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At least 775 records · Page 43Linked to original sources

Kinetics of viral shedding provide insights into the epidemiology of viral hemorrhagic septicemia in Pacific herring

Losses from infectious diseases are an important component of natural mortality among marine fish species, but factors controlling the ecology of these diseases and their potential responses to anthropogenic changes are poorly understood. We used viral hemorrhagic septicemia virus (VHSV) and a laboratory stock of Pacific herring Clupea pallasii to investigate the kinetics of viral shedding and its effect on disease transmission and host mortality. Outbreaks of acute disease, accompanied by mortality and viral shedding, were initiated after waterborne exposure of herring to concentrations of VHSV as low as 101 plaque-forming units (pfu) ml–1. Shed virus in flow-through tanks was first detected 4 to 5 d post-exposure, peaked after 6 to 10 d, and was no longer detected after 16 d. Shedding rates, calculated from density, flow and waterborne virus titer reached 1.8 to 5.0 × 108 pfu fish–1 d–1. Onset of viral shedding was dose-dependent and preceded initial mortality by 2 d. At 21 d, cumulative mortality in treatment groups ranged from 81 to 100% and was dependent not on challenge dose, but on the kinetics and level of viral shedding by infected fish in the tank. Possible consequences of the viral shedding and disease kinetics are discussed in the context of epizootic initiation and perpetuation among populations of wild Pacific herring.

