Geology topics

Courtney Grady

Publications and source records attributed to Courtney Grady.

3 recordsLinked to original sources

USGS2012

Induction of anti-viral genes during acute infection with Viral hemorrhagic septicemia virus (VHSV) genogroup IVa in Pacific herring ( Clupea pallasii )

Infection with the aquatic rhabdovirus Viral hemorrhagic septicemia virus (VHSV) genogroup IVa results in high mortality in Pacific herring ( Clupea pallasii ) and is hypothesized to be a potential limiting factor for herring recovery. To investigate anti-viral immunity in the Pacific herring, four immune response genes were identified: the myxovirus resistance ( Clpa- Mx), a major histocompatibility complex IB (named Clpa- UAA.001), the inducible immunoproteosome subunit 9 ( Clpa- PSMB9) and the neutrophil chemotactic factor ( Clpa- LECT2). Reverse transcriptase quantitative PCR (RT-qPCR) assays were developed based on these gene sequences to investigate the host immune response to acute VHSV infection following both injection and immersion challenge. Virus levels were measured by both plaque assay and RT-qPCR and peaked at day 6 during the 10-day exposure period for both groups of fish. The interferon stimulated genes ( Clpa- Mx, −UAA.001, and −PSMB9) were significantly up-regulated in response to VHSV infection at both 6 and 10 days post-infection in both spleen and fin. Results from this study indicate that Pacific herring mount a robust, early antiviral response in both fin and spleen tissues. The immunological tools developed in this study will be useful for future studies to investigate antiviral immunity in Pacific herring.

Fish and Shellfish Immunology↗

USGS2010

Amplification and transport of an endemic fish disease by an introduced species

The introduction of American shad from the Atlantic to the Pacific coast of North America in the late 1800’s and the subsequent population expansion in the 1980’s resulted in the amplification of Ichthyophonus sp., a Mesomycetozoean parasite of wild marine fishes. Sequence analysis of the ribosomal DNA gene complex (small subunit and internal transcribed spacer regions) and Ichthyophonus epidemiological characteristics indicate a low probability that Ichthyophonus was co-introduced with American shad from the Atlantic; rather, Ichthyophonus was likely endemic to marine areas of the Pacific region and amplified by the expanding population of a highly susceptible host species. The migratory life history of shad resulted in the transport of amplified Ichthyophonus from its endemic region in the NE Pacific to the Columbia River watershed. An Ichthyophonus epizootic occurred among American shad in the Columbia River during 2007, when infection prevalence was 72%, and 57% of the infections were scored as moderate or heavy intensities. The epizootic occurred near the record peak of shad biomass in the Columbia River, and corresponded to an influx of 1,595 mt of infected shad tissues into the Columbia River. A high potential for parasite spillback and the establishment of a freshwater Ichthyophonus life cycle in the Columbia River results from currently elevated infection pressures, broad host range, plasticity in Ichthyophonus life history stages, and precedents for establishment of the parasite in other freshwater systems. The results raise questions regarding the risk for sympatric salmonids and the role of Ichthyophonus as a population-limiting factor affecting American shad in the Columbia River.

Biological Invasions↗

USGS2010

Kinetics of viral shedding provide insights into the epidemiology of viral hemorrhagic septicemia in Pacific herring

Losses from infectious diseases are an important component of natural mortality among marine fish species, but factors controlling the ecology of these diseases and their potential responses to anthropogenic changes are poorly understood. We used viral hemorrhagic septicemia virus (VHSV) and a laboratory stock of Pacific herring Clupea pallasii to investigate the kinetics of viral shedding and its effect on disease transmission and host mortality. Outbreaks of acute disease, accompanied by mortality and viral shedding, were initiated after waterborne exposure of herring to concentrations of VHSV as low as 101 plaque-forming units (pfu) ml–1. Shed virus in flow-through tanks was first detected 4 to 5 d post-exposure, peaked after 6 to 10 d, and was no longer detected after 16 d. Shedding rates, calculated from density, flow and waterborne virus titer reached 1.8 to 5.0 × 108 pfu fish–1 d–1. Onset of viral shedding was dose-dependent and preceded initial mortality by 2 d. At 21 d, cumulative mortality in treatment groups ranged from 81 to 100% and was dependent not on challenge dose, but on the kinetics and level of viral shedding by infected fish in the tank. Possible consequences of the viral shedding and disease kinetics are discussed in the context of epizootic initiation and perpetuation among populations of wild Pacific herring.

Marine Ecology Progress Series↗