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The Central Valley of California (CVC) and Mid‐Atlantic (MA) in the U.S. are both critical sites for nationwide food security, and many waterfowl species annually, especially during the winter, providing feeding and roosting locations for a variety of species. Mapping waterfowl distributions, using NEXRAD, may aid in the adaptive management of important waterfowl habitat and allow various government agencies to better understand the interface between wild and domestic birds and commercial agricultural practices. We used 9 years (2014–2023) of data from the US NEXRAD network to model winter waterfowl relative abundance in the CVC and MA as a function of weather, temporal period, environmental conditions, and landcover characteristics using boosted regression tree modelling. We were able to quantify the variability in effect size of 28 different covariates across space and time within two geographic regions which are critical to nationwide waterfowl management and host a high density of nationally important commercial agriculture. In general, weather, geographic (distance to features), and landcover condition (wetness index) predictors had the strongest relative effect on predicting wintering waterfowl relative abundance in both regions, while effects of land cover composition were more regionally and temporally specific. Increased daily mean temperature was a major predictor of increasing relative waterfowl abundance in both regions throughout the winter. Increasing precipitation had differing effects within regions, increasing relative waterfowl abundance in the MA, while decreasing in general within the CVC. Increasing relative waterfowl abundance in the CVC are strongly tied to the flooding of the landscape and rice availability, whereas waterfowl in the MA, where water is less limiting, are generally governed by waste grain availability and emergent wetland on the landscape. Waterfowl relative abundance in the MA was generally higher nearer to the Atlantic coast and lakes, while in the CVC they were higher nearer to lakes. Our findings promote a better understanding of spatial associations of waterfowl to landscape features and may aid in conservation and biosecurity management protocols.

The efficacy of commercially available recombinant herpesvirus of turkeys-infectious bursal disease (rHVT-IBD) virus vaccines was studied in broiler chickens derived from an IBDV-vaccinated breeder flock at 30 wk of age (Trial 1) and 60 wk of age (Trial 2). In parallel, specific-pathogen-free (SPF) white leghorn chickens were used to evaluate vaccine efficacy to control for the effects of maternally derived antibodies (MDA) associated with the broiler chickens. Broilers and SPF leghorns were vaccinated subcutaneously in the neck at 1 day of age with Vaxxitek® HVT+IBD or Vectormune® HVT-IBD vaccines and were placed in isolators. On 10, 14, 18, 22, and 26 days postvaccination (DPV), vaccinated and nonvaccinated broilers and SPF leghorns were bled prior to challenge via the oral-nasal route with infectious bursal disease (IBD) reference strains ST-C, Delaware variant E (Del E), or contemporary field isolates DMV/5038/07 or FF6. Microscopic lesion assessment of the bursa was useful for assessing IBDV challenge in both rHVT-IBD-vaccinated broiler and SPF leghorn chickens. In general, rHVT-IBD vaccines induced greater protection as the time between vaccination and challenge increased. Based on incidence of microscopic lesions (IML) of bursa tissue, Vaxxitek HVT+IBD vaccination of SPF leghorns induced protection by 18 DPV and continued to protect 22 DPV and 26 DPV in Trials 1 and 2. Vectormune HVT-IBD vaccine induced protection of SPF leghorns by 18 or 22 DPV in Trial 1, depending upon the IBDV challenge strain. However, the onset of protection was delayed until 22 or 26 DPV in Trial 2. With either commercial vaccine, rHVT-IBD vaccination of broiler chickens was not as effective as was observed in SPF leghorns, based on IML of bursa tissue. However, Vaxxitek HVT+IBD vaccination protected broilers following challenge with ST-C in both Trial 1 (30-wk-old breeder progeny) and Trial 2 (60-wk-old breeder progeny). Partial protection against FF6 (Trial 1) and DMV/5038/07 (Trial 2) challenges was observed. Vectormune HVT-IBD vaccination protected broilers vs. FF6 challenge in Trial 1. In Trial 2, the vaccine did not offer protection on the basis of IML of bursa tissue. The results indicate that 1) bursa/body weight ratios were not consistently useful as a tool for assessing IBDV challenge in broiler chickens with anti-IBDV MDA compared to assessment by IML of bursa tissue, though were useful for assessing protection in SPF leghorns; and 2) both vaccines may offer some protection to older broilers; however, a window of susceptibility exists between the waning of MDA and the development of vaccine-induced antibodies. The SPF studies showed that some vaccinated chickens were not protected from an IBDV challenge earlier than 14 DPV while broiler studies showed that MDA was not fully protective beyond 10 DPV. Because these vaccines did not protect chickens from an IBDV challenge during this window of susceptibility, our data show that breeder vaccination programs for IBDV must aim to maximize anti-IBDV MDA in progeny to protect against early IBDV challenge.

