Viruses from salmon farms are low risk to wild fish

Viruses from salmon farms are not likely to harm wild salmon.

The idea that salmon farms can “amplify” a natural virus to the point that it will harm wild salmon is pure speculation not backed up by facts.

Since salmon farmers are having trouble with the IHN virus right now, let’s talk about this virus specifically.

IHN is an RNA virus, which replicate themselves very quickly. In fact, RNA viruses replicate so quickly that a single infectious particle can reproduce itself three times a second!

However, RNA viruses do not “proof-read” themselves during the replication process like DNA does. Skipping this step allows for more rapid replication but leads to a high level of errors — mutations — when RNA viruses reproduce.

An RNA virus happily reproducing itself.
An RNA virus happily reproducing itself.

This sounds like a recipe for disaster, doesn’t it? IHN gets into a salmon farm, where there are lots of hosts, replicates a huge amount of itself and mutations are inevitable. Isn’t something terrible inevitable?

No, it isn’t. There is no reason to assume that any of those mutations will make the virus suddenly more harmful to the infected farmed salmon, or to the wild fish swimming by.

In fact, research suggests that most of those mutations are random noise. A normal virus population is full of mutants which do nothing to alter the virus’ overall survival strategy (infect a particular host, replicate, repeat).

Virus populations normally consist of a widely dispersed mutant distribution rather than a homogeneous one formed by a single, most-fit, wild-type sequence.

In the case of the IHN virus, although it will certainly replicate quickly and mutate, it is extremely unlikely that a mutation will evolve on a salmon farm which is suddenly harmful to wild salmon swimming by. Wild salmon are already highly resistant to the disease and often carry it as hosts without any ill effect. It’s incredibly unlikely that a random mutation from a farm will suddenly overturn hundreds, if not thousands, of years of evolution and start killing wild salmon when it hasn’t before. Viruses live to replicate themselves. If they kill their hosts, they can’t replicate.

But suppose such a harmful mutation did happen. It’s very unlikely that the few fish swimming by which would be exposed to such a harmful mutation would survive to spread it.

If they did, it’s practically impossible that the new more harmful virus strain would somehow out-compete and and replace all the other strains of IHN already out in the ocean. What’s more likely is that the harmful strain would kill its hosts, eliminating further chances for it to reproduce and spread itself.

Harmful mutation is “snot” likely

Sneezing a cloudConsider this analogy. There is a portable building full of kindergartners in the middle of a sports field. These kids are all highly susceptible to the flu virus. There are windows on all sides of the building and they are all open.

Outside, in the sports field, other kindergartners are running around, playing. These kids all have a natural resistance to the flu virus. Occasionally they pass close to the open windows.

One kid passing close to the open windows sneezes through the window, spraying saliva and mucus at several of the kids inside. Since they have no resistance to the flu virus, they quickly get sick with the flu and spread it to other kids in the classroom.

Now the entire portable full of kids are sneezing and coughing out the windows. Occasionally, one of the outside kids passes by and passes through air carrying mucus and saliva from the sick kids inside.

Like all the other kids running around the field, this one already has a natural resistance to this virus. How likely is it that he is going to suddenly get sick? How likely is it that the virus inside the portable is suddenly going to mutate into a form which will make the kids outside sick? If it does, how likely is it that the outside kid running past the window is going to get sick but still keep running around enough to pass it on to the other kids running around the field?

We think it’s pretty unlikely the sick kids in the portable will have any effect on the health of the kids running around the field.

Environment prompts evolution

Back to salmon, it’s important to understand that the only cases where IHN virus has been observed to do any harm to wild salmon is in hatcheries, where man-made spawning channels contain a high density of eggs and young salmon. When spawning salmon return to those channels, if they are carrying the IHN virus (and they regularly do) the high density situation in the spawning channel can lead to high infection rates, and mortalities among the young salmon. The environment is different from the environment where the virus and wild salmon have co-existed for millennia, resulting in a different outcome.

But in natural spawning settings, there is a low risk of IHN virus harming young salmon because the natural densities of young salmon in freshwater are low.

On the other hand, farmed Atlantic salmon are highly susceptible because they are raised in densities higher than how fish normally school in the ocean. And, more importantly, farmed Atlantic salmon come from a different ocean and did not evolve alongside the virus, developing a natural resistance to it. This plus a higher density changes the environment for the virus, resulting in different outcomes.

Let’s look at a real-world example. The Hagerman Valley in Idaho is home to a large number of rainbow trout farms, which are relatively isolated from nearby rivers and from the ocean. There are very few, if any, new introductions of IHN virus particles into the valley. For 21 years, scientists tracked and studied the evolution of the virus and found that over time the relatively few strains present in the valley grew into many.

