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Gael Kurath

Publications and source records attributed to Gael Kurath.

At least 19 recordsLinked to original sources

Region-specific understanding of virus transmission to support salmonid health at hatcheries in three regions of the Pacific Northwest, North America

Juvenile salmonid mortality due to infectious haematopoietic necrosis virus (IHNV) can be a major burden on fish hatcheries. We consider possible IHNV transmission routes and specialist–generalist patterns across three regions in the Pacific Northwest of North America: Coastal Washington and Oregon (CWO), Lower Columbia River Basin (LCRB) and Snake River Basin (SRB) to obtain multi-region inference about IHNV transmission and specialization. While individual regions have been studied previously, our consideration of three regions to identify consistent trends or localized patterns is novel. The most consistent patterns we found were that most exposure to IHNV was from migrating adult salmonids and that the IHNV lineage MD specialized in steelhead and rainbow trout. Our results were consistent with LCRB being a source of IHNV and the SRB and CWO being sinks. Results specific to particular regions include the role of local geography on exposure and influence of hatchery complexes on transmission, which highlights the need to understand local hatchery operations before disease ecology can be understood and suitable hatchery management can be planned. Results demonstrate the need for spatially and temporally explicit quantitative approaches to understand disease dynamics and inform management.

Oregon, Washington

Virulence evolution of a salmonid virus following a host jump

Emergent viral diseases remain a critical obstacle to welfare across landscapes and species, encompassing humans, wildlife, and agriculture. Following a jump to a novel host, the severity of disease resulting from infection is a critical determinant of the overall emergent pathogen threat. Conventional wisdom posits that virulence, defined here as host mortality, attenuates to intermediate levels as a pathogen adapts to a novel host, but this is largely based on data from just one system, myxoma virus, which was intentionally introduced as a biocontrol agent in rabbits ( Oryctolagus cuniculus ) in mid-1900s Australia. In this study, we demonstrate that infectious hematopoietic necrosis virus (IHNV), which made a host jump from sockeye salmon ( Oncorhynchus nerka , ancestral host) to rainbow trout ( O. mykiss , novel host), has not conformed to classical theory. We quantified virulence in the ancestral and novel hosts using common garden in vivo experiments with 16 archival IHNV isolates collected from 1972-2017, which span the period from shortly after the host jump and the subsequent 45 years of host adaptation. These virus isolates also represent two distinct phylogenetic genogroups, each associated with either the ancestral or novel host. The experiments were replicated across two research facilities, two challenges dosages, and two temperatures. While isolates from the ancestral genogroup showed no temporal change in virulence in either host, isolates from the novel viral genogroup displayed a significant increase in virulence over time in the novel host. Some possible indication of a virus temperature adaption after the host jump was also present. Potential drivers of virulence evolution are discussed. This represents one of only a handful of systems in which the evolution of increased virulence has been empirically characterized after a host jump and subsequent adaptation. It contributes to a growing body of evidence that contradicts the classical case study of myxoma virus attenuation after adaptation.

PLoS Pathogens

Evaluation of 6PPD-quinone lethal toxicity and sublethal effects on disease resistance and swimming fitness in coastal cutthroat trout (Oncorhynchus clarkii clarkii)

6PPD-quinone (6PPDQ), derived from the tire-protectant 6PPD reacting with ozone, is an emerging contaminant of concern owing to its role in coho salmon ( Oncorhynchus kisutch ) deaths via urban runoff mortality syndrome (URMS). Given the impact of 6PPDQ on aquatic life in urban streams, we addressed the acute toxicity of 6PPDQ exposure on coastal cutthroat trout (CCT) ( Oncorhynchus clarkii clarkii ), a species sympatric with coho salmon in natal watersheds. Using static exposures coupled with analytical chemistry, we determined the 24-h LC 50 values for alevin (297.2 ng/L), swim-up fry (39.6 ng/L), 5-month parr (103.3 ng/L), and 13-month juveniles (185.9 ng/L)─values similar to toxicity observed in coho salmon. Additionally, the 96-h LC 50 (77.6 ng/L) was 2.4 times more lethal for juvenile CCT. We assessed potential effects of sublethal 6PPDQ exposure on disease resistance to infectious hematopoietic necrosis (IHN), an endemic viral disease of Pacific salmon, and to swimming performance. Sublethal 6PPDQ (53.6 ng/L) did not affect survival of parr exposed to IHN virus compared to virus alone. Conversely, 6PPDQ exposure as low as 72.2 ng/L significantly reduced 15- and 24-month juvenile swimming performance, and 120.5 ng/L 6PPDQ increased blood hematocrit. Overall, CCT are the second most sensitive species tested to date for 6PPDQ sensitivity which further emphasizes the need for identifying alternatives to 6PPD.

Environmental Science and Technology

Heterologous exchanges of glycoprotein and non-virion protein in novirhabdoviruses: Assessment of virlence in yellow perch (Perca flavescens) and rainbow trout (Oncorhynchus mykiss)

Infectious hematopoietic necrosis virus (IHNV) and viral hemorrhagic septicemia virus (VHSV) are rhabdoviruses in two different species belonging to the Novirhabdovirus genus. IHNV has a narrow host range restricted to trout and salmon species, and viruses in the M genogroup of IHNV have high virulence in rainbow trout ( Oncorhynchus mykiss ). In contrast, the VHSV genotype IVb that invaded the Great Lakes in the United States has a broad host range, with high virulence in yellow perch ( Perca flavescens ), but not in rainbow trout. By using reverse-genetic systems of IHNV-M and VHSV-IVb strains, we generated six IHNV:VHSV chimeric viruses in which the glycoprotein (G), non-virion-protein (NV), or both G and NV genes of IHNV-M were replaced with the analogous genes from VHSV-IVb, and vice versa. These chimeric viruses were used to challenge groups of rainbow trout and yellow perch. The parental recombinants rIHNV-M and rVHSV-IVb were highly virulent in rainbow trout and yellow perch, respectively. Parental rIHNV-M was avirulent in yellow perch, and chimeric rIHNV carrying G, NV, or G and NV genes from VHSV-IVb remained low in virulence in yellow perch. Similarly, the parental rVHSV-IVb exhibited low virulence in rainbow trout, and chimeric rVHSV with substituted G, NV, or G and NV genes from IHNV-M remained avirulent in rainbow trout. Thus, the G and NV genes of either virus were not sufficient to confer high host-specific virulence when exchanged into a heterologous species genome. Some exchanges of G and/or NV genes caused a loss of host-specific virulence, providing insights into possible roles in viral virulence or fitness, and interactions between viral proteins.

Viruses

Local and systemic replicative fitness for viruses in specialist, generalist, and non-specialist interactions with salmonid hosts

Host tissues represent diverse resources or barriers for pathogen replicative fitness. We tested whether viruses in specialist, generalist, and non-specialist interactions replicate differently in local entry tissue (fin), and systemic target tissue (kidney) using infectious hematopoietic necrosis virus (IHNV) and three salmonid fish hosts. Virus tissue replication was host specific, but one feature was shared by specialists and the generalist which was uncommon in the non-specialist interactions: high host entry and replication capacity in the local tissue after contact. Moreover, specialists showed increased replication in systemic target tissues early after host contact. By comparing ancestral and derived IHNV viruses, we also characterized replication tradeoffs associated with specialist and generalist evolution. Compared with the ancestral virus, a derived specialist gained early local replicative fitness in the new host but lost replicative fitness in the ancestral host. By contrast, a derived generalist showed small replication losses relative to the ancestral virus in the ancestral host but increased early replication in the local tissue of novel hosts. This study shows that the mechanisms of specialism and generalism are host specific and that local and systemic replication can contribute differently to overall within host replicative fitness for specialist and generalist viruses.