Background Avian influenza (AI) viruses infect numerous avian species, and low pathogenicity (LP) AI viruses of the H7 subtype are typically reported to produce mild or subclinical infections in both wild aquatic birds and domestic poultry. However relatively little work has been done to compare LPAI viruses from different avian species for their ability to cause disease in domestic poultry under the same conditions. In this study twelve H7 LPAI virus isolates from North America were each evaluated for their comparative pathogenesis in chickens, ducks, and turkeys. Results All 12 isolates were able to infect all three species at a dose of 10 6 50% egg infectious doses based on seroconversion, although not all animals seroconverted with each isolate-species combination. The severity of disease varied among isolate and species combinations, but there was a consistent trend for clinical disease to be most severe in turkeys where all 12 isolates induced disease, and mortality was observed in turkeys exposed to 9 of the 12 viruses. Turkeys also shed virus by the oral and cloacal routes at significantly higher titers than either ducks or chickens at numerous time points. Only 3 isolates induced observable clinical disease in ducks and only 6 isolates induced disease in chickens, which was generally very mild and did not result in mortality. Full genome sequence was completed for all 12 isolates and some isolates did have features consistent with adaptation to poultry (e.g. NA stalk deletions), however none of these features correlated with disease severity. Conclusions The data suggests that turkeys may be more susceptible to clinical disease from the H7 LPAI viruses included in this study than either chickens or ducks. However the severity of disease and degree of virus shed was not clearly correlated with any isolate or group of isolates, but relied on specific species and isolate combinations.

Background Wild waterfowl, including ducks, represent the classic reservoir for low pathogenicity avian influenza (LPAI) viruses and play a major role in the worldwide dissemination of AIV. AIVs belonging to the hemagglutinin (H) 7 subtype are of epidemiological and economic importance due to their potential to mutate into a highly pathogenic form of the virus. Thus far, however, relatively little work has been conducted on elucidating the host-pathogen interactions of ducks and H7 LPAIVs. In the current study, three H7 LPAIVs isolated from either chicken, duck, or turkey avian species were evaluated for their comparative effect on the transcriptional innate immune response of ducks. Results Three H7 LPAIV isolates, chicken-origin (A/chicken/Maryland/MinhMa/2004), duck-origin (A/pintail/Minnesota/423/1999), and turkey-origin (A/turkey/Virginia/SEP-67/2002) were used to infect Pekin ducks. At 3 days post-infection, RNA from spleen tissue was used for transcriptional analysis using the Avian Innate Immune Microarray (AIIM) and quantitative real-time RT-PCR (qRT-PCR). Microarray analysis revealed that a core set of 61 genes was differentially regulated in response to all three LPAIVs. Furthermore, we observed 101, 135, and 628 differentially expressed genes unique to infection with the chicken-, duck-, or turkey-origin LPAIV isolates, respectively. qRT-PCR results revealed significant (p<0.05) induction of IL-1β, IL-2, and IFNγ transcription, with the greatest induction observed upon infection with the chicken-origin isolate. Several key innate immune pathways were activated in response to LPAIV infection including the toll-like receptor and RIG-I-like receptor pathways. Conclusions Pekin ducks elicit a unique innate immune response to different species-of-origin H7 LPAIV isolates. However, twelve identifiable genes and their associated cell signaling pathways (RIG-I, NOD, TLR) are differentially expressed regardless of isolate origin. This core set of genes are critical to the duck immune response to AI. These data provide insight into the potential mechanisms employed by ducks to tolerate AI viral infection.

