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[Dave]

WatershedWatch and Craig Orr have always been aligned with anti salmon farmers.   Why do you think they and Routledge sampled Cultus Lake Cutthroat ... I suggest potential funding opportunities drove that little program (that could have had so much more scientific value had a control site been used); they were looking for that elusive link Ms. Morton suggested as the cause for the near extirpation of Cultus sockeye, but of course failed.
But had they found something even close to plausible huge money would have been available from well meaning but misinformed funders for their particular research
Just my $.02 of course

[chris gadsden]

WatershedWatch and Craig Orr have always been aligned with anti salmon farmers.   Why do you think they and Routledge sampled Cultus Lake Cutthroat ... I suggest potential funding opportunities drove that little program (that could have had so much more scientific value had a control site been used); they were looking for that elusive link Ms. Morton suggested as the cause for the near extirpation of Cultus sockeye, but of course failed.
But had they found something even close to plausible huge money would have been available from well meaning but misinformed funders for their particular research
Just my $.02 of course

Yes, good guys that really know the issue.

[work2fish]

WatershedWatch and Craig Orr have always been aligned with anti salmon farmers.   Why do you think they and Routledge sampled Cultus Lake Cutthroat ... I suggest potential funding opportunities drove that little program (that could have had so much more scientific value had a control site been used); they were looking for that elusive link Ms. Morton suggested as the cause for the near extirpation of Cultus sockeye, but of course failed.
But had they found something even close to plausible huge money would have been available from well meaning but misinformed funders for their particular research
Just my $.02 of course

  Not sure I follow your arguement.  So they decided for whatever reason to sample Cultas lake, and failed to find what they were looking for in your opinion, but found PVR in cut throat, which had previously never been detected in BC fresh water. Further tests genetically linked it as 99% similar to norway strains. 

So because they were funded by anti-fish farmers, this is a bad thing?  I'm not sure how more testing, and gathering more information by anyone is a bad thing, regardless of thier initial motivation.  Either the science will be reproducable or it won't.  All this does is provide data previously unavailable, and ask more questions that can be followed up by further studies. To some thier results are still troubling since some scientists think there is a link between PVR and HSMI which does cause damage in salmon, and that the strain seems to originate from Noraway-aka fish farms.

With research scientists, funding is always an issue, especially when it's privatly funded.  You find your funding from people with common interests. In this case anti-farmers were looking for a link to the decline of cultus lake sockeye, so what?

[Dave]

You raise good points work2fish, but I’m not arguing anything.  I’m suggesting Cultus Lake was chosen for sampling for political reasons and because Ms. Morton had earlier stated the CL sockeye run was failing due to a European virus … some face saving was needed so her collaborators tried to help her out.   And there’s nothing wrong with that because as you said this was new information but had they included samples of cutthroat trout from Chilliwack Lake, a stock showing productivity quite opposite to Cultus, the study would have had more relevance.
Again, I'm hardly on speaking terms with these people  so this is just my opinion.

[alwaysfishn]

  Not sure I follow your arguement.  So they decided for whatever reason to sample Cultas lake, and failed to find what they were looking for in your opinion, but found PVR in cut throat, which had previously never been detected in BC fresh water. Further tests genetically linked it as 99% similar to norway strains. 

So because they were funded by anti-fish farmers, this is a bad thing?  I'm not sure how more testing, and gathering more information by anyone is a bad thing, regardless of thier initial motivation.  Either the science will be reproducable or it won't.  All this does is provide data previously unavailable, and ask more questions that can be followed up by further studies. To some thier results are still troubling since some scientists think there is a link between PVR and HSMI which does cause damage in salmon, and that the strain seems to originate from Noraway-aka fish farms.

With research scientists, funding is always an issue, especially when it's privatly funded.  You find your funding from people with common interests. In this case anti-farmers were looking for a link to the decline of cultus lake sockeye, so what?

Great post!

