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Results for “Infection and Immunity”

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At least 91 records · Page 5Linked to original sources
USGS2008

Transcriptional profiling of MHC class I genes in rainbow trout infected with infectious hematopoietic necrosis virus

Major histocompatibility complex (MHC) molecules are important mediators of cell-mediated immunity in vertebrates. MHC class IA molecules are important for host anti-viral immunity as they present intracellular antigens and regulate natural killer cell (NK) activity. MHC class Ib molecules on the other hand are less understood and have demonstrated diverse immune and non-immune functions in mammals. Rainbow trout possess a single classical MHC IA locus ( Onmy -UBA) that is believed to function similar to that of mammalian MHC class Ia. Numerous MHC class Ib genes with undetermined functions have also been described in trout. Here we utilize quantitative reverse transcriptase PCR (qRT-PCR) techniques to survey the levels of basal and inducible transcription for selected trout MHC class Ib genes, sIgM and sentinels of IFN induction in response to viral infection. Basal transcription of all the class Ib genes examined in this study was lower than Onmy -UBA in naïve fish. UBA, along with all of the non-classical genes were induced in fish infected with virus but not in control fish. Our results support a non-classical designation for the majority of the class IB genes surveyed in this study based upon expression levels while also indicating that they may play an important role in anti-viral immunity in trout.

Molecular Immunology↗
USGS2001

The effects of electroshock on immune function and disease progression in juvenile spring chinook salmon

Although much is known about the effects of electroshock on fish physiology, consequences to the immune system and disease progression have not received attention. Our objectives were to determine the effects of electroshock on selected immune function in juvenile spring chinook salmon Oncorhynchus tshawytscha, the mechanism of any observed alteration, and the effects of electroshock on disease progression. We found that the ability of anterior kidney leukocytes to generate antibody-producing cells (APC) was suppressed 3 h after a pulsed-DC electroshock (300 V, 50 Hz, 8 ms pulse width) but recovered within 24 h. This response was similar in timing and magnitude to that of fish subjected to an acute handling stress. The mechanism of suppression is hypothesized to be via an elevation of plasma cortisol concentrations in response to stress. Other monitored immune functions, skin mucous lysozyme levels, and respiratory burst activity were not affected by exposure to electroshock. The progression of a Renibacterium salmoninarum (RS) infection may have been altered after exposure to an electroshock. The electroshock did not affect infection severity or the number of mortalities, but may have accelerated the time to death. The limited duration of APC suppression and lack of effects on lysozyme and respiratory burst, as well as infection severity and mortality levels in RS-infected fish, led us to conclude that electrofishing under the conditions we tested is a safe procedure in regards to immunity and disease.

Transactions of the American Fisheries Society↗
USGS2013

The innate immune response may be important for surviving plague in wild Gunnison's prairie dogs

Prairie dogs (Cynomys spp.) are highly susceptible to Yersinia pestis, with ≥99% mortality reported from multiple studies of plague epizootics. A colony of Gunnison's prairie dogs (Cynomys gunnisoni) in the Aubrey Valley (AV) of northern Arizona appears to have survived several regional epizootics of plague, whereas nearby colonies have been severely affected by Y. pestis. To examine potential mechanisms accounting for survival in the AV colony, we conducted a laboratory Y. pestis challenge experiment on 60 wild-caught prairie dogs from AV and from a nearby, large colony with frequent past outbreaks of plague, Espee (n = 30 per colony). Test animals were challenged subcutaneously with the fully virulent Y. pestis strain CO92 at three doses: 50, 5,000, and 50,000 colony-forming units (cfu); this range is lethal in black-tailed prairie dogs (Cynomys ludovicianus). Contrary to our expectations, only 40% of the animals died. Although mortality trended higher in the Espee colony (50%) compared with AV (30%), the differences among infectious doses were not statistically significant. Only 39% of the survivors developed moderate to high antibody levels to Y. pestis, indicating that mechanisms other than humoral immunity are important in resistance to plague. The ratio of neutrophils to lymphocytes was not correlated with plague survival in this study. However, several immune proteins with roles in innate immunity (VCAM-1, CXCL-1, and vWF) were upregulated during plague infection and warrant further inquiry into their role for protection against this disease. These results suggest plague resistance exists in wild populations of the Gunnison's prairie dog and provide important directions for future studies.