Marine Ecology Progress Series↗

Costimulatory receptors in a teleost fish: Typical CD28, elusive CTLA4

T cell activation requires both specific recognition of the peptide-MHC complex by the TCR and additional signals delivered by costimulatory receptors. We have identified rainbow trout sequences similar to CD28 (rbtCD28) and CTLA4 (rbtCTLA4). rbtCD28 and rbtCTLA4 are composed of an extracellular Ig-superfamily V domain, a transmembrane region, and a cytoplasmic tail. The presence of a conserved ligand binding site within the V domain of both molecules suggests that these receptors likely recognize the fish homologues of the B7 family. The mRNA expression pattern of rbtCD28 and rbtCTLA4 in naive trout is reminiscent to that reported in humans and mice, because rbtCTLA4 expression within trout leukocytes was quickly up-regulated following PHA stimulation and virus infection. The cytoplasmic tail of rbtCD28 possesses a typical motif that is conserved in mammalian costimulatory receptors for signaling purposes. A chimeric receptor made of the extracellular domain of human CD28 fused to the cytoplasmic tail of rbtCD28 promoted TCR-induced IL-2 production in a human T cell line, indicating that rbtCD28 is indeed a positive costimulator. The cytoplasmic tail of rbtCTLA4 lacked obvious signaling motifs and accordingly failed to signal when fused to the huCD28 extracellular domain. Interestingly, rbtCTLA4 and rbtCD28 are not positioned on the same chromosome and thus do not belong to a unique costimulatory cluster as in mammals. Finally, our results raise questions about the origin and evolution of positive and negative costimulation in vertebrate immune systems. T cell activation is initiated through complex cell-to-cell interactions. TCRs expressed on the surface of T cells first recognize antigenic peptides presented by MHC molecules on the surface of APCs. TCRs and other surface receptors and ligands stabilize the contact between T cells and APCs, which triggers signal transduction pathways resulting in T cell activation. According to the two-signal model ( 1 , 2 ), T cell activation by Ag requires both specific recognition of the peptide by the TCR (signal 1) and additional signals delivered by other costimulatory receptors (signal 2). Among the known costimulatory receptors, CD28 and CTLA4 (also known as CD152), which are expressed on T cells and bind their corresponding ligands B7-1/B7-2 (CD80/CD86) on APCs, represent a well-studied system in mammals ( 3 ). CD28 is a glycosylated homodimeric protein expressed on the surface of double-positive thymocytes, mature CD4 + T cells, CD11b − CD8 + T cells, and γδ CD3 + T cells ( 4 , 5 ). CD28 is expressed at higher levels on activated T cells than on resting cells ( 6 ). In mammals, CD28 binds to B7-1 and B7-2, which are expressed on the surface of APCs, and delivers a critical costimulatory signal to T lymphocytes. In the absence of CD28 ligation, TCR binding either induces apoptosis or anergy in T cells ( 5 ). Engagement of CD28 alone cannot activate T cells, even if synergetic effects are provided via stimulation by T cell mitogens or anti-CD3 treatment ( 7 ). A tyrosine-based motif in cytoplasmic tail of CD28 functions as a binding site for the p85 PI3K subunit when it is phosphorylated ( 8 , 9 ). Other CD28 intracytoplasmic motifs, which associates with IL-2-inducible tyrosine kinase, lymphocyte-specific tyrosine kinase, and the adaptor growth-factor receptor bound protein-2 are responsible for signal transduction ( 10 , 11 , 12 ). The binding of growth-factor receptor bound protein-2 to CD28 also activates the GTPase RAS ( 13 ). CD28 signaling is also thought to contribute to the mobilization of lipid rafts to the immunological synapse ( 14 ), the region of contact between T cell and APC, which lowers the overall threshold of TCR engagement required for effective cytokine production and proliferation ( 15 ). In contrast, CTLA4 is a powerful negative regulator of T cell activation and was first cloned via differential screening of a cytotoxic T cell cDNA library ( 16 ). CD28 and CTLA4 belong to the same family and share high sequence similarity to each other ( 16 , 17 ). Both receptors interact with B7-1 and/or B7-2 but induce different signals: CD28 amplifies signaling triggered by the TCR-CD3 complex, whereas CTLA4 generates negative signals that inhibit T cell activation ( 18 ). CTLA4 has higher affinity for B7-1 and B7-2 compared with CD28, and its expression is also induced by TCR engagement ( 19 ). The mechanisms of CTLA4-mediated suppression likely involve both competition with CD28 for B7-1/B7-2 binding and potent inhibitory signals delivered by CTLA4 ( 20 ). The inhibitory signaling mechanisms triggered by CTLA4 are not clear. The CTLA4 cytoplasmic tail lacks typical ITIM motifs and shares with CD28 a p85 binding site ( 21 ). Thus, the extent of an immune response is likely controlled through the finely tuned expression of costimulatory receptors from the CD28/CTLA4 family on the surface of activated T cells ( 22 , 23 ). Very little is known about T cell responses and activation in bony fish. TCR-αβ cDNAs ( 24 , 25 , 26 , 27 ) and polymorphic class IA and class IIA/B MHC molecules ( 28 , 29 , 30 ) have been reported in several species, suggesting that the fish TCR recognizes antigenic peptides presented by MHC molecules similar to that of mammals. T cell-mediated responses in fish are supported by several lines of evidence. Allograft rejection provided the first experimental indications suggesting that bony fish possess a functional T cell-mediated immune response ( 31 , 32 ). In vitro assays for allospecific cytotoxicity have also been established using clonal and nonclonal catfish cell lines ( 33 , 34 ) or clonal rainbow trout ( 35 ). Autologous cell-mediated specific lysis of virus-infected syngenic target cells has also been reported in cloned goldfish ( 36 , 37 ). Finally, both public and private T cell-specific expansions have been observed in rainbow trout during secondary immune responses to viral hemorrhagic septicemia virus (VHSV), 3 a fish rhabdovirus, using TCR-β CDR3-length spectratyping ( 38 ). TCR-MHC-peptide interactions induce signaling events through CD3 in mammals and most likely in lower vertebrates because a complete set of CD3 genes, including TCR ζ, CD3 ε, and CD3 γδ, has been found in Pufferfish and Xenopus ( 39 , 40 ). CD8α has been identified in rainbow trout ( 41 ); however, the cytoplasmic tail lacks the consensus p56 lck motif, suggesting that TCR/CD3/CD8-mediated signaling events may be different in teleosts. In this study, we have identified and initially characterized two members of the CD28 family in rainbow trout, rbtCD28 and rbtCTLA4. Their sequence features and expression patterns suggest that they are the likely homologues of mammalian CD28 and CTLA4. The potential costimulatory capacities of these fish receptors were investigated using a human T cell line expressing chimeric receptors composed of the extracellular domain of human CD28 (hCD28) fused to the cytoplasmic tail of rbtCD28 or rbtCTLA4. The chimeric hCD28-rbtCD28 receptor mediated enhanced TCR-induced IL-2 production, suggesting a costimulatory function for rbtCD28. In contrast, the divergent cytoplasmic tail from rbtCTLA4 did not mediate similar signaling activities. This study therefore provides the first characterization of costimulatory receptors in lower vertebrates.

