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USGS2006

Comparison of methods used to diagnose generalized inflammatory disease in manatees (Trichechus manatus latirostris)

Manatees ( Trichechus manatus latirostris ) are afflicted with inflammatory and infectious disease secondary to human interaction, such as boat strike and entanglement, as well as “cold stress syndrome” and pneumonia. White-blood-cell count and fever, primary indicators of systemic inflammation in most species, are insensitive in diagnosing inflammatory disease in manatees. Acute phase-response proteins, such as haptoglobin and serum amyloid A, have proven to be sensitive measures of inflammation/infection in domestic large animal species. This study assessed diagnosis of generalized inflammatory disease by different methods including total white-blood-cell count, albumin: globulin ratio, gel electrophoresis analysis, C-reactive protein, alpha 1 acid glycoprotein, haptoglobin, fibrinogen, and serum amyloid A. Samples were collected from 71 apparently healthy and 27 diseased animals during diagnostic medical examination. Serum amyloid A, measured by ELISA, followed by albumin:globulin ratio, measured by plasma gel electrophoresis, were most sensitive in diagnosing inflammatory disease, with diagnostic sensitivity and specificity of approximately 90%. The reference interval for serum amyloid A is <10–50 μg/ml with an equivocal interval of 51–70 μg/ml. The reference interval for albumin:globulin ratio by plasma gel electrophoresis is 0.7–1.1. Albumin: globulin ratio, calculated using biochemical techniques, was not accurate due to overestimation of albumin by bromcresol green dye-binding methodology. Albumin:globulin ratio, measured by serum gel electrophoresis, has a low sensitivity of 15% due to the lack of fibrinogen in the sample. Haptoglobin, measured by hemoglobin titration, had a reference interval of 0.4–2.4 mg/ml, a diagnostic sensitivity of 60%, and a diagnostic specificity of 93%. The haptoglobin assay is significantly affected by hemolysis. Fibrinogen, measured by heat precipitation, has a reference interval of 100–400 mg/dl, a diagnostic sensitivity of 40%, and a diagnostic specificity of 95%.

Journal of Zoo and Wildlife Medicine↗

USGS2019

Modeling elk‐to‐livestock transmission risk to predict hotspots of brucellosis spillover

Wildlife reservoirs of infectious disease are a major source of human‐wildlife conflict because of the risk of potential spillover associated with commingling of wildlife and livestock. In the Greater Yellowstone Ecosystem, the presence of brucellosis ( Brucella abortus ) in free‐ranging elk ( Cervus canadensis ) populations is of significant management concern because of the risk of disease transmission from elk to livestock. We identified how spillover risk changes through space and time by developing resource selection functions using telemetry data from 223 female elk to predict the relative probability of female elk occurrence daily during the transmission risk period. We combined these spatiotemporal predictions with elk seroprevalence, demography, and transmission timing data to identify when and where abortions (the primary transmission route of brucellosis) were most likely to occur. Additionally, we integrated our predictions of transmission risk with spatiotemporal data on areas of potential livestock use to estimate the daily risk to livestock. We predicted that approximately half of the transmission risk occurred on areas where livestock may be present (i.e., private property or grazing allotments). Of the transmission risk that occurred in livestock areas, 98% of it was on private ranchlands as opposed to state or federal grazing allotments. Disease prevalence, transmission timing, host abundance, and host distribution were all important factors in determining the potential for spillover risk. Our fine‐resolution (250‐m spatial, 1‐day temporal), large‐scale (17,732 km 2 ) predictions of potential elk‐to‐livestock transmission risk provide wildlife and livestock managers with a useful tool to identify higher risk areas in space and time and proactively focus actions in these areas to separate elk and livestock to reduce spillover risk.

