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[work2fish]

Sorry it's not my job to educate you. The papers are readily available to anyone on the internet.  You could also try subscribing to a few journals if you're really interested, and besides, while you may lead a horse to water, you can't make it drink.  I'm also not interested in arguing the merits of pro or anti-fish farmers.  For the most part they both need a good bath with soap and a fire hose.

As for the rest of your arguments, most of what you're saying about disease is irrelevant to this discussion, or like your previous statements on reoviruses just plain wrong.  The rest is just rhetoric about Don and Morton, and Routlage, and not worth the time to address.  Yes, they are not my favorite researchers either, but neither is a government lab that has failed to find anything, and litterally has no suspects into the decline of CL sockeye.  Again, it's irrelevant. The relevant facts are:

1. Routlage found PRV in cultas lake sockeye.

2. While PRV still needs to be isolated in cell culture, it has been linked as the most plausible cause of HMSI, by well respected and highly published biologists that have nothing to do with Morton et al. Here's your homework, go read: "Immunohistochemical detection of piscine reovirus (PRV) in hearts of Atlantic salmon coincide with the course of heart and skeletal muscle inflammation", the authors names are in my previous post if you have issues finding it. Spoiler alert, the title gives away the story.

3. PRV was sequenced to be more than 99% similar to Norwegien strains of the virus.  According to your own post, Marty found it in 75% of farmed salmon tested.  Sorry I didn't vet this source, I'll take your word for it.

4. The only source of Norwegian virus (or the most likely source, outside of aliens, act of god, or other) is the Norwegian fish farms.   I doubt it swam here on it's own.

5. If a=b and a=c then b=c, or if PRV has been found in CL, and the PRV is from Norway, and fish farms stock is Norwegian in origin, then fish farms are the most likely source of PRV in cultas lake.

6. Just because something is infected with a virus and shows no obvious signs of disease, does not mean it is fitness to reproduce is not compromised.  Until tests are done that show no effect on spawning fitness, this cannot be ruled out.  Absence of evidence is not evidence of absence.  This is why Marty's reasoning that no obvious signs of disease = no problem is  flawed logic.

7. PRV has now been shown to be exposed to the CL Sockeye from both freshwater and saltwater sources, freshwater- due to the infected cutthroat trout (thanks again Routlage), which may be a simple reservoir for the disease, (though virology of the pathogen has not been studied in depth in this animal, and it may be more than a reservoir), and fish farms effecting both sides of their ocean migrations.

8. As you stated previously: "HSMI primarily affects juvenile fish.  Think about…if most of them had this deadly virus they would not have survived past the juvenile stage." even if this is true, and HMSI only effects juvenile fish which has not been proved, (otherwise please point me to a study showing it only effects juvenile fish, or even a study on PRV's Virulence), we now know the cultas lake sockeye can be exposed to the virus through resident trout, and on outward migration as they swim past the farms.  Even if it only effects juvenile fish, as you stated if most of them had this virus, they would not survive past this stage, though there is no research to support this hypothesis.

9. Until a study has been done on the virology of PRV, and how it relates to sockeye's fitness to reproduce and survive from egg to adult, it cannot be ruled out as a cause of the decline in sockeye salmon in Cultas lake, since it's now known that sockeye are exposed to the virus at all life stages.

Best bet would be for someone to do follow-up analysis on Millar's samples that showed the genetic signature for pre-spawn mortality.  Hopefully her or someone like her is doing something like a Random Multiplex (RT)-PCR to try to determine the pathogen or pathogens responsible for the signature, and the most likely cause of the sockeye decline. They have a signature, they have samples, all that's required is to isolate the pathogen producing the signature, and they have the smoking gun.

[curious]

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.

Salmon feedlots have been here closer to 30 years, about 10 years before Fraser sockeye salmon productivity dropped drasticly.

[work2fish]

Salmon feedlots have been here closer to 30 years, about 10 years before Fraser sockeye salmon productivity dropped drastically.

So what?

It doesn't mean they haven't or are not having an effect.  We don't know when PRV came from Norway, or even if it is the virus causing the pre-spawn mortality signature in Sockeye.

Until we know exactly what pathogen or group of pathogens are responsible for the pre-spawn mortality signature in these fish, anything else is speculation.  The fish farms are a possible source, or at least a possible source of amplification of the virus(es) responsible, and should not be discounted so easily.

[curious]

So what?

So we should turn a blind eye to the fish farms and stall till the wild salmon are gone?
Maybe you aren't familiar with the steady decline, other than a one off year, or consider it serious.