The pro-feedlot crowd tends to react to any activity that may lead to further proof that the feedlots are killing wild salmon. Then they argue that the science being conducted is faulty and lacks credibility.

These kind of studies need to be done...... by someone. Unfortunately DFO doesn't appear to be interested in finding anything that may lead to further proof that the feedlots are killing wild salmon either.

[Bassonator]

Great post!

The pro-feedlot crowd tends to react to any activity that may lead to further proof that the feedlots are killing wild salmon. Then they argue that the science being conducted is faulty and lacks credibility.

These kind of studies need to be done...... by someone. Unfortunately DFO doesn't appear to be interested in finding anything that may lead to further proof that the feedlots are killing wild salmon either.

You see AF now who am I a non science guy to believe you a financial planner or Dave, Abs or Shuswap.....

[work2fish]

You raise good points work2fish, but I’m not arguing anything.  I’m suggesting Cultus Lake was chosen for sampling for political reasons and because Ms. Morton had earlier stated the CL sockeye run was failing due to a European virus … some face saving was needed so her collaborators tried to help her out.   And there’s nothing wrong with that because as you said this was new information but had they included samples of cutthroat trout from Chilliwack Lake, a stock showing productivity quite opposite to Cultus, the study would have had more relevance.
Again, I'm hardly on speaking terms with these people  so this is just my opinion.

  No worries, as I said I didn't get it, as it came across as there being an issue. 

Good point, and that would defintily add more value to sample more lakes and have a better comparison.  Hopefully someone does sample the lake.  I'd assume it could always be done as follow-up work, building on thier first results.

[shuswapsteve]

The problem from my perspective is that mere presence of piscine reovirus (PRV) is getting kind of blown out of proportion.  Personally, I have no issue with someone private trying to look into things like this.  For instance, researchers from BC universities (i.e. UBC) are quite active in the Fraser watershed doing salmon research.  I know a few of them quite well and they are very competent people who very professional in their approach.  They collaborate with DFO and ENGOs like the Pacific Salmon Foundation and do good work which is transparent and defensible.  In contrast, those private individuals in the anti-fish farm camp (i.e. people like Don Staniford) looking for viruses are the complete opposite, in my opinion.

The mere presence of PRV does not prove anything, but what I do have a problem with are the conclusions made afterwards which are more speculation at this point than fact.  Reoviruses get their name from the respiratory and enteric orphans – meaning that they were commonly associated with the respiratory and digestive system, but not with disease.  The “O” in reovirus stands for orphan – meaning they are viruses without a disease.

Suspicions of HSMI are based on one study from Palacios et al 2010 which found a link between PVR and HSMI.  Soon after Ms Morton found PRV in farmed salmon purchased in stores and started calling the PRV the “heart and skeletal muscle inflammation virus” which is misleading and should have been balanced with some objectivity considering the evidence gathered to date.  For instance, if you look at local evidence you will find something completely different.  As I stated before on this forum, believe it or not, most healthy broiler chickens (80-90%) from the Fraser Valley would be positive for reovirus.  Recent testing of 150 healthy, wild pink salmon on our coast showed no positive PCR test results the virus and no suspicious heart lesions (Saksida et al. 2012).  In 2010, Dr. Gary Marty found that 75% of the farmed salmon he tested were positive for PRV, but found no signs of disease.

It is important to note that Ms Morton did not find HSMI in her samples and neither did Rick Routledge with the cutthroat trout in Cultus Lake.  Just because you find a virus in the host does not necessarily mean that the host is suffering from a disease.  There is a difference between a virus and a disease.  You need to examine the tissues – preferably someone who is fish pathologist.  Neither Morton nor Routledge did this necessary follow-up to confirm their suspicions.  Neither Morton nor Routledge are fish pathologists or virologists.  Viruses are actually part of a larger equation which can involve environmental conditions, individual fitness, physiological stress, etc.  Fish farm critics like Morton and Staniford use “viruses” and “diseases” interchangeably - misinforming the public as a result.  Thus, a positive PCR test for PRV does not mean that the host has HSMI.  Morton’s findings in market sized fish may not have been in vain totally because they are good evidence that the virus was not the cause of disease in those fish.  HSMI primarily affects juvenile fish.  Think about…if most of them had this deadly virus they would not have survived past the juvenile stage.

