The study commissioned by the Suzuki Foundation reviewed a number of possible factors that could have contributed to the low productivity of the 2000 brood year. When I read the executive summary I did find that the authors concluded that one of the factors was the high spawner densities. This is also found in the abstract of the main report. However, the authors said that although this egg to fry survival was low – it was not devastating. Now it was not the only factor, but it was suggested by the authors. The authors of the study also discuss the role of environmental impacts (sea surface temperatures, air temperatures, and stream discharge) and conclude that low survival was not the result of this although measurements in the study were based on the closest surrogate site (Port Hardy) and not direct stream measurements from the key study streams. They also suggest that with large number fish farms in the immediate area that sea lice had a serious impact on the survival of the 2000 brood and they go into reasons behind that hypothesis such as low rainfall, high salinities, lice burden levels, and juvenile residency in the area. However, they also conclude that there is no direct evidence of a causal link between sea lice on farmed salmon in the area and mortality of wild juvenile salmon. This also goes for the other factors in the study – there is no direct evidence to determine what caused this mortality. In a nutshell, they conclude this low survival is the result of cumulative impacts throughout the life history of this Pink Salmon brood year.
They also suggest that there is no evidence to indicate that sea lice are the primary invader (primary cause of death) or the secondary invader (opportunistic parasite on an already weakened host with a compromised immune system). In my opinion, this is where it was important at the time to do the proper fish pathology on these juvenile Pink Salmon to rule in or out any bacterial or viral infection. This was not done. How do we know if these juveniles were already compromised before they were infected with sea lice? We don’t. I don’t fully agree with the author’s contention that the lack of fish farm cooperation was the cause of not being able to find out if sea lice were the primary or secondary invader. The authors say that primary invaders (such as bacterial and viral pathogens) are not unusual in the sea farm industry so given that there is overlap between farmed and wild fish in the immediate area then lateral transmission is possible. I agree having knowledge of any bacterial or viral outbreak at those fish farms in the vicinity could have been helpful; however, that should not have prevented the necessarily sampling of juvenile Pink Salmon and subsequent diagnostic investigation (i.e. bacteriology, virology, and histology) at the time. In my opinion, the authors basically assumed that any bacterial and viral infections would have come from near by fish farms, but this ignores that fact that these pathogens are endemic and already exist in wild populations in BC. Cohen Technical Report #1 reviews all these endemic pathogens. That same report says that most of our current knowledge of salmonid diseases at the time of that technical report was based on research from cultured fish from either government hatcheries or aquaculture. There is an absence of this data from wild population because historically most this effort has been put into cultured fish (This is one of the Cohen recommendations. Studies like the Fish Health Initiative between DFO and Genome BC will hopefully shed more light on this.). When you look at a subsequent report (Marty et al 2010) on that same issue years later they conclude that this proper diagnostic work should have been done to the wild fish to rule in or out other compromising conditions. The role of this potential mortality in 2001 is unknown.
Relationship of farm salmon, sea lice, and wild salmon populations
http://faculty.vetmed.ucdavis.edu/faculty/gdmarty/2010PNAS107_52_22599-22604.pdf
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Topic: The Cohen Report (Read 11644 times)