Susceptibility of Three Stocks of Pacific Herring to Viral Hemorrhagic Septicemia

Abstract

Laboratory challenges using specific-pathogen-free Pacific herring Clupea pallasii from three distinct populations indicated that stock origin had no effect on susceptibility to viral hemorrhagic septicemia (VHS). All of the populations were highly susceptible to the disease upon initial exposure, with significantly greater cumulative mortalities occurring in the exposed treatment groups (56.3-64.3%) than in the unexposed control groups (0.8-9.0%). Interstock differences in cumulative mortality were not significant. The virus loads in the tissues of fish experiencing mortality were 10-10,000 times higher during the acute phase of the epizootics (day 13 postexposure) than during the recovery phase (days 30-42). Survivors of the epizootics were refractory to subsequent VHS, with reexposure of VHS survivors resulting in significantly less cumulative mortality (1.2-4.0%) than among positive controls (38.1-64.4%); interstock differences in susceptibility did not occur after reexposure. These results indicate that data from experiments designed to understand the ecology of VHS virus in a given stock of Pacific herring are broadly applicable to stocks throughout the northeastern Pacific.

Chronic and persistent viral hemorrhagic septicemia virus infections in Pacific herring

“…After surviving a sub acute outbreak of VHS, Pacific herring became solidly immune to the acute form of the disease (but not necessarily to re-infection), and the level of protection conferred was similar to that of herring surviving acute VHS manifestations (Kocan et al 2001, Hershberger et al 2007, 2010b. Although the immunological mechanisms of this adaptive response remain unknown, the resulting immunity following recovery from either the acute or chronic form of the disease has important implications in forecasting the potential for future VHS epizootics in wild populations.…”

“…Once exposed, laboratory stocks of Pacific herring typically experience acute disease followed by rapid mortality (Kocan et al 1997), and epizootics in the wild are likely initiated as a result of a combination of environmental stressors and concentration or amplification mechanisms associated with viral shedding from infected individuals within a school (Hershberger et al 2010a). Individuals that survive these epizootics become refractory to disease, indicating the involvement of a protective adaptive immune response (Kocan et al 2001, Hershberger et al 2007, 2010b). …”

“…Additionally, VHSV titers in the brain of infected Pacific herring were generally as high as or higher than those in kidney/spleen pools, a pattern of viral tropism that is similar to reports of chronic and neurotropic forms of VHS in European rainbow trout VHS (Smail 1999). These results support the recommendations of the OIE (2009) that standard procedures for determining VHSV prevalence in wild fish populations should include collection of brain tissue as well as samples from the heart, kidney, and spleen for viral assays.After surviving a sub acute outbreak of VHS, Pacific herring became solidly immune to the acute form of the disease (but not necessarily to re-infection), and the level of protection conferred was similar to that of herring surviving acute VHS manifestations (Kocan et al 2001, Hershberger et al 2007, 2010b. Although the immunological mechanisms of this adaptive response remain unknown, the resulting immunity following recovery from either the acute or chronic form of the disease has important implications in forecasting the potential for future VHS epizootics in wild populations.…”

Principles underlying the epizootiology of viral hemorrhagic septicemia in Pacific herring and other fishes throughout the North Pacific Ocean

“…Recurring epizootics of VHS have caused fish kills in Pacific herring and other forage fishes . These observations are supported by numerous controlled laboratory studies that indicate that naïve Pacific herring are highly susceptible to VHS (Kocan et al 1997;Hershberger et al 2007Hershberger et al , 2010c. Pacific herring, therefore, may be considered an exceptionally susceptible host species, with waterborne exposure levels as low as 10 1 virus particles (plaque-forming units, PFU)·mL -1 capable of initiating epizootics in laboratory exposures (Hershberger et al 2011a).…”

“…VHS progression in susceptible Pacific herring can be extremely rapid, with detectable levels of virus occurring in the tissues of exposed herring as early as 2 days PE, and mortality from the disease occurring as early as 4 days PE (Kocan et al 1997;Hershberger et al 2010c). However, the pace, intensity, and outcome of the disease are highly dependent on several variables, including exposure level and duration, temperature, diet, water exchange rate, and other factors (Hershberger et al 2011a.…”