Palacios, G., Lovoll, M., Tengs, T., Hornig, M., Hutchison, S., Hui, J., Kongtorp, R.T., Savji, N., Bussetti, A.V., Solovyov, A., Kristoffersen, A.B., Celone, C., Street, C., Trifonov, V., Hirschberg, D.L., Rabadan, R., Egholm, M., Rimstad, E. & Lipkin, W.I. 2010. Heart and skeletal muscle inflammation of farmed salmon is associated with infection with a novel reovirus. PloS One 5(7), e11487.   

Saksida, S.M., G.D. Marty, S. St-Hilaire, S.R.M. Jones, H.A. Manchester, C.L. Diamond, and J. Bidulka.  2012.  Parasites and hepatic lesions among pink salmon, Oncorhynchus gorbuscha (Walbaum), during early seawater residence. J. Fish Dis. 35:137-151.

[work2fish]

The problem from my perspective is that mere presence of piscine reovirus (PRV) is getting kind of blown out of proportion.  Personally, I have no issue with someone private trying to look into things like this.  For instance, researchers from BC universities (i.e. UBC) are quite active in the Fraser watershed doing salmon research.  I know a few of them quite well and they are very competent people who very professional in their approach.  They collaborate with DFO and ENGOs like the Pacific Salmon Foundation and do good work which is transparent and defensible.  In contrast, those private individuals in the anti-fish farm camp (i.e. people like Don Staniford) looking for viruses are the complete opposite, in my opinion.

I'm not aware of any research by Don, and I'm sure like research from pro farm activists it would have to stand on it's scientific merits.  Personally I don't really care where the research comes from, what their previous bias is, so long as the science is good.  If it's not, it won't be reproductable, and will not become part of the "general consensus" in the scientific community.

The mere presence of PRV does not prove anything, but what I do have a problem with are the conclusions made afterwards which are more speculation at this point than fact.  Reoviruses get their name from the respiratory and enteric orphans – meaning that they were commonly associated with the respiratory and digestive system, but not with disease.  The “O” in reovirus stands for orphan – meaning they are viruses without a disease.

 
Reoviruses were first thought to be "orphaned" viruses without disease, but as scientific understanding has evolved on this, and we now know this is not necessarily the case.  Just because it was once thought that these viruses were orphans without disease, doesn't mean that all viruses in the Reovirus family do not cause disease.  The understanding has evolved, but the naming has not.  It's not the first time an assumption has made in naming something, and the name has remained despite the fact.  In general the understanding of viruses is still fairly limited in terms of their interaction on gene expression and their effect on the host, so making assumptions is always a silly endeavor, as is the incorrect assumption that reoviruses do not cause disease.   Even though the word Alligator comes from the Spanish word for lizard, an alligator is still not a lizard.  As an example of renoviruses causing disease, you only have to look at how a grass carp reovirus is causing severe mortality in China.

Suspicions of HSMI are based on one study from Palacios et al 2010 which found a link between PVR and HSMI.  Soon after Ms Morton found PRV in farmed salmon purchased in stores and started calling the PRV the “heart and skeletal muscle inflammation virus” which is misleading and should have been balanced with some objectivity considering the evidence gathered to date.  For instance, if you look at local evidence you will find something completely different.  As I stated before on this forum, believe it or not, most healthy broiler chickens (80-90%) from the Fraser Valley would be positive for reovirus.  Recent testing of 150 healthy, wild pink salmon on our coast showed no positive PCR test results the virus and no suspicious heart lesions (Saksida et al. 2012).