Arizona↗
USGS1997

Immunogenicity of synthetic peptides representing neutralizing epitopes on the glycoprotein of infectious hematopoietic necrosis virus

Three peptides, P76, P226, and P268 representing 3 putative antigen~c determinants on the glycoprotein of infectious hematopoietic necrosis virus (IHNV), were synthesized and injected into rainbow trout Oncorhynchus mykiss to assess their immunogen~city. Antisera extracted from the immunized trout were analyzed uslng an enzyme linked imrnunosorbent assay (ELISA) for the presence of antibodies that could bind to the peptides or to intact virions of IHNV. The antisera were also tested for neutralizing activity against IHNV by a complement-mediated neutralization assay. In general, recognition of the peptides and IHNV was low and only a few antibody binding patterns were demonstrated. Antisera from fish injected with P76 constructs recognized the homologous peptide more than the heterologous peptides, whereas antisera from fish inoculated with either P226 or P268 constructs recognized P76 equally, or better, than the homologous peptide; however, there was a high degree of individual variation within each treatment group. Neutralization actlvlty was demonstrated by serum from a single flsh lnlected with one of the pept~des (P268) and from 7 of 10 positive control f~sh Infected with an attenuated strain of IHNV Possible explanations for the dichotomous immune responses are discussed. These results indicate we need to improve our overall understanding of the

Diseases of Aquatic Organisms↗
USGS2004

Immunomodulation and disease resistance in postyearling rainbow trout infected with Myxobolus cerebralis, the causative agent of whirling disease

Myxobolus cerebralis , the myxosporean parasite that causes whirling disease, has a number of deleterious effects on its salmonid host. Although it is well established that juvenile salmonids in the active stages of whirling disease mount an immune response to the pathogen, the occurrence and longevity of any related immunomodulatory effects are unknown. In this study, postyearling rainbow trout Oncorhynchus mykiss infected with M. cerebralis were examined for leukocyte functions and for resistance to Yersinia ruckeri , a bacterial pathogen of salmonids. Compared with uninfected controls, M. cerebralis -infected fish showed lower proliferative lymphocyte responses to four mitogens (concanavalin A, pokeweed mitogen, phytohemagglutinin, and lipopolysaccharide). Conversely, M. cerebralis -infected fish displayed greater bactericidal activity of anterior kidney macrophages than did uninfected fish. After bath challenges with Y. ruckeri , M. cerebralis -infected fish had slightly lower survival and a more rapid onset of mortality than did the control fish. Renal tissue and fecal samples from M. cerebralis -infected and uninfected survivors were cultured for the presence of Y. ruckeri , and no difference in prevalence was noted between the two groups. Because immunomodulatory changes in the M. cerebralis -infected fish involved functional enhancement and suppression of different leukocyte populations, disease resistance among M. cerebralis -infected fish in the later stages of whirling disease will probably vary with the secondary pathogen and the nature of immune response the pathogen evokes.

Journal of Aquatic Animal Health↗
USGS2020

Immune and sex-biased gene expression in the threatened Mojave desert tortoise, Gopherus agassizii

The immune system of ectotherms, particularly non-avian reptiles, remains poorly characterized regarding the genes involved in immune function, and their function in wild populations. We used RNA-Seq to explore the systemic response of Mojave desert tortoise ( Gopherus agassizii ) gene expression to three levels of Mycoplasma infection to better understand the host response to this bacterial pathogen. We found over an order of magnitude more genes differentially expressed between male and female tortoises (1,037 genes) than differentially expressed among immune groups (40 genes). There were 8 genes differentially expressed among both variables that can be considered sex-biased immune genes in this tortoise. Among experimental immune groups we find enriched GO biological processes for cysteine catabolism, regulation of type 1 interferon production, and regulation of cytokine production involved in immune response. Sex-biased transcription involves iron ion transport, iron ion homeostasis, and regulation of interferon-beta production to be enriched. More detailed work is needed to assess the seasonal response of the candidate genes found here. How seasonal fluctuation of testosterone and corticosterone modulate the immunosuppression of males and their susceptibility to Mycoplasma infection also warrants further investigation, as well as the importance of iron in the immune function and sex-biased differences of this species. Finally, future transcriptional studies should avoid drawing blood from tortoises via subcarapacial venipuncture as the variable aspiration of lymphatic fluid will confound the differential expression of genes.

