H
handee
Guest
quote:Originally posted by agentaqua
Handee,
I’m not sure how the rest of the posters on this forum feel – but I am getting tired of your arguments based on personal attacks. If I were the moderator; I’d be getting nervous about letting the personal attacks, slander and libel continue.
>> My "personal attacks" are used to defend "attacks" on DFO scientists whom you accuse of somehow benefitting from the sea lice debate. My "attacks" are merely arguments that the main researcher suggesting their is a sea lice issue, has far greater motivations and far greater resources of money and power than a pure academic scientist from DFO who are actually experst in the field to which Morton and her co authors are students. I think juxtapositioning of Morton vs the DFO scientists is fair game. Besides calling someone a billionaire is not exactly insulting. Saying she misrepresnts her own science to the media is a matter of public record and I challenge you to find any DFO scientist that has done so towards her.
I do appreciate the debate on the science – when it does occasionally happen.
However, I will cease to respond to your malicious attacks on fish farm critics. It’s anti-productive and detracts from the issues we need to understand and deal with when we are discussing the impacts of the open net-cage technology. Maybe that’s why you insist on trying to deflect the debate – but I’m not buying-in any more. motivations if you will grant the same civility towards the scientists at DFO.
>>Iam fine to not bring up any thing personal about Morton and her motivations if you will grant the same civility towards the scientists at DFO. But next time you accuse Jones of stopping an experiment early because he was afraid the results would hurt salmon farmers, in other words , utterly lacking scientific integrity, I'll be all over you, matching your innuendo with hard evidence that Morton has repeatedly misrepresented her own results and that her predictions have not come true and that she is anything but an expert. You behave and I'll behave. Truce.
I will tidy-up with discussing a few points from some of your last posts…
Fish do flash when they get an external parasite – possibly in an attempt to dislodge that parasite. This happens for both sea lice (saltwater) and Trichodina ( or “Trich” in freshwater). I’m sure sockeyefry will even confirm this.
>>When fish “flash” – they advertise to predators, which in turn - increases predation. That’s part of the sub-lethal effects that lead to increased predation and population-level effects. >> Yes I know they flash and I have seen the science- there are many many environmental factors that make them flash and lice is one of them and lice have been in the ocean for millenia. this fact tells us nothing. so yes, I assume if salmon farms were contributing a signifiant amount of lice to the environment and they were infecting a wild salmon we may have a problem. Fortunately the weight of evidence to support that hypothesis is not there.
Another sub-lethal effect that has population-level effects – is growth rates. As motile sea lice create wounds (which can also allow viruses and bacteria to enter) and increases osmotic stress to fish – these hosts then have to spend much more energy pumping sodium out of their bodies at the gills. This is in addition to the energy lost directly to the parasite.
>>Yes that has been shown in the lab where the fish are exposed to unnaturally high doses of nauplii in an tank where they cannot access fresh water which may instantly remove the lice and thus not suffer any consequence. In lab tests, under these extreme conditions none of the infected juveniles dies from the infection. One would suppose they would be less likely to die from an infection in nature where they can easily remove the lice and they are exposed to much lower concentrations.
All of this energy loss means the fish grows slower (if at all in some cases), which again has population-level effects. The larger a fish is and grows – the faster it can escape predators. All of these points are well researched and covered, and available in the scientific literature.
>> they only would grow slower if they were under .3 grams and in a lab and were sea trout. dont confuse lab tests done on sea trout with the effect on wild Pacific stocks (Morton did that in her first paper).
You seem incapable of understanding what an enhanced run is, or what a spawning channel is. If you don’t understand after it has been explained to you – then you are demonstrating your lack of experience and incapacity to everyone on this forum. I find it ironic and arrogant that you told Cuttlefish that he doesn’t:”seem equipped to read scientific studies”.
In addition, your other statement to Cuttlefish: “the net water movement is strongly seaward- otherwise the inlets would fill up” similarly displays your ignorance of fjord estuarine science. It all the water only ran out of the inlet – the inlet would then become empty and dry.
The net SURFACE water movement is seaward, while high saline ocean water is entrained along the bottom. Then there are also the effects of tide and wind. We already covered this topic at length.
