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At least 865 records · Page 48Linked to original sources

Exposure of Alaska brown bears (Ursus arctos) to bacterial, viral, and parasitic agents varies spatiotemporally and may be influenced by age

We collected blood and serum from 155 brown bears ( Ursus arctos ) inhabiting five locations in Alaska during 2013–16 and tested samples for evidence of prior exposure to a suite of bacterial, viral, and parasitic agents. Antibody seroprevalence among Alaska brown bears was estimated to be 15% for Brucella spp., 10% for Francisella tularensis , 7% for Leptospira spp., 18% for canine adenovirus type 1 (CAV-1), 5% for canine distemper virus (CDV), 5% for canine parvovirus, 5% for influenza A virus (IAV), and 44% for Toxoplasma gondii . No samples were seropositive for antibodies to Trichinella spp. Point estimates of prior exposure to pathogens among brown bears at previously unsampled locations generally fell within the range of estimates for previously or contemporaneously sampled bears in Alaska. Statistical support was found for variation in antibody seroprevalence among bears by location or age cohort for CAV-1, CDV, IAV, and Toxoplasma gondii . There was limited concordance in comparisons between our results and previous serosurveys regarding spatial and age-related trends in antibody seroprevalence among Alaska brown bears suggestive of temporal variation. However, we found evidence that the seroprevalence of CAV-1 antibodies is consistently high in bears inhabiting SW Alaska and the cumulative probability of exposure may increase with age. We found evidence for seroconversion or seroreversion to six different infectious agents in one or more bears. Results of this study increase our collective understanding of disease risk to both Alaska brown bear populations and humans that utilize this resource.

Alaska↗

Poecivirus is present in individuals with beak deformities in seven species of North American birds

Avian keratin disorder (AKD), a disease of unknown etiology characterized by debilitating beak overgrowth, has increasingly affected wild bird populations since the 1990s. A novel picornavirus, poecivirus, is closely correlated with disease status in Black-capped Chickadees ( Poecile atricapillus ) in Alaska. However, our knowledge of the relationship between poecivirus and beak deformities in other species and other geographic areas remains limited. The growing geographic scope and number of species affected by AKD-like beak deformities require a better understanding of the causative agent to evaluate the population-level impacts of this epizootic. Here, we tested eight individuals from six avian species with AKD-consistent deformities for the presence of poecivirus: Mew Gull ( Larus canus ), Hairy Woodpecker ( Picoides villosus ), Black-billed Magpie ( Pica hudsonia ), American Crow ( Corvus brachyrhynchos ), Red-breasted Nuthatch ( Sitta canadensis ), and Blackpoll Warbler ( Setophaga striata ). The birds were sampled in Alaska and Maine (1999−2016). We used targeted PCR followed by Sanger sequencing to test for the presence of poecivirus in each specimen and to obtain viral genome sequence from virus-positive host individuals. We detected poecivirus in all individuals tested, but not in negative controls (water and tissue samples). Furthermore, we used unbiased metagenomic sequencing to test for the presence of other pathogens in six of these specimens (Hairy Woodpecker, two American Crows, two Red-breasted Nuthatches, Blackpoll Warbler). This analysis yielded additional viral sequences from several specimens, including the complete coding region of poecivirus from one Red-breasted Nuthatch, which we confirmed via targeted PCR followed by Sanger sequencing. This study demonstrates that poecivirus is present in individuals with AKD-consistent deformities from six avian species other than Black-capped Chickadee. While further investigation will be required to explore whether there exists a causal link between this virus and AKD, this study demonstrates that poecivirus is not geographically restricted to Alaska, but rather occurs elsewhere in North America.