PLoS ONE↗
USGS2006

Ichthyophonus-induced cardiac damage: a mechanism for reduced swimming stamina in salmonids

Swimming stamina, measured as time-to-fatigue, was reduced by approximately two-thirds in rainbow trout experimentally infected with Ichthyophonus. Intensity of Ichthyophonus infection was most severe in cardiac muscle but multiple organs were infected to a lesser extent. The mean heart weight of infected fish was 40% greater than that of uninfected fish, the result of parasite biomass, infiltration of immune cells and fibrotic (granuloma) tissue surrounding the parasite. Diminished swimming stamina is hypothesized to be due to cardiac failure resulting from the combination of parasite-damaged heart muscle and low myocardial oxygen supply during sustained aerobic exercise. Loss of stamina in Ichthyophonus-infected salmonids could explain the poor performance previously reported for wild Chinook and sockeye salmon stocks during their spawning migration. ?? 2006 Blackwell Publishing Ltd.

Journal of Fish Diseases↗
USGS2017

Replication and shedding kinetics of infectious hematopoietic necrosis virus in juvenile rainbow trout

Viral replication and shedding are key components of transmission and fitness, the kinetics of which are heavily dependent on virus, host, and environmental factors. To date, no studies have quantified the shedding kinetics of infectious hematopoietic necrosis virus (IHNV) in rainbow trout ( Oncorhynchus mykiss ), or how they are associated with replication, making it difficult to ascertain the transmission dynamics of this pathogen of high agricultural and conservation importance. Here, the replication and shedding kinetics of two M genogroup IHNV genotypes were examined in their naturally co-evolved rainbow trout host. Within host virus replication began rapidly, approaching maximum values by day 3 post-infection, after which viral load was maintained or gradually dropped through day 7. Host innate immune response measured as stimulation of Mx-1 gene expression generally followed within host viral loads. Shedding also began very quickly and peaked within 2 days, defining a generally uniform early peak period of shedding from 1 to 4 days after exposure to virus. This was followed by a post-peak period where shedding declined, such that the majority of fish were no longer shedding by day 12 post-infection. Despite similar kinetics, the average shedding rate over the course of infection was significantly lower in mixed compared to single genotype infections, suggesting a competition effect, however, this did not significantly impact the total amount of virus shed. The data also indicated that the duration of shedding, rather than peak amount of virus shed, was correlated with fish mortality. Generally, the majority of virus produced during infection appeared to be shed into the environment rather than maintained in the host, although there was more retention of within host virus during the post-peak period. Viral virulence was correlated with shedding, such that the more virulent of the two genotypes shed more total virus. This fundamental understanding of IHNV shedding kinetics and variation at the individual fish level could assist with management decisions about how to respond to disease outbreaks when they occur.

Virus Research↗
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↗
USGS2025

Host responses and viral traits interact to shape the impacts of climate warming on highly pathogenic avian influenza in migratory waterfowl

Emerging infectious diseases pose threats to wildlife populations, as exemplified by recent outbreaks of avian influenza viruses in wild birds. Climate change can affect infection dynamics in wildlife through direct effects on pathogens (e.g., environmental decay rates) and changes to host ecology, including shifting migration patterns. Here, we adapt an existing mechanistic model that couples migration and infection to study how traits of highly pathogenic avian influenza (HPAI) viruses contribute to HPAI outcomes in migratory waterfowl, then apply this model to explore potential impacts of climate change on HPAI dynamics. We find that the simulated impacts of HPAI on the host population under baseline climate conditions varied from no impact to 100% mortality, depending on viral traits. In most cases, traits related to transmission (i.e., contact rates, shedding rates) were more important for HPAI establishment probability, infection prevalence, and mortality than were other viral traits (e.g., environmental temperature sensitivity, cross-protective immunity). We then simulated the effects of climate change (i.e., altered temperature regimes) on HPAI dynamics both via viral environmental decay and via changes in bird migration phenology. In these simulations, we found that a 9-day advancement in spring migration timing increased the duration of HPAI outbreaks by increasing time birds spent at their breeding grounds, leading to higher mortality and fewer infections. In contrast, increased viral decay in warmer years had a smaller, but opposite impact. These patterns depended on the primary transmission mode of HPAI (i.e., direct vs. environmental) and its sensitivity to environmental temperatures. Together, these results suggest that climate change is likely to increase the impacts of HPAI on waterfowl populations if HPAI relies strongly on direct transmission and birds advance their spring migration. Further integrating host-viral co-evolution and other climatic changes (e.g., salinity, humidity) could provide more precise predictions of how HPAI dynamics could change in the future.