Montana↗

USGS2022

Progression of infection and detection of Pseudoloma neurophilia in zebrafish Danio rerio Hamilton by PCR and histology

Pseudoloma neurophilia is a critical threat to the zebrafish ( Danio rerio ) model, as it is the most common infectious agent found in research facilities. In this study, our objectives were two-fold: (1) compare the application of diagnostic tools for P. neurophilia and (2) track the progression of infection using PCR and histology. The first experiment showed that whole-body analysis by qPCR (WB-qPCR) can be a standardized process, providing a streamlined diagnostic protocol, without the need for extraction of specific tissues. Evaluating the course of infection in experimentally infected fish, we showed key dynamics in infection. Starting with a low dose exposure of 8000 spores/fish, the prevalence remained low until 92 days post-exposure (dpe), followed by a 30%–40% prevalence by histology or 40%–90% by PCR until the end of the experiment at 334 dpe. WB-qPCR positively detected infection in more fish than histology throughout the study, as WB-qPCR detected the parasite as early as 4 dpe, whereas it was undetected by histology until 92 dpe. We also added a second slide for histologic analyses, showing an increase in detection rate from 24% to 26% when we combined all data from our experiments, but this increase was not statistically significant.

Journal of Fish Diseases↗

USGSDate not supplied

Characterizing the interface between wild ducks and poultry to evaluate the potential of transmission of avian pathogens

Background Characterizing the interface between wild and domestic animal populations is increasingly recognized as essential in the context of emerging infectious diseases (EIDs) that are transmitted by wildlife. More specifically, the spatial and temporal distribution of contact rates between wild and domestic hosts is a key parameter for modeling EIDs transmission dynamics. We integrated satellite telemetry, remote sensing and ground-based surveys to evaluate the spatio-temporal dynamics of indirect contacts between wild and domestic birds to estimate the risk that avian pathogens such as avian influenza and Newcastle viruses will be transmitted between wildlife to poultry. We monitored comb ducks ( Sarkidiornis melanotos melanotos ) with satellite transmitters for seven months in an extensive Afro-tropical wetland (the Inner Niger Delta) in Mali and characterise the spatial distribution of backyard poultry in villages. We modelled the spatial distribution of wild ducks using 250-meter spatial resolution and 8-days temporal resolution remotely-sensed environmental indicators based on a Maxent niche modelling method. Results Our results show a strong seasonal variation in potential contact rate between wild ducks and poultry. We found that the exposure of poultry to wild birds was greatest at the end of the dry season and the beginning of the rainy season, when comb ducks disperse from natural water bodies to irrigated areas near villages. Conclusions Our study provides at a local scale a quantitative evidence of the seasonal variability of contact rate between wild and domestic bird populations. It illustrates a GIS-based methodology for estimating epidemiological contact rates at the wildlife and livestock interface integrating high-resolution satellite telemetry and remote sensing data.

Inner Niger Delta↗

USGS2013

Estimating transmission of avian influenza in wild birds from incomplete epizootic data: implications for surveillance and disease spreac

Estimating disease transmission in wildlife populations is critical to understand host–pathogen dynamics, predict disease risks and prioritize surveillance activities. However, obtaining reliable estimates for free-ranging populations is extremely challenging. In particular, disease surveillance programs may routinely miss the onset or end of epizootics and peak prevalence, limiting the ability to evaluate infectious processes. We used profile likelihood to estimate the force of infection (FOI) in a low pathogenic avian influenza virus (LPAIv) epizootic model from censored time series of LPAIv prevalence in hatch-year waterfowl (order Anseriformes) at postbreeding and migration sites in North America. We found a mean LPAIv FOI of 0·12 day −1 [95% CI, 0·00–0·39], corresponding to an incidence rate of 0·11 day −1 , with geographic heterogeneity (min–max: 0·02–0·23 day −1 ) among study sites. These high infection rates indicate that most hatch-year waterfowl are likely infected with LPAIv early in the fall migration. Comparison of model-predicted and observed immunity confirmed our assumption of naïve hatch-year waterfowl and suggested long-term immunity (>6 months) for adults. Using the mean LPAIv incidence rate, we predict a shorter and lower epizootic curve for highly pathogenic avian influenza virus (HPAIv; 5 weeks with peak prevalence of 28% and 30% mortality) than LPAIv (8 weeks with peak prevalence of 50%). These findings indicate it is harder to detect HPAIv than LPAIv with swabs from live birds, which are commonly used during disease surveillance. Synthesis and applications . Our study highlights the potential of integrating incomplete surveillance data with epizootic models to quantify disease transmission and immunity. This modelling approach provides an important tool to understand spatial and temporal epizootic dynamics and inform disease surveillance. Our findings suggest focusing highly pathogenic avian influenza virus (HPAIv) surveillance on postbreeding areas where mortality of immunologically naïve hatch-year birds is most likely to occur, and collecting serology to enhance HPAIv detection. Our modelling approach can integrate various types of disease data facilitating its use with data from other surveillance programs (as illustrated by the estimation of infection rate during an HPAIv outbreak in mute swans Cygnus olor in Europe).