Understanding timing and distribution of virus spread is critical to global commercial and wildlife biosecurity management. A highly pathogenic avian influenza virus (HPAIv) global panzootic, affecting ~600 bird and mammal species globally and over 83 million birds across North America (December 2023), poses a serious global threat to animals and public health. We combined a large, long‐term waterfowl GPS tracking dataset (16 species) with on‐ground disease surveillance data (county‐level HPAIv detections) to create a novel empirical model that evaluated spatiotemporal exposure and predicted future spread and potential arrival of HPAIv via GPS tracked migratory waterfowl through 2022. Our model was effective for wild waterfowl, but predictions lagged HPAIv detections in poultry facilities and among some highly impacted nonmigratory species. Our results offer critical advance warning for applied biosecurity management and planning and demonstrate the importance and utility of extensive multispecies tracking to highlight potential high‐risk disease spread locations and more effectively manage outbreaks.

Wild waterfowl and shorebirds in the Delaware-Maryland-Virginia (Delmarva) Peninsula region within the Atlantic Flyway were sampled as part of the Early Detection of Highly Pathogenic H5N1 Avian Influenza (AI) in Wild Migratory Birds program. The U.S. Department of Agriculture (USDA) and state wildlife agencies submitted 7858 samples for AI virus (AIV) testing by real-time reverse transcription PCR (rRT-PCR) to the University of Delaware Poultry Health System from April 2007 to March 2011. Virus isolation attempts were performed on samples with matrix gene cycle threshold (Ct) values ≤33.9. Using rRT-PCR, AIV was detected in 14% (1091/7857) of the samples. In species with sample sizes >100, American black duck (Anas rubripes; 28%), ruddy turnstone (Arenaria interpres; 27%), American green-winged teal (Anas crecca; 21%), semipalmated sandpiper (Calidris pusilla; 27%), greater snow goose (Chen caerulescens atlanticus; 12%), mallard (Anas platyrhynchos; 10%), and northern pintail (Anas acuta; 14%) showed the highest rates of AIV detection. Forty-two AIVs were recovered from eight species: American black duck, mallard, ruddy turnstone, American green-winged teal, greater snow goose, Canada goose (Branta canadensis), ring-necked duck (Aythya collaris), and mallard × American black duck (Anas platyrhynchos × Anas rubripes). Recovered H5 (n = 2) and H7 (n = 2) viruses were found to be low pathogenicity by the USDA National Veterinary Services Laboratory. Additional AIVs represented a diversity of subtype combinations: H1–H4, H6, and H10 and H11 and N subtypes N1–N9 and N6–N9. The rate of AIV recovery from swabbings was inversely related to Ct value, ranging from 50% for Ct values of 16.0–18.9 to 5.1% for Ct values of 31–33.9.

The effect of pooling 11 or 5 oropharyngeal (O/P) swabbings on detecting avian influenza virus (AIV) by real-time reverse transcription (RRT)–PCR was evaluated. The model used for the evaluation was designed to minimize viral load and, thus, assess the effect of the pooling on detection. Two-week-old broiler chickens were inoculated via the intranasal route with the low pathogenicity chicken/Maryland/Minh Ma/04 H7N2 strain or remained uninoculated. On days 2, 3, 4, 5, 7, 9, 11, and 14 postinoculation (PI), O/P swabbings were collected from individual infected birds and pooled with either 10 or 4 O/P swabs from uninfected broilers to produce 10 replicate pools of 11 or 5 swabbings, respectively. AIV was readily detected (80%–100%) by RRT-PCR in the pools of 11 and pools of 5 swabbings from days 2 through 5 PI. Detection in pools of both types decreased to similar levels on day 7 (40% for the pools of 11 and 50% for the pools of 5). AIV was not detected on day 9, 11, and 14 PI in pools of either size. On a given sample day PI, mean cycle threshold (Ct) values were consistently higher (lower genome levels) in the pools of 11 compared to the pools of 5. These differences were statistically significant on days 3 and 5 PI, yet Ct values associated with both types of pools were clearly interpretable as AIV positive.