Alaska, California, Oregon↗
USGS2010

Early viral replication and induced or constitutive immunity in rainbow trout families with differential resistance to Infectious hematopoietic necrosis virus (IHNV)

The main objective of this study was to assess correlates of innate resistance in rainbow trout full-sibling families that differ in susceptibility to Infectious hematopoietic necrosis virus (IHNV). As part of a commercial breeding program, full-sibling families were challenged with IHNV by waterborne exposure at the 1 g size to determine susceptibility to IHNV. Progeny from select families (N = 7 families) that varied in susceptibility (ranging from 32 to 90% cumulative percent mortality (CPM)) were challenged again at the 10 g size by intra-peritoneal injection and overall mortality, early viral replication and immune responses were evaluated. Mortality challenges included 20–40 fish per family while viral replication and immune response studies included 6 fish per family at each time point (24, 48 and 72 h post-infection (hpi)). CPM at the 1 g size was significantly correlated with CPM at the 10 g size, indicating that inherent resistance was a stable trait irrespective of size. In the larger fish, viral load was measured by quantitative reverse-transcriptase PCR in the anterior kidney and was a significant predictor of family disease outcome at 48 hpi. Type I interferon (IFN) transcript levels were significantly correlated with an individual's viral load at 48 and 72 hpi, while type II IFN gene expression was significantly correlated with an individual's viral load at 24 and 48 hpi. Mean family type I but not type II IFN gene expression was weakly associated with susceptibility at 72 hpi. There was no association between mean family susceptibility and the constitutive expression of a range of innate immune genes (e.g. type I and II IFN pathway genes, cytokine and viral recognition receptor genes). The majority of survivors from the challenge had detectable serum neutralizing antibody titers but no trend was observed among families. This result suggests that even the most resistant families experienced sufficient levels of viral replication to trigger specific immunity. In summary, disease outcome for each family was determined very early in the infection process and resistance was associated with lower early viral replication.

Fish and Shellfish Immunology↗
USGS2024

Potential impact of annual vaccination with reformulated COVID-19 vaccines: Lessons from the US COVID-19 scenario modeling hub

Background Coronavirus Disease 2019 (COVID-19) continues to cause significant hospitalizations and deaths in the United States. Its continued burden and the impact of annually reformulated vaccines remain unclear. Here, we present projections of COVID-19 hospitalizations and deaths in the United States for the next 2 years under 2 plausible assumptions about immune escape (20% per year and 50% per year) and 3 possible CDC recommendations for the use of annually reformulated vaccines (no recommendation, vaccination for those aged 65 years and over, vaccination for all eligible age groups based on FDA approval). Methods and findings The COVID-19 Scenario Modeling Hub solicited projections of COVID-19 hospitalization and deaths between April 15, 2023 and April 15, 2025 under 6 scenarios representing the intersection of considered levels of immune escape and vaccination. Annually reformulated vaccines are assumed to be 65% effective against symptomatic infection with strains circulating on June 15 of each year and to become available on September 1. Age- and state-specific coverage in recommended groups was assumed to match that seen for the first (fall 2021) COVID-19 booster. State and national projections from 8 modeling teams were ensembled to produce projections for each scenario and expected reductions in disease outcomes due to vaccination over the projection period. From April 15, 2023 to April 15, 2025, COVID-19 is projected to cause annual epidemics peaking November to January. In the most pessimistic scenario (high immune escape, no vaccination recommendation), we project 2.1 million (90% projection interval (PI) [1,438,000, 4,270,000]) hospitalizations and 209,000 (90% PI [139,000, 461,000]) deaths, exceeding pre-pandemic mortality of influenza and pneumonia. In high immune escape scenarios, vaccination of those aged 65+ results in 230,000 (95% confidence interval (CI) [104,000, 355,000]) fewer hospitalizations and 33,000 (95% CI [12,000, 54,000]) fewer deaths, while vaccination of all eligible individuals results in 431,000 (95% CI: 264,000–598,000) fewer hospitalizations and 49,000 (95% CI [29,000, 69,000]) fewer deaths. Conclusions COVID-19 is projected to be a significant public health threat over the coming 2 years. Broad vaccination has the potential to substantially reduce the burden of this disease, saving tens of thousands of lives each year.