Journal of Applied Ecology↗

USGS2022

A serological survey of Francisella tularensis exposure in wildlife on the Arctic Coastal Plain of Alaska

Tularemia is an infectious zoonotic disease caused by one of several subspecies of Francisella tularensis bacteria. Infections by F. tularensis are common throughout the northern hemisphere and have been detected in more than 250 wildlife species. In Alaska, US, where the pathogen was first identified in 1938, studies have identified F. tularensis antibodies in a diverse suite of taxa, including insects, birds, and mammals. However, few such investigations have been conducted recently and knowledge about the current distribution and disease ecology of F. tularensis is limited, particularly in Arctic Alaska, an area undergoing rapid environmental changes from climate warming. To help address these information gaps and provide insights about patterns of exposure among wildlife, we assessed the seroprevalence of F. tularensis antibodies in mammals and tundra-nesting geese from the Arctic Coastal Plain of Alaska, 2014–17. With a commercially available slide agglutination test, we detected antibodies in 14.7% of all individuals sampled ( n =722), with titers ranging from 1:20 to 1:320. We detected significant differences in seroprevalence between family groups, with Canidae (foxes, Vulpes spp.) and Sciuridae (Arctic ground squirrel, Spermophilus parryii ) having the highest seroprevalence at 21.5% and 33.3%, respectively. Mean seroprevalence for Ursidae (polar bears, Ursus maritimus ) was 13.3%, whereas Cervidae (caribou, Rangifer tarandus ) had comparatively low seroprevalence at 6.5%. Antibodies were detected in all Anatidae species sampled, with Black Brant ( Branta bernicla nigricans ) having the highest seroprevalence at 13.6%. The detection of F. tularensis antibodies across multiple taxa from the Arctic Coastal Plain and its nearshore marine region provides evidence of exposure to this pathogen throughout the region and highlights the need for renewed surveillance in Alaska.

Alaska↗

USGS2013

Genomic analysis of avian influenza viruses from waterfowl in Western Alaska, USA

The Yukon-Kuskokwim Delta (Y-K Delta) in western Alaska is an immense and important breeding ground for waterfowl. Migratory birds from the Pacific Americas, Central Pacific, and East Asian-Australasian flyways converge in this region, providing opportunities for intermixing of North American- and Eurasian-origin hosts and infectious agents, such as avian influenza virus (AIV). We characterized the genomes of 90 low pathogenic (LP) AIV isolates from 11 species of waterfowl sampled on the Y-K Delta between 2006 and 2009 as part of an interagency surveillance program for the detection of the H5N1 highly pathogenic (HP) strain of AIV. We found evidence for subtype and genetic differences between viruses from swans and geese, dabbling ducks, and sea ducks. At least one gene segment in 39% of all isolates was Eurasian in origin. Target species (those ranked as having a relatively high potential to introduce HP H5N1 AIV to North America) were no more likely than nontarget species to carry viruses with genes of Eurasian origin. These findings provide evidence that the frequency at which viral gene segments of Eurasian origin are detected does not result from a strong species effect, but rather we suspect it is linked to the geographic location of the Y-K Delta in western Alaska where flyways from different continents overlap. This study provides support for retaining the Y-K Delta as a high priority region for the surveillance of Asian avian pathogens such as HP H5N1 AIV.