 
That may have been accurate a few months or years ago, as there was little understanding on the new virus, but there is more than one study that links HMSI and PRV, including this one: Immunohistochemical detection of piscine reovirus (PRV) in hearts of Atlantic salmon coincide with the course of heart and skeletal muscle inflammation (HSMI) Øystein W Finstad1*, Knut Falk2, Marie Løvoll2, Øystein Evensen3 and Espen Rimstad1

And the general concensus is that PRV is associated with HMSI, as discussed at the 14th annual meeting of national reference laboratories for fish diseases.  Where the so far unpublished work of Dr. Tengs was discussed and presented by Irene Orpetveit from the National Veterinary Institute on the isolation of the renovirus by cell culture from fish, including those that show no clinical signs.

While I'm always open to the possibility of this changing based on new research, I think that's highly unlikely based on those studies and the manner in which they investigated the link, that PRV is not associated with HMSI, though the mechanism and how they relate still requires further study.

In 2010, Dr. Gary Marty found that 75% of the farmed salmon he tested were positive for PRV, but found no signs of disease.

 
This is not uncommon with viral infections, and does not speak to the health of the host, it's ability to fight off other diseases, or it's fitness to reproduce.  It would also depend on the life cycle of the animal in question and when they are examined.  It could be as simple as these fish were harvested before they developed any disease as a result of the infection.   There are many factors that could account for this, since all of the fish Marty looks at are pre-spawn, and never go through the spawning phase or acclimation to freshwater. It could also be that the effect PRV has on Atlantic Salmon is different than it's effect on Pacific Salmon.  So saying these fish showed no signs of disease despite testing positive for the virus is irrelevant.  Look at Hep C and it's effects, and how it's quite common to not show signs of disease despite being infected with a disease causing pathogen.  It also seems to be Marty's fall back line, that if there's no sign of disease, there's nothing wrong with the fish.

It is important to note that Ms Morton did not find HSMI in her samples and neither did Rick Routledge with the cutthroat trout in Cultus Lake.  Just because you find a virus in the host does not necessarily mean that the host is suffering from a disease.  There is a difference between a virus and a disease.  You need to examine the tissues – preferably someone who is fish pathologist.  Neither Morton nor Routledge did this necessary followup to confirm their suspicions.  Neither Morton nor Routledge are fish pathologists or virologists.  Viruses are actually part of a larger equation which can involve environmental conditions, individual fitness, physiological stress, etc.  Fish farm critics like Morton and Staniford use “viruses” and “diseases” interchangeably - misinforming the public as a result.  Thus, a positive PCR test for PRV does not mean that the host has HSMI.  Morton’s findings in market sized fish may not have been in vain totally because they are good evidence that the virus was not the cause of disease in those fish.  HSMI primarily affects juvenile fish.  Think about…if most of them had this deadly virus they would not have survived past the juvenile stage.

Their study showed that cutthroat trout are infected with PRV.  I don't think it was the intent of their study to show that PRV causes HMSI, or that PRV causes HMSI in cuthroat trout.  The important information from their study is that PRV, which is commonly understood to be associated with HMSI, (though it may not meet your burden of proof), was found in cuthroat trout in fresh water, in a system that is experiencing issues with sockeye salmon decline.  As to the effects of PRV on this system and the salmon that reproduce in this system, that is still unknown.  Considering the papers that do show a link of HMSI and PRV, and that PRV has now been found in this fresh water system, it is still a possibility that PRV is in part responsible for the decline of salmon, until proven otherwise. It also still fits with the work done by Kristi Miller that showed a pre-spawn mortality signature in salmon related to an unknown viral infection effecting spawning fitness, and prespawn mortality.

While I might object the activists jumping the gun, and their overly alarmist rhetoric in general, in this case I think they may be on the right path, or at least this definitely deserves some detailed followup studies. 

It also shows that fish-farms impact on wild salmon should not be discounted so easily, since the PRV that has been detected has been sequenced to be over 99% identical to Norwegian strains of the virus, making fish farms it's most likely source.

[alwaysfishn]

Very informative post work2fish. I also like your objective viewpoint.

