The single biggest threat to ALL Pacific salmon is indeed those "open netpen fish farms"!
The part everyone seems to keep missing "IT IS NOT" overfishing, or the destruction of their habitat that is causing the present wild salmon decines in both BC and Puget Sound. Sorry, to keep trying to inform; however, the Columbia (which has NO fish farms is actually seeing an increase in their salmon stock returns, while both BC (all stocks) and Pugut Sound (most) are still showing declines. The only ONE COMMON FACTOR or lack there of is - OPEN NETPEN FISH FARMS!
Open netpen fish farms have been killing off entire enviroments and entire wild salmon stocks ALL over the world! If anyone believes they aren't killing off the Pacific salmon, I can only suggest - you are a FOOL! You (we) can restore whatever habitat you wish; however, until ALL those open netpen fish farms are OUT of the water both Atlantic and Pacific wild salmon, as Dr Kristy Miller has stated - they are just "dead fish swimming"! Please note and think about, all those "Pacific COHO" in those open netpens of Gregs that are now spreading the DEADLY IHN disease to ALL the migrating wild salmon passing those open netpens?
FYI… in case you don’t know and it is well documented, IHN is “highly contagious” and if those Atlantic salmon and Pacific Coho have a strain BC/Puget Sound fish have not built up a resistance and then they are exposed, it is/has the potential of being VERY DEADLY to "ALL" BC and Puget Sound wild salmon! In case one doesn't know or remember, my Puget Sound Chinook are currently swimming around ALL those infected pens. If one doesn't think IHN hasn't been brought back to Puget Sound by those fish... you are again a FOOL - it already has been!
Here is part of a couple of studies and I do quote:
Infectious hematopoietic necrosis (IHN): The virus known as IHN attacks the liver of salmon or steelhead. The fish are more susceptible to IHN when water temperatures are cold. The disease is "vertically transmitted" which means that it can be passed from fluids within the gut of female fish to eggs of the next generation. Chen (1984) suggested that various strains of IHN exist, and if salmonids evolve with a specific strain they will develop resistance to it. He suggested that if IHN were transferred from one basin to another, its virulence could be substantially increased. Juvenile salmonid mortality at large northern California hatcheries has been very high due to IHN outbreaks (Kier Assoc., 1991).
Horizontal transmission of the IHN virus occurs readily in both saltwater and freshwater (Traxler et al. 1998). Although there is anecdotal information that vertical transmission of IHNV occurs, no laboratory study has been able to demonstrate the event (Traxler et al. 1997, Bootland and Leong 1999). Ribonuclease protection assays and nucleotide sequencing of IHNV isolates collected over a 20 year period found that the isolates can be grouped into three separate regional isotypes: northwest coast (Oregon to Alaska), California, and Idaho (Hsu et al. 1986, Emmenegger et al. 2000, Troyer et al. 2000, Emmenegger and Kurath 2002). Different salmonid species appear to be sensitive to different genetic isotypes. For example sockeye salmon,
Oncorhynchus nerka, are susceptible to the northwest coast IHNV isolates while chinook salmon,
Oncorhynchus tshawytscha, are more susceptible to the Californian isolates. Rainbow trout,
Oncorhynchus mykiss, are susceptible to the Idaho isolate.
Most of the losses associated with IHN, in sockeye salmon, occur in the freshwater alevin and swim-up stages. Disease in the seawater sockeye stages has not been as commonly observed, however, the northwest isolates are quite homogeneous indicating that continual mixing of the isolates has occurred over the generations. The only location where this appears possible would be in the ocean (Williams and Amend 1976, Traxler and Rankin 1989, Emmenegger et al. 2000). One such place could be the “Alaskan gyre”, the common feeding grounds for all sockeye populations north of Oregon (Emmenegger et al. 2000, Emmenegger and Kurath 2002).
Lab transmission studies have found that Atlantic salmon are very susceptible to IHNV infections (Traxler et al 1993). In 1992, IHN was diagnosed in a population of farmed Atlantic salmon, S
almo salar, in British Columbia (BC). Over the next four years, the disease spread to 13 separate farm sites within a 20 km radius of the index case (St-Hilaire 2000, St-Hilaire et al.2001). In the summer of 2001, nine years after the first epizootic, IHN was again diagnosed in a population of farmed Atlantic salmon. As in the 1992 epizootic, mortality as a result of the disease has been significant.
Lag time between suspicion and confirmation of an infection
For sites where mortality data was examined, in 82% of the cases IHN was suspected prior to any substantial jump in mortality. This indicates a high level of diligence in fish health monitoring at the sites. The concern, however, is the length of time between suspicion and confirmation of IHN. This ranged from five to twenty-one days, with an average of 15.7 days.
Here is a study, as asked on the impact of those open netpens... and I do suggest reading it very closely:
'A Global Assessment of Salmon Aquaculture Impacts on Wild Salmonids'
http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0060033