[work2fish]

So we should turn a blind eye to the fish farms and stall till the wild salmon are gone?
Maybe you aren't familiar with the steady decline, other than a one off year, or consider it serious.

You seem to be arguing with yourself.  In one post you say "Salmon feedlots have been here closer to 30 years, about 10 years before Fraser sockeye salmon productivity dropped drastically. " implying feedlots have had no effect, and in the next you're implying they they are responsible, asking if we should turn a blind eye until wild salmon are gone.

I consider the decline serious,  and I'm not saying they are not a possible cause, or contributing factor, but there is not enough evidence to prove it yet.  Though it is a good hypothesis.

Yes I think the precautionary principle should have been applied, and they shouldn't be in the ocean on migration routes of wild salmon, but unless the government is willing to force their removal, nothing will get done.  If research is done that shows a definite link, then government would have a valid reason for their removal or movement, until then chances are nothing will be done.

[work2fish]

Salmon feedlots have been here closer to 30 years, about 10 years before Fraser sockeye salmon productivity dropped drastically.

Sorry curious I misinterpreted your meaning from this as an argument discounting the link between farming and the decline, not in response to this:

[/quote]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.[/quote]

ISAV, and the premature conclusion that Morton made that it was responsible for the decline of salmon is somewhat irrelevant to the discussion on PRV, though until virulence studies have been done we can't discount the possibility that it is acting in concert with PRV or another organism adding to the decline in sockeye salmon.  Anti fish farm proponents may contend it originates from Norway, like the more virulent strains that decimated the farming industry in Chile, but that hasn't been proven and is unlikely based on Millar's work. Until the entire DNA sequence is analyzed and compared to the other strains, making a guess on origin or time of origin is also premature.

[Dave]

Yes, they are not my favorite researchers either, but neither is a government lab that has failed to find anything, and litterally has no suspects into the decline of CL sockeye. 

I've been away from this issue for a while but the general concensus among respected scientists was Cultus Lake sockeye populations started crashing when overharvested as by catch during the once huge Weaver Creek sockeye fishery - that's certainly when staff at the Cultus Lake Laboratory started noticing the declination. Combined with early entry into freshwater, exacerbating a kidney parasite called Parvicapsula minibicornis, degradation of spawning habitat at Lindell Beach and winter month predation by Northern Pikeminnow and those same cutthroat found to have PRV, decimated this population to the point where hatchery intervention now is the only reason these fish still exist.
Again, many of these questions would have been answered had Chilliwack Lake cutthroat been sampled … Orr and Routledge would have had their ‘smoking gun’ if those cutthroat were PRV free and we would probably not be discussing this if they were found  to  have PRV.
I'm surprised and curious why these fish weren't sampled at the same time.

[work2fish]

I've been away from this issue for a while but the general concensus among respected scientists was Cultus Lake sockeye populations started crashing when overharvested as by catch during the once huge Weaver Creek sockeye fishery - that's certainly when staff at the Cultus Lake Laboratory started noticing the declination. Combined with early entry into freshwater, exacerbating a kidney parasite called Parvicapsula minibicornis, degradation of spawning habitat at Lindell Beach and winter month predation by Northern Pikeminnow and those same cutthroat found to have PRV, decimated this population to the point where hatchery intervention now is the only reason these fish still exist.
Again, many of these questions would have been answered had Chilliwack Lake cutthroat been sampled … Orr and Routledge would have had their ‘smoking gun’ if those cutthroat were PRV free and we would probably not be discussing this if they were found  to  have PRV.
I'm surprised and curious why these fish weren't sampled at the same time.

I'm more surprised and curious why he's the first researcher to sample and test either population.

Even if both populations are infected with PRV, until we know more about he virulence of PRV, speculating that it couldn't be the cause even if both populations are infected is just that speculation.  It might be the combination of several factors increases the virulence of the pathogen.

[absolon]

Until we have learned more about the virus the hypothesis that it is of fish farm and specifically Norwegian origin and that it is related to the decline in sockeye numbers also remains speculation.

We have no shortage of valid hypotheses to explain the decline. The debate as it currently exists contributes nothing toward finding the answer.

[shuswapsteve]

work2fish,

Although I do not agree with everyone on this forum, I am always open to hear different points of view and have been willing to share information to those that seem to be genuinely interested, knowledgeable and respectful.  For instance, I sent a particular member on this forum a couple of papers already on something somewhat related to what we are talking about.  I was not looking to you to educate me; however, I was interested in understanding your point of view, so that I might learn something myself.  Although I like to think of myself as an educated person there is always something to learn which I did not know before.  I was trying to remain open to your views.