Journal of General Virology

Characterization of maternal immunity following vaccination of broodstock against IHNV or Flavobacterium psychrophilum in rainbow trout (Oncorhynchus mykiss)

Infectious hematopoietic necrosis (IHN) is a significant viral disease affecting salmonids, whereas Flavobacterium psychrophilum (Fp), the causative agent of bacterial coldwater disease (BCWD), remains one of the most significant bacterial pathogens of salmonids. We explored maternal immunity in the context of IHN and BCWD management in rainbow trout ( Oncorhynchus mykiss ) aquaculture. Two experimental trials were conducted where different groups of female broodstock were immunized prior to spawning with an IHNV DNA vaccine or a live attenuated F. psychrophilum (Fp B.17-ILM) vaccine alone, or in combination. Progeny were challenged with either a low or high dose of IHNV at 13 days post hatch (dph) and 32 dph or challenged with F. psychrophilum at 13 dph. Mortality following a low-dose IHNV challenge at 13 dph was significantly lower in progeny from vaccinated broodstock vs. unvaccinated broodstock, but no significant differences were observed at 32 dph. Mortality due to BCWD was also significantly reduced in 13 dph fry that originated from broodstock immunized with the Fp B.17-ILM vaccine. After vaccination broodstock developed specific or neutralizing antibodies respectively to F. psychrophilum and IHNV; however, antibody titers in eggs and fry were undetectable. In the eggs and fry mRNA transcripts of the complement components C3 and C5 were detected at much higher levels in progeny from vaccinated broodstock and showed a significantly increased and rapid response post-challenge compared with unvaccinated broodstock. After challenges pro-inflammatory cytokine expression was immediately and considerably elevated in the fry from vaccinated broodstock vs. unvaccinated broodstock, whereas adaptive immune genes were elevated to a lesser degree. Results suggest that maternal transfer of innate and adaptive factors at the transcript level occurred because development of lymphomyeloid organs is not complete in such young fry. In addition to documenting maternally derived immunity in teleosts, this study demonstrates that broodstock vaccination can confer some degree of protection to progeny against viral and bacterial pathogens.

Fish and Shellfish Immunology

Coproduction and modeling spatial contact networks prevent bias about infectious hematopoietic necrosis virus transmission for Snake River Basin salmonids

Much remains unknown about variation in pathogen transmission across the geographic range of a free-ranging fish or animal species and about the influence of movement (associated with husbandry practices or animal behavior) on pathogen transmission. Salmonid hatcheries are an ideal system in which to study these processes. Salmonid hatcheries are managed for endangered species recovery, supplementation of threatened or at-risk fish stocks, support of fisheries, and ecosystem stability. Infectious hematopoietic necrosis virus (IHNV) is a rhabdovirus of significant concern to salmon aquaculture. Landscape IHNV transmission dynamics previously had been estimated only for salmonid hatcheries in the Lower Columbia River Basin (LCRB). The objectives of this study were to estimate IHNV transmission dynamics in a unique geographic region, the Snake River Basin (SRB), and to quantitatively estimate the effect of model coproduction on inference because previous assessments of coproduction have been qualitative. In contrast to the LCRB, the SRB has hatchery complexes consisting of a main hatchery and ≥1 satellite facility. Knowledge about hatchery complexes was held by a subset of project researchers but would not have been available to project modelers without coproduction. Project modelers generated and tested multiple versions of Bayesian susceptible-exposedinfected models to realistically represent the SRB and estimate the effect of coproduction. Models estimated the frequency of transmission routes, route-specific infection probabilities, and infection probabilities for combinations of salmonid hosts and IHNV lineages. Model results indicated that in the SRB, avoiding exposure to IHNV-positive adult salmonids is the most important action to prevent juvenile infections. Migrating adult salmonids exposed juvenile cohort-sites most frequently, and the infection probability was greatest following exposure to migrating adults. Without coproduction, the frequency of exposure by migrating adults would have been overestimated by 70 cohort-sites, and the infection probability following exposure to migrating adults would have been underestimated by∼0.09. The coproduced model had less uncertainty in the infection probability if no transmission route could be identified (Bayesian credible interval (BCI) width = 0.12) compared to the model without coproduction (BCI width = 0.34). Evidence for virus lineage MD specialization on steelhead and rainbow trout (both Oncorhynchus mykiss) was apparent without model coproduction. In the SRB, we found a greater probability of virus lineage UC infection in Chinook salmon (Oncorhynchus tshawytscha) compared to in O. mykiss, whereas in the LCRB, UC more clearly exhibited a generalist approach. Coproduction influenced estimates that depended on transmission routes, which operated differently at main hatcheries and satellite sites within hatchery complexes. Hatchery complexes are found outside of the SRB and are not specific to salmonid hatcheries alone. There is great potential for coproduction and modeling spatial contact networks to advance understanding about infectious disease transmission in complex production systems and surrounding free-ranging animal populations.