Journal of Immunology↗

Identification of Chelonid herpesvirus 5 (ChHV5) in endangered green turtles (Chelonia mydas) with fibropapillomatosis in Asia

Fibropapillomatosis (FP), a debilitating tumor disease of sea turtles, was first identified in green turtles [ Chelonia mydas (Linnaeus, 1758)] in Florida in 1938. In recent decades, FP has been observed globally and is an emerging panzootic disease in sea turtles. However, few reports of FP in Asia exist. Here, we provide the first evidence of Chelonid herpesvirus 5 (ChHV5) DNA associated with FP in endangered green turtles from Taiwan, through molecular characterization, phylogenetic analysis, and histopathological examination. In our study, ChHV5 was successfully detected by PCR in the FP tumor lesions of green turtles. The sequences were found to be consistent with those of tumor-inducing viruses shown to affect sea turtles in the other parts of the world. ChHV5 RNA from the FP tissues was further detected by RT-PCR, indicating active replication of the viruses inside FP tumors. In addition to the molecular evidence of ChHV5 in FP, epidermal intranuclear inclusions were identified in tumor lesions upon histopathological examination. This further suggests that ChHV5 should be in a transcriptionally active (i.e., non-latent) state in FP tumors of affected green turtles. The phylogenetic tree revealed that ChHV5 from the green turtles in Taiwan were closest to the ChHV5 from Hawaii, Puerto Rico, and Sao Tome. For conservation of endangered sea turtles, ChHV5 should be considered an emerging virus, which threatens sea turtles in marine waters in Asia.

Bulletin of Marine Science↗

Distributions of host heterogeneity in susceptibility show signatures of pathogen geographic structure in an insect baculovirus

Segregated variation between populations is a fundamental evolutionary process leading to parasite specialization, yet the resulting impacts on infection heterogeneity within populations are theoretically and empirically understudied. We asked whether the distribution of host susceptibility to infection within populations carries the signatures of geographic structure from pathogen local adaptation, maladaptation, or generalism in a nuclear polyhedrosis virus that infects the Gulf Fritillary butterfly Dione vanillae . For this virus, there is genetic support for two geographically distinct groups within San Diego County, based on whole genome sequencing of 16 virus isolates. Reciprocal laboratory infections showed evidence of two contrasting viral life history strategies: a ‘generalist’ phenotype that consistently infected variable hosts and a ‘specialist’ that performed slightly better in its local host population. As predicted by our theoretical model, the more consistent infection displayed by the generalist across populations corresponded to lower heterogeneity in susceptibility within populations, modeled as gamma distribution. Furthermore, the generalist phenotype was collected over a wider geographic range despite having a tenfold-lower mean infection rate than the specialist, suggesting that a strategy of more consistent infection provides key fitness advantages across diverse host populations. Intriguingly, when there is variation in host susceptibility, interpretations of pathogen local adaptation are dose-dependent. Measuring infectivity across multiple doses enables estimation of the whole distribution of susceptibility, which provides more reliable identification of pathogen specialization to its local host. Our work demonstrates how trait distributions and not only their mean values can carry quantifiable signatures of eco-evolutionary processes in interspecific interactions.

BioRxiv↗

Perspectives on the diagnosis, epizootiology, and control of the 1973 duck plague epizootic in wild waterfowl at Lake Andes, South Dakota

