Infectious diseases are common in marine environments, but the effects of a changing climate on marine pathogens are not well understood. Here we review current knowledge about how the climate drives ...host-pathogen interactions and infectious disease outbreaks. Climate-related impacts on marine diseases are being documented in corals, shellfish, finfish, and humans; these impacts are less clearly linked for other organisms. Oceans and people are inextricably linked, and marine diseases can both directly and indirectly affect human health, livelihoods, and well-being. We recommend an adaptive management approach to better increase the resilience of ocean systems vulnerable to marine diseases in a changing climate. Land-based management methods of quarantining, culling, and vaccinating are not successful in the ocean; therefore, forecasting conditions that lead to outbreaks and designing tools/approaches to influence these conditions may be the best way to manage marine disease.
When estimating mortality from disease with fish population models, common disease surveillance data such as infection prevalence are not always informative, especially for fast-acting diseases that ...may go unobserved in infrequently sampled populations. In these cases, seroprevalence — the proportion of fish with measurable antibody levels in their blood — may be more informative. In cases of life-long immunity, seroprevalence data require less frequent sampling intervals than infection prevalence data and can reflect the cumulative exposure history of fish. We simulation tested the usefulness of seroprevalence data in an age-structured fish stock assessment model using viral hemorrhagic septicemia virus (VHSV) in Pacific herring (Clupea pallasii) as a case study. We developed a novel epidemiological model to simulate population dynamics and seroprevalence data and fitted to these data in an integrated catch-at-age model with equations that estimate age- and time-varying mortality from disease. We found that simulated seroprevalence data can provide accurate estimates of infection history and disease-associated mortality. Importantly, even models that misspecified nonstationary processes in background or disease-associated mortality, but included seroprevalence data, accurately estimated annual infection and population abundance.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Echinoderms, positioned taxonomically at the base of deuterostomes, provide an important system for the study of the evolution of the immune system. However, there is little known about the cellular ...components and genes associated with echinoderm immunity. The 2013-2014 sea star wasting disease outbreak is an emergent, rapidly spreading disease, which has led to large population declines of asteroids in the North American Pacific. While evidence suggests that the signs of this disease, twisting arms and lesions, may be attributed to a viral infection, the host response to infection is still poorly understood. In order to examine transcriptional responses of the sea star Pycnopodia helianthoides to sea star wasting disease, we injected a viral sized fraction (0.2 μm) homogenate prepared from symptomatic P. helianthoides into apparently healthy stars. Nine days following injection, when all stars were displaying signs of the disease, specimens were sacrificed and coelomocytes were extracted for RNA-seq analyses. A number of immune genes, including those involved in Toll signaling pathways, complement cascade, melanization response, and arachidonic acid metabolism, were differentially expressed. Furthermore, genes involved in nervous system processes and tissue remodeling were also differentially expressed, pointing to transcriptional changes underlying the signs of sea star wasting disease. The genomic resources presented here not only increase understanding of host response to sea star wasting disease, but also provide greater insight into the mechanisms underlying immune function in echinoderms.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
We characterized a natural sea louse epizootic of Caligus clemensi and the effects of parasitism on Pacific herring Clupea pallasii in Port Angeles Harbor, WA, USA. Infestation prevalence on newly ...metamorphosed age 0 Pacific herring reached 100% prevalence by mid-August. At this time, the mean louse intensity was 4.6 lice/fish, and a positive correlation occurred between louse intensity and herring body length. The epizootic then waned, with infestation prevalence decreasing to less than 25% and the mean parasite intensity falling below 1 louse. While skin injuries were not detected, motile lice preferentially aggregated around head and anterior dorsal areas. However, louse tropism became evenly distributed over the body as the parasite intensity increased. Louse-induced mortality in herring was negligible in controlled experiments. These results indicate that Caligus clemensi epizootics reach high prevalence, but also fade from mid-summer to early fall. Due to the predominant presence of motile copepod stages, we suggest that the epizootic fades because lice complete their life cycle and dislodge from the host; however, multiple explanations for epidemic fading are possible.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Nuclear inclusion X (NIX), the etiological agent of bacterial gill disease in Pacific razor clams
Siliqua patula
, was associated with host mortality events in coastal Washington State, USA, during ...the mid-1980s. Ongoing observations of truncated razor clam size distributions in Kalaloch Beach, Washington, raised concerns that NIX continues to impact populations. We conducted a series of spatial and longitudinal NIX surveillances, examined archived razor clam gill tissue, and used population estimates from stock assessments to test whether (1) the prevalence and intensity of NIX infections is higher at Kalaloch Beach relative to nearby beaches, (2) infected gill tissue has features consistent with historical descriptions of NIX-associated histopathology, and (3) annual clam survival is inversely related to NIX infection prevalence and intensity. NIX prevalence exceeded 85% at all sampled locations, and infection intensity was the highest at Kalaloch Beach by 0.9-2.6 orders of magnitude. Kalaloch Beach clams revealed histopathology consistent with previous NIX epidemics, including enlarged and/or rupturing branchial epithelial cells, branchial necrosis, and high hemocyte densities. Estimated annual survival was 22% at Kalaloch Beach, and ranged between 57 and 99% at other study sites. NIX infection intensity (via quantitative PCR) was not significantly correlated with annual survival; however, annual survival was lowest at Kalaloch Beach, where infection intensities were highest, suggesting that clams can tolerate infections up to a lethal threshold. Collectively these data support the hypothesis that high NIX intensities are associated with host mortality. NIX-associated mortality appears to be more pronounced at Kalaloch Beach relative to other Washington beaches.
Pacific herring (
), a cornerstone of marine food webs, generally spawn on marine macroalgae in shallow nearshore areas that are disproportionately at risk from oil spills. Herring embryos are also ...highly susceptible to toxicity from chemicals leaching from oil stranded in intertidal and subtidal zones. The water-soluble components of crude oil trigger an adverse outcome pathway that involves disruption of the physiological functions of cardiomyocytes in the embryonic herring heart. In previous studies, impaired ionoregulation (calcium and potassium cycling) in response to specific polycyclic aromatic hydrocarbons (PAHs) corresponds to lethal embryolarval heart failure or subtle chamber malformations at the high and low ends of the PAH exposure range, respectively. Sublethal cardiotoxicity, which involves an abnormal outgrowth (ballooning) of the cardiac ventricular chamber soon after hatching, subsequently compromises juvenile heart structure and function, leading to pathological hypertrophy of the ventricle and reduced individual fitness, measured as cardiorespiratory performance. Previous studies have not established a threshold for these sublethal and delayed-in-time effects, even with total (∑)PAH exposures as low as 29 ng/g of wet weight (tissue dose). Here, we extend these earlier findings showing that (1)
gene expression provides an oil exposure metric that is more sensitive than typical quantitation of PAHs via GC-MS and (2) heart morphometrics in herring embryos provide a similarly sensitive measure of toxic response. Early life stage injury to herring (impaired heart development) thus occurs below the quantitation limits for PAHs in both water and embryonic tissues as a conventional basis for assessing oil-induced losses to coastal marine ecosystems.
In recent decades, evidence has accumulated to suggest that the widespread and highly variable parasite
Ichthyophonus hoferi
is actually a species complex. Highly plastic morphology and a general ...lack of defining structures has contributed to the likely underestimate of biodiversity within this group. Molecular methods are a logical next step in the description of these parasites, but markers used to date have been too conserved to resolve species boundaries. Here we use mitochondrial encoded cytochrome-c oxidase (MTCO1) gene sequences and phylogenic analysis to compare
Ichthyophonus
spp. isolates from several marine and anadromous fish hosts. The resulting phylogeny displays lineage separation among isolates and possible host/niche segregation not previously described. The parasite type that infects Pacific herring
Clupea pallasii
, Atlantic herring
C. harengus
, Atlantic salmon
Salmo salar
, and Pacific staghorn sculpin
Oligocottus maculosus
(Clade A) is different from that which infects Chinook salmon
Oncorhynchus tshawytscha,
walleye pollock
Gadus chalcogrammus
, Greenland halibut
Reinhardtius hippoglossoides
, and Pacific halibut
Hippoglossus stenolepsis
(Clade B). MTCO1 sequences confirmed the presence of a more divergent
Ichthyophonus
sp. isolated from American shad
Alosa sapidissima
in rivers of eastern North America (Clade C), while American shad introduced to the Pacific Ocean are infected with the same parasite that infects Pacific herring (Clade A). Currently there are no consensus criteria for delimiting species within
Ichthyophonidae
, but MTCO1 sequences hold promise as a potential species identifying marker and useful epizootiological tool.