Idaho, Oregon, Washington

Variation in within-host replication kinetics among virus genotypes provides evidence of specialist and generalist infection strategies across three salmonid host species

Theory of the evolution of pathogen specialization suggests that a specialist pathogen gains high fitness in one host, but this comes with fitness loss in other hosts. By contrast, a generalist pathogen does not achieve high fitness in any host, but gains ecological fitness by exploiting different hosts, and has higher fitness than specialists in nonspecialized hosts. As a result, specialist pathogens are predicted to have greater variation in fitness across hosts, and generalists would have lower fitness variation across hosts. We test these hypotheses by measuring pathogen replicative fitness as within-host viral loads from the onset of infection to the beginning of virus clearance, using the rhabdovirus infectious hematopoietic necrosis virus (IHNV) in salmonid fish. Based on field prevalence and virulence studies, the IHNV subgroups UP, MD, and L are specialists, causing infection and mortality in sockeye salmon, steelhead, and Chinook salmon juveniles, respectively. The UC subgroup evolved naturally from a UP ancestor and is a generalist infecting all three host species but without causing severe disease. We show that the specialist subgroups had the highest peak and mean viral loads in the hosts in which they are specialized, and they had low viral loads in nonspecialized hosts, resulting in large variation in viral load across hosts. Viral kinetics show that the mechanisms of specialization involve the ability to both maximize early virus replication and avoid clearance at later times, with different mechanisms of specialization evident in different host–virus combinations. Additional nuances in the data included different fitness levels for nonspecialist interactions, reflecting different trade-offs for specialist viruses in other hosts. The generalist UC subgroup reached intermediate viral loads in all hosts and showed the smallest variation in fitness across hosts. The evolution of the UC generalist from an ancestral UP sockeye specialist was associated with fitness increases in steelhead and Chinook salmon, but only slight decreases in fitness in sockeye salmon, consistent with low- or no-cost generalism. Our results support major elements of the specialist–generalist theory, providing evidence of a specialist–generalist continuum in a vertebrate pathogen. These results also quantify within-host replicative fitness trade-offs resulting from the natural evolution of specialist and generalist virus lineages in multi-host ecosystems

Virus Evolution

Genetics reveal long-distance virus transmission links in Pacific salmon

In the coastal region of Washington State, a major pathogen emergence event occurred between 2007 and 2011 in which steelhead trout ( Oncorhynchus mykiss ) experienced a high incidence of infection and disease outbreaks due to the rhabdovirus infectious hematopoietic necrosis virus (IHNV). Genetic typing showed that the introduced viruses were in the steelhead-specific MD subgroup of IHNV and indicated the most likely source was a virus from the nearby Columbia River Basin. In the current study, full-length viral glycoprotein (G) gene sequences were determined for 55 IHNV isolates from both coastal and Columbia fish populations to identify specific source populations and infer mechanisms of transmission to coastal steelhead. We identified three transmission links based on exact fullG genotype matches between Columbia and coastal fish. In all cases, the likely source population was infected juvenile fish, and sink populations were adult fish returning to coastal rivers to spawn. The time intervals between detection in source and sink populations varied from 6 months to nearly 4 years, suggesting different transmission pathways. Surprisingly, distances between source and sink populations varied between 140 and 1000 km. These results confirm repeated introductions of virus from Columbia River Basin fish as the cause of emergence of MD virus on the Washington coast from 2007 to 2011. View Full-Text

Washington

Shedding kinetics of Infectious Hematopoietic Necrosis Virus (IHNV) in juvenile spring- and fall-run Chinook salmon of the Columbia River Basin

