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Julia A. Langenberg

Publications and source records attributed to Julia A. Langenberg.

4 recordsLinked to original sources

Applying a Bayesian weighted surveillance approach to detect chronic wasting disease in white‐tailed deer

Surveillance is critical for early detection of emerging and re‐emerging infectious diseases. Weighted surveillance leverages heterogeneity in infection risk to increase sampling efficiency. Here, we apply a Bayesian approach to estimate weights for 16 surveillance classes of white‐tailed deer in Wisconsin, USA, relative to hunter‐harvested yearling males. We used these weights to conduct a surveillance programme for detecting chronic wasting disease (CWD) in white‐tailed deer at Shenandoah National Park (SHEN) in Virginia, USA. Generally, for surveillance, risk of infection increased with age and was greater in males. Clinical suspect deer had the highest risk, with weight estimates of 33.33 and 9.09 for community‐reported and hunter‐reported suspect deer, respectively. Fawns had the lowest risk with an estimated weight of 0.001. We used surveillance weights for Wisconsin deer to determine sampling effort required to detect a CWD‐positive case in SHEN if prevalence in yearling males ≥0.025. The sampling required to detect CWD was 37–91 adult deer, depending on the adult male:female ratio in the surveillance stream. We collected rectal biopsies from 49 female and 21 male adult deer, and 10 additional samples from vehicle‐killed deer. CWD was not detected and we concluded with 95% probability that prevalence in the reference population (yearling males) was between 0.0% and 3.6%. Synthesis and applications . Our approach allows managers to estimate relative surveillance weights for different host classes and quantify limits of disease detection in real time when only a sample of animals from a population can be tested, resulting in considerable cost savings for agencies performing wildlife disease detection surveillance. Additionally, it provides a rigorous means of estimating prevalence limits when a disease/pathogen is not detected in a sample set. It is therefore applicable to other wildlife, domestic animal and human disease systems, which can be characterized by surveillance classes with heterogeneous probability of infection. This methodology is also extendable to other disciplines such as invasive species, environmental toxicology, and generally, any ecological question seeking to efficiently use scarce financial and human resources to maximize the detection probability of a rare event.

Journal of Applied Ecology

Mortality patterns and detection bias from carcass data: An example from wolf recovery in Wisconsin

We developed models and provide computer code to make carcass recovery data more useful to wildlife managers. With these tools, wildlife managers can understand the spatial, temporal (e.g., across time periods, seasons), and demographic patterns in mortality causes from carcass recovery datasets. From datasets of radio-collared and non-collared carcasses, managers can calculate the detection bias by mortality cause in a non-collared carcass dataset compared to a collared carcass dataset. As a first step, we provide a standard procedure to assign mortality causes to carcasses. We provide an example of these methods for radio-collared wolves ( n  = 208) and non-collared wolves ( n  = 668) found dead in Wisconsin (1979–2012). We analyzed differences in mortality cause relative to season, age and sex classes, wolf harvest zones, and recovery phase (1979–1995: initial recovery, 1996–2002: early growth, 2003–2012: late growth). Seasonally, illegal kills and natural deaths were proportionally higher in winter (Oct–Mar) than summer (Apr–Sep) for collared wolves, whereas vehicle strikes and legal kills were higher in summer than winter. Spatially, more illegally killed collared wolves occurred in eastern wolf harvest zones where wolves reestablished more slowly and in the central forest region where optimal habitat is isolated by agriculture. Natural mortalities of collared wolves (e.g., disease, intraspecific strife, or starvation) were highest in western wolf harvest zones where wolves established earlier and existed at higher densities. Calculating detection bias in the non-collared dataset revealed that more than half of the non-collared carcasses on the landscape are not found. The lowest detection probabilities for non-collared carcasses (0.113–0.176) occurred in winter for natural, illegal, and unknown mortality causes.

Wisconsin

Rejoinder: Sifting through model space

Observational data sets generated by complex processes are common in ecology. Traditionally these have been very challenging to analyze because of the limitations of available statistical tools. This seems to be changing, and these are exciting times to be involved with ecological statistics, not just because of the neo-Bayesian revival but also because of the proliferation of computationally intensive methods in general. It is now possible to fit much richer models to observational data than in the relatively recent past, which in turn has stimulated much interest in how to evaluate and compare such models. In such an immature, vibrant, and rapidly growing field, not everyone is going to agree on the best way to do things. This is reflected in the contrast of opinions offered by the discussants. Each offers a thoughtful and thought-provoking critique of our work that reflects the current thinking in a non-negligible segment of the ecological data analysis community. We want to thank them for their insights.

Ecology

Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: complement component C1q and Prnp polymorphisms

The genetic basis of susceptibility to chronic wasting disease (CWD) in free-ranging cervids is of great interest. Association studies of disease susceptibility in free-ranging populations, however, face considerable challenges including: the need for large sample sizes when disease is rare, animals of unknown pedigree create a risk of spurious results due to population admixture, and the inability to control disease exposure or dose. We used an innovative matched case&ndash;control design and conditional logistic regression to evaluate associations between polymorphisms of complement C1q and prion protein (Prnp) genes and CWD infection in white-tailed deer from the CWD endemic area in south-central Wisconsin. To reduce problems due to admixture or disease-risk confounding, we used neutral genetic (microsatellite) data to identify closely related CWD-positive ( n = 68) and CWD-negative ( n = 91) female deer to serve as matched cases and controls. Cases and controls were also matched on factors (sex, location, age) previously demonstrated to affect CWD infection risk. For Prnp, deer with at least one Serine (S) at amino acid 96 were significantly less likely to be CWD-positive relative to deer homozygous for Glycine (G). This is the first characterization of genes associated with the complement system in white-tailed deer. No tests for association between any C1q polymorphism and CWD infection were significant at p < 0.05. After controlling for Prnp, we found weak support for an elevated risk of CWD infection in deer with at least one Glycine (G) at amino acid 56 of the C1qC gene. While we documented numerous amino acid polymorphisms in C1q genes none appear to be strongly associated with CWD susceptibility.

Wisconsin