more than 20,000 deer have been removed from a >2,500‐km2 disease eradication zone surrounding the three initial cases. Nearly all deer removed were tested for CWD infection and sex, age, and harvest location were recorded. Our analysis used data from a 310‐km2 core study area where disease prevalence was higher than surrounding areas. We found no difference in harvest rates between CWD infected and noninfected deer. Our results show that the probability of infection increased with age and that adult males were more likely to be infected than adult females. Six fawns tested positive for CWD, five fawns from the core study area, including the youngest (5 months) free‐ranging cervid to test positive. The increase in male prevalence with age is nearly twice the increase found in females. We concluded that CWD is not randomly distributed among deer and that differential transmission among sex and age classes is likely driving the observed patterns in disease prevalence. We discuss alternative hypotheses for CWD transmission and spread and, in addition, discuss several possible nonlinear relationships between prevalence and age. Understanding CWD transmission in free‐ranging cervid populations will be essential to the development of strategies to manage this disease in areas where CWD is found, as well as for surveillance strategies in areas where CWD threatens to spread.
Predicting the spread of wildlife disease is critical for identifying populations at risk, targeting surveillance and designing proactive management programmes. We used a landscape genetics approach to identify landscape features that influenced gene flow and the distribution of chronic wasting disease (CWD) in Wisconsin white-tailed deer. CWD prevalence was negatively correlated with genetic differentiation of study area deer from deer in the area of disease origin (core-area). Genetic differentiation was greatest, and CWD prevalence lowest, in areas separated from the core-area by the Wisconsin River, indicating that this river reduced deer gene flow and probably disease spread. Features of the landscape that influence host dispersal and spatial patterns of disease can be identified based on host spatial genetic structure. Landscape genetics may be used to predict high-risk populations based on their genetic connection to infected populations and to target disease surveillance, control and preventative activities.
Underlying dynamic event processes unfolding in continuous time give rise to spatiotemporal patterns that are sometimes observable at only a few discrete times. Such event processes may be modulated simultaneously over several spatial (e.g., latitude and longitude) and temporal (e.g., age, calendar time, and cohort) dimensions. The ecological challenge is to understand the dynamic latent processes that were integrated over several dimensions (space and time) to produce the observed pattern: a so-called inverse problem. An example of such a problem is characterizing epidemiological rate processes from spatially referenced age-specific prevalence data for a wildlife disease such as chronic wasting disease (CWD). With age-specific prevalence data, the exact infection times are not observed, which complicates the direct estimation of rates. However, the relationship between the observed data and the unobserved rate variables can be described with likelihood equations. Typically, for problems with multiple timescales, the likelihoods are integral equations without closed forms. The complexity of the likelihoods often makes traditional maximum-likelihood approaches untenable. Here, using seven years of hunter-harvest prevalence data from the CWD epidemic in white-tailed deer (Odocoileus virginianus) in Wisconsin, USA, we develop and explore a Bayesian approach that allows for a detailed examination of factors modulating the infection rates over space, age, and time, and their interactions. Our approach relies on the Bayesian ability to borrow strength from neighbors in both space and time. Synthesizing a number of areas of event time analysis (current-status data, age/period/cohort models, Bayesian spatial shared frailty models), our general framework has very broad ecological applicability beyond disease prevalence data to a number of important ecological event time analyses, including general survival studies with multiple time dimensions for which existing methodology is limited. We observed strong associations of infection rates with age, gender, and location. The infection rate appears to be increasing with time. We could not detect growth hotspots, or location by time interactions, which suggests that spatial variation in infection rates is determined primarily by when the disease arrives locally, rather than how fast it grows. We emphasize assumptions and the potential consequences of their violations.
ABSTRACT:Chronic wasting disease (CWD) is a fatal, emerging disease of cervids associated with transmissible protease-resistant prion proteins. The potential for CWD to cause dramatic declines in deer and elk populations and perceived human health risks associated with consuming CWDcontaminated venison have led wildlife agencies to embark on extensive CWD control programs, typically involving culling to reduce deer populations. We characterized the spatial distribution of CWD in white-tailed deer (Odocoileus virginianus) in Wisconsin to facilitate CWD management. We found that CWD prevalence declined with distance from a central location, was locally correlated at a scale of 3.6 km, and was correlated with deer habitat abundance. The latter result is consistent with patterns expected for a positive relationship between density and prevalence of CWD. We recommend management activities focused on culling in geographic areas with high prevalence to have the greatest probability of removing infected individuals. Further research is needed to elucidate the factors involved in CWD spread and infection rates, especially the role of density-dependent transmission.
Starting in the 1970s, many populations of large-bodied mammalian carnivores began to recover from centuries of human-caused eradication and habitat destruction. The recovery of several such populations has since slowed or reversed due to mortality caused by humans. Illegal killing (poaching) is a primary cause of death in many carnivore populations. Law enforcement agencies face difficulties in preventing poaching and scientists face challenges in measuring it. Both challenges are exacerbated when evidence is concealed or ignored. We present data on deaths of 937 Wisconsin gray wolves (Canis lupus) from October 1979 to April 2012 during a period in which wolves were recolonizing historic range mainly under federal government protection. We found and partially remedied sampling and measurement biases in the source data by reexamining necropsy reports and reconstructing the numbers and causes of some wolf deaths that were never reported. From 431 deaths and disappearances of radiocollared wolves aged > 7.5 months, we estimated human causes accounted for two-thirds of reported and reconstructed deaths, including poaching in 39–45%, vehicle collisions in 13%, legal killing by state agents in 6%, and nonhuman causes in 36–42%. Our estimate of poaching remained an underestimate because of persistent sources of uncertainty and systematic underreporting. Unreported deaths accounted for over two-thirds of all mortality annually among wolves > 7.5 months old. One-half of all poached wolves went unreported, or > 80% of poached wolves not being monitored by radiotelemetry went unreported. The annual mortality rate averaged 18% ± 10% for monitored wolves but 47% ± 19% for unmonitored wolves. That difference appeared to be due largely to radiocollaring being concentrated in the core areas of wolf range, as well as higher rates of human-caused mortality in the periphery of wolf range. We detected an average 4% decline in wolf population growth in the last 5 years of the study. Because our estimates of poaching risk and overall mortality rate exceeded official estimates after 2012, we present all data for transparency and replication. More recent additions of public hunting quotas after 2012 appear unsustainable without effective curtailment of poaching. Effective antipoaching enforcement will require more accurate estimates of poaching rate, location, and timing than currently available. Independent scientific review of methods and data will improve antipoaching policies for large carnivore conservation, especially for controversial species facing high levels of human-induced mortality.
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