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Viruses associated with diseases of walleye, sauger, and walleye x sauger hybrids
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Virus disease of sockeye salmon
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Channel catfish virus disease
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Approved procedure for determining absence of infectious pancreatic necrosis (IPN) virus in certain fish and fish products
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Characterization of a rhabdovirus isolated from carpione Salmo trutta carpio in Italy
A virus, strain 583, was isolated from carpione Salmo trutta carpio fry exhibiting high mortality. The virus was not neutralized by rabbit antisera against the fish rhabdoviruses viral haemorrhagic septicaemia virus (VHSV), infectious hematopoietic necrosis virus, eel rhabdovirus European X, spring viraemia of carp virus or pike fry rhabdovirus, or against the birnavirus infectious pancreatic necrosis virus. The virus replicated in several fish cell lines incubated at 20 to 25*C and grew optimally in the bluegill fry (BF-2) and fathead minnow (FHM) cell lines. Electron microscopy of infected BF-2 cell cultures revealed the presence of typical rhabdovirus particles, and immunofluorescent staining was observed using various polyclonal and monoclonal antibodies (MAbs) against Egtved virus, the causative agent of viral haemorrhagic septicaemia. The staining by a MAb against the nucleoprotein (N) of VHSV was particularly strong, a MAb against the glycoprotein (G) gave a moderate reaction, whereas a second MAb against the G protein and MAbs against the matrix proteins, M_(1) and M_(2), of VHSV did not react. Fluorescence titres using 3 rabbit antisera against whole Egtved virus varied between negative and moderately positive. Western blotting using polyclonal and monoclonal sera confirmed that both the N and G proteins of the carpione virus shared some epitopes with those of VHSV, but the M_(1) and M_(2) proteins did not. SDS-PAGE showed the structural proteins of the carpione virus produced a pattern typical of members of the Lyssavirus genus of the Rhabdoviridae and the molecular weights were very similar to those of VHSV, except for the M_(2) protein which was somewhat smaller. Infection trials showed the carpione virus induced high mortalities in carpione fry but not in rainbow trout Oncorhynchus mykiss fry. The carpione virus was clearly distinguishable from Egtved virus despite limited serological cross reaction. Since it was also easily distinguishable by immunofluorescence from the other fish rhabdoviruses included in the present study as well as in studies published elsewhere, it is concluded that the virus is a previously undescribed one. It is proposed that the virus be given the preliminary designation 'carpione rhabdovirus'.
Avian influenza shedding patterns in waterfowl: implications for surveillance, environmental transmission, and disease spread
Despite the recognized importance of fecal/oral transmission of low pathogenic avian influenza (LPAI) via contaminated wetlands, little is known about the length, quantity, or route of AI virus shed by wild waterfowl. We used published laboratory challenge studies to evaluate the length and quantity of low pathogenic (LP) and highly pathogenic (HP) virus shed via oral and cloacal routes by AI-infected ducks and geese, and how these factors might influence AI epidemiology and virus detection. We used survival analysis to estimate the duration of infection (from virus inoculation to the last day virus was shed) and nonlinear models to evaluate temporal patterns in virus shedding. We found higher mean virus titer and longer median infectious period for LPAI-infected ducks (10–11.5 days in oral and cloacal swabs) than HPAI-infected ducks (5 days) and geese (7.5 days). Based on the median bird infectious dose, we found that environmental contamination is two times higher for LPAI- than HPAI-infectious ducks, which implies that susceptible birds may have a higher probability of infection during LPAI than HPAI outbreaks. Less environmental contamination during the course of infection and previously documented shorter environmental persistence for HPAI than LPAI suggest that the environment is a less favorable reservoir for HPAI. The longer infectious period, higher virus titers, and subclinical infections with LPAI viruses favor the spread of these viruses by migratory birds in comparison to HPAI. Given the lack of detection of HPAI viruses through worldwide surveillance, we suggest monitoring for AI should aim at improving our understanding of AI dynamics (in particular, the role of the environment and immunity) using long-term comprehensive live bird, serologic, and environmental sampling at targeted areas. Our findings on LPAI and HPAI shedding patterns over time provide essential information to parameterize environmental transmission and virus spread in predictive epizootiologic models of disease risks.
