I read this the other day and it's kind of the report Morton wish Cohen would have came out with but didn't, in my opinion. Although it did highlight some gaps I didn't find it very objective. In fact, the authors conveniently manoeuvred through the literature to make their point, but when you go to some of those cited studies in the references there is some missing context in Morton/Routledge article. There is a broader understanding missing and it can be found in a few of the references. In regards to PRV, the authors steered clear of most of the recent literature. Instead they picked only one quote from one of the studies from Dr. Garver. Well, Garver had more to say than that which I have posted on this forum already.
Honestly, if folks want a more objective view it would be better to read the studies in the references, but especially this one:
http://onlinelibrary.wiley.com/doi/10.1111/eva.12164/full
Doesn't sound like DFO or our government is following the precautionary principle when you read what you posted. Seems to me like more evidence that fish farms should be condemmed. Are you sure you read the study that you posted? I thought you were a supporter that was fine with fish farms.
From your link.
Potential for exchange between wild and cultured salmon
As wild salmon populations in North America and Norway have been declining in both numbers and productivity, aquaculture production has been increasing (Ford and Myers
2008; Walker and Winton
2010). There is growing evidence that in some regions, aquaculture may be a primary cause of declines in wild populations (Ford and Myers
2008). Reductions in fitness due to genetic introgression of farmed escapees (where endemic species are cultured) and transfer of disease are the main issues of concern (Heggberget et al.
1993). Disease exchange from aquaculture to wild fish may occur through the introduction of novel microparasites by translocations of eggs or juvenile fish, or as a result of artificially high carrier states of endemic microparasites due to high density rearing environments (Krkošek et al.
2006). Additionally, net pen farming could increase concentrations of myxozoan parasites by creating optimal environments for their intermediate invertebrate hosts (e.g., annelid worms) in the eutrophic environment under salmon pens (Johnsen et al.
1993), potentially increasing their impact on both farmed and wild migrating populations (Bakke and Harris
1998).
In aquaculture, fish can be reared at densities more than a thousand times those in natural environments (Pulkkinen et al.
2010). A fundamental principle of epidemiology is that populations should be most subject to host-specific infectious disease when they are at high densities (Lafferty and Gerber
2002). This is a key tenet of the premise that populations in a culture environment will be more affected by disease than wild populations; given what we know about disease outbreaks on farms, this does appear to be the case (Ibieta et al.
2011). In the section on microbial evolution above, we discussed the factors in addition to density present in a culture environment that facilitate rapid evolution of enhanced virulence. However, most evidence to date suggests that it is not the highly virulent microparasites produced by high density salmon culture that are the greatest risk to wild populations (Anderson
1979; Bakke and Harris
1998; Biering et al.
2013). For example, molecular monitoring of wild Atlantic Salmon and sea trout (
S. trutta) in Norway revealed that only one of the five emerging viruses (PRV but not IPNV, SAV, ISAV, or PCMV) impacting the salmon aquaculture industry was present in >1.5% of wild fish, nor were the two most pathogenic bacterial microbes,
R. salmoninarum and
A.
salmonicida present at appreciable levels among the 500 fish surveyed (Biering et al.
2013). These prevalence rates differed dramatically from those associated with the Norwegian aquaculture industry, which had been experiencing particularly high incidence of IPNV and SAV. The question is, did affeced wild fish simply die unsampled or is there really a much lower infection pressure on wild fish (McVicar
1997)?
Studies from terrestrial systems indicate that cultured animals can be important carriers of disease, even if the cultured species suffers little pathology (Lafferty and Gerber
2002). Terrestrial examples of domestic/wild impacts of disease exchange are abundant and have involved bacterial, fungal, viral, and protozoan infectious agents that have reduced wild populations of affected species by 80–90%, occasionally causing local extinction (reviewed in Lafferty and Gerber
2002). In the aquatic realm, a survey from ProMED-mail in 2000 revealed that hatcheries and aquaculture facilities were associated with the North American spread of ISAV and salmon sarcoma virus in Atlantic Salmon, and whirling disease (
M. