The Effect of Maternal Antibodies on Clinical Response to Infection with Epizootic Hemorrhagic Disease Virus in White-Tailed Deer (Odocoileus virginianus) Fawns.

We investigated whether naturally acquired maternal antibodies to epizootic hemorrhagic disease virus serotype 2 (EHDV-2) would protect white-tailed deer (Odocoileus virginianus) fawns against infection and clinical disease following an EHDV-2 challenge. We compared viremia and clinical response in 27-47-d-old, experimentally infected fawns with and without maternally derived antibodies to EHDV-2. Mild to moderate clinical signs were observed in four seronegative (maternal antibody-negative) fawns, which were viremic from 3 to 14 d postinoculation. Individual peak blood virus titers for seronegative fawns ranged from 104.3 to 106.3 median tissue culture infective doses (TCID50)/mL. In contrast, clinical signs were not observed in seropositive (maternal antibody-positive) fawns and a transient low-level viremia (≤102.4 TCID50/mL) occurred in two of six fawns. Our results indicated that the presence of maternally derived EHDV-2 antibodies in fawns prevents or greatly reduces clinical disease and the level and duration of EHDV-2 viremia.

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.

Prevalence of Influenza A Viruses in Ducks Sampled in Northwestern Minnesota and Evidence for Predominance of H3N8 and H4N6 Subtypes in Mallards, 2007-2016.

Long-term comprehensive studies of avian influenza virus subtypes in ducks not only contribute to understanding variations and patterns of subtype diversity, but also can be important in defining seasonal and temporal risks associated with transmission of potentially highly pathogenic H5 and H7 subtypes to domestic poultry. We analyzed influenza A virus (IAV) surveillance data from dabbling ducks collected at an important migratory stopover site in northwestern Minnesota from 2007-2016 and identified prevalence and subtype diversity throughout this period. In total, 13,228 cloacal and oropharyngeal swabs from waterfowl were tested over the 10-year period; the majority of these waterfowl were mallards sampled from late August through late September (n = 9133). From these, 1768 IAVs were isolated (19.4% mean annual prevalence, ranging from 11.0% in 2007 to 32.8% in 2011), and both hemagglutinin (HA) and neuraminidase were identified for 1588. Although subtype diversity and prevalence varied by year, H3 and H4 HA subtypes predominated in all years, accounting for 65.7% of the observed HA subtype diversity. The mechanisms driving this consistent pattern of subtype diversity and predominance are not understood but may include factors at the host, population, and virus level.

Prevalencia de virus de influenza A en patos muestreados en el noroeste de Minnesota y evidencia de predominio de los subtipos H3N8 y H4N6 en patos de collar entre los años 2007 al 2016. Los estudios exhaustivos a largo plazo de subtipos de virus de la influenza aviar en patos no solo contribuyen a comprender las variaciones y patrones de diversidad de subtipos, sino que también pueden ser importantes para definir los riesgos estacionales y temporales asociados con la transmisión de subtipos H5 y H7 potencialmente altamente patógenos para la avicultura comercial. Analizamos los datos de vigilancia del virus de la influenza A de patos chapoteadores recolectados en un sitio de descanso migratorio importante en el noroeste de Minnesota desde el año 2007 al 2016 y se identificó la prevalencia y la diversidad de subtipos a lo largo de este período. En total, 13,228 hisopos cloacales y orofaríngeos de aves acuáticas se analizaron durante el período de diez años; la mayoría de estas aves acuáticas eran patos silvestres muestreados desde finales de agosto hasta finales de septiembre (n = 9133). De estas muestras, 1768 virus de la influenza aviar fueron aislados (prevalencia anual media de 19.4%, y con un rango de 11.0% en el 2007 a 32.8% en 2011), y tanto la hemaglutinina (HA) como la neuraminidasa fueron identificadas para 1588 virus. Aunque la diversidad de subtipos y la prevalencia variaron por año, los subtipos de hemaglutinina H3 y H4 predominaron en todos los años, representando el 65.7% de la diversidad de subtipos observada para la hemaglutinina. Los mecanismos que impulsan este patrón consistente de diversidad de subtipos y predominio no se comprenden, pero pueden incluir factores a nivel del hospedador, de la población y del virus. Abbreviations: CL = cloacal; HA = hemagglutinin; IAV = influenza A virus; NA = neuraminidase; NWR = National Wildlife Refuge; RRT-PCR = real-time reverse transcriptase PCR; WMA = Wildlife Management Area.

EXPERIMENTAL INFECTION OF WHITE-TAILED DEER (ODOCOILEUS VIRGINIANUS) WITH BLUETONGUE VIRUS SEROTYPE 3.

Bluetongue virus serotype 3 (BTV-3) has been found in the US since 1999 and was recently identified in white-tailed deer (WTD; Odocoileus virginianus) found dead in Virginia, US and West Virginia, US in 2016. Bluetongue viruses are known to cause pathologic changes in WTD; however, the relative virulence and pathogenicity of BTV-3 in WTD is unknown. In our study, eight WTD fawns, 6-12 wk old, were needle inoculated subcutaneously with a field isolate of BTV-3, with one fawn shaminoculated as a control during July 2017; all were monitored to determine the pathogenicity of BTV-3 in WTD. All inoculated fawns developed viremias that were first detected on postinoculation day (PID), 3 with peak titers on PID 5 by both quantitative reverse-transcription PCR (qRT-PCR) and virus isolation. The sham-inoculated control fawn also became viremic on PID 12, presumably through contact with infected fawns. Mild clinical signs, including periorbital edema and hyperemia, were first seen on PID 5. None of the fawns developed a significant febrile response, clinical pathology changes, or BTV-3 neutralizing antibodies. The cytokines TNF-α, IL-1ß, and IFN-α were not detected by commercial enzyme-linked immunosorbent assays developed for bovids. The absence of severe clinical disease, fibrinogenemia, thrombocytopenia, and leukopenia, along with the lack of seroconversion and a detectable cytokine response during the study period, is atypical when compared to previous experimental BTV serotype infections in WTD but may be related to the young age of these deer, possible attenuation of the BTV-3 strain used, innate resistance or, in some cases to maternally derived antibody to other BTV serotypes.