An epizootic of duck plague occurred in early 1973 in a population of 163,500 wild waterfowl, primarily mallards (Anas platyrhynchos), wintering on Lake Andes and the nearby Missouri River in southeastern South Dakota (USA). The diagnosis was based on pathologic lesions and confirmed by virus isolation. Control measures included quarantine, attempts to reduce virus contamination of the area, dispersal of waterfowl, and monitoring of wild waterfowl populations for mortality. The epizootic resulted in documented mortality of 18% and estimated mortality of 26% of the waterfowl at risk. Prompt implementation of control measures might have limited mortality to approximately 8%. Losses during the epizootic were equivalent to 0.12% of the annual mortality in the North American 1996 fall population of 80,000,000 wild ducks. The most likely sources of the infection were free-flying wild mallard or American black duck (Anas rubripes) carriers from the upper midwestern or northeastern United States. Duck plague serum neutralization antibodies were demonstrated in 31% of 395 apparently healthy mallards sampled prior to dispersal of the flock at Lake Andes, suggesting that tens of thousands of potential duck plague carriers entered the wild waterfowl populations of all four major flyways. Consequently, the absence of major epizootics of duck plague in wild waterfowl in the subsequent two decades is evidence that substantial numbers of duck plague carriers can occur in wild waterfowl populations without resulting in epizootic mortalities. The failure to isolate duck plague virus from apparently healthy mallards sampled during the epizootic raises questions concerning the validity of conclusions regarding the status of duck plague in wild waterfowl based upon negative results of random surveys conducted in the absence of epizootics. © Wildlife Disease Association 1997.

South Dakota↗

The 1992 epizootic of Newcastle disease in double-crested cormorants in North America

In the summer of 1992, morbidity and mortality in juvenile double-crested cormorants (Phalacrocorax auritus; DCC) attributable to Newcastle disease virus (NDV) was observed for the first time in seven northern USA states and one Canadian province, and recurred in three western Canadian provinces. Based on clinical signs and laboratory diagnostic findings, DCC mortality from NDV occurred in 59 of the 63 nesting colonies and two of three non-colony sites investigated. An estimate of in excess of 20,000 DCC died, with mortality rates ranging from < 1 to 37% in Great Lakes colonies to 20 to 92% in Minnesota (USA) and North and South Dakota (USA) colonies. Sick juvenile white pelicans (Pelecanus erythrorhynchos) exhibiting signs similar to sick cormorants, and dead pelicans were observed in Minnesota and North Dakota. Mortality rates in pelican colonies were as high as in the adjacent cormorant colonies, but no cause for the mortality of an estimated 5,000 pelicans was determined. No evidence of NDV was found in other species nesting in proximity to affected cormorants. Although the source of the NDV infection is unknown in cormorants, the simultaneous onset of the epizootics in juvenile birds over a wide geographic area implies that the virus was acquired by adults prior to migration and was carried back to nest sites, exposing susceptible nestlings. The possible transmission of this virus from free-ranging wild birds to domestic poultry is a concern. Based on repeated epizootics in cormorants since 1990, NDV seems to be established in DCC.

Journal of Wildlife Diseases↗

Pathogen prevalence in American black bears (Ursus americanus) of the Jemez Mountains, New Mexico, USA

Informed management of American black bears ( Ursus americanus ) requires knowledge of the distribution and pathology of diseases affecting the species. Little information is available on pathogen prevalence from black bear populations in the Southwest, US, and it is unknown how these infections may influence black bear populations or disease transmission. We captured New Mexico black bears ( Ursus americanus amblyceps ) during 2016–17 as part of a long-term monitoring project and opportunistically collected 36 blood samples from 12 female and 17 male black bears. We wanted to determine prior exposure to canine distemper virus, canine parvovirus, Yersinia pestis , Francisella tularensis , West Nile virus, Toxoplasma gondii , and the tick-borne pathogens, Anaplasma spp., Ehrlichia spp., Borrelia burgdorferi , Rickettsia spp., and Babesia spp. Approximately half (55%, 16/29) of the individuals sampled had antibodies to Y. pestis , and 37% (10/27) had antibodies to T. gondii . Prevalence of antibodies to West Nile virus, F. tularensis , and canine parvovirus were lower (i.e., 11, 10, and 3%, respectively). We detected no antibodies to canine distemper, B. burgdorferi , Rickettsia spp., or Babesia spp. We documented changes in antibody titer levels for both sexes of several recaptured black bears. Our data will inform managers of pathogen prevalence and distribution in black bears in north-central New Mexico and provide a vital baseline dataset for future pathogen monitoring. Additionally, these data support actions to minimize exposure through handling wild individuals or through hunter harvest activities.