Alaska↗

USGS2024

Viral pathogen detection in U.S. game-farm mallard (Anas platyrhynchos) flags spillover risk to wild birds

The threat posed by emerging infectious diseases is a major concern for global public health, animal health and food security, and the role of birds in transmission is increasingly under scrutiny. Each year, millions of mass-reared game-farm birds are released into the wild, presenting a unique and a poorly understood risk to wild and susceptible bird populations, and to human health. In particular, the shedding of enteric pathogens through excrement into bodies of water at shared migratory stop-over sites, and breeding and wintering grounds, could facilitate multi-species long-distance pathogen dispersal and infection of high numbers of naive endemic birds annually. The Mallard ( Anas platyrhynchos ) is the most abundant of all duck species, migratory across much of its range, and an important game species for pen-rearing and release. Major recent population declines along the US Atlantic coast has been attributed to game-farm and wild mallard interbreeding and the introduction maladaptive traits into wild populations. However, pathogen transmission and zoonosis among game-farms Mallard may also impact these populations, as well as wildlife and human health. Here, we screened 16 game-farm Mallard from Wisconsin, United States, for enteric viral pathogens using metatranscriptomic data. Four families of viral pathogens were identified – Picobirnaviridae (Genogroup I), Caliciviridae (Duck Nacovirus ), Picornaviridae (Duck Aalivirus ) and Sedoreoviridae (Duck Rotavirus G). To our knowledge, this is the first report of Aalivirus in the Americas, and the first report of Calicivirus outside domestic chicken and turkey flocks in the United States. Our findings highlight the risk of viral pathogen spillover from peri-domestically reared game birds to naive wild bird populations.

Frontiers Earth Science Journal↗

USGS2012

Space-time models for a panzootic in bats, with a focus on the endangered Indiana bat

Knowledge of current trends of quickly spreading infectious wildlife diseases is vital to efficient and effective management. We developed space-time mixed-effects logistic regressions to characterize a disease, white-nose syndrome (WNS), quickly spreading among endangered Indiana bats ( Myotis sodalis ) in eastern North America. Our goal was to calculate and map the risk probability faced by uninfected colonies of hibernating Indiana bats. Model covariates included annual distance from and direction to nearest sources of infection, geolocational information, size of the Indiana bat populations within each wintering population, and total annual size of populations known or suspected to be affected by WNS. We considered temporal, spatial, and spatiotemporal formulae through the use of random effects for year, complex (a collection of interacting hibernacula), and yearxcomplex. Since first documented in 2006, WNS has spread across much of the range of the Indiana bat. No sizeable wintering population now occurs outside of the migrational distance of an infected source. Annual rates of newly affected wintering Indiana bat populations between winter 2007 to 2008 and 2010 to 2011 were 4, 6, 8, and 12%; this rate increased each year at a rate of 3%. If this increasing rate of newly affected populations continues, all wintering populations may be affected by 2016. Our models indicated the probability of a wintering population exhibiting infection was a linear function of proximity to affected Indiana bat populations and size of the at-risk population. Geographic location was also important, suggesting broad-scale influences. For every 50-km increase in distance from a WNS-affected population, risk of disease declined by 6% (95% CI=5.2-5.7%); for every increase of 1,000 Indiana bats, there was an 8% (95% CI = 1-21%) increase in disease risk. The increasing rate of infection seems to be associated with the movement of this disease into the core of the Indiana bat range. Our spatially explicit estimates of disease risk may aid managers in prioritizing surveillance and management for wintering populations of Indiana bats and help understand the risk faced by other hibernating bat species.

Journal of Wildlife Diseases↗

USGS2017

A systematic surveillance programme for infectious salmon anaemia virus supports its absence in the Pacific Northwest of the United States

In response to reported findings of infectious salmon anaemia virus (ISAV) in British Columbia (BC), Canada, in 2011, U.S. national, state and tribal fisheries managers and fish health specialists developed and implemented a collaborative ISAV surveillance plan for the Pacific Northwest region of the United States. Accordingly, over a 3-1/2-year period, 4,962 salmonids were sampled and successfully tested by real-time reverse-transcription PCR. The sample set included multiple tissues from free-ranging Pacific salmonids from coastal regions of Alaska and Washington and farmed Atlantic salmon ( Salmo salar L.) from Washington, all representing fish exposed to marine environments. The survey design targeted physiologically compromised or moribund animals more vulnerable to infection as well as species considered susceptible to ISAV. Samples were handled with a documented chain of custody and testing protocols, and criteria for interpretation of test results were defined in advance. All 4,962 completed tests were negative for ISAV RNA. Results of this surveillance effort provide sound evidence to support the absence of ISAV in represented populations of free-ranging and marine-farmed salmonids on the northwest coast of the United States.

