Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) that affects members of the cervidae family. The infectious agent is a misfolded isoform (PrP^SC) of the host prion protein (PrP^C). The replication of PrP^SC initiates a cascade of developmental changes that spread from cell to cell, individual to individual, and that for some TSEs, has crossed the species barrier. CWD can be transmitted horizontally and vertically, and it is the only TSE that affects free-ranging wildlife. While other TSEs are under control and even declining, infection rates of CWD continue to grow and the disease distribution continues to expand in North America and around the world. Since the first reported case in 1967, CWD has spread infecting captive and free-ranging cervids in 26 states in the US, 3 Canadian provinces, 3 European countries and has been found in captive cervids in South Korea. CWD causes considerable ecologic, economic and sociologic impact, as this is a 100% fatal highly contagious infectious disease, with no treatment or cure available. Because some TSEs have crossed the species barrier, the zoonotic potential of CWD is a concern for human health and continues to be investigated. Here we review the characteristics of the CWD prion protein, mechanisms of transmission and the role of genetics. We discuss the characteristics that contribute to prevalence and distribution. We also discuss the impact of CWD and review the management strategies that have been used to prevent and control the spread of CWD.

Bluetongue (BT) and epizootic hemorrhagic disease (EHD) cases have increased worldwide, causing significant economic loss to ruminant livestock production and detrimental effects to susceptible wildlife populations. In recent decades, hemorrhagic disease cases have been reported over expanding geographic areas in the United States. Effective BT and EHD prevention and control strategies for livestock and monitoring of these diseases in wildlife populations depend on an accurate understanding of the distribution of BT and EHD viruses in domestic and wild ruminants and their vectors, the Culicoides biting midges that transmit them. However, national maps showing the distribution of BT and EHD viruses and the presence of Culicoides vectors are incomplete or not available at all. Thus, efforts to accurately describe the potential risk of these viruses on ruminant populations are obstructed by the lack of systematic and routine surveillance of their hosts and vectors. In this review, we: (1) outline animal health impacts of BT and EHD in the USA; (2) describe current knowledge of the distribution and abundance of BT and EHD and their vectors in the USA; and (3) highlight the importance of disease (BT and EHD) and vector surveillance for ruminant populations.

The North American river otter (Lontra canadensis) is a biomonitor for organohalogenated compounds (OHCs) associated with a wide range of deleterious health effects in wildlife and humans. We determined concentrations of twenty OHCs in livers of 23 river otters salvaged by the Illinois Department of Natural Resources from 2009 to 2011, determined sex-dependent distribution of OHCs, and compared our results to the reported concentrations of four OHCs in Illinois river otters from 1984 to 1989. Since these contaminants have been banned for over 30 years, we predicted smaller mean concentrations than those previously reported in Illinois otters. We detected eleven of twenty OHCs; PCBs (polychlorinated biphenyls), dieldrin, and 4,4'-DDE (dichlorodiphenyldichloroethylene) were present in the greatest mean concentrations. We report the largest mean concentration of dieldrin to date in the liver of North American river otters (mean: 174, range: 14.4-534 parts per billion wet wt [ppb]). Mean PCB concentrations were significantly higher in males (mean: 851; range: 30-3450 ppb) than females (mean: 282; range: 40-850 ppb; p=0.04). Mean concentrations of dieldrin were greater than those detected in otters from 1984 to 1989 (mean: 90; range: 30-130 ppb; p<0.05). Our results suggest OHC exposure remains a concern. Future research in Illinois should focus on evaluating OHCs exposures, particularly dieldrin, at the watershed level.

We investigated the effect of varying storage time and storage temperature on fungal species’ isolation as part of a case study of Illinois cave sediment samples. A deeper understanding of cave fungal communities may influence eco-epidemiology studies of emerging or re-emerging cave fungal pathogens. Using culture-dependent techniques, we isolated geophilic fungi from homogeneous cave sediment samples from three Illinois caves. Each sample was stored under five different temperatures ranging from −80 °C to 22 °C. Cave sediment was periodically removed at five different time periods from 48 h to 1 year, serially diluted with distilled water, lawn plated onto two different media, and monitored for fungal colonies. We isolated colonies and confirmed identity through nrDNA sequence similarity. Our results suggest that storage time was more important than storage temperature for the isolation of a wide diversity of geophilic fungal taxa. Importantly, our results show that varying storage conditions will alter both the kind of taxa and abundance of those taxa, suggesting that comparative studies of fungal diversity across studies should employ similar storage conditions. Lastly, future investigations should utilize multiple genetic markers because the fungal barcode region lacked species-level resolution for many isolates within common Illinois geophilic fungal genera.

Epizootic hemorrhagic disease (EHD) leads to high mortality in white-tailed deer (Odocoileus virginianus) and is caused by a double-stranded RNA (dsRNA) virus. Toll-like receptor 3 (TLR3) plays a role in host immune detection and response to dsRNA viruses. We, therefore, examined the role of genetic variation within the TLR3 gene in EHD among 84 Illinois wild white-tailed deer (26 EHD-positive deer and 58 EHD-negative controls). The entire coding region of the TLR3 gene was sequenced: 2715 base pairs encoding 904 amino acids. We identified 85 haplotypes with 77 single nucleotide polymorphisms (SNPs), of which 45 were synonymous mutations and 32 were non-synonymous. Two non-synonymous SNPs differed significantly in frequency between EHD-positive and EHD-negative deer. In the EHD-positive deer, phenylalanine was relatively less likely to be encoded at codon positions 59 and 116, whereas leucine and serine (respectively) were detected less frequently in EHD-negative deer. Both amino acid substitutions were predicted to impact protein structure or function. Understanding associations between TLR3 polymorphisms and EHD provides insights into the role of host genetics in outbreaks of EHD in deer, which may allow wildlife agencies to better understand the severity of outbreaks.

Chronic wasting disease (CWD) is a fatal neurodegenerative prion disease of cervids that can be transmitted through direct physical contact, indirect contact with a contaminated environment, or vertical transmission. CWD is characterized by a long incubation period followed by symptoms like loss of appetite resulting from the destruction of brain tissue. While the consequences for infected animals are clear, a previous study from our laboratory showing lower body weights in the foetuses of CWD-positive female deer suggests those consequences may be intergenerational. In this study, we addressed the impact of maternal CWD infection on foetal head development (as a proxy for brain growth) in wild white-tailed deer using data from CWD management efforts in northern Illinois, U.S.A. Multivariate, multilevel, Bayesian Gamma regression found that maternal CWD infection reduced foetal head nose-occipital length and crown-jaw circumference by 6.76% and frontal-occipital length by 11.31%. These findings suggest impeded brain development in the offspring of CWD-infected female deer, which could reduce fawns' survival and success after birth and lead to a decline in population fitness over time. This study is the first to demonstrate the detrimental effects of a prion disease on foetal brain development in any animal species regardless of whether vertical transmission has occurred.