Alaska, Maine↗

Investigating microbial size classes associated with the transmission of stony coral tissue loss disease (SCTLD)

Effective treatment and prevention of any disease necessitates knowledge of the causative agent, yet the causative agents of most coral diseases remain unknown, in part due to the difficulty of distinguishing the pathogenic microbe(s) among the complex microbial backdrop of coral hosts. Stony coral tissue loss disease (SCTLD) is a particularly destructive disease of unknown etiology, capable of transmitting through the water column and killing entire colonies within a matter of weeks. Here we used a previously described method to (i) isolate diseased and apparently healthy coral colonies within individual mesocosms containing filtered seawater with low microbial background levels; (ii) incubate for several days to enrich the water with coral-shed microbes; (iii) use tangential-flow filtration to concentrate the microbial community in the mesocosm water; and then (iv) filter the resulting concentrate through a sequential series of different pore-sized filters. To investigate the size class of microorganism(s) associated with SCTLD transmission, we used 0.8 µm pore size filters to capture microeukaryotes and expelled zooxanthellae, 0.22 µm pore size filters to capture bacteria and large viruses, and 0.025 µm pore size filters to capture smaller viruses. In an attempt to further refine which size fraction(s) contained the transmissible element of SCTLD, we then applied these filters to healthy “receiver” coral fragments and monitored them for the onset of SCTLD signs over three separate experimental runs. However, several factors outside of our control confounded the transmission results, rendering them inconclusive. As the bulk of prior studies of SCTLD in coral tissues have primarily investigated the associated bacterial community, we chose to characterize the prokaryotic community associated with all mesocosm 0.22 µm pore size filters using Illumina sequencing of the V4 region of the 16S rRNA gene. We identified overlaps with prior SCTLD studies, including the presence of numerous previously identified SCTLD bioindicators within our mesocosms. The identification in our mesocosms of specific bacterial amplicon sequence variants that also appear across prior studies spanning different collection years, geographic regions, source material, and coral species, suggests that bacteria may play some role in the disease.

PeerJ↗

Woodcock reovirus

This chapter provides information on a recently identified disease of the American woodcock. Little is known about the disease or the virus that causes it. It has been included in this Manual to enhance awareness that such a disease exists and to stimulate additional interest in further investigations to define the importance of woodcock reovirus. More information about this disease is needed because it is not known whether or not this virus is a factor in the decline of woodcock populations within the United States.

Information and Technology Report↗

Jaundice and bilirubinemia as manifestations of canine distemper in raccoons and ferrets

1) Two strains of distemper virus have been isolated from wild raccoons and one strain from ferrets. 2) All strains isolated have induced bilirubinemia in raccoons and ferrets. Many raccoons with bilirubinemia also had jaundice. 3) Identification of these strains as members of the canine distemper virus complex has been by clinical and pathological findings consistent with this diagnosis as well as by cross-immunity tests.

American Journal of Veterinary Research↗

Seasonal movements and migration of Pallas's Gulls Larus ichthyaetus from Qinghai Lake, China

We studied the seasonal movements and migration often Pallas's Gulls Larus ichthyaetus trom Qinghai Lake to assess migratory routes and stopover areas. Each individual was captured and equipped with an 18 g solar-powered Platform Transmitter Terminal (PIT) to track its movements from September 2007 to May 2008. Six individuals remained near Qinghai Lake until the PTTs stopped transmitting. Three individuals flew 50-330 km from Qinghai Lake to nearby salt lakes. One individual departed on 8 December and flew over 1,700 km south-west to arrive at coastal Bangladesh on 9 January 2008. Two individuals flew in October to the Brahmaputra River in Assam, India, remaining in the area for at least one month until one stopped transmitting. The second individual travelled southwest to coastal Bangladesh. Of the two individuals overwintering in Bangladesh, one remained for 67 days before migrating north. The second bird departed after 96 days, and it returned to Qinghai on 10 May 2008 after 48 days in migration. Both individuals that overwintered in coastal Bangladesh arrived much later than the outbreaks of Highly Pathogenic Avian Influenza (HP AI H5N I) in poultry in 2007. This disparity in timing would tentatively suggest that this species was not involved in long-distance movements of the virus. Instead, the converse may be true: previous work demonstrates the potential for virus spill-over trom poultry into gulls and other wild bird species upon arrival into locations with widespread HPAI H5NI outbreaks and environmental contamination.