A limited outbreak of nephropathogenic infectious bronchitis (NIB) occurred in three Delmarva (DMV) commercial broiler chicken flocks in 2011. Isolates of NIB virus (NIBV)—DMV/1639/11, DMV/3432/11, and DMV/3902/11—were characterized by sequence analysis of the N-terminal subunit (S1) of the spike (S) gene. Findings indicated that the isolates were identical to each other and to PA/9579A/10, a 2010 isolate from poultry in Pennsylvania. The 2010 and 2011 isolates appear to have originated from a 1997–2000 NIB outbreak in Pennsylvania. DMV/1639/11 and PA/9579A/10 were determined to be nephropathogenic in susceptible chickens, yielding virus reisolations from kidney and inducing characteristic interstitial nephritis microscopic lesions. In a controlled laboratory study, 40% of chickens vaccinated with a combination live vaccine containing infectious bronchitis virus (IBV) strains Massachusetts (Mass) + Connecticut (Conn) were positive on virus isolation attempts after challenge with DMV/1639/11, compared with only 13% of Mass + Arkansas (Ark) vaccinates. Both combination vaccines gave partial protection against the development of DMV/1639/11-induced renal lesions. Although numerically fewer chickens vaccinated with Mass + Conn had interstitial nephritis compared with those vaccinated with Mass + Ark, neither vaccine combination offered greater protection (P < 0.05) than observed in unvaccinated chickens challenged with DMV/1639/11. Mass + Ark vaccinations, applied under commercial conditions in the hatchery (spray) and on-farm (spray), did not protect the trachea or kidney from DMV/1639/11 challenge. Serologic testing of broiler flocks found <3% (2 of 69) tested to possess specific antibodies to DMV/1639/11, indicating the virus had not become established in the region. Caracterización del virus nefropatogénico de la bronquitis infecciosa DMV/1639/11 aislado de pollos de engorde en el área de Delmarva en el año 2011. Se presentó un brote limitado de bronquitis infecciosa nefropatogénica (NIB) en tres parvadas comerciales de pollos de engorde en el año 2011 en el área de Delmarva. Se caracterizaron los aislamientos de virus nefropatogénicos de bronquitis infecciosa DMV/1639/11, DMV/3432/11 y DMV/3902/11 se caracterizaron mediante el análisis de la secuencia del gene de la subunidad S1 de la espícula (S). Los resultados indicaron que los aislamientos eran idénticos entre sí y con el aislamiento PA/9579A/10, que es un aislamiento de aves comerciales en Pennsylvania del año 2010. Las cepas de los años 2010 y 2011 parecen haberse originado a partir de un brote de bronquitis infecciosa nefropatogénica que se presentó entre los años 1997 al 2000 en Pennsylvania. Se determinó que los aislamientos DMV/1639/11 y PA/9579A/10 eran nefropatogénicos en pollos susceptibles, que eran reaislados del riñón e inducían las lesiones de nefritis intersticial microscópica característica. En un estudio controlado de laboratorio, el 40% de los pollos vacunados con una vacuna viva que contenía la combinación cepas Massachussets (Mass) y Connecticut (Conn) fueron positivos a los intentos de aislamiento del virus después del desafío con el virus DMV/1639/11, en comparación con sólo el 13% de los pollos vacunados con la combinación Massachussets y Arkansas (Ark). Ambas combinaciones de vacunas confirieron una protección parcial contra el desarrollo de las lesiones renales inducidas por el virus DMV/1639/11. Aunque un número menor de los pollos vacunados con la combinación Massachussets y Connecticut mostraron nefritis intersticial en comparación con los pollos vacunados con Massachussets y Arkansas, ninguna combinación de vacunas ofreció una mayor protección (P < 0.05) que la observada en los pollos no vacunados y desafiados con el virus DMV/1639/11. Las vacunaciones con la combinación Massachussets y Arkansas, aplicadas en condiciones comerciales en la planta de incubación (aerosol) y en las explotaciones agrícolas (aerosol), no protegieron a la tráquea o a los riñones ante el desafío con el virus DMV/1639/11. Las pruebas serológicas demostraron que menos del 3% de las parvadas (2 de 69) poseían anticuerpos específicos contra el virus DMV/1639/11, lo que indica que el virus no se había establecido en la región.