Pacific Northwest↗

USGS2014

Genetic variation in bacterial kidney disease (BKD) susceptibility in Lake Michigan Chinook Salmon and its progenitor population from the Puget Sound

Mass mortality events in wild fish due to infectious diseases are troubling, especially given the potential for long-term, population-level consequences. Evolutionary theory predicts that populations with sufficient genetic variation will adapt in response to pathogen pressure. Chinook Salmon Oncorhynchus tshawytscha were introduced into Lake Michigan in the late 1960s from a Washington State hatchery population. In the late 1980s, collapse of the forage base and nutritional stress in Lake Michigan were thought to contribute to die-offs of Chinook Salmon due to bacterial kidney disease (BKD). Previously, we demonstrated that Lake Michigan Chinook Salmon from a Wisconsin hatchery have greater survival following BKD challenge relative to their progenitor population. Here, we evaluated whether the phenotypic divergence of these populations in BKD susceptibility was due to selection rather than genetic drift. Comparison of the overall magnitude of quantitative trait to neutral marker divergence between the populations suggested selection had occurred but a direct test of quantitative trait divergence was not significant, preventing the rejection of the null hypothesis of differentiation through genetic drift. Estimates of phenotypic variation (V P ), additive genetic variation (V A ) and narrow-sense heritability (h 2 ) were consistently higher in the Wisconsin relative to the Washington population. If selection had acted on the Wisconsin population there was no evidence of a concomitant loss of genetic variation in BKD susceptibility. The Renibacterium salmoninarum exposures were conducted at both 14°C and 9°C; the warmer temperature accelerated time to death in both populations and there was no evidence of phenotypic plasticity or a genotype-by-environment (G × E) interaction. High h 2 estimates for BKD susceptibility in the Wisconsin population, combined with a lack of phenotypic plasticity, predicts that future adaptive gains in BKD resistance are still possible and that these adaptive gains would be stable under the temperature range evaluated here.

Washington;Wisconsin↗

USGS2001

Negligible risk associated with the movement of processed rainbow trout, Oncorhynchus mykiss (Walbaum), from an infectious haematopoietic necrosis virus (IHNV) endemic area

To assess the risk of transmission of infectious haematopoietic necrosis virus (IHNV) associated with the movement of processed rainbow trout, Oncorhynchus mykiss, from an area where the virus is endemic, 240 freshly eviscerated fish (225-500 g) exhibiting spinal curvature or spinal compression types of deformities were tested for IHNV by virus isolation and polymerase chain reaction (PCR) techniques. Commercially produced rainbow trout, approximately 1-year-old, that exhibited spinal deformities were considered to have had a high likelihood of having survived an outbreak of IHN. Serological analysis of fish exhibiting spinal curvature or spinal compression types of deformities for anti-IHNV antibodies resulted, in 71 and 50% of the serum samples, respectively, with detectable neutralization activity suggesting previous infection with IHNV. A portion of the skin and muscle in the area of the deformity was collected, as well as brain tissue from each commercially processed fish. Tissue homogenates were tested for IHNV using the epithelioma papulosum cyprini (EPC) cell line pretreated with polyethylene glycol and the chinook salmon embryo (CHSE-214) cell line using standard methods. Nested, reverse transcriptase (RT)-PCR for the detection of IHNV used the central 1231 bp portion of the glycoprotein (G) challenge studies and is suggested as a mechanism responsible for virus clearance. These results provide scientific information that can be used to assess the risk associated with the movement of processed rainbow trout from an IHNV endemic area.

Journal of Fish Diseases↗

USGS2018

Applying a Bayesian weighted surveillance approach to detect chronic wasting disease in white‐tailed deer