New Mexico↗

Overview of recent DNA vaccine development for fish

Since the first description of DNA vaccines for fish in 1996, numerous studies of genetic immunisation against the rhabdovirus pathogens infectious haematopoietic necrosis virus (IHNV) and viral haemorrhagic septicaemia virus (VHSV) have established their potential as both highly efficacious biologicals and useful basic research tools. Single small doses of rhabdovirus DNA constructs provide extremely strong protection against severe viral challenge under a variety of conditions. DNA vaccines for several other important fish viruses, bacteria, and parasites are under investigation, but they have not yet shown high efficacy. Therefore, current research is focussed on mechanistic studies to understand the basis of protection, and on improvement of the nucleic acid vaccine applications against a wider range of fish pathogens.

Conference Paper↗

Model-based evaluation of highly and low pathogenic avian influenza dynamics in wild birds

There is growing interest in avian influenza (AI) epidemiology to predict disease risk in wild and domestic birds, and prevent transmission to humans. However, understanding the epidemic dynamics of highly pathogenic (HPAI) viruses remains challenging because they have rarely been detected in wild birds. We used modeling to integrate available scientific information from laboratory and field studies, evaluate AI dynamics in individual hosts and waterfowl populations, and identify key areas for future research. We developed a Susceptible-Exposed-Infectious-Recovered (SEIR) model and used published laboratory challenge studies to estimate epidemiological parameters (rate of infection, latency period, recovery and mortality rates), considering the importance of age classes, and virus pathogenicity. Infectious contact leads to infection and virus shedding within 1–2 days, followed by relatively slower period for recovery or mortality. We found a shorter infectious period for HPAI than low pathogenic (LP) AI, which may explain that HPAI has been much harder to detect than LPAI during surveillance programs. Our model predicted a rapid LPAI epidemic curve, with a median duration of infection of 50–60 days and no fatalities. In contrast, HPAI dynamics had lower prevalence and higher mortality, especially in young birds. Based on field data from LPAI studies, our model suggests to increase surveillance for HPAI in post-breeding areas, because the presence of immunologically naïve young birds is predicted to cause higher HPAI prevalence and bird losses during this season. Our results indicate a better understanding of the transmission, infection, and immunity-related processes is required to refine predictions of AI risk and spread, improve surveillance for HPAI in wild birds, and develop disease control strategies to reduce potential transmission to domestic birds and/or humans.

PLoS ONE↗

Persistent infections of fish cell lines by paramyxovirus isolates from Chinook salmon ( Oncorhynchus tschawytscha )

We have reported the isolation of a paramyxovirus from stocks of adult chinook salmon ( Oncorhynchus tshawytscha ) returning to coastal rivers of Oregon, USA (Winton et al 1985). The isolates were obtained from kidney and spleen tissues using the chinook salmon embryo cell line, CHSE-214. Initial cytopathic effect (CPE) was slow to develop, requiring 28 days incubation at 18°C. The virus replicated in CHSE-214, chum heart (CHH-1), kokanee ovary (K0-6), coho salmon embryo (CSE-119), and fathead minnow (FHM) cell lines where it produced a lytic type of CPE. The virus was stable at pH 3-11 and iodo-deoxyuridine did not inhibit wiral replication. Infectivity was lost after treatment with chloroform indicating the presence of essential lipids. The density of virions in CsCl was 1.2 g/ml. The virus hemagglutinated cells of 11 of 14 species of birds, mammals, and fish tested. Electron microscopy of infected cells revealed enveloped particles 125-250 nm in dia. containing coiled nucleocapsids and examination of freon-treated virions showed the nucleocapsid was a helix approximately 18 nm in dia. and > 1000 nm in length (Winton et al 1985). In addition to causing hemagglutination, members of the Paramyxoviridae are known for the ability to establish persistent infections of cell lines (Choppin and Compans 1975). The purpose of this study was to determine if the paramyxovirus isolates from salmon were able to establish persistent infections in fish cell lines and to study the nature of the infection.