The only times I get to browse the forums these days seems to be late at night (my child demands my attentions when she is awake).  Along with my work taking me out of town lately (some of the places I go to have limited or no internet) I do not get much time to just go hunting around on the internet.  I did not feel the need at the time to provide you an insight of my day in order to explain why I asked you, so I just left that alone.  I like to hunt for this sort of stuff myself, but I thought that if you had those particular papers handy it could save me the time in finding them myself.  Sometimes only the abstract is easily found, so I was hoping you had the whole document.  I asked nicely; however, if it presented a great burden to you I apologize for even asking.

I disagree with your assertion that what I am saying about disease is irrelevant to this discussion.  In fact, what I have been saying about the difference between viruses and diseases is foundational to the whole discussion.  Just because a fish has PRV does not necessarily mean that it will develop HSMI.  Dr. Marty did find PRV in 75% of farm fish tested, but he did not find HSMI.  Actually your prior description on how a person like Dr. Marty goes about this testing is not accurate.  You make a few assumptions which could have been cleared up if you looked into it further.  If you look into it, farm fish carcasses to be sampled are those that have grown well prior to death and have red or pink gills for the most part.  These are fish that have recently died which may or may not have disease.  These fish provide the best diagnostic value to people like Dr. Marty because it is more than likely if disease is present it will be in these particular fish.  In addition, it is probably the most representative sample of robust fish on a farm without sampling every single fish.  Samples are taken for a variety of tests which include histopathology, bacteriology and virology.  Despite what you might believe, the diagnostic testing is quite rigorous and follows accredited techniques.  They do not get out a dissecting kit, cut open the fish and look with their naked eyes and say a simple “yes” or “no” to the presence of disease and then move on to the next fish.  In addition, it is not just one sign that determines the presence of a disease – it could more than two that are needed to make that determination (this is what many anti-fish farm activists do not understand).  To my knowledge, HSMI has never been detected in BC fish farms.  I can go into more of this in depth and provide some references, but I do not think it is my job to educate you either.  Sorry, but I am not feeling very motivated to exchange additional information considering your condescending remarks in your last post (which included “Here's your homework”.  That was a very classy remark).

As for bringing up the activists, you did this in your second post and I responded with my opinion.  In addition, the thread is technically about Don Staniford and relates to his trial win as well as his views.  The rhetoric is being spread by people like Don Staniford and Ms Morton.  Even you mentioned that the work should be reproducible.  Well, if you go to where these conclusions are coming from you will not find any details which satisfy this.  The results are sometimes posted, the methods used are virtually non-existent, and the conclusions are often misleading.  If people like that want to be taken seriously for doing this important work then they need to act seriously which I am sure you agree with.  If you do not wish to address this I can respect that, but I will not be restrained by the same bounds considering these two individuals have openly criticized government scientists and their professionalism.  In my opinion, it is totally relevant to the discussion in this thread.

[shuswapsteve]

I would like to finish off by addressing your relevant facts:

1. Routlage found PRV in Cultus lake sockeye.

Are you certain about this fact?  Could you be talking about cutthroat trout?

2. While PRV still needs to be isolated in cell culture, it has been linked as the most plausible cause of HMSI, by well respected and highly published biologists that have nothing to do with Morton et al. Here's your homework, go read: "Immunohistochemical detection of piscine reovirus (PRV) in hearts of Atlantic salmon coincide with the course of heart and skeletal muscle inflammation", the authors names are in my previous post if you have issues finding it. Spoiler alert, the title gives away the story.

I do not doubt what you found and the science behind it, but if you read the paper like I have you will notice that there might be some factors which do not allow the disease to develop on BC fish farms.  Perhaps how fish husbandry is conducted in BC aquaculture is a factor – I am not sure.  The authors explicitly state that PRV can be quite common in fish farms that have Atlantic Salmon and that the detection of PRV alone does not establish the presence of HSMI.  I cannot ignore what Dr. Saksida and Dr. Marty have found locally or what Routledge and Morton failed to find (i.e. HSMI).  Despite this I do concede that the association appears to be very plausible according to this study.  I learned something that I did not know before and I appreciate you sharing it.

3. PRV was sequenced to be more than 99% similar to Norwegian strains of the virus.  According to your own post, Marty found it in 75% of farmed salmon tested.  Sorry I didn't vet this source, I'll take your word for it.

4. The only source of Norwegian virus (or the most likely source, outside of aliens, act of god, or other) is the Norwegian fish farms.   I doubt it swam here on it's own.