>> Yes I was aware I was over simplifying. Stucchi and Jones have demonstrated in detail the water movement in the fjords and how it relates to sea lice naupli movements. It was all ignored by Krkosek and his model makes the ridiculous assumption that wild fish near fish farms have higher levels of sea lice CAUSED by the fish farm. He also ignores plankton tow drag results that show no extra lice naupli are found near salmon farms. My point was that no matter how many arguments are made, the results so far show that the farther away from the freshwater source the more sea lice are caried by the salmon.
You also seem incapable of understanding or admitting that humans harvesting a wild food resource is what is natural – not the current industrialized and corporate-controlled food resource. Are there problems with how our resources are managed – with corporate control and greed as surrogates for sustainability – yes.
Killing wild fish to eat ensures fish are valued; the key is to ensure that is done sustainably. Your arguments to the contrary only show your obvious bias that you want people to buy your farmed product from you (or your fish farming buddies)– so that you (or your fish farming buddies) can get rich. You’re not fooling anyone but yourself.
>>this is just too weak a point to warrant yet another response. things that were natural when the earths population was less than a billion are no longer relevant. This is not about right or wrong, its about what works and doesnt work. we have tried to manage commercial harvesting of wild species with little success and massive failure. The definition of insanity is trying the same thing over and over expecting a different result. If 6 billion people want seafood, they sure as hell cant get it the same way it was got when there was only a billion people. Its "natural" to adjust to changing circumstance; its insane to keep trying the failed experiment of commercial fishing.
You keep confusing diseases with parasites. If sea lice are on fish, they drain resources. That drain can be substantial - even lethal - if the fish is small, or the lice numerous. If you can’t or won’t understand this – there is little more I can do to educate you.
>> Sorry AA it is you that are confused. infection by parasite does not equal disease. Other wise every wild fish out there is diseased. Have you ever caught a salmon without sea lice? Being infected is normal. You are infected, iam infected. we only suffere from disease if we endure stress- and sometimes not even then. Wild salmon were infected before fish farms came along and after fish farms came along. That is not up for debate. the debate is "do salmon farm produce a significant amount of sea lice to effect wild salmon health?" so far there is not good evidence that this is happening. In fact it looks like pacific salmon have an innate resistance to sea lice. I farmed for 10 years and never treated for sea lice. If you are infected with 2 lice and Iam infected by 1 lice are you sicker than me? Not necessarily, you can observe those fish 2 weeks later an dneither will have lice or show any effects. then some lice come and then they go. If it were the case then the fish with 2 lice would always dies before the fish with 1 lice. Even with 40 lice they may well have a full life. thats because infection does not equal disease. there is a measurable effect in the lab, that does not mean it is a significant effect. I know you dont get this. the world is very black and white to you and this doesn't fit. But the world is complex and mysterious and observations back this up.
If you want to argue that you can’t use the exact numbers (in number of parasites per gram of host weight) for sea lice-induced mortality from Bjorn and Finstead’s work on Atlantics to other species – you would be right. The levels would be similar – but not identical.
However, in the absence of species-specific information, those numbers have to be seen as a “best case” scenario, and use the precautionary approach until more accurate numbers come-in.
>> Thats nonsense. The tests were done in a lab on sea trout under ideal lice growing conditions [aka not natural] and we have lab studies done on Pacifics. the latter results trump. and still we have reason to believe that the effect would be far far milder in the wild. Thank goodness Mortons mis-citing of Bjorn and Finstead was not taken seriously by anyone who mattered. Besides, we still have no reason that to think that lice in the wild contribute significantly to wild salmon mortality. sea lice may not even constitute a spot in the top 100 causes of salmon mortality. in fact, and I know this will seem absurd, we may even find that lice infected wild salmon are resistsant to certain disease that lice free salmon are not. Its like bug feces on food. we wash our food to get rid of bugs and bug****- but if we wash it too much we deprive our system of essential Vitamin B. Too much or too little bug **** can be dangerous. The same MAY go for sea lice. AA, we dont know. SOME people pretend they know, and misrepresent themselves as knowing, but we are still just learning about the 300 species of sea lice that we know of so far.
As far as a comparison between Atlantic smolts and juvenile pinks go – pinks are way smaller and more at-risk than the Atlantic smolts.