Forktail↗

Severe bill deformity of an American Kestrel wintering in California

During a recent survey for West Nile virus in wild birds around the Sonny Bono Salton Sea National Wildlife Refuge, Imperial County, California (Dusek et al. 2010), we captured a female American Kestrel ( Falco sparverius ) with a severe bill deformity (Figure 1). The kestrel was captured on 9 March 2006, at 08:45, approximately 0.25 km south of the intersection of Wiest and Lindsey roads (33° 08' 42' N, 115° 26' 59' W) and 6 km east-northeast of Calipatria. It was caught on a bal-chatri trap baited with a domestic mouse (Berger and Mueller 1959), as were all the 208 kestrels captured during this study. The bird was initially perched on a high transmission line running along Wiest Road and was caught within 10 minutes of our setting the trap. In examining the bird, we observed that the maxilla beyond the cere was missing. The upper bill structure from the palatine process, which included part of the maxilla, the entire premaxilla, and the external rhamphotheca (the hardened keratin layer cover­ ing the premaxilla) was missing rostral to the bird's cere and nares (Threlfall 1968, Lucas and Stettenheim 1972, Proctor and Lynch 1993). The epidermal layer of the cere appeared to have fused over the remaining area between the nares where the upper bill normally would have been. The deformation did not appear to be recent or related to our trapping, as there were no obvious abrasions or open wounds in the region surrounding the nares and oropharynx or signs of recent trauma surrounding the oropharynx area. Both nares were clearly defined, and the tongue protruded from the open oropharynx area. After completing the physical examination, measurements, and obtaining a blood sample for testing for West Nile virus, we released the kestrel at the location of capture. After its release, we monitored the kestrel's behavior for approximately 30 minutes but did not observe any additional hunting.

California↗

Ills in the pipeline: Emerging infectious diseases and wildlife

In the recent film Contagion, a medical thriller released in fall 2011, the fictitious MEV-1 virus—passed from bat to pig to humans—spreads across the globe as easily as the common cold, killing millions of humans and causing mass hysteria as medical researchers race to find a cure. Though it's Hollywood hyperbole, the film holds a kernel of truth: Researchers believe that the close proximity of Malaysian hog farms to forested areas—the natural habitat for fruit bats—allowed the previously unknown Nipah virus to spill from bats into pigs and subsequently into people, resulting in more than 100 human deaths (Epstein et al. 2006). There is no doubt that in recent times we have seen an unprecedented number of emerging infectious diseases, defined by the Institute for Medicine as new, reemerging, or drug-resistant infections whose incidence has increased or whose incidence threatens to increase in the near future. Many of these have a wildlife origin (Taylor et al. 2001). While this jump may be due, in part, to increased vigilance and reporting, there is a general consensus that current global conditions are creating a situation that is very favorable to the transmission of microbes that cause diseases. (For reviews, see Daszak et al. 2001 and Keesing et al. 2010). Likewise, it's increasingly important that wildlife professionals become aware of how and why new infectious diseases spread and what, if anything, can be done to minimize impacts on wildlife.

The Wildlife Professional↗

Pathogens associated with native and exotic trout populations in Shenandoah National Park and the relationships to fish stocking practices

Restrictive fish stocking policies in National Parks were developed as early as 1936 in order to preserve native fish assemblages and historic genetic diversity. Despite recent efforts to understand the effects of non-native or exotic fish introductions, park managers have limited information regarding the effects of these introductions on native fish communities. Shenandoah National Park was established in 1936 and brook trout (Salvelinus fontinalis) restoration within selected streams in the park began in 1937 in collaboration with the Virginia Department of Game and Inland Fisheries (VDGIF). An analysis of tissue samples from brook, brown (Salmo trutta), and rainbow trout (Oncorhynchus mykiss) from 29 streams within the park from 1998–2002 revealed the presence of Renibacterium salmoninarum, Yersinia ruckeri, and infectious pancreatic necrosis virus (IPNv). In order to investigate the relationships of the occurrence of fish pathogens with stocking histories we classified the streams into three categories: 1) streams with no record of stocking, 2) streams that are known to have been stocked historically, and 3) streams that were historically stocked within the park and continue to be stocked downstream of the park boundary. The occurrences of pathogens were summarized relative to this stocking history. Renibacterium salmoninarum, the causative agent of bacterial kidney disease, was the most prevalent pathogen found, occurring in all three species and stream stocking categories, and appears to be endemic to the park. Two other pathogens, Yersinia ruckeri and infectious pancreatic necrosis virus were also described from brook trout populations within the park. IPNv was only found in brook trout populations in streams with prior stocking histories. Yersinia ruckeri was only found in brook trout in steams that have never been stocked and like R. salmoninarum, is likely endemic.

Virginia↗

Infectious diseases, parasites, and biological toxins in sea ducks

This chapter addresses disease agents in the broad sense, including viruses, bacteria, fungi, protozoan and helminth parasites, and biological toxins. Some of these agents are known to cause mortality in sea ducks, some are thought to be incidental findings, and the significance of others is yet poorly understood. Although the focus of the chapter is on free-living sea ducks, the study of disease in this taxonomic group has been relatively limited and examples from captive sea ducks and other wild waterfowl are used to illustrate the pathogenicity of certain diseases. Much of the early work in sea ducks consisted of anecdotal and descriptive reports of parasites, but it was soon recognized that diseases such as avian cholera, renal coccidiosis, and intestinal infections with acanthocephalans were causes of mortality in wild populations. More recently, adenoviruses, reoviruses, and the newly emergent Wellfleet Bay virus, for example, also have been linked to die-offs of sea ducks. Declining populations of animals are particularly vulnerable to the threats posed by disease and it is important that we improve our understanding of the significance of disease in sea ducks. To conclude, we offer our recommendations for future directions in this field.

Book chapter↗

Scale-dependent approaches to modeling spatial epidemiology of chronic wasting disease.