Surveillance is critical for early detection of emerging and re‐emerging infectious diseases. Weighted surveillance leverages heterogeneity in infection risk to increase sampling efficiency. Here, we apply a Bayesian approach to estimate weights for 16 surveillance classes of white‐tailed deer in Wisconsin, USA, relative to hunter‐harvested yearling males. We used these weights to conduct a surveillance programme for detecting chronic wasting disease (CWD) in white‐tailed deer at Shenandoah National Park (SHEN) in Virginia, USA. Generally, for surveillance, risk of infection increased with age and was greater in males. Clinical suspect deer had the highest risk, with weight estimates of 33.33 and 9.09 for community‐reported and hunter‐reported suspect deer, respectively. Fawns had the lowest risk with an estimated weight of 0.001. We used surveillance weights for Wisconsin deer to determine sampling effort required to detect a CWD‐positive case in SHEN if prevalence in yearling males ≥0.025. The sampling required to detect CWD was 37–91 adult deer, depending on the adult male:female ratio in the surveillance stream. We collected rectal biopsies from 49 female and 21 male adult deer, and 10 additional samples from vehicle‐killed deer. CWD was not detected and we concluded with 95% probability that prevalence in the reference population (yearling males) was between 0.0% and 3.6%. Synthesis and applications . Our approach allows managers to estimate relative surveillance weights for different host classes and quantify limits of disease detection in real time when only a sample of animals from a population can be tested, resulting in considerable cost savings for agencies performing wildlife disease detection surveillance. Additionally, it provides a rigorous means of estimating prevalence limits when a disease/pathogen is not detected in a sample set. It is therefore applicable to other wildlife, domestic animal and human disease systems, which can be characterized by surveillance classes with heterogeneous probability of infection. This methodology is also extendable to other disciplines such as invasive species, environmental toxicology, and generally, any ecological question seeking to efficiently use scarce financial and human resources to maximize the detection probability of a rare event.

Journal of Applied Ecology↗

USGS2008

Buruli ulcer disease prevalence in Benin, West Africa: Associations with land use/cover and the identification of disease clusters

Background: Buruli ulcer (BU) disease, caused by infection with the environmental mycobacterium M. ulcerans, is an emerging infectious disease in many tropical and sub-tropical countries. Although vectors and modes of transmission remain unknown, it is hypothesized that the transmission of BU disease is associated with human activities in or around aquatic environments, and that characteristics of the landscape (e.g., land use/cover) play a role in mediating BU disease. Several studies performed at relatively small spatial scales (e.g., within a single village or region of a country) support these hypotheses; however, if BU disease is associated with land use/cover characteristics, either through spatial constraints on vector-host dynamics or by mediating human activities, then large-scale (i.e., country-wide) associations should also emerge. The objectives of this study were to (1) investigate associations between BU disease prevalence in villages in Benin, West Africa and surrounding land use/cover patterns and other map-based characteristics, and (2) identify areas with greater and lower than expected prevalence rates (i.e., disease clusters) to assist with the development of prevention and control programs. Results: Our landscape-based models identified low elevation, rural villages surrounded by forest land cover, and located in drainage basins with variable wetness patterns as being associated with higher BU disease prevalence rates. We also identified five spatial disease clusters. Three of the five clusters contained villages with greater than expected prevalence rates and two clusters contained villages with lower than expected prevalence rates. Those villages with greater than expected BU disease prevalence rates spanned a fairly narrow region of south-central Benin. Conclusion: Our analyses suggest that interactions between natural land cover and human alterations to the landscape likely play a role in the dynamics of BU disease. For example, urbanization, potentially by providing access to protected water sources, may reduce the likelihood of becoming infected with BU disease. Villages located at low elevations may have higher BU disease prevalence rates due to their close spatial proximity to high risk environments. In addition, forest land cover and drainage basins with variable wetness patterns may be important for providing suitable growth conditions for M. ulcerans, influencing the distribution and abundance of vectors, or mediating vector-human interactions. The identification of disease clusters in this study provides direction for future research aimed at better understanding these and other environmental and social determinants involved in BU disease outbreaks. ?? 2008 Wagner et al; licensee BioMed Central Ltd.