Duck plague
Duck plague is caused by a herpesvirus. Infection often results in an acute, contagious, and fatal disease. As with many other herpesviruses, duck plague virus can establish inapparent infections in birds that survive exposure to it, a state referred to as latency. During latency, the virus cannot be detected by standard methods for virus isolation. Studies of domestic species of waterfowl have detected multiple strains of the virus that vary in their ability to cause disease and death. Little is known about the response of wild waterfowl to strain differences. Duck plague outbreaks are thought to be caused when birds that carry the virus shed it through fecal or oral discharge, thus releasing the virus into food and water with which susceptible birds may have contact. Experimental studies have demonstrated spontaneous virus shedding by duck plague carriers during spring. Changes in the duration of daylight and onset of breeding are thought to be physiological stresses that stimulate virus shedding at this time of year. The carriers are immune to the disease, but the virus shed by them causes infection and disease among susceptible waterfowl. Bird-to-bird contact and contact with virus that has contaminated the environment perpetuate an outbreak. Scavenging and decomposition of carcasses of infected birds also contaminate the environment by releasing viruses from tissues and body fluids. Virus transmission through the egg has been reported, but the role of the egg in the disease cycle remains to be resolved.
Highly pathogenic avian influenza is an emerging disease threat to wild birds in North America
Prior to the emergence of the A/goose/Guangdong/1/1996 (Gs/GD) H5N1 influenza A virus, the long-held and well-supported paradigm was that highly pathogenic avian influenza (HPAI) outbreaks were restricted to poultry, the result of cross-species transmission of precursor viruses from wild aquatic birds that subsequently gained pathogenicity in domestic birds. Therefore, management agencies typically adopted a prevention, control, and eradication strategy that included strict biosecurity for domestic bird production, isolation of infected and exposed flocks, and prompt depopulation. In most cases, this strategy has proved sufficient for eradicating HPAI. Since 2002, this paradigm has been challenged with many detections of viral descendants of the Gs/GD lineage among wild birds, most of which have been associated with sporadic mortality events. Since the emergence and evolution of the genetically distinct clade 2.3.4.4 Gs/GD lineage HPAI viruses in approximately 2010, there have been further increases in the occurrence of HPAI in wild birds and geographic spread through migratory bird movement. A prominent example is the introduction of clade 2.3.4.4 Gs/GD HPAI viruses from East Asia to North America via migratory birds in autumn 2014 that ultimately led to the largest outbreak of HPAI in the history of the United States. Given the apparent maintenance of Gs/GD lineage HPAI viruses in a global avian reservoir; bidirectional virus exchange between wild and domestic birds facilitating the continued adaptation of Gs/GD HPAI viruses in wild bird hosts; the current frequency of HPAI outbreaks in wild birds globally, and particularly in Eurasia where Gs/GD HPAI viruses may now be enzootic; and ongoing dispersal of AI viruses from East Asia to North America via migratory birds, HPAI now represents an emerging disease threat to North American wildlife. This recent paradigm shift implies that management of HPAI in domestic birds alone may no longer be sufficient to eradicate HPAI viruses from a given country or region. Rather, agencies managing wild birds and their habitats may consider the development or adoption of mitigation strategies to minimize introductions to poultry, to reduce negative impacts on wild bird populations, and to diminish adverse effects to stakeholders using wildlife resources. The main objective of this review is, therefore, to provide information that will assist wildlife managers in developing mitigation strategies or approaches for dealing with outbreaks of Gs/GD HPAI in wild birds in the form of preparedness, surveillance, research, communications, and targeted management actions. Resultant outbreak response plans and actions may represent meaningful steps of wildlife managers toward the use of collaborative and multi-jurisdictional One Health approaches when it comes to the detection, investigation, and mitigation of emerging viruses at the human-domestic animal-wildlife interface.
Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia
Highly pathogenic avian influenza (HPAI) viruses of the H5 A/goose/Guangdong/1/96 lineage can cause severe disease in poultry and wild birds, and occasionally in humans. In recent years, H5 HPAI viruses of this lineage infecting poultry in Asia have spilled over into wild birds and spread via bird migration to countries in Europe, Africa, and North America. In 2016/2017, this spillover resulted in the largest HPAI epidemic on record in Europe and was associated with an unusually high frequency of reassortments between H5 HPAI viruses and cocirculating low-pathogenic avian influenza viruses. Here, we show that the seven main H5 reassortant viruses had various combinations of gene segments 1, 2, 3, 5, and 6. Using detailed time-resolved phylogenetic analysis, most of these gene segments likely originated from wild birds and at dates and locations that corresponded to their hosts’ migratory cycles. However, some gene segments in two reassortant viruses likely originated from domestic anseriforms, either in spring 2016 in east China or in autumn 2016 in central Europe. Our results demonstrate that, in addition to domestic anseriforms in Asia, both migratory wild birds and domestic anseriforms in Europe are relevant sources of gene segments for recent reassortant H5 HPAI viruses. The ease with which these H5 HPAI viruses reassort, in combination with repeated spillovers of H5 HPAI viruses into wild birds, increases the risk of emergence of a reassortant virus that persists in wild bird populations yet remains highly pathogenic for poultry.
USGS role and response to highly pathogenic avian influenza
Avian influenza viruses are naturally occurring in wild birds such as ducks, geese, swans, and gulls. These viruses generally do not cause illness in wild birds, however, when spread to poultry they can be highly pathogenic and cause illness and death in backyard and commercial farms. Outbreaks may cause devastating agricultural economic losses and some viral strains have the potential to infect people directly. Furthermore, the combination of avian influenza viruses with mammalian viruses can result in strains with the ability to transmit from person to person, possibly leading to viruses with pandemic potential. All known pandemic influenza viruses have had some genetic material of avian origin. Since 1996, a strain of highly pathogenic avian influenza (HPAI) virus, H5N1, has caused infection in wild birds, losses to poultry farms in Eurasia and North Africa, and led to the deaths of several hundred people. Spread of the H5N1 virus and other influenza strains from China was likely facilitated by migratory birds. In December 2014, HPAI was detected in poultry in Canada and migratory birds in the United States. Since then, HPAI viruses have spread to large parts of the United States and will likely continue to spread through migratory bird flyways and other mechanisms throughout North America. In the United States, HPAI viruses have severely affected the poultry industry with millions of domestic birds dead or culled. These strains of HPAI are not known to cause disease in humans; however, the Centers for Disease Control and Prevention (CDC) advise caution when in close contact with infected birds. Experts agree that HPAI strains currently circulating in wild birds of North America will likely persist for the next few years. This unprecedented situation presents risks to the poultry industry, natural resource management, and potentially human health. Scientific knowledge and decision support tools are urgently needed to understand factors affecting the persistence of HPAI in wild birds, to forecast future spread of HPAI by wild birds, and to detect novel strains of HPAI that may emerge.