This e-book is the product of a second workshop that was funded and promoted by the United States Geological Survey to enhance cooperation between states for the management of chronic wasting disease (CWD). The first workshop addressed issues surrounding the statistical design and collection of surveillance data for CWD. The second workshop, from which this document arose, followed logically from the first workshop and focused on appropriate methods for analysis, interpretation, and use of CWD surveillance and related epidemiology data. Consequently, the emphasis of this e-book is on modeling approaches to describe and gain insight of the spatial epidemiology of CWD. We designed this e-book for wildlife managers and biologists who are responsible for the surveillance of CWD in their state or agency. We chose spatial methods that are popular or common in the spatial epidemiology literature and evaluated them for their relevance to modeling CWD. Our opinion of the usefulness and relevance of each method was based on the type of field data commonly collected as part of CWD surveillance programs and what we know about CWD biology, ecology, and epidemiology. Specifically, we expected the field data to consist primarily of the infection status of a harvested or culled sample along with its date of collection (not date of infection), location, and demographic status. We evaluated methods in light of the fact that CWD does not appear to spread rapidly through wild populations, relative to more highly contagious viruses, and can be spread directly from animal to animal or indirectly through environmental contamination. We discovered that many of the wellpublished methods were developed for fast-spreading human diseases, such as influenza and measles. While these methods are applicable to fast spreading wildlife diseases, such as foot-and-mouth disease or West Nile virus, many are not likely to work well for CWD. Only limited data exist to evaluate geographic and spatial spread because many locations where we find CWD tend to be locations where samples have just been taken or sample sizes have just become large enough to have a high probability of detecting a low prevalence. Consequently, methods that work well to describe or predict the spread of foot-and-mouth disease throughout England, which occurred within a year, do not work well for describing or predicting CWD spread. We did not exclude methods that we regarded as inappropriate; rather, we included methods that are commonly used for disease epidemiology and then discussed their applicability for modeling the spatial epidemiology of CWD. We hope including inappropriate methods with an explanation of why they are ill-suited for CWD will make it easier to drop them from consideration and explain to others why they were not recommended for spatial modeling of CWD. We organized the three chapters by scale and extent for which each method was developed or best suited. The first chapter covers methods appropriate to multi-jurisdictional or multi-state modeling, which we call “regional” scale. The second chapter covers methods appropriate for within state areas such as wildlife management units or metapopulations, which we call “landscape” scale. The third chapter covers methods appropriate for population or individual-based modeling, which we call “fine” scale. We know this rubric is somewhat artificial because many methods work at multiple scales. We hope, however, that this structure addresses some of the challenges faced by managers that work at local, regional, state, and national scales. Further, the resolution of empirical data often changes with spatial scale, which affects the utility of different modeling approaches. For example, individual-based models work best at modeling spread within populations, while risk analysis is most useful for summarizing data over larger scales such as a region. Because some methods are applicable at several scales, however, we included a graphic at the beginning of each method that indicates the range of scales for which it applies. For example, the graphic to the right indicates that the method is most applicable for regional-scale modeling. There is also a question of resolution as well as scale and extent for each method. CWD surveillance data have been collected over large areas, such as a wildlife management unit or state, but the resolution of the data may be fine scale with GPS locations for many samples. For each method, we described the required resolution of the data and describe the type of data required, as well as what questions the method could answer and how useful the method is, given typical CWD data. For each scale, we presented a focal approach that would be useful for understanding the spatial pattern and epidemiology of CWD, as well as being a useful tool for CWD management. The focal approaches include risk analysis and micromaps for the regional scale, cluster analysis for the landscape scale, and individual based modeling for the fine scale of within population. For each of these methods, we used simulated data and walked through the method step by step to fully illustrate the “how to”, with specifics about what is input and output, as well as what questions the method addresses. We also provided a summary table to, at a glance, describe the scale, questions that can be addressed, and general data required for each method described in this e-book. We hope that this review will be helpful to biologists and managers by increasing the utility of their surveillance data, and ultimately be useful for increasing our understanding of CWD and allowing wildlife biologists and managers to move beyond retroactive fire-fighting to proactive preventative action.

Book↗

Sacramento River chinook disease

Epizootics among chinook salmon fingerlings at the Coleman National Fish Hatchery have occurred periodically since 1941. A virus or virus-like filterable agent has been demonstrated to be the causative agent of this disease.

Leaflet↗

Isolation of a reovirus from coho salmon ( Oncorhynchus kisutch ) in Oregon, USA

Reoviruses isolated from aquatic animals share certain common characteristics: (1) a typical reovirus-like morphology which shows an icosahedral particle with a double capsid that is approximately 75 nm in diameter; (2) a genome with eleven segments of double-stranded RNA (dsRNA) distributed as three large, three medium and five small segments with a total molecular weight of approximately 15 x 106; (3) a virion composed of five major and several minor structural proteins that range in molecular weight from 32,000 to 137,000; and (4) form plaque-like syncytia in monolayer cultures of fish cells. Intact virus particles have buoyant densities in CsCl of 1.34 to 1.36 g/ml. The viruses have been isolated from fish and shellfish collected in both the marine and freshwater environments and will replicate in several fish cell lines (Plumb et al., 1979; Meyers and Hirai, 1980; Winton et al., 1981; Nagabayashi and Mori, 1983; Hedrick et al., 1984; Chen and Jiang, 1984). The original four aquatic reovirus isolates have been compared by Winton et al., 1987.

Book chapter↗

Exxon Valdez oil spill restoration project final report: Prince William Sound Herring disease program (HDP), restoration project 070819

Surveys of pathogens in Pacific herring from 2007 – 2010 indicated that Ichthyophonus , viral hemorrhagic septicemia virus, and erythrocytic necrosis virus are endemic in Prince William Sound and throughout the NE Pacific. Laboratory studies with VHSV indicated that multiple herring stocks are equally susceptible to the resulting disease, Pacific herring shed copious levels of VHSV (as high at 5x10 8 plaque-forming units/day) shortly after exposure, chronic and persistent infections can occur in Pacific herring, susceptibility of Pacific herring to VHS extends to the larval life stages but not the embryonic stages, and the prior exposure history of Pacific herring to VHSV can be determined post hoc. Laboratory studies involving Ichthyophonus indicated that schizonts can be inactivated with chlorine and iodine solutions, the parasite can survive for extended periods in saltwater but not freshwater, a low potential exists for cross contamination between in vitro explant cultures, infectious schizonts are released from the skin surface of infected herring, schizonts are not uniformly distributed throughout the skeletal muscle of infected Pacific herring, multiple types of Ichthyophonus exist with different genotypes and phenotypic traits, and temperature is an important factor influencing the infectivity of Ichthyophonus . Additional field and laboratory studies indicated that Ichthyophonus negatively influences the swimming performance of infected hosts and the negative impacts effects are exacerbated by increasing temperatures, American shad are an important reservoir of Ichthyophonus in the NE Pacific, Pacific herring are not susceptible to infectious hematopoietic necrosis (IHN), and Pacific herring will accept surgically implanted acoustic tags with negligible impacts on survival.

Alaska, Washington↗

Genomes reveal genetic diversity of Piscine orthoreovirus in farmed and free-ranging salmonids from Canada and USA

Piscine orthoreovirus (PRV-1) is a segmented RNA virus which is commonly found in salmonids in the Atlantic and Pacific Oceans. PRV-1 causes the Heart and Skeletal Muscle Inflammation (HSMI) disease in Atlantic salmon and is associated with several other disease conditions. Previous phylogenetic studies of genome segment 1 (S1) identified four main genogroups of PRV-1 (S1 genogroups I – IV). The goal of the present study was to use Bayesian phylogenetic inference to expand our understanding of the spatial, temporal and host patterns of PRV-1 from the waters of the northeast Pacific. To that end, we determined the coding genome sequences of 14 PRV-1 samples that were selected to improve our knowledge of genetic diversity across a broader temporal, geographic and host range, including the first reported genome sequences from the northwest Atlantic (Eastern Canada). Nucleotide and amino acid sequences of the concatenated genomes and their individual segments revealed that established sequences from the northeast Pacific were monophyletic in all analyses. Bayesian inference phylogenetic trees of S1 sequences using BEAST and MrBayes also found that sequences from the northeast Pacific grouped separately from sequences from other areas. One PRV-1 sample (WCAN_BC17_AS_2017) from an escaped Atlantic salmon, collected in British Columbia but derived from Icelandic broodstock, grouped with other S1 sequences from Iceland. Our concatenated genome and S1 analysis demonstrated that PRV-1 from the northeast Pacific is genetically distinct but descended from PRV-1 from the North Atlantic. However, the analyses were inconclusive as to the timing and exact source of introduction into the northeast Pacific, either from eastern North America or European waters of the North Atlantic. There was no evidence that PRV-1 was evolving differently between free-ranging Pacific Salmon and farmed Atlantic Salmon. The northeast Pacific PRV-1 sequences fall within genogroup II based on the classification of Garseth et al. (2013), which also includes North Atlantic sequences from Eastern Canada, Iceland and Norway. The additional full genome sequences herein strengthen our understanding of phylogeographical patterns related to the northeast Pacific, but a more balanced representation of full PRV-1 genomes from across its range, as well additional sequencing of archived samples, are still needed to better understand global relationships including potential transmission links among regions.