International Journal of Health Geographics↗

USGS2020

Anticipating future learning affects current control decisions: A comparison between passive and active adaptive management in an epidemiological setting

Infectious disease epidemics present a difficult task for policymakers, requiring the implementation of control strategies under significant time constraints and uncertainty. Mathematical models can be used to predict the outcome of control interventions, providing useful information to policymakers in the event of such an epidemic. However, these models suffer in the early stages of an outbreak from a lack of accurate, relevant information regarding the dynamics and spread of the disease and the efficacy of control. As such, recommendations provided by these models are often incorporated in an ad hoc fashion, as and when more reliable information becomes available. In this work, we show that such trial-and-error-type approaches to management, which do not formally take into account the resolution of uncertainty and how control actions affect this, can lead to sub-optimal management outcomes. We compare three approaches to managing a theoretical epidemic: a non-adaptive management (AM) approach that does not use real-time outbreak information to adapt control, a passive AM approach that incorporates real-time information if and when it becomes available, and an active AM approach that explicitly incorporates the future resolution of uncertainty through gathering real-time information into its initial recommendations. The structured framework of active AM encourages the specification of quantifiable objectives, models of system behaviour and possible control and monitoring actions, followed by an iterative learning and control phase that is able to employ complex control optimisations and resolve system uncertainty. The result is a management framework that is able to provide dynamic, long-term projections to help policymakers meet the objectives of management. We investigate in detail the effect of different methods of incorporating up-to-date outbreak information. We find that, even in a highly simplified system, the method of incorporating new data can lead to different results that may influence initial policy decisions, with an active AM approach to management providing better information that can lead to more desirable outcomes from an epidemic.

Journal of Theoretical Biology↗

USGS2017

Pneumonia in bighorn sheep: Risk and resilience

Infectious disease was an important driver of historic declines and extirpations of bighorn sheep (Ovis canadensis) in North America and continues to impede population restoration and management. Domestic sheep have long been linked to pneumonia outbreaks in bighorn sheep and this association has now been confirmed in 13 captive commingling experiments. However, ecological and etiological complexities still hinder our understanding and control of the disease. We provide an overview of the current state of knowledge about the biology and management of respiratory disease in bighorn sheep and propose strategies for moving forward. Epizootic pneumonia in bighorn sheep is polymicrobial. Mycoplasma ovipneumoniae, a bacterium host-specific to Caprinae and commonly carried by healthy domestic sheep and goats appears to be a necessary primary agent. All-age epizootics following introduction of M. ovipneumoniae along with other pathogens into bighorn sheep populations are usually severe (median mortality 47%) but fatality rates vary widely, from 15 – 100%. Disease severity may be influenced by the strain of M. ovipneumoniae, by secondary bacterial and viral pathogens, and by factors affecting transmission and host immunity. Once introduced, M. ovipneumoniae can persist in bighorn sheep populations for decades. Carrier dams transmit the pathogen to their susceptible lambs, triggering fatal pneumonia outbreaks in nursery groups, which limits recruitment and slows or prevents population recovery. The result is that demographic costs of pathogen persistence often outweigh the impacts of the initial invasion and die-off. There is currently no effective vaccine or antibiotic for domestic or wild sheep and to date, no management actions have been successful in reducing morbidity, mortality, or disease spread once pathogen invasion has occurred. Molecular-based strain typing suggests that spillover of M. ovipneumoniae into bighorn sheep populations from domestic small ruminants is ongoing, and that consequences of pathogen invasion are amplified by movements of infected bighorn sheep. Therefore, current disease management strategies focus on reducing risk of spillover from reservoir populations of domestic small ruminants and on limiting transmission among bighorn sheep. A broad array of approaches has been tried and more are needed to prevent pathogen introduction, induce disease fadeout in persistently infected populations, and promote population resilience across the diverse landscapes bighorn sheep inhabit. A comprehensive examination of disease dynamics across populations could help elucidate how disease fades out naturally and if population resilience can be increased in the face of infection. Cross-jurisdictional adaptive management experiments and transdisciplinary collaboration, including partnerships with members of the domestic sheep and goat community, are needed to facilitate innovation and speed progress towards sustainable solutions for managing pneumonia to protect and restore bighorn sheep populations.

California, Idaho, Nevada, Oregon, Utah, Washingto↗

USGS2011

Restricted growth of U-type infectious haematopoietic necrosis virus (IHNV) in rainbow trout cells may be linked to casein kinase II activity

Previously, we demonstrated that a representative M genogroup type strain of infectious haematopoietic necrosis virus (IHNV) from rainbow trout grows well in rainbow trout‐derived RTG‐2 cells, but a U genogroup type strain from sockeye salmon has restricted growth, associated with reduced genome replication and mRNA transcription. Here, we analysed further the mechanisms for this growth restriction of U‐type IHNV in RTG‐2 cells, using strategies that assessed differences in viral genes, host immune regulation and phosphorylation. To determine whether the viral glycoprotein (G) or non‐virion (NV) protein was responsible for the growth restriction, four recombinant IHNV viruses were generated in which the G gene of an infectious IHNV clone was replaced by the G gene of U‐ or M‐type IHNV and the NV gene was replaced by NV of U‐ or M‐type IHNV. There was no significant difference in the growth of these recombinants in RTG‐2 cells, indicating that G and NV proteins are not major factors responsible for the differential growth of the U‐ and M‐type strains. Poly I:C pretreatment of RTG‐2 cells suppressed the growth of both U‐ and M‐type IHNV, although the M virus continued to replicate at a reduced level. Both viruses induced type 1 interferon (IFN1) and the IFN1 stimulated gene Mx1, but the expression levels in M‐infected cells were significantly higher than in U‐infected cells and an inhibitor of the IFN1‐inducible protein kinase PKR, 2‐aminopurine (2‐AP), did not affect the growth of U‐ or M‐type IHNV in RTG‐2 cells. These data did not indicate a role for the IFN1 system in the restricted growth of U‐type IHNV in RTG‐2 cells. Prediction of kinase‐specific phosphorylation sites in the viral phosphoprotein (P) using the NetPhosK program revealed differences between U‐ and M‐type P genes at five phosphorylation sites. Pretreatment of RTG‐2 cells with a PKC inhibitor or a p38MAPK inhibitor did not affect the growth of the U‐ and M‐type viruses. However, 100 μ m of the casein kinase II (CKII) inhibitor, 5,6‐dichloro‐1‐β‐ d ‐ribofuranosylbenzimidazole (DRB), reduced the titre of the U type 8.3‐fold at 24 h post‐infection. In contrast, 100 μ m of the CKII inhibitor reduced the titre of the M type only 1.3‐fold at 48 h post‐infection. Our data suggest that the different growth of U‐ and M‐type IHNV in RTG‐2 cells may be linked to a differential requirement for cellular protein kinases such as CKII for their growth.

Journal of Fish Diseases↗

USGS2009

Infectious haematopoietic necrosis virus genogroup-specific virulence mechanisms in sockeye salmon, Oncorhynchus nerka (Walbaum), from Redfish Lake, Idaho

Characterization of infectious haematopoietic necrosis virus (IHNV) field isolates from North America has established three main genogroups (U, M and L) that differ in host-specific virulence. In sockeye salmon, Oncorhynchus nerka, the U genogroup is highly virulent, whereas the M genogroup is nearly non-pathogenic. In this study, we sought to characterize the virus-host dynamics that contribute to genogroup-specific virulence in a captive stock of sockeye salmon from Redfish Lake in Idaho. Juvenile sockeye salmon were challenged by immersion and injection with either a representative U or M viral strain and sampled periodically until 14 days post-infection (p.i.). Fish challenged with each strain had positive viral titre by day 3, regardless of challenge route, but the fish exposed to the M genogroup virus had significantly lower virus titres than fish exposed to the U genogroup virus. Gene expression analysis by quantitative reverse transcriptase PCR was used to simultaneously assess viral load and host interferon (IFN) response in the anterior kidney. Viral load was significantly higher in the U-challenged fish relative to M-challenged fish. Both viruses induced expression of the IFN-stimulated genes (ISGs), but expression was usually significantly lower in the M-challenged group, particularly at later time points (7 and 14 days p.i.). However, ISG expression was comparable with 3 days post-immersion challenge despite a significant difference in viral load. Our data indicated that the M genogroup virus entered the host, replicated and spread in the sockeye salmon tissues, but to a lesser extent than the U genogroup. Both virus types induced a host IFN response, but the high virulence strain (U) continued to replicate in the presence of this response, whereas the low virulence strain (M) was cleared below detectable levels. We hypothesize that high virulence is associated with early in vivo replication allowing the virus to achieve a threshold level, which the host innate immune system cannot control. ?? 2009 Blackwell Publishing Ltd.

Journal of Fish Diseases↗