5. If a=b and a=c then b=c, or if PRV has been found in CL, and the PRV is from Norway, and fish farms stock is Norwegian in origin, then fish farms are the most likely source of PRV in cultas lake.

I suggest to you that you are taking bits and pieces of media headlines to form these opinions; however, if you look at the actual facts of this you might have a slightly different view.  The reporting of this PRV viral sequence is fairly recent (2010) and has not been officially described or seen using electron microscopy so there is very little information on the how long it has been here or where it came from.  If it were to be discovered in BC first then Norway would be saying it was 99% BC strain.  Merely saying that the BC and Norway strains are 99% identical does not tell us where this originated.  Viruses do not come out of thin air – they come from the wild (as do many pathogens).  However, the role of farms spreading PRV is unknown, so I agree that should be looked at more – specifically looking at wild fish.  I used the ISAV work by Dr. Miller as example of how much we still do not know and the gaps that remain in our knowledge about the impact of pathogens on the survival of wild salmon off our coast.  You will find that most of these studies on pathogens in BC have been done on farm fish and at hatcheries.  Given these gaps (which were presented at the Cohen Inquiry) I believe it is premature at this point to making any conclusions in this regard as to the source of viruses like PRV.  Again, I would like to provide you references for this, but it is not my job to educate you.

6. Just because something is infected with a virus and shows no obvious signs of disease, does not mean it is fitness to reproduce is not compromised.  Until tests are done that show no effect on spawning fitness, this cannot be ruled out.  Absence of evidence is not evidence of absence.  This is why Marty's reasoning that no obvious signs of disease = no problem is  flawed logic

I believe you have totally misinterpreted Dr. Marty in this regard.  He does not say “no obvious signs of disease = no problem”.  He is talking about the presence of disease – not that the fish is not affected in some other way.  He is not saying fitness is unaffected.  I agree with you that an effect on spawning fitness cannot be ruled out and should be investigated, specifically in wild fish.  However, PRV seems to be very common in Atlantic Salmon and does not appear to be a great threat to their health in BC fish farms at least.  You do not have to take my word for this.  If you disagree with this then go find out for yourself like I did.

7. PRV has now been shown to be exposed to the CL Sockeye from both freshwater and saltwater sources, freshwater- due to the infected cutthroat trout (thanks again Routlage), which may be a simple reservoir for the disease, (though virology of the pathogen has not been studied in depth in this animal, and it may be more than a reservoir), and fish farms effecting both sides of their ocean migrations.

How is PRV that has been detected in some freshwater specimens of cutthroat trout and on BC fish farms “effecting” Cultus Lake Sockeye on both sides of their ocean migrations?  Do you care to expand on this recent discovery for me please?  Are you suggesting that PRV is spreading horizontally from cutthroat to juvenile Sockeye in the lake?  If so, how do you know this?

8. As you stated previously: "HSMI primarily affects juvenile fish.  Think about…if most of them had this deadly virus they would not have survived past the juvenile stage." even if this is true, and HMSI only effects juvenile fish which has not been proved, (otherwise please point me to a study showing it only effects juvenile fish, or even a study on PRV's Virulence), we now know the cultas lake sockeye can be exposed to the virus through resident trout, and on outward migration as they swim past the farms.  Even if it only effects juvenile fish, as you stated if most of them had this virus, they would not survive past this stage, though there is no research to support this hypothesis.

Actually there is research to support this.  It was an accidental oversight on my part to not include the reference in my previous post.  I apologize for that; but given your recent remarks I will have to decline being open to showing you what I have.  However, if you read Finstad et al 2012 closely it might lead you in the right direction.  You can either choose to believe me or not.  At this point of the discussion with you I am indifferent.  I wish I did not feel that way, but I do.

9. Until a study has been done on the virology of PRV, and how it relates to sockeye's fitness to reproduce and survive from egg to adult, it cannot be ruled out as a cause of the decline in sockeye salmon in Cultas lake, since it's now known that sockeye are exposed to the virus at all life stages.

Well, before we put the cart before the horse we would first have to find PRV in Cultus Sockeye before we can see how it relates to fitness to reproduce and survive from egg to adult.  It would also have to be put into context with other things impacting Cultus Lake Sockeye.  There are members on this forum with more specific knowledge about Cultus Lake Sockeye so I will defer to them.  However, I do agree with you that work on this should be considered.  No argument there.

[curious]

Sorry curious I misinterpreted your meaning from this as an argument discounting the link between farming and the decline, not in response to this:

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.

No problem work2fish. I'm happy that you got the correct meaning