Book chapter↗

Airborne pathogens from dairy manure aerial irrigation and the human health risk

Dairy manure, like the fecal excrement from any domesticated or wild animal, can contain pathogens capable of infecting humans and causing illness or even death. Pathogens in dairy manure can be broadly divided into categories of taxonomy or infectiousness. Dividing by taxonomy there are three pathogen groups in dairy manure: viruses (e.g., bovine rotavirus), bacteria (e.g., Salmonella species), and protozoa (e.g., Cryptosporidium parvum). There are two categories of infectiousness for pathogens found in animals: those that are zoonotic and those that are not. A zoonotic pathogen is one that can infect both human and animal hosts. Some zoonotic pathogens found in dairy manure cause illness in both hosts (e.g., Salmonella) while other zoonotic pathogens, like Escherichia coli O157:H7, (enterohemorrhagic E. coli (EHEC)) cause illness only in humans. As a general rule, the gastrointestinal viruses found in dairy manure are not zoonotic. While there are exceptions (e.g., rare reports of bovine rotavirus infecting children), for the most part the viruses in dairy manure are not a human health concern. The primary concerns are the zoonotic bacteria and protozoa in dairy manure.

Report↗

Novel circoviruses detected in feces of Sonoran felids

Sonoran felids are threatened by drought and habitat fragmentation. Vector range expansion and anthropogenic factors such as habitat encroachment and climate change are altering viral evolutionary dynamics and exposure. However, little is known about the diversity of viruses present in these populations. Small felid populations with lower genetic diversity are likely to be most threatened with extinction by emerging diseases, as with other selective pressures, due to having less adaptive potential. We used a metagenomic approach to identify novel circoviruses, which may have a negative impact on the population viability, from confirmed bobcat ( Lynx rufus ) and puma ( Puma concolor ) scats collected in Sonora, Mexico. Given some circoviruses are known to cause disease in their hosts, such as porcine and avian circoviruses, we took a non-invasive approach using scat to identify circoviruses in free-roaming bobcats and puma. Three circovirus genomes were determined, and, based on the current species demarcation, they represent two novel species. Phylogenetic analyses reveal that one circovirus species is more closely related to rodent associated circoviruses and the other to bat associated circoviruses, sharing highest genome-wide pairwise identity of approximately 70% and 63%, respectively. At this time, it is unknown whether these scat-derived circoviruses infect felids, their prey, or another organism that might have had contact with the scat in the environment. Further studies should be conducted to elucidate the host of these viruses and assess health impacts in felids

Sonoran Desert↗

Genomic and epidemiological investigations reveal chromosomal integration of the acipenserid herpesvirus 3 genome in Lake Sturgeon Acipenser fulvescens

DNA sequence from a new alloherpesvirus named acipenserid herpesvirus 3 (AciHV-3) was found in sturgeon species that are vulnerable to decline globally. A study was undertaken to develop a better understanding of the virus genome and to develop diagnostic tools to support an epidemiological investigation. A 184,426 bp genome was assembled from PacBio HiFi sequences generated with DNA from a Lake Sturgeon Acipenser fulvescens gonad cell line. The AciHV-3 genome was contiguous with host chromosomal DNA and was structured with telomere-like terminal direct repeat regions, five internal direct repeat regions and a U region that included intact open reading frames encoding alloherpesvirus core proteins. Diagnostic testing conducted with a newly developed and analytically validated qPCR assay established the ubiquitous presence and high titer of AciHV-3 DNA in somatic and germline tissues from wild Lake Sturgeon in the Hudson Bay drainage basin. Phylogenetic reconstructions confirm that the monophyletic AciHV-3 lineage shares a common ancestor with AciHV-1 and that AciHV-3 taxa cluster according to their sturgeon host. The same genotype of AciHV-3 is found in disjunctive Lake Sturgeon populations within and among drainage basins. The results support the hypotheses that AciHV-3 has established latency through germline chromosomal integration, is vertically transmitted via a Mendelian pattern of inheritance, is evolving in a manner consistent with a replication competent virus and has co-evolved with its host reaching genetic fixation in Lake Sturgeon populations in central Canada.

Hudson Bay drainage basin↗

Avian Influenza spread and transmission dynamics

The spread of highly pathogenic avian influenza (HPAI) viruses of type A of subtype H5N1 has been a serious threat to global public health. Understanding the roles of various (migratory, wild, poultry) bird species in the transmission of these viruses is critical for designing and implementing effective control and intervention measures. Developing appropriate models and mathematical techniques to understand these roles and to evaluate the effectiveness of mitigation strategies have been a challenge. Recent development of the global health surveillance (especially satellite tracking and GIS techniques) and the mathematical theory of dynamical systems combined have gradually shown the promise of some cutting-edge methodologies and techniques in mathematical biology to meet this challenge.