USGS highly pathogenic avian influenza research strategy
Avian influenza viruses are naturally occurring in wild birds such as ducks, geese, swans, and gulls. These viruses generally do not cause illness in wild birds, however, when spread to poultry they can be highly pathogenic and cause illness and death in backyard and commercial farms. Outbreaks may cause devastating agricultural economic losses and some viral strains have the potential to infect people directly. Furthermore, the combination of avian influenza viruses with mammalian viruses can result in strains with the ability to transmit from person to person, possibly leading to viruses with pandemic potential. All known pandemic influenza viruses have had some genetic material of avian origin. Since 1996, a strain of highly pathogenic avian influenza (HPAI) virus, H5N1, has caused infection in wild birds, losses to poultry farms in Eurasia and North Africa, and led to the deaths of several hundred people. Spread of the H5N1 virus and other influenza strains from China was likely facilitated by migratory birds. In December 2014, HPAI was detected in poultry in Canada and migratory birds in the United States. Since then, HPAI viruses have spread to large parts of the United States and will likely continue to spread through migratory bird flyways and other mechanisms throughout North America. In the United States, HPAI viruses have severely affected the poultry industry with millions of domestic birds dead or culled. These strains of HPAI are not known to cause disease in humans; however, the Centers for Disease Control and Prevention (CDC) advise caution when in close contact with infected birds. Experts agree that HPAI strains currently circulating in wild birds of North America will likely persist for the next few years. This unprecedented situation presents risks to the poultry industry, natural resource management, and potentially human health. Scientific knowledge and decision support tools are urgently needed to understand factors affecting the persistence of HPAI in wild birds, to forecast future spread of HPAI by wild birds, and to detect novel strains of HPAI that may emerge.
Assessing the risks posed by SARS-CoV-2 in and via North American bats — Decision framing and rapid risk assessment
The novel β-coronavirus, SARS-CoV-2, may pose a threat to North American bat populations if bats are exposed to the virus through interaction with humans, if the virus can subsequently infect bats and be transmitted among them, and if the virus causes morbidity or mortality in bats. Further, if SARS-CoV-2 became established in bat populations, it could possibly serve as a source for new infection in humans, domesticated animals, or other wild animals. Wildlife management agencies in the United States are concerned about these potential risks and have begun to issue guidance regarding work that brings humans into contact with bats, but decision making is difficult because of the high degree of uncertainty about many of the relevant processes that could lead to virus transmission and establishment. The risk assessment described in this report was undertaken to provide management agencies with an understanding of the likelihood that the various steps in the causal pathways would lead to SARS-CoV-2 infection of North American bats from people. This assessment focused on the active season for bats in the temperate zone of North America (April 15 through November 15), and used Myotis lucifugus (little brown bats) as a surrogate species. At the time of this work (April 2020), no empirical data about the effects of SARS-CoV-2 on North American bats were available, so a formal process of expert judgment was used to elicit estimates of the underlying parameters. Twelve experts in bat ecology, epidemiology, virology, and wildlife disease from the United States, United Kingdom, and Australia participated in the elicitation. A Monte Carlo simulation model was used to integrate the parameter estimates elicited from the experts and to predict the likelihood of exposure and infection in bats through a series of transmission pathways, with particular attention to capturing uncertainty in the predictions. Given the current state of knowledge as expressed by the expert panel, the results of this assessment indicate that there is a non-negligible risk of transmission of SARS-CoV-2 from humans to bats. For example, if a research scientist were shedding SARS-CoV-2 virus while handling bats under the field protocols used in North America prior to the COVID-19 pandemic, the risk model indicates that 50 percent (uncertainty, 15–84 percent) of those bats could be exposed to virus, and 17 percent (uncertainty, 3–51 percent) could become infected. Use of personal protective equipment, especially a respirator, is expected to reduce the exposure risk. The expert panel estimated that exposure risk from research scientists could be reduced 94–96 percent (uncertainty, 86–99 percent) through proper use of appropriate N95 respirators (a type of mechanical filter worn over the nose and mouth), dedicated clothing (such as Tyvek coveralls), and gloves. Should any North American bats become infected with SARS-CoV-2, the expert panel estimated that there is an approximately 33-percent chance the virus could spread within a bat population. This study, conducted by the U.S. Geological Survey in cooperation with the U.S. Fish and Wildlife Service, identified several critical uncertainties that could affect the estimate of risks associated with SARS-CoV-2 entering bat populations—notably, the underlying probability that a human would be shedding virus while working with bats, the likelihood of the virus replicating in bat tissue, and the likelihood of transmission of the virus within bat populations. Ongoing empirical work during May–October 2020 may shed light on these issues. Follow-up work is needed to better understand the probability of transmission of SARS-CoV-2 to bats from the general public; the manner in which the probabilities of exposure, infection, and transmission would differ during hibernation compared to the breeding season; and the likelihood of important effects, like morbidity and mortality in bats, the possibility of zoonosis from a North American bat reservoir, and effects of and on other wildlife.