Preliminary evidence suggests that Chinook salmon Oncorhynchus tshawytscha from the Yukon River may be more susceptible to Ichthyophonus sp. infections than Chinook from stocks further south. To ...investigate this hypothesis in a controlled environment, we experimentally challenged juvenile Chinook from the Yukon River and from the Salish Sea with Ichthyophonus sp. and evaluated mortality, infection prevalence and infection load over time. We found that juvenile Chinook salmon from a Yukon River stock were more susceptible to ichthyophoniasis than were those from a Salish Sea stock. After feeding with tissues from infected Pacific herring Clupea pallasii, Chinook salmon from both stocks became infected. The infection was persistent and progressive in Yukon River stock fish, where infections sometimes progressed to mortality, and histological examinations revealed parasite dissemination and proliferation throughout the host tissues. In Salish Sea-origin fish, however, infections were largely transient; host mortalities were rare, and parasite stages were largely cleared from most tissues after 3-4 wk. Susceptibility differences were evidenced by greater cumulative mortality, infection prevalence, parasite density, proportion of fish demonstrating a cellular response, and intensity of the cellular response among fish from the Yukon River stock. These observed differences between Chinook salmon stocks were consistent when parasite exposures occurred in both freshwater and seawater. These results support the hypothesis that a longer-standing host-pathogen relationship, resulting in decreased disease susceptibility, exists among Salish Sea Chinook salmon than among Yukon River conspecifics.
The susceptibility of yellow perch Perca flavescens, rainbow trout Oncorhynchus mykiss, Chinook salmon O. tshawytscha, koi Cyprinus carpio koi, and Pacific herring Clupea pallasii to 4 strains of ...viral hemorrhagic septicemia virus (VHSV) was assessed. Fish were challenged via intraperitoneal injection with high (1 × 106 plaque-forming units, PFU) and low (1 × 103 PFU) doses of a European strain (genotype Ia), and North American strains from the West coast (genotype IVa), Great Lakes (genotype IVb), and the East coast (genotype IVc). Pacific herring were exposed to the same VHSV strains, but at a single dose of 5 × 103 PFU ml-1 by immersion in static seawater. Overall, yellow perch were the most susceptible, with cumulative percent mortality (CPM) ranging from 84 to 100%, and 30 to 93% in fish injected with high or low doses of virus, respectively. Rainbow trout and Chinook salmon experienced higher mortalities (47 to 98% CPM) after exposure to strain Ia than to the other virus genotypes. Pacific herring were most susceptible to strain IVa with an average CPM of 80% and moderately susceptible (42 to 52% CPM) to the other genotypes. Koi had very low susceptibility (≤5.0% CPM) to all 4 VHSV strains. Fish tested at 7 d post challenge were positive for all virus strains, with yellow perch having the highest prevalence and concentrations of virus, and koi the lowest. While genotype Ia had higher virulence in salmonid species, there was little difference in virulence or host-specificity between isolates from subtypes IVa, IVb, and IVc.
Although viral hemorrhagic septicemia virus (VHSV) typically occurs at low prevalence and intensity in natural populations of Pacific herring (Clupea pallasii) and other marine fishes in the ...Northeast Pacific Ocean, epizootics of the resulting disease (VHS) periodically occur, often in association with observed fish kills. Here we identify a list of principles, based on a combination of field studies, controlled laboratory experiments, and previously unpublished observations, that govern the epizootiology of VHS in Pacific herring. A thorough understanding of these principles provides the basis for identifying risk factors that predispose certain marine fish populations to VHS epizootics, including the lack of population resistance, presence of chronic viral carriers in a population, copious viral shedding by infected individuals, cool water temperatures, limited water circulation patterns, and gregarious host behavioral patterns. Further, these principles are used to define the epizootiological stages of the disease in Pacific herring, including the susceptible (where susceptible individuals predominate a school or subpopulation), enzootic (where infection prevalence and intensity are often below the limits of reasonable laboratory detection), disease amplification (where infection prevalence and intensity increase rapidly), outbreak (often accompanied by host mortalities with high virus loads and active shedding), recovery (in which the mortality rate and virus load decline owing to an active host immune response), and refractory stages (characterized by little or no susceptibility and where viral clearance occurs in most VHS survivors). In addition to providing a foundation for quantitatively assessing the potential risks of future VHS epizootics in Pacific herring, these principles provide insights into the epizootiology of VHS in other fish communities where susceptible species exist.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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