Faroe Islands↗

Crossroads of highly pathogenic H5N1: overlap between wild and domestic birds in the Black Sea-Mediterranean impacts global transmission

Understanding transmission dynamics that link wild and domestic animals is a key element of predicting the emergence of infectious disease, an event that has highest likelihood of occurring wherever human livelihoods depend on agriculture and animal trade. Contact between poultry and wild birds is a key driver of the emergence of highly pathogenic avian influenza (HPAI), a process that allows for host-switching and accelerated reassortment, diversification and spread of virus between otherwise unconnected regions. This study addresses questions relevant to the spillover of HPAI at a transmission hotspot: what is the nature of the wild bird-poultry interface in Egypt and adjacent Black Sea-Mediterranean countries and how has this contributed to outbreaks occurring worldwide? Using a spatio-temporal model of infection risk informed by satellite tracking of waterfowl and viral phylogenetics, this study identified ecological conditions that contribute to spillover in this understudied region. Results indicated that multiple ducks (Northern Shoveler and Northern Pintail) hosted segments that shared ancestry with HPAI H5 from both clade 2.2.1 and clade 2.3.4 supporting the role of Anseriformes in linking viral populations in East Asia and Africa over large-distances. Quantifying the interface between wild ducks and H5N1-infected poultry revealed an increasing interface in late winter peaking in early spring when ducks expanded their range before migration, with key differences in the timing of poultry contact risk between local and long-distance migrants.

Virus Evolution↗

Freshwater mussels show elevated viral richness and intensity during a mortality event

Freshwater mussels (Unionida) are among the world’s most imperiled taxa, but the relationship between freshwater mussel mortality events and infectious disease is largely unstudied. We surveyed viromes of a widespread and abundant species (mucket, Actinonaias ligamentina ; syn: Ortmanniana ligamentina ) experiencing a mortality event of unknown etiology in the Huron River, Michigan, in 2019–2020 and compared them to viromes from mucket in a healthy population in the St. Croix River, Wisconsin and a population from the Clinch River, Virginia and Tennessee, where a mortality event was affecting the congeneric pheasantshell ( Actinonaias pectorosa ; syn: Ortmanniana pectorosa ) population. We identified 38 viruses, most of which were associated with mussels collected during the Huron River mortality event. Viral richness and cumulative viral read depths were significantly higher in moribund mussels from the Huron River than in healthy controls from each of the three populations. Our results demonstrate significant increases in the number and intensity of viral infections for freshwater mussels experiencing mortality events, whereas individuals from healthy populations have a substantially reduced virome comprising a limited number of species at low viral read depths.

Michigan, Tennessee, Virginia, Wisconsin↗

Perpetuation of avian influenza from molt to fall migration in wild Swan Geese (Anser cygnoides): An agent-based modeling approach

Wild waterfowl are considered to be the reservoir of avian influenza, but their distinct annual life cycle stages and their contribution to disease dynamics are not well understood. Studies of the highly pathogenic avian influenza (HPAI) virus have primarily focused on wintering grounds, where human and poultry densities are high year-round, compared with breeding grounds, where migratory waterfowl are more isolated. Few if any studies of avian influenza have focused on the molting stage where wild waterfowl congregate in a few selected wetlands and undergo the simultaneous molt of wing and tail feathers during a vulnerable flightless period. The molting stage may be one of the most important periods for the perpetuation of the disease in waterfowl, since during this stage, immunologically naïve young birds and adults freely intermix prior to the fall migration. Our study incorporated empirical data from virological field samplings and markings of Swan Geese ( Anser cygnoides ) on their breeding grounds in Mongolia in an integrated agent-based model (ABM) that included susceptible–exposed–infectious–recovered (SEIR) states. Our ABM results provided unique insights and indicated that individual movements between different molting wetlands and the transmission rate were the key predictors of HPAI perpetuation. While wetland extent was not a significant predictor of HPAI perpetuation, it had a large effect on the number of infections and associated death toll. Our results indicate that conserving undisturbed habitats for wild waterfowl during the molting stage of the breeding season could reduce the risk of HPAI transmission.

Viruses↗