[work2fish]

Very informative post work2fish. I also like your objective viewpoint.

Thanks!

[Dave]

I agree and appreciate your input work2fish. You obviously know your stuff - if you don't mind saying, what is your background?  If you prefer not to answer that question that's fine too; just keep posting!

[work2fish]

I agree and appreciate your input work2fish. You obviously know your stuff - if you don't mind saying, what is your background?  If you prefer not to answer that question that's fine too; just keep posting!

Thanks Dave, I'll try.

I tend to try to keep my private life private, but my main focus is technology.  Like most though I've worked in a variety of industries including forestry, commercial fishing, geology, project management etc.

I'm just generally curious and believe anything is learnable if you dissect until it's in small enough pieces to understand.

[chris gadsden]

Very informative post work2fish. I also like your objective viewpoint.

Yes, thanks for this.

[shuswapsteve]

Personally I don't really care where the research comes from, what their previous bias is, so long as the science is good.  If it's not, it won't be reproducible, and will not become part of the "general consensus" in the scientific community.

No dispute there at all.

Reoviruses were first thought to be "orphaned" viruses without disease, but as scientific understanding has evolved on this, and we now know this is not necessarily the case.  Just because it was once thought that these viruses were orphans without disease, doesn't mean that all viruses in the Reovirus family do not cause disease.  The understanding has evolved, but the naming has not.  It's not the first time an assumption has made in naming something, and the name has remained despite the fact.  In general the understanding of viruses is still fairly limited in terms of their interaction on gene expression and their effect on the host, so making assumptions is always a silly endeavor, as is the incorrect assumption that reoviruses do not cause disease.   Even though the word Alligator comes from the Spanish word for lizard, an alligator is still not a lizard.  As an example of renoviruses causing disease, you only have to look at how a grass carp reovirus is causing severe mortality in China.

Thanks for the information on reoviruses I was not aware of.  I would not mind reading the references if you have them handy.  I am open to the possibility of changing my mind also on recent discoveries of PRV in salmon here, but the work done to date by people like Ms Morton and Rick Routledge does not constitute a well thought-out approach in my opinion.  All we have are PCR results with conclusions posted on blogs and some mainstream media sites as well as vague results on another website (i.e. Dept. of Wild Salmon).

Merely testing for the presence of virus does not prove disease.  The two words are not interchangeable, but anti-fish farm activists (like Don Staniford) are doing just that.  What I would have liked to have seen is a better plan from those that reported these local discoveries.  Published findings which included methods and detailed results would have also been very helpful.  This should have included actual histological work to see if disease was detected and sampling from adjacent areas like Chilliwack Lake.  In addition, there is the issue between presence versus the prevalence of a pathogen so a statistically defensible sample size should also be a consideration for future work.  However, despite these shortcomings the inferences about PRV and HSMI locally were still made.  This included alarming the general public about the PRV getting into the water system from cleaning farmed fish at home.  This was irresponsible and definitely premature given what I already mentioned.

This is not uncommon with viral infections, and does not speak to the health of the host, it's ability to fight off other diseases, or it's fitness to reproduce.  It would also depend on the life cycle of the animal in question and when they are examined.  It could be as simple as these fish were harvested before they developed any disease as a result of the infection.   There are many factors that could account for this, since all of the fish Marty looks at are pre-spawn, and never go through the spawning phase or acclimation to freshwater. It could also be that the effect PRV has on Atlantic Salmon is different than it's effect on Pacific Salmon.  So saying these fish showed no signs of disease despite testing positive for the virus is irrelevant.  Look at Hep C and it's effects, and how it's quite common to not show signs of disease despite being infected with a disease causing pathogen.  It also seems to be Marty's fall back line, that if there's no sign of disease, there's nothing wrong with the fish

.