PLOS Medicine↗
USGS2025

Exposure of wild mammals inhabiting Alaska to influenza A(H5N1) virus

Serum samples from wild mammals inhabiting Alaska, USA, showed that 4 species, including Ursus arctos bears and Vulpes vulpes foxes, were exposed to influenza A(H5N1) viruses. Results indicated some mammals in Alaska survived H5N1 virus infection. Surveillance efforts may be improved by incorporating information on susceptibility and detectable immune responses among wild mammals.

Alaska↗
USGS2014

A lack of crowding? Body size does not decrease with density for two behavior-manipulating parasites

For trophically transmitted parasites that manipulate the phenotype of their hosts, whether the parasites do or do not experience resource competition depends on such factors as the size of the parasites relative to their hosts, the intensity of infection, the extent to which parasites share the cost of defending against the host’s immune system or manipulating their host, and the extent to which parasites share transmission goals. Despite theoretical expectations for situations in which either no, or positive, or negative density-dependence should be observed, most studies document only negative density-dependence for trophically transmitted parasites. However, this trend may be an artifact of most studies having focused on systems in which parasites are large relative to their hosts. Yet, systems are common where parasites are small relative to their hosts, and these trophically transmitted parasites may be less likely to experience resource limitation. We looked for signs of density-dependence in Euhaplorchis californiensis (EUHA) and Renicola buchanani (RENB), two manipulative trematode parasites infecting wild-caught California killifish (Fundulus parvipinnis). These parasites are small relative to killifish (suggesting resources are not limiting), and are associated with changes in killifish behavior that are dependent on parasite-intensity and that increase predation rates by the parasites’ shared final host (indicating the possibility for cost sharing). We did not observe negative density-dependence in either species, indicating that resources are not limiting. In fact, observed patterns indicate possible mild positive density-dependence for EUHA. Although experimental confirmation is required, our findings suggest that some behavior-manipulating parasites suffer no reduction in size, and may even benefit when "crowded" by conspecifics.

Integrative and Comparative Biology↗
USGS2022

Microbiomes associated with avian malaria survival differ between susceptible Hawaiian honeycreepers and sympatric malaria-resistant introduced birds

Of the estimated 55 Hawaiian honeycreepers (subfamily Carduelinae) only 17 species remain, nine of which the International Union for Conservation of Nature considers endangered. Among the most pressing threats to honeycreeper survival is avian malaria, caused by the introduced blood parasite Plasmodium relictum , which is increasing in distribution in Hawaiʻi as a result of climate change. Preventing further honeycreeper decline will require innovative conservation strategies that confront malaria from multiple angles. Research on mammals has revealed strong connections between gut microbiome composition and malaria susceptibility, illuminating a potential novel approach to malaria control through the manipulation of gut microbiota. One honeycreeper species, Hawaiʻi ʻamakihi ( Chlorodrepanis virens ), persists in areas of high malaria prevalence, indicating they have acquired some level of immunity. To investigate if avian host-specific microbes may be associated with malaria survival, we characterized cloacal microbiomes and malaria infection for 174 ʻamakihi and 172 malaria-resistant warbling white-eyes ( Zosterops japonicus ) from Hawaiʻi Island using 16S rRNA gene metabarcoding and quantitative polymerase chain reaction. Neither microbial alpha nor beta diversity covaried with infection, but 149 microbes showed positive associations with malaria survivors. Among these were Escherichia and Lactobacillus spp . , which appear to mitigate malaria severity in mammalian hosts, revealing promising candidates for future probiotic research for augmenting malaria immunity in sensitive endangered species.