This investigation sought to characterize the shedding of infectious hematopoietic necrosis virus (IHNV) in two populations of Columbia River Basin (CRB) Chinook salmon ( Oncorhynchus tshawytscha ). Juvenile spring- and fall-run Chinook salmon were exposed by immersion to each of three IHN virus strains from the UC, MD, and L subgroups, and then monitored for viral shedding from individual fish for 30 days. Detectable quantities of UC, MD and L IHN virus were shed by a subset of fish from each host population (1–9 out of 10 fish total in each treatment group). Viral shedding kinetics were consistent, with a rapid onset of shedding, peak shedding by 2–3 days, and then a rapid decline to below detectable levels by 7 days’ post-exposure to IHNV. Intraspecies variation was observed as spring Chinook salmon shed more UC virus than fall fish: spring Chinook salmon shed UC virus in greater numbers of fish, with 22-fold higher mean peak shedding magnitude, 33-fold higher mean total virus shed per fish, and 900-fold higher total virus shed per treatment group. The L and MD viruses had comparable shedding at intermediate levels in each host population. All viral shedding occurred well before host mortality began, and shedding magnitude did not correlate with virulence differences. Overall, the greater shedding of UC virus from spring Chinook salmon, combined with low virulence, indicates a uniquely high transmission potential that may explain the predominance of UC viruses in CRB Chinook salmon. This also suggests that spring-run fish may contribute more to the ecology of IHNV in the CRB than fall-run Chinook salmon.

Oregon, Washington

Comparative susceptibilities of selected California Chinook salmon and steelhead populations to isolates of L Genogroup Infectious Hematopoietic Necrosis Virus (IHNV)

Salmonid species demonstrate varied susceptibility to the viral pathogen infectious hematopoietic necrosis virus (IHNV). In California conservation hatcheries, juvenile Chinook salmon ( Oncorhynchus tshawytscha) have experienced disease outbreaks due to L genogroup IHNV since the 1940s, while indigenous steelhead (anadromous O. mykiss) appear relatively resistant. To characterize factors contributing to the losses of California salmonid fish due to IHNV, three populations of Chinook salmon and two populations of steelhead native to California watersheds were compared in controlled waterborne challenges with California L genogroup IHNV isolates at viral doses of 10 4 –10 6 pfu mL −1 . Chinook salmon fry were moderately to highly susceptible (CPM = 47–87%) when exposed to subgroup LI and LII IHNV. Susceptibility to mortality decreased with increasing age and also with a higher temperature. Mortality for steelhead fry exposed to two IHNV isolates was low (CPM = 1.3–33%). There was little intraspecies variation in susceptibility among populations of Chinook salmon and no differences in virulence between viruses strains. Viral persistence was demonstrated by the isolation of low levels of infectious IHNV from the skin of two juvenile Chinook salmon at 215 d post exposure. The persistence of the virus among Chinook salmon used for stocking into Lake Oroville may be an explanation for the severe epidemics of IHN at the Feather River hatchery in 1998–2002.

California

Revised taxonomy of rhabdoviruses infecting fish and marine mammals

Rhabdoviridae is a large family of negative-sense (-) RNA viruses that includes important pathogens of ray-finned fish and marine mammals. As for all viruses, the taxonomic assignment of rhabdoviruses occurs through a process implemented by the International Committee on Taxonomy of Viruses (ICTV). A recent revision of taxonomy conducted in conjunction with the ICTV Rhabdoviridae Study Group has resulted in the establishment of three new subfamilies ( Alpharhabdovirinae , Betarhabdovirinae , and Gammarhabdovirinae ) within the Rhabdoviridae , as well as three new genera ( Cetarhavirus , Siniperhavirus , and Scophrhavirus ) and seven new species for viruses infecting fish or marine mammals. All rhabdovirus species have also now been named or renamed to comply with the binomial format adopted by the ICTV in 2021, comprising the genus name followed by a species epithet. Phylogenetic analyses of L protein (RNA-dependent RNA polymerase) sequences of (-) RNA viruses indicate that members of the genus Novirhabdovirus (subfamily Gammarhabdovirinae ) do not cluster within the Rhabdoviridae , suggesting the need for a review of their current classification.