>>HUH? We just discussed the Jones results and saw there is evidence that there is only a tiny window of opportunity for lice to infect and have a measurable effect on pink salmon. To infect a pink salmon that is under .7 grams the lice would have to cohabitate with the pink fry in virtually freshwater (WAAY upstream from any farm) for a period of days at unnaturally high concentrations. The Jones study shows that nature pretty well designed things so that by the time the pink had any exposure to lice from natural hosts his innate resistance was in place. It also showed that even under .7grams the lice seems to have little effect.
Yes, some sea lice can be knocked-off with most conventional fishing methodologies that fish with nets. What percentage is done by which nets is still undetermined (which I find strange why this has not yet been indexed) – but Beamish and DFO continue on trawling and claiming they can tell how much sea lice might have been on the abraided fish regardless of the obvious inconsistencies in that assumption.
>> Actually counting abrasions in parasitiology is a very established, reasonable methodology as referecnced in their paper. Or do you think all parasitologists from decades past are also in cahoots with DFO scientists?
There have been other nets (e.g. the Norwegian “Ocean-Fish-Lift”) developed to specifically address this issue – nets which Beamish et al. do not use. Check-out:
http://www.npafc.org/new/publications/Technical%20Report/TR4/page%2033(Holst).pdf
>> you mean nets that neither</u> Morton nor Beamish used.
Sticklebacks do not commonly have gravid (or even adult) sea lice on them. They therefore cannot be a source, but instead help juvenile salmon by being a sink for lice. If you understood sea lice at all – you would quickly make the connection.
>>Listen, Im not the one pretending to completely understand sea lice. You and Morton are. iam saying that Morton and Krkosek assumed no other hosts and DFO found one on the first try. There is more research to be done. Parasites often use a complex set of hosts to keep their life cycle going. Morton et al assumed that ONLY farm salmon could be a host and were instantly proven wrong. they also ignored studies done in the [fish farm free] Bering sea by Trudel(2006) who concluded
"This study demonstrated salmon examined in the Eastern Bering Sea infested with sea lice remained in coastal waters throughout the year. We suggest that lice on salmon that over winter in coastal waters will contribute to the infestation of salmon smolts migrating to sea in the spring through the release of lice naulpii."
Morton and Krkosek didnt refute or address this fact, they ignored it, and the stickleback finding, and went ahead and created a model assuming salmon farms were the ONLY possible source. It wa sonly after publishing and being publicly admonished that they created the "gravid lice defense" and pretended that it mattered. the topic wasnt even addressed in their paper. Note ALL DFO sea lice studies cite Morton and Krkosek thoroughly.
Another statement that demonstrates your lack of understanding of sea lice is your statement: “reason lice are more abundant on more fish near the farms rather than nearer the source of their home stream is because...the farms ar emore seaward”. Actually, in Ireland and Scotland – McKibben found the sea lice from the farms piled-up near the estuary due to tide and wind effects. You also forgot to mention that the reason lice plumes are more dense near fish farms is because the gravid female lice on the net-caged fish extrude naupilar lice stages.
>>You want to switch geography now? i have been to these places and I assure you there is no comparison with the Broughton. I have not read the McKibben paper, i will be interested in how he sampled, because our results , from either side of the debate do NOT show this. and who cares if stickleback have gravid or not gravid lice? we know they are part of the picture and all Morton and Krkosek studies have ignored this fact.
I quoted McVicar directly (forgot to put the quotes around it). That’s why I couldn’t therefore help but be amused at your assertion that I: “misrepresented MCvicar”.
I can only you assume that you believe he is a “friendly” and everything he says must support open net-pen technology because he is a ex-fish farmer turned into a veterinarian from Scotland. Your ignorance and neurotic tendencies are showing here.
>> Any enemy of junk science is a friend of mine. BTW congratulations you quoted mcVicar, but as usual you misinterpret what he means. McVicar is outraged at being misquoted by Krkosek et al.
;1. It is essential that the information used from quoted scientific papers is accurate. For example McVicar (1997, 2004) did not implicate farms in the infestations and collapse of wild sea trout and Atlantic salmon populations in Europe, but made reference to other publications where this was claimed. Both of these papers actually threw doubt on that claim.
I didnt say you misrepresented him, I said they did. You have a fondness for thinking you can win an argument with a soundbite. That's in line with a media-based campaign, or a marketting campaign, not a quest for understanding through scientific investigation. Please show me one incident where DFO scientists have mis-cited a paper by Krkosek or Morton?
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