Book chapter↗

Risk of invasive waterfowl interaction with poultry production: Understanding potential for avian pathogen transmission via species distribution models

Recent outbreaks of highly pathogenic avian influenza have devastated poultry production across the United States, with more than 77 million birds culled in 2022–2024 alone. Wild waterfowl, including various invasive species, host numerous pathogens, including highly pathogenic avian influenza virus (HPAIV), and have been implicated as catalysts of disease outbreaks among native fauna and domestic birds. In major poultry-producing states like Arkansas, USA, where the poultry sector is responsible for significant economic activity (>$4 billion USD in 2022), understanding the risk of invasive waterfowl interactions with domestic poultry is critical. Here, we assessed the risk of invasive waterfowl-poultry interaction in Arkansas by comparing the density of poultry production sites (chicken houses) to areas of high habitat suitability for two invasive waterfowl species, (Egyptian Goose [ Alopochen aegyptiaca ] and Mute Swan [ Cygnus olor ]), known to host significant pathogens, including avian influenza viruses. The percentage of urban land cover was the most important habitat characteristic for both invasive waterfowl species. At the 95% confidence interval, chicken house densities in areas highly suitable for both species (Egyptian Goose = 0.91 ± 0.11 chicken houses/km 2 ; Mute Swan = 0.61 ± 0.03 chicken houses/km 2 ) were three to five times higher than chicken house densities across the state (0.17 ± 0.01 chicken houses/km 2 ). We show that northwestern and western Arkansas, both areas of high importance for poultry production, are also at high risk of invasive waterfowl presence. Our results suggest that targeted monitoring efforts for waterfowl-poultry contact in these areas could help mitigate the risk of avian pathogen exposure in Arkansas and similar regions with high poultry production.

Biological Invasions↗

Waterfowl recently infected with low pathogenic avian influenza exhibit reduced local movement and delayed migration

Understanding relationships between infection and wildlife movement patterns is important for predicting pathogen spread, especially for multispecies pathogens and those that can spread to humans and domestic animals, such as avian influenza viruses (AIVs). Although infection with low pathogenic AIVs is generally considered asymptomatic in wild birds, prior work has shown that influenza-infected birds occasionally delay migration and/or reduce local movements relative to their uninfected counterparts. However, most observational research to date has focused on a few species in northern Europe; given that influenza viruses are widespread globally and outbreaks of highly pathogenic strains are increasingly common, it is important to explore influenza–movement relationships across more species and regions. Here, we used telemetry data to investigate relationships between influenza infection and movement behavior in 165 individuals from four species of North American waterfowl that overwinter in California, USA. We studied both large-scale migratory and local overwintering movements and found that relationships between influenza infection and movement patterns varied among species. Northern pintails ( Anas acuta ) with antibodies to avian influenza, indicating prior infection, made migratory stopovers that averaged 12 days longer than those with no influenza antibodies. In contrast, greater white-fronted geese ( Anser albifrons ) with antibodies to avian influenza made migratory stopovers that averaged 15 days shorter than those with no antibodies. Canvasbacks ( Aythya valisineria ) that were actively infected with influenza upon capture in the winter delayed spring migration by an average of 28 days relative to birds that were uninfected at the time of capture. At the local scale, northern pintails and canvasbacks that were actively infected with influenza used areas that were 7.6 and 4.9 times smaller than those of uninfected ducks, respectively, during the period of presumed active influenza infection. We found no evidence for an influence of active influenza infection on local movements of mallards ( Anas platyrhynchos ). These results suggest that avian influenza can influence waterfowl movements and illustrate that the relationships between avian influenza infection and wild bird movements are context- and species-dependent. More generally, understanding and predicting the spread of multihost pathogens requires studying multiple taxa across space and time.