Animals

Temperature variation and host immunity regulate viral persistence in a salmonid host

Environmental variation has important effects on host–pathogen interactions, affecting large-scale ecological processes such as the severity and frequency of epidemics. However, less is known about how the environment interacts with host immunity to modulate virus fitness within hosts. Here, we studied the interaction between host immune responses and water temperature on the long-term persistence of a model vertebrate virus, infectious hematopoietic necrosis virus (IHNV) in steelhead trout ( Oncorhynchus mykiss ). We first used cell culture methods to factor out strong host immune responses, allowing us to test the effect of temperature on viral replication. We found that 15 ∘ "> ∘ C water temperature accelerated IHNV replication compared to the colder 10 and 8 ∘ "> ∘ C temperatures. We then conducted in vivo experiments to quantify the effect of 6, 10, and 15 ∘ "> ∘ C water temperatures on IHNV persistence over 8 months. Fish held at 15 and 10 ∘ "> ∘ C were found to have higher prevalence of neutralizing antibodies compared to fish held at 6 ∘ "> ∘ C. We found that IHNV persisted for a shorter time at warmer temperatures and resulted in an overall lower fish mortality compared to colder temperatures. These results support the hypothesis that temperature and host immune responses interact to modulate virus persistence within hosts. When immune responses were minimized (i.e., in vitro) virus replication was higher at warmer temperatures. However, with a full potential for host immune responses (i.e., in vivo experiments) longer virus persistence and higher long-term virulence was favored in colder temperatures. We also found that the viral RNA that persisted at later time points (179 and 270 days post-exposure) was mostly localized in the kidney and spleen tissues. These tissues are composed of hematopoietic cells that are favored targets of the virus. By partitioning the effect of temperature on host and pathogen responses, our results help to better understand environmental drivers of host–pathogen interactions within hosts, providing insights into potential host–pathogen responses to climate change.

Pathogens

Virus shedding kinetics and unconventional virulence tradeoffs

Tradeoff theory, which postulates that virulence provides both transmission costs and benefits for pathogens, has become widely adopted by the scientific community. Although theoretical literature exploring virulence-tradeoffs is vast, empirical studies validating various assumptions still remain sparse. In particular, truncation of transmission duration as a cost of virulence has been difficult to quantify with robust controlled in vivo studies. We sought to fill this knowledge gap by investigating how transmission rate and duration were associated with virulence for infectious hematopoietic necrosis virus (IHNV) in rainbow trout ( Oncorhynchus mykiss ). Using host mortality to quantify virulence and viral shedding to quantify transmission, we found that IHNV did not conform to classical tradeoff theory. More virulent genotypes of the virus were found to have longer transmission durations due to lower recovery rates of infected hosts, but the relationship was not saturating as assumed by tradeoff theory. Furthermore, the impact of host mortality on limiting transmission duration was minimal and greatly outweighed by recovery. Transmission rate differences between high and low virulence genotypes were also small and inconsistent. Ultimately, more virulent genotypes were found to have the overall fitness advantage, and there was no apparent constraint on the evolution of increased virulence for IHNV. However, using a mathematical model parameterized with experimental data, it was found that host culling resurrected the virulence tradeoff and provided low virulence genotypes with the advantage. Human-induced or natural culling, as well as host population fragmentation, may be some of the mechanisms by which virulence diversity is maintained in nature. This work highlights the importance of considering non-classical virulence tradeoffs.

PLoS Pathogens

Virulence and infectivity of UC, MD and L strains of infectious hematopoietic necrosis virus (IHNV) in four populations of Columbia River Basin Chinook salmon

Infectious Hematopoietic Necrosis Virus (IHNV) infects juvenile salmonid fish in conservation hatcheries and aquaculture facilities, and in some cases, causes lethal disease. This study assesses intra-specific variation in the IHNV susceptibility of Chinook salmon ( Oncorhynchus tshawytscha ) in the Columbia River Basin (CRB), in the northwestern United States. The virulence and infectivity of IHNV strains from three divergent virus genogroups are measured in four Chinook salmon populations, including spring-run and fall-run fish from the lower or upper regions of the CRB. Following controlled laboratory exposures, our results show that the positive control L strain had significantly higher virulence, and the UC and MD strains that predominate in the CRB had equivalently low virulence, consistent with field observations. By several experimental measures, there was little variation in host susceptibility to infection or disease. However, a small number of exceptions suggested that the lower CRB spring-run Chinook salmon population may be less susceptible than other populations tested. The UC and MD viruses did not differ in infectivity, indicating that the observed asymmetric field prevalence in which IHNV detected in CRB Chinook salmon is 83% UC and 17% MD is not due to the UC virus being more infectious. Overall, we report little intra-species variation in CRB Chinook salmon susceptibility to UC or MD IHNV infection or disease, and suggest that other factors may instead influence the ecology of IHNV in the CRB.

Columbia River Basin

Effects of stocking density on stress response and susceptibility to infectious hematopoietic necrosis virus in rainbow trout

The goals of this study were to examine the effect of stocking density on the stress response and disease susceptibility in juvenile rainbow trout ( Oncorhynchus mykiss ). Fish were sorted into one of 2 stocking densities (high density "HD", 20-40 kg/m 3 ) or (low density, "LD", 4-8 kg/m 3 ) and 3 stress indices (cortisol levels in serum and water, and neutrophil: lymphocyte (N:L) ratios from blood smears) were measured at multiple time points over 21 d. Serum cortisol was significantly increased at 1 h in LD samples and at 14 d in HD samples. Water cortisol concentrations were significantly higher in LD tanks as compared with HD tanks on day 14. N:L ratios were significantly higher in HD tanks on day 14 as compared with LD tanks and with baseline. The effect of stocking density on mortality after exposure to infectious hematopoietic necrosis virus (IHNV) was compared between fish held in HD or LD conditions, with or without prior acclimation to the different density conditions. No significant differences in survival were found between HD and LD treatments or between acclimated and nonacclimated treatments. Cumulative results indicate that 1) 1 to 4 gram rainbow trout did not generally demonstrate significant differences in stress indices at the density conditions tested over a 21-d period, 2) independent differences were found in 3 stress indices at day 14 after sorting into LD and HD holding conditions; and 3) LD and HD stocking densities did not have a significant effect on mortality due to IHNV.

Journal of the American Association for Laboratory

Fish Rhabdoviruses (Rhabdoviridae)

The family Rhabdoviridae currently has 18 genera accepted by the International Committee for Virus Taxonomy (ICTV), and three of those genera contain fish rhabdoviruses. In the genera Novirhabdovirus, Sprivivirus, and Perhabdovirus all viruses infect fish hosts, and there are no fish viruses in any of the other 15 rhabdovirus genera. In the overall phylogeny of the Rhabdoviridae the three fish virus genera are well separated from each other, and the novirhabdovirus genus occupies a position basal to all other genera.

Book chapter

Infectious hematopoietic necrosis virus specialization in a multihost salmonid system

Many pathogens interact and evolve in communities where more than one host species is present, yet our understanding of host–pathogen specialization is mostly informed by laboratory studies with single species. Managing diseases in the wild, however, requires understanding how host–pathogen specialization affects hosts in diverse communities. Juvenile salmonid mortality in hatcheries caused by infectious hematopoietic necrosis virus (IHNV) has important implications for salmonid conservation programs. Here, we evaluate evidence for IHNV specialization on three salmonid hosts and assess how this influences intra‐ and interspecific transmission in hatchery‐reared salmonids. We expect that while more generalist viral lineages should pose an equal risk of infection across host types, viral specialization will increase intraspecific transmission. We used Bayesian models and data from 24 hatcheries in the Columbia River Basin to reconstruct the exposure history of hatcheries with two IHNV lineages, MD and UC, allowing us to estimate the probability of juvenile infection with these lineages in three salmonid host types. Our results show that lineage MD is specialized on steelhead trout and perhaps rainbow trout (both Oncorhynchus mykiss ), whereas lineage UC displayed a generalist phenotype across steelhead trout, rainbow trout, and Chinook salmon. Furthermore, our results suggest the presence of specialist–generalist trade‐offs because, while lineage UC had moderate probabilities of infection across host types, lineage MD had a small probability of infection in its nonadapted host type, Chinook salmon. Thus, in addition to quantifying probabilities of infection of socially and economically important salmonid hosts with different IHNV lineages, our results provide insights into the trade‐offs that viral lineages incur in multihost communities. Our results suggest that knowledge of the specialist/generalist strategies of circulating viral lineages could be useful in salmonid conservation programs to control disease.

Oregon, Washington