Hawaii↗
USGS2006

Parasitic Cowbirds have increased immunity to West Nile and other mosquitoborne encephalitis viruses

The rapid geographic spread of West Nile Virus [WNV, Flaviviridae, Flavivirus] across the United States has stimulated interest in comparative host infection studies of avian species to delineate competent reservoir hosts critical for viral amplification. Striking taxonomic differences in avian susceptibility have been noted, offering the opportunity to strategically select species on the basis of life history traits to examine aspects of pathogen virulence or host immunity. We hypothesized that avian brood parasites would show increased resistance to pathogens compared to related taxa, because they have been exposed in their evolutionary history to a wide array of infectious organisms from their different parenting species. The Brown-headed Cowbird (Molothrus ater) is a generalist brood parasite that parasitizes 200+ North American species. Elevated exposure to other species? parasites may have created an unusual degree of pathogen resistance. We compared the relative susceptibility of adult cowbirds to three closely-related non-parasitic species, Red-winged blackbirds, Tricolored blackbirds and Brewer?s blackbirds, to invading NY99 strain of WNV that is highly virulent for many passeriform birds. Previously we had experimentally infected these species with two North American mosquitoborne encephalitis viruses, western equine encephalomyelitis virus [WEEV, Togaviridae, Alphavirus] and St. Louis encephalitis virus [SLEV, Flaviviridae, Flavivirus]. Our results showed that cowbirds exhibited significantly lower viremia responses against all three viruses as well as after co-infection with both WEEV and WNV than did the three related, non-parasitic species. These data supported our hypothesis and indicated that cowbirds were more resistant to infection to both native and introduced viruses.

Book chapter↗
USGS2026

Transcriptional changes in wild Yukon River Chinook Salmon associated with Ichthyophonus infections

Objective We compared differentially expressed genes in Chinook Salmon Oncorhynchus tshawytscha with three divergent Ichthyophonus statuses (undetected, subclinical infections, or clinical disease; n = 100) to investigate associated transcriptomic responses. Disease associated with the fish parasite Ichthyophonus sp. was first diagnosed in adult Chinook Salmon from the Yukon River in the late 1980s and has subsequently been implicated in premature host mortality. Methods Chinook Salmon tissue sample collections and Ichthyophonus infection data were leveraged from a multi-agency collaboration during summer 2022 at three locations along the main-stem Yukon River that spanned nearly 2,000 km of freshwater migration (lower, middle, and upper river). We sequenced the transcriptome and compared this to infection status based on routine diagnostic procedures. Results Among the 17,569 genes for which messenger RNA was detected, we identified a transcription signature in the skeletal muscle that was associated with Ichthyophonus infections and included 53 differentially expressed genes. The differentially expressed genes and their pathways included those known for involvement in immune functions, energy synthesis, cellular breakdown, and reproduction—all processes that are known to be influenced by senescence during spawning migrations. Conclusions Results demonstrate a clear transcriptional difference between diseased fish (clinical disease group) and those in which Ichthyophonus was undetected, including identifying candidate markers for infection in this population. These results provide a foundation for development of nonlethal biomarkers to evaluate potential Ichthyophonus infections in Chinook Salmon based on gene transcription, protein products, or gene variants (e.g., polymorphisms).

Journal of Aquatic Animal Health↗
USGS2004

High doses of corticosteroid suppress resistance to Ichthyophonus in starry flounder

Application of pharmacological doses of the corticosteroid dexamethasone phosphate to starry flounder Platichthys stellatus resulted in a predisposition to clinical ichthyophoniasis and a progression from latent Ichthyophonus infections to patent, histologically identifiable infections. Among Ichthyophonus -challenged starry flounder, the prevalences of clinical infections and histologically identifiable infections were significantly greater in two groups that received dexamethasone (100% and 31%, respectively) than in the respective control groups (8% and 0%). Proliferation of Ichthyophonus infections in corticosteroid-treated groups may have resulted from suppression of the cellular immune response that typically follows corticosteroid application; however, further studies are needed to determine whether these effects occur at lower, physiological concentrations of corticosteroids.

Journal of Aquatic Animal Health↗