Stability of viral hemorrhagic septicemia virus (VHSV) in freshwater and seawater at various temperatures

Abstract

Three North American and 1 European viral hemorrhagic septicemia virus (VHSV) isolates taken from either a marine, freshwater, or estuarine host were assessed for survivability in raw and filtered freshwater and seawater at temperatures ranging from 4 to 30°C. All 4 isolates were substantially more stable in freshwater than in seawater, and higher survival was observed at lower water temperatures. The average time required for 99.9% inactivation of VHSV in raw freshwater at 15°C was 13 d, while in raw seawater VHSV was inactivated within an average of 4 d. No consistent correlation was observed between the origin and the stability of the virus isolates. Freshwater isolates were not always the most stable in freshwater; similarly, seawater isolates were not consistently more stable in seawater. Virus survival was greatly enhanced in filtered freshwater with some virus strains remaining infective after 1 yr at 4°C. KEY WORDS: Viral hemorrhagic septicemia virus · Virus inactivation · Great Lakes VHSV · Genotype IVb · Virus survival · Environmental factors/effects Resale or republication not permitted without written consent of the publisherDis Aquat Org 82: [171][172][173][174][175][176][177][178] 2008 (Meyers & Winton 1995, Stone et al. 1997, Dixon 1999, Einer-Jensen et al. 2004, Snow et al. 2004.Historically, VHSV in North America had only been recovered from marine, estuarine and anadromous fish populations occurring in coastal waters of the Pacific Ocean from Alaska to California and the Atlantic Ocean waters of Maine, New Brunswick and Nova Scotia (Meyers & Winton 1995, Olivier 2002, Hedrick et al. 2003. However, in the spring of 2005, VHSV was isolated for the first time from a mass mortality event in a freshwater environment in North America. The virus was isolated from dead or dying freshwater drum Aplodinotus grunniens in Lake Ontario (Lumsden et al. 2007). Following this initial discovery, an archived viral isolate obtained from diseased muskellunge Esox masquinongy in Lake St. Clair in 2003 was identified as VHSV, indicating the earliest detection of the virus in the Great Lakes (Elsayed et al. 2006). The virus has also been associated with large mortalities of round gobies Neogobius melanostomus in Lake Ontario and the Saint Lawrence River (Groocock et al. 2007). To date, this freshwater strain of VHSV has been isolated from 28 species of fish in the Great Lakes regions of Canada and the USA including Lake Michigan, Lake Huron, Lake St. Clair, Lake Erie, Lake Ontario, the Saint Lawrence River and from inland lakes in New York, Michigan, Wisconsin and Ohio (USDA & APHIS 2007).Phylogenetic analyses based on nucleotide sequence of nucleo-and glycoprotein genes illustrated that VHSV isolates group into 4 major genotypes that generally correlate with geographic location (Benmansour et al. 1997, Einer-Jensen et al. 2004Snow et al. 2004. Genotype I encompasses European freshwater and north European marine isolates; Genotype II represents marine isolates originating from the Baltic Sea; Genot...

Replication and persistence of VHSV IVb in freshwater turtles

“…The VHSV IVb has been reported to persist for more than 10 d in fresh water at 15°C (Hawley & Garver 2008), but our data implies something much briefer. This difference may be due to intermittent shedding combined with a shorter period of viability (attributable to the far higher amount of organic material present in our turtle containers).…”

“…Fish-eating birds are a candidate for concern, but their gastric fluids are likely to inactivate the virus (Peters & Neukirch 1986), and their body temperatures are far above the limit for VHSV IVb replication in vitro (Hawley & Garver 2008). Thus, VHSV IVb is unlikely to survive transit through a bird, nor will it be able to establish a low level infection in a bird host.…”

Chronic and persistent viral hemorrhagic septicemia virus infections in Pacific herring

“…Losses due to VHS are generally highest at temperatures between 9 and 12°C, at which the disease becomes increasingly acute (OIE 2009); however, temperature optima for VHS epizootics are somewhat dependent on host species (Enzmann et al 1993). The disease rarely occurs at temperatures above 18°C even after experimental challenge (Castric & de Kinkelin 1984, Arkush et al 2006, possibly because the fish immune response to VHSV increases with temperature (Konrad 1986), the synthesis of protective interferon (de Kinkelin et al 1982) occurs more quickly at elevated temperatures (Dorson & de Kinkelin 1974), waterborne stability of VHSV decreases with temperature (Parry & Dixon 1997, Hawley & Garver 2008, and in vitro replication of VHSV decreases rapidly at temperatures greater than 20 to 25°C (de Kinkelin & Scherrer 1970, Isshiki et al 2001, Arkush et al 2006. Additionally, abrupt changes in temperature to chronically infected Japanese flounder have been reported to result in exacerbation of VHS (Iida et al 2003); however, an analogous response among chronically infected Pacific herring did not occur (data not shown).…”

Using 96-well tissue culture polystyrene plates and a fluorescence plate reader as tools to study the survival and inactivation of viruses on surfaces

“…For example, VHSV survived in freshwater for 5 or more days at 25°C, increasing to more than 25 days at 4°C. However, the survival of some isolate was much lower in seawater, dropping to around 12 days at 4°C and about 1 day at 20°C (Hawley and Garver 2008). Interestingly, filtering freshwater but not seawater increased VHSV survival time, this hints at an association in freshwater with particles, although these might be living rather than inert (Hawley and Garver 2008).…”