Demographic Risk Factors Vary in the Invasion Front of Chronic Wasting Disease in West Virginia, USA.

After detecting chronic wasting disease (CWD) in white-tailed deer (Odocoileus virginianus) in Hampshire County, West Virginia, USA, in 2005, we investigated the change of CWD apparent prevalence and potential factors influencing infection risk during the invasion front. Over eight sampling years (2006-2012 and 2017) during a 12-yr period within a 101-km2-area monitoring zone, we sampled and tested a total of 853 deer for CWD by ELISA and immunohistochemistry. Bayesian logistic regression of risk factors included collection year, age class, sex, and adjusted body weight (weight after accounting for sex, age, kidney fat index, and number of fetuses). In the whole-herd model (n=634), collection year, age, and adjusted body weight were associated with increased odds of CWD, whereas an age-weight interaction had a negative relationship. We found that males drove the positive associations with age and adjusted body weight, whereas females were responsible for the negative interaction effect. These findings suggest potential behavioral and physiological mechanisms related to sex that may influence CWD exposure. Older males exhibited higher CWD prevalence, aligning with previous studies. Notably, the novel finding of adjusted body weight as a risk factor in males warrants further investigation, and this study highlights the need for future research on social behavior and its role in CWD transmission within white-tailed deer populations.

Detection of Chronic Wasting Disease Prions in Fetal Tissues of Free-Ranging White-Tailed Deer.

The transmission of chronic wasting disease (CWD) has largely been attributed to contact with infectious prions shed in excretions (saliva, urine, feces, blood) by direct animal-to-animal exposure or indirect contact with the environment. Less-well studied has been the role that mother-to-offspring transmission may play in the facile transmission of CWD, and whether mother-to-offspring transmission before birth may contribute to the extensive spread of CWD. We thereby focused on a population of free-ranging white-tailed deer from West Virginia, USA, in which CWD has been detected. Fetal tissues, ranging from 113 to 158 days of gestation, were harvested from the uteri of CWD+ dams in the asymptomatic phase of infection. Using serial protein misfolding amplification (sPMCA), we detected evidence of prion seeds in 7 of 14 fetuses (50%) from 7 of 9 pregnancies (78%), with the earliest detection at 113 gestational days. This is the first report of CWD detection in free ranging white-tailed deer fetal tissues. Further investigation within cervid populations across North America will help define the role and impact of mother-to-offspring vertical transmission of CWD.

LIMITED DETECTION OF ANTIBODIES TO CLADE 2.3.4.4 A/GOOSE/GUANGDONG/1/1996 LINEAGE HIGHLY PATHOGENIC H5 AVIAN INFLUENZA VIRUS IN NORTH AMERICAN WATERFOWL.

During 2014, highly pathogenic (HP) influenza A viruses (IAVs) of the A/Goose/Guangdong/1/1996 lineage (GsGD-HP-H5), originating from Asia, were detected in domestic poultry and wild birds in Canada and the US. These clade 2.3.4.4 GsGD-HP-H5 viruses included reassortants possessing North American lineage gene segments; were detected in wild birds in the Pacific, Central, and Mississippi flyways; and caused the largest HP IAV outbreak in poultry in US history. To determine if an antibody response indicative of previous infection with clade 2.3.4.4 GsGD-HP-H5 IAV could be detected in North American wild waterfowl sampled before, during, and after the 2014-15 outbreak, sera from 2,793 geese and 3,715 ducks were tested by blocking enzyme-linked immunosorbent assay and hemagglutination inhibition (HI) tests using both clade 2.3.4.4 GsGD-HPH5 and North American lineage low pathogenic (LP) H5 IAV antigens. We detected an antibody response meeting a comparative titer-based criteria (HI titer observed with 2.3.4.4 GsGD-HP-H5 antigens exceeded the titer observed for LP H5 antigen by two or more dilutions) for previous infection with clade 2.3.4.4 GsGD-HP-H5 IAV in only five birds, one Blue-winged Teal (Spatula discors) sampled during the outbreak and three Mallards (Anas platyrhynchos) and one Canada Goose (Branta canadensis) sampled during the post-outbreak period. These serologic results are consistent with the spatiotemporal extent of the outbreak in wild birds in North America during 2014 and 2015 and limited exposure of waterfowl to GsGD-HP-H5 IAV, particularly in the central and eastern US.

Avian oncogenesis induced by lymphoproliferative disease virus: a neglected or emerging retroviral pathogen?

Lymphoproliferative disease virus (LPDV) is an exogenous oncogenic retrovirus that induces lymphoid tumors in some galliform species of birds. Historically, outbreaks of LPDV have been reported from Europe and Israel. Although the virus has previously never been detected in North America, herein we describe the widespread distribution, genetic diversity, pathogenesis, and evolution of LPDV in the United States. Characterization of the provirus genome of the index LPDV case from North America demonstrated an 88% nucleotide identity to the Israeli prototype strain. Although phylogenetic analysis indicated that the majority of viruses fell into a single North American lineage, a small subset of viruses from South Carolina were most closely related to the Israeli prototype. These results suggest that LPDV was transferred between continents to initiate outbreaks of disease. However, the direction (New World to Old World or vice versa), mechanism, and time frame of the transcontinental spread currently remain unknown.

Epizootiology of an epizootic hemorrhagic disease outbreak in West Virginia.

An outbreak of epizootic hemorrhagic disease virus, serotype 2 (EHDV-2) was responsible for localized white-tailed deer (Odocoileus virginianus) mortality in Hardy and Hampshire counties, West Virginia (USA), in the summer and fall of 1993. Using available historical data on regional herd immunity, data opportunistically collected during the epizootic, and postepizootic sampling of hunter-harvested deer, we grossly estimate certain epidemiologic parameters and compare findings to a hypothesis about hemorrhagic disease outbreaks in the Appalachian Mountains. During the epizootic, 57.9 km(2) were actively searched and 228 dead deer were found. Epizootic hemorrhagic disease virus, serotype 2 was isolated from seven of nine deer sampled in Hardy and Hampshire counties. Preepizootic exposure of deer to EHD viruses was unknown, but available data suggest that it was negligible. The geographic distribution of the outbreak was defined by plotting the locations of dead deer found during the outbreak, as well as the locations of deer harvested by hunters after the outbreak that had antibodies to EHDV-2 on a map sectioned into 16.65 km(2) rectangular sections. Sections that included one or more dead deer or hunter-harvested deer with antibodies to EHDV-2 were included in the defined outbreak area. Postoutbreak sampling revealed monospecific EHDV-2 antibodies in 12% of deer harvested by hunters within the defined outbreak area. Based on the available data and accepting certain assumptions, gross calculations suggest that this outbreak appears to have been isolated and probably killed a high percentage of the deer that were infected. This is consistent with the hypothesis that sporadic hemorrhagic disease outbreaks in the Appalachian Mountains are usually localized and severe.