That is my point.  The presence of a pathogen does not mean equal the presence of a disease.  There are many factors (some I already mentioned) that are more important than the pathogen itself when it comes to disease.  Although her results still need to be confirmed, Dr. Kristi Miller study of ISAV in farmed Chinook (presented during the Cohen Inquiry on Dec 15, 2011) is another example of how the presence of a pathogen does not equal disease.  She found that the prevalence of ISAV was the same between healthy fish and unhealthy fish.  Her study was much more defensible than Ms Morton’s recent work because Dr. Miller’s viral results were linked to data from a licensed veterinarian that sampled the fish and a board-certified veterinary pathologist that examined sections of the organs under the microscope.  By doing this it is much better to see if the sick fish were sick and if the healthy fish were healthy.  If you ask Dr. Marty, a board certified fish pathologist, you will find out that it is not a fall back line at all.  Those that do this work are experienced enough to be diligent to this level of detail.  This is what people like Ms Morton and Rick Routledge need to start doing before going to the media or posting on blogs.  If the work is that important then it should treated as such.

Their study showed that cutthroat trout are infected with PRV.  I don't think it was the intent of their study to show that PRV causes HMSI, or that PRV causes HMSI in cuthroat trout.  The important information from their study is that PRV, which is commonly understood to be associated with HMSI, (though it may not meet your burden of proof), was found in cuthroat trout in fresh water, in a system that is experiencing issues with sockeye salmon decline.  As to the effects of PRV on this system and the salmon that reproduce in this system, that is still unknown.  Considering the papers that do show a link of HMSI and PRV, and that PRV has now been found in this fresh water system, it is still a possibility that PRV is in part responsible for the decline of salmon, until proven otherwise. It also still fits with the work done by Kristi Miller that showed a pre-spawn mortality signature in salmon related to an unknown viral infection effecting spawning fitness, and prespawn mortality.

I disagree.  I believe it was the intent of people like Ms Morton (not so much Rick Routledge) to show, inferring from their local work, that PRV causes HMSI and that only plausible explanation that this is coming from BC salmon farms.  If you check out Ms Morton’s blog and the “Common Sense Canadian” website (trying to control my laughter with that name) you can see the fear that has already being generated based on the limited samples taken.  Look at the poster of a mother holding her child in a supermarket on the Salmon Are Sacred website and it pretty clear what the intent was.

May not meet my burden of proof?  If conclusions were limited to what they found without the alarmist remarks it would have been alright, but some anti-fish farm activists like Ms Morton or Don Staniford feel that need to get this to the blogs or press as soon as possible supersedes a well thought-out objective approach.  For instance, I would have preferred to see this work done much better to see if there was indeed a connection here locally; however, all we have are positive results which are not proof on their own.  It does not inspire much confidence when the fish chosen for a study of such importance are purchased from a store with no change of custody provided, no sampling methodology provided and no evidence of any tissue sampling (which is required to see if HSMI is indeed present).

While I might object the activists jumping the gun, and their overly alarmist rhetoric in general, in this case I think they may be on the right path, or at least this definitely deserves some detailed followup studies.  

It also shows that fish-farms impact on wild salmon should not be discounted so easily, since the PRV that has been detected has been sequenced to be over 99% identical to Norwegian strains of the virus, making fish farms it's most likely source.

While I agree that being able to document the presence of PRV is not a bad thing and deserves some detailed follow-up, I disagree with the assertion of them being on the right path.  The reason I say this is based on what I just said above.  I do not see much professionalism and objectivity from anti-fish farm activists.  They need to put together a better study design which includes: rationale, sampling protocols (using accepted techniques), sample size to address their hypothesis and biosecurity measures taken to prevent contamination.  I am aware that the PRV found here was 99% identical to Norwegian strains; however, I also know that it was Dr. Miller’s opinion that the ISAV sequences that she found in preserved samples that she retested using a different primer could have been present in our waters for as long as 25 years or more – long before salmon farms even began in BC.  Despite this, fish farm activists contend that ISAV here must also be of foreign origin. Given what we know about ISAV alone, I think it is premature to say that BC fish farms are the most likely source of PRV.  Thank you for your detailed and thoughtful contribution, work2fish.