A limited outbreak of nephropathogenic infectious bronchitis (NIB) occurred in three Delmarva (DMV) commercial broiler chicken flocks in 2011. Isolates of NIB virus (NIBV)-DMV/1639/11, DMV/3432/11, and DMV/3902/11-were characterized by sequence analysis of the N-terminal subunit (S1) of the spike (S) gene. Findings indicated that the isolates were identical to each other and to PA/9579A/10, a 2010 isolate from poultry in Pennsylvania. The 2010 and 2011 isolates appear to have originated from a 1997-2000 NIB outbreak in Pennsylvania. DMV/1639/11 and PA/9579A/10 were determined to be nephropathogenic in susceptible chickens, yielding virus reisolations from kidney and inducing characteristic interstitial nephritis microscopic lesions. In a controlled laboratory study, 40% of chickens vaccinated with a combination live vaccine containing infectious bronchitis virus (IBV) strains Massachusetts (Mass) + Connecticut (Conn) were positive on virus isolation attempts after challenge with DMV/1639/11, compared with only 13% of Mass + Arkansas (Ark) vaccinates. Both combination vaccines gave partial protection against the development of DMV/1639/11-induced renal lesions. Although numerically fewer chickens vaccinated with Mass + Conn had interstitial nephritis compared with those vaccinated with Mass + Ark, neither vaccine combination offered greater protection (P < 0.05) than observed in unvaccinated chickens challenged with DMV/1639/11. Mass + Ark vaccinations, applied under commercial conditions in the hatchery (spray) and on-farm (spray), did not protect the trachea or kidney from DMV/1639/11 challenge. Serologic testing of broiler flocks found <3% (2 of 69) tested to possess specific antibodies to DMV/1639/11, indicating the virus had not become established in the region. Caracterizacion del virus nefropatogenico de la bronquitis infecciosa DMV/1639/11 aislado de pollos de engorde en el area de Delmarva en el ano 2011.

Background: Marek’s disease (MD) is a pathology affecting chickens caused by Marek’s disease virus (MDV), an acute transforming alphaherpesvirus of the genus Mardivirus. MD is characterized by paralysis, immune suppression, and the rapid formation of T-cell (primarily CD4+) lymphomas. Over the last 50 years, losses due to MDV infection have been controlled worldwide through vaccination; however, these live-attenuated vaccines are non-sterilizing and potentially contributed to the virulence evolution of MDV field strains. Mutations common to field strains that can overcome vaccine protection were identified in the C-terminal proline-rich repeats of the oncoprotein Meq (Marek’s EcoRI-Q-encoded protein). These mutations in meq have been found to be distinct to their region of origin, with high virulence strains obtained in Europe differing from those having evolved in the US. The present work reports on meq mutations identified in MDV field strains in Nigeria, arising at farms employing different vaccination practices. Materials and Methods: DNA was isolated from FTA cards obtained at 12 farms affected by increased MD in the Plateau State, Nigeria. These sequences included partial whole genomes as well as targeted sequences of the meq oncogenes from these strains. Several of the meq genes were cloned for expression and their localization ability to interact with the chicken NF-IL3 protein, a putative Meq dimerization partner, were assessed. Results: Sequence analysis of the meq genes from these Nigerian field strains revealed an RB1B-like lineage co-circulating with a European Polen5-like lineage, as well as recombinants harboring a combination of these mutations. In a number of these isolates, Meq mutations accumulated in both N-terminal and C-terminal domains. Discussion: Our data, suggest a direct effect of the vaccine strategy on the selection of Meq mutations. Moreover, we posit the evolution of the next higher level of virulence MDVs, a very virulent plus plus pathotype (vv++).