Exxon Valdez oil spill long-term herring research and monitoring program final report
This study includes annual field surveys of Ichthyophonus, viral hemorrhagic septicemia virus, and erythrocytic necrosis virus in adult and juvenile Pacific herring (Clupea pallasii) in Prince William Sound, Alaska and several reference populations in Alaska, British Columbia, and Washington. Results from controlled experimental studies with Ichthyophonus indicated that: • Pacific herring could become infected after repeated feedings on simulated infected offal, • Gross external signs of ichthyophoniasis can persist for extended periods without causing direct host mortality, • A novel tool (chromogenic in situ hybridization) was developed to confirm the presence of Ichthyophonus in histological sections, • A circulating stage of Ichthyophonus was detected in the blood of infected hosts, • Ichthyophonus remains viable in a fish carcass for up to 4 weeks and remains infectious for at least 5 days post mortem, • Six distinct genetic types of Ichthyophonus were identified in different hosts throughout the world, • Tissue explant culture was confirmed to be more sensitive than qPCR for detecting low - intensity Ichthyophonus infections directly from fish tissues. Results from controlled experimental studies with viral hemorrhagic septicemia virus indicated that: • Cooler temperatures are more conducive to viral hemorrhagic septicemia epizootics in Pacific herring, • A blocking ELISA was developed to detect fish antibodies to viral hemorrhagic septicemia virus, • A more sensitive plaque neutralization test was optimized to detect herring neutralizing antibodies to viral hemorrhagic septicemia virus, • The relative susceptibility of Pacific herring to other viral hemorrhagic septicemia virus genotypes was assessed, experimental spill-over, amplification, and spill-back was demonstrated between Atlantic salmon (Salmo salar) and Pacific herring, • The efficacy of homologous and heterologous DNA vaccines against viral hemorrhagic septicemia virus was demonstrated in Pacific herring. Controlled experimental studies with erythrocytic necrosis virus resulted in the development of a conventional PCR technique that is capable of the virus in the blood and the development of a quantitative PCR technique that is capable of detecting the virus in any herring tissues.
Waterfowl show spatiotemporal trends in influenza A H5 and H7 infections but limited taxonomic variation
Influenza A viruses in wild birds pose threats to the poultry industry, wild birds, and human health under certain conditions. Of particular importance are wild waterfowl, which are the primary reservoir of low pathogenicity influenza viruses that ultimately cause high pathogenicity outbreaks in poultry farms. Despite much work on the drivers of influenza A virus prevalence, the underlying viral subtype dynamics are still mostly unexplored. Nevertheless, understanding these dynamics, particularly for the agriculturally significant H5 and H7 subtypes, is important for mitigating the risk of outbreaks in domestic poultry farms. Here, using an expansive surveillance database, we take a large-scale look at the spatial, temporal, and taxonomic drivers in the prevalence of these two subtypes among influenza A positive wild waterfowl. We document spatiotemporal trends that are consistent with past work, particularly an uptick in H5 viruses in late autumn and H7 viruses in spring. Interestingly, despite large species differences in temporal trends in overall influenza A virus prevalence, we document only modest differences in the relative abundance of these two subtypes and little, if any, temporal differences among species. As such, it appears that differences in species' phenology, physiology, and behaviors that influence overall susceptibility to influenza A viruses play a much lesser role in relative susceptibility to different subtypes. Instead, species likely freely pass viruses among each other regardless of subtype. Importantly, despite the similarities among species documented here, individual species still may play important roles in moving viruses across large geographic areas or sustaining local outbreaks through their different migratory behaviors.