Ecosphere↗

Sampling for disease surveillance: Assessing effects on blue-winged teal survival and recovery

Outbreaks of highly pathogenic avian influenza virus in wild animals highlight the need for disease surveillance in wild birds to improve our understanding of their role as reservoirs and dispersers, and potential threats to domestic poultry and wild bird populations. Surveillance for avian influenza varies in its approach, objectives, and coordination with other monitoring efforts. For waterfowl, a common host to avian influenza viruses, banding represents a concerted effort of capturing and marking thousands of individuals annually to estimate survival and harvest rates, but users of these data have generally taken a conservative approach to remove any banded birds from analyses that had a sample taken for disease surveillance during capture. We tested for differences in survival and encounter probabilities of blue-winged teal ( Spatula discors ) marked ( n = 21,702 teal) and sampled for disease surveillance ( n = 4,216) during the nonbreeding season in Louisiana, USA, from 2016 to 2023. Although we found no consistent effect of collecting biological samples on survival probability, including an additional test showing no detectable effects of sampling for disease surveillance with oropharyngeal and cloacal swabs versus sampling with swabs and a syringe-drawn blood sample, wide 95% credible intervals on the posterior survival estimates (mean 0.36 difference between upper and lower values across all year-sex-sampling groups; 0.44 for sampling type groups) indicated low statistical power to detect an effect. Seber recovery probability during the first interval following sampling was lower among birds sampled using swabs only, but we assume this stems from low sample sizes rather than an effect of collecting biological samples. Because recovery probabilities can vary as a function of individual covariates, we also examined direct recovery probabilities and observed no meaningful effect of disease surveillance sampling type but strong effects of capture date, suggesting the effect on Seber recovery probability may have been due to heterogeneity in exposure to natural and harvest mortality risks. Although we suggest that aligning disease surveillance sample collection efforts with landscape-scale waterfowl banding efforts may have little effect on observed demographic rates, additional studies with larger sample sizes are likely needed to provide the statistical power necessary to formally conclude no effect of biological sampling on survival probabilities.

Louisiana↗

Feathers and flu: Identifying data gaps in avian influenza host dynamics to prioritize wildlife conservation

Highly pathogenic avian influenza viruses (HPAIV) have had disastrous, worldwide effects on wild birds and domestic poultry since the emergence of the A/goose/Guangdong/1/1996 (Gs/GD/96) lineage. The currently circulating H5N1 clade 2.3.4.4b has an expanded set of susceptible hosts, including many migratory wild birds, and is associated with higher transmission rates, increased susceptibility among wild bird hosts, and a greater number of wildlife reservoirs. Certain wild bird life-history strategies and behaviors have been suggested to explain avian hosts’ susceptibility and exposure to HPAIV. These biological traits include gregariousness, such as colonial nesting and mixed flock foraging, predation or scavenging on wild birds, and association with aquatic habitats. Variation in host infection responses (e.g., infectability, shedding rates and duration, mortality rate, antibody development) informs the overall infection risk across avian species, yet the specific role of biological traits is often inconsistent and unclear across taxa. Moreover, the interactions and potential compounding effects among these biological traits remain largely unknown. To develop a more holistic understanding of cumulative risk across bird species, we integrate existing information on infection risk factors (i.e., susceptibility, immunological response, and behavioral traits) into a qualitative multivariate analysis. This approach enabled us to examine how infection risk factors relate to biological traits (e.g., phylogeny, physiology, behavior, species range) and to begin disentangling their complex interactions. We quantified and summarized these risk factors across host species and qualitatively ranked species by their viral responses along a proposed HPAIV response continuum, guided by expectations of traits and metrics associated with competence or vulnerability to HPAIV. In doing so, we aimed to better understand how viral responses and biological traits synergistically interact to influence cumulative risk across wild bird species. This work broadly expands on the previous avian influenza literature, which has focused on Anseriformes and Charadriiformes as primary viral reservoirs. We tie our findings to effective disease management responses with links to risk components, including descriptions of potential surveillance strategies applied to research and One Health goals, as well as a fuller understanding of how resources may be better deployed for rapid response when spillovers do inevitably occur. Additionally, we identified numerous areas where vital epidemiological information is lacking to best characterize the spread of these viruses. Ultimately, this improved understanding will help identify and inform disease management needs and decision making.

Wildlife Monographs↗