The presence of a general trend toward divergence over time suggests that the virus is actively evolving in the valley rather than exhibiting the relative genetic stasis observed in Alaska and the Washington state coastal region (Emmenegger et al. 2000, Emmenegger & Kurath 2002).

The generation of this diversity may have been facilitated by conditions specific to Hagerman Valley aquaculture. Year-round trout production with the constant introduction of immunologically naïve fish may allow more rounds of viral replication per year than in anadromous hatchery or wild fish, where low-level chronic or carrier infection may be more common.

In addition, partitioning of fish populations into numerous facilities, each with numerous rearing units may result in a lack of competition and purifying selection, allowing multiple variants to be simultaneously maintained. Rapid evolution of IHNV may also have been initiated by the process of virus adaptation to the unique Hagerman Valley environment which includes the rainbow trout host and constant 15°C water temperature.

Bracken fern
Bracken ferns have been around for 55 million years, longer than us humans (or even hominids!) They haven’t evolved much since then because they haven’t needed to do so.

There are several reasons why the virus was able to evolve such diversity. Being isolated into an artificial system is at the top of the list. And it’s important to note that in the ocean, the IHN virus is in relative genetic stasis because it is experiencing no environmental pressures to significantly change itself.

And even in the Hagerman Valley example, there is no evidence after 21 years that the virus had mutated to be more harmful.

Amplification is for music

There is simply no good reason to assume that a salmon farm will somehow “amplify” a naturally-occurring virus to the point that it will be harmful to the wild salmon which already carry it.

And there is certainly no good reason to assume that random mutations of the virus at an infected farm will do any harm to wild salmon.

Once again, we point out that the ocean is full of viruses. Fish swim through them every day. The ocean is not “pristine” in the sense that it is free of viruses and diseases. Nature is brutal, and in the ocean just like on land creatures get sick and die.

Wild salmon have evolved to be incredibly hardy to viruses and diseases. It’s grasping at straws to suggest that a string of incredibly unlikely scenarios, which get more unlikely as they stack one on the other,  is going to do any harm to wild salmon.

And it’s cynical and manipulative for anti-salmon farming fanatics to suggest this, especially the ones such as Alexandra Morton who purport to be scientific experts.

We hope people will ignore the silly speculations and research the science for themselves, and they will see the risks posed by salmon farms in B.C. are very low to wild fish.


4 thoughts on “Viruses from salmon farms are low risk to wild fish”

  1. The list author presented a challenge.

    Information sources.

    Most scientific and engineering papers now flag any conflicts in their papers; eg disclosure if sponsored by First Nations, fish farms, governments, etc. No one says that a connection implies unethical science. Only that disclosure allows the reader to judge whether the paper is truly impartial. I work in an industry (nothing to do with fisheries) where I am obliged by regulation to disclose any real or perceived conflicts of interest in any report. It is not the relationship that is important, it is the failure to disclose the relationship that is important

    Back to the subject matter.

    This is a vast, fast developing research area. Since I am not a molecular biologist, and this is not my day job, I have to be careful in my selection of reference material.

    My argument is that fish farm advocates are slow to recognise the density dependence of impact of various viruses on wild and farm salmon, are slow in BC to identify research results that confirm or refute the association and rarely if ever publish audits of virus surveillance and control programs. They may exist, but the ordinary citizen with a day job cannot access them.

    My argument is that BC has to do a better job of marine spatial planning to minimise virus transmission and maximise economic return.

    Seems reasonable to me.

    In the area of density dependent viruses and pathogens, I was impressed by these three papers and summary

    1) Sea lice as a density-dependent constraint to salmonid farming : Jansen PA, Kristoffersen AB, Viljugrein H, Jimenez D, Aldrin M, Stien A. PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES 2012; 279 (1737):2330-8

    2) Tracing pathways for ISA: Review of recent Ph.D theses by T Lyngstad: Norwegian School of Veterinary Science, July 2012

    3) Use of molecular epidemiology to trace transmission pathways for infectious salmon anaemia virus (ISAV) in Norwegian salmon farming.: Epidemics. 2011 Mar;3(1):1-11. Epub 2010 Nov 24. By Lyngstad TM, Hjortaas MJ, Kristoffersen AB, Markussen T, Karlsen ET, Jonassen CM, Jansen PA.

    In the case of sea lice in Norway, the authors argue that sea lice epidemics are related to the biomass of individual farms and the spatial density of the farms. They argue that there are limits on fish farm locations in order to avoid lice outbreaks. In the case of the ISA and the work by Lyngstad, the authors demonstrate that the ISA virus outbreaks in Norway relate in part to proximity to infected fish farms and also to outbreaks of virulent forms of ISA among low virulent variants of the ISA virus. The mechanism of rapid virus mutation is incompletely known but the same threat exists in BC with the IHN virus.

    The Norwegian researchers are identifying the importance of spatial marine planning to minimise risks of destructive sea lice epidemics or ISA virus outbreaks.

    From my point of view, there is a lack of good published research in BC that would help identify virus transmission pathways. If it exists, it seems very well hidden.

    In terms of overview, I found these two papers of value

    4) Viruses of Fish: An Overview of Significant Pathogens : Viruses 2011, 3, 2025-2046; doi:10.3390/v3112025 Review:Mark Crane * and Alex Hyatt

    5) Emerging viral diseases of fish and shrimp: Vet. Res. (2010) 41:51 :Peter J. Walker and James R. Winton

    Both papers identify the risks associated with introduction of new species into ecosystems where there are natural viruses and the risk of mutation is substantial. It may be that this research is ongoing in BC but there seems to be a dearth of readily accessible research results that help ordinary citizens understand the risk profiles of the aquaculture industry and the fisheries regulators.

    For example, I had to find out from a US publication that the IHN virus associated with the recent outbreak on west Vancouver Island was different from the IHN virus associated with the recent outbreak at Bainbridge Island, Puget Sound. Interesting and unexplained. Yet the ordinary citizen has no idea how our fisheries scientists are addressing or propose to address the reasons.

    Further the Norwegians and the Americans publish results of audits and case studies of virus ecology: such as

    6) 15-2010: Evaluation of the surveillance and control programme for VHS and IHN The National Veterinary Institute ,Norway and:

    7) Spread of the Emerging Viral Hemorrhagic Septicemia Virus Strain, Genotype IVb, in Michigan, USA Mohamed Faisal 1,2,* et al. Viruses. 2012 May;4(5):734-60. Epub 2012 May 3.

    Perhaps the Cohen Commission findings and recommendations will result in a level playing field where scientific data will be accessible and independent.

    Otherwise we will still have a regrettable scientific schism between the fish farm and wild salmon advocates.

    1. Thank you for providing these papers, we have read at least half of these but some are new to us.

      From my point of view, there is a lack of good published research in BC that would help identify virus transmission pathways. If it exists, it seems very well hidden.

      We completely agree with you here. We know there is a lot of good research being done by BC scientists, who have been more than willing to talk about their work with us, but not enough is getting published. The DFO scientists we know are frustrated about this and would prefer to be completely open and public with their work and see more of it published. They are also dissatisfied with DFO’s communications policy, which appears to be to say as little as possible. Contrast this with NOAA, which is exemplary when it comes to providing the public with good, scientific information.

      We also agree that marine spatial planning is important, and salmon farmers need to be part of these discussions to make sure their farms are considered, and so that farms can be placed in locations which are most appropriate for the farmed fish and for the surrounding environment.

      there seems to be a dearth of readily accessible research results that help ordinary citizens understand the risk profiles of the aquaculture industry

      We have to somewhat disagree with you here. Disease data has been made publicly available since 2003 on the Internet. This data includes information about what sort of bacteria, diseases and viruses were found on farms. The numbers are all there. The only thing this data does not do is present the information on a site-by-site basis, but groups it by area. But the exact numbers of disease, virus, tests and PCR results are all there and this has been available to the public for nearly a decade.

      I had to find out from a US publication that the IHN virus associated with the recent outbreak on west Vancouver Island was different from the IHN virus associated with the recent outbreak at Bainbridge Island, Puget Sound.

      That’s very interesting. It shows that the virus has not spread from farm to farm. It’s not surprising that there would be variations in the virus in regions hundreds of miles apart, though. Are you able to share the source?

      And although the viruses may be slightly variant from Clayoquot Sound to Puget Sound, they are still in the same clade (U) which is found from Alaska to Oregon.

      Here in BC we have heard that the virus which infected farms this spring and summer is exactly the same as the virus which was observed in samples of wild sockeye sampled this year.

      Perhaps the Cohen Commission findings and recommendations will result in a level playing field where scientific data will be accessible and independent.

      We sure hope so. Scientific data should be available for all to access, verify and share.

  2. This is very well worded.

    The only difficulty I have with it is that there is no citation to independent fish virus experts to back up some of the assertions.

    Can you please provide those citations ?

    1. Thank you.

      Please explain what you mean by “independent.” We have cited a wide variety of research here, and have selected it for its scientific merit. If you have any reasons why the research we have cited is not acceptable, we’d love to hear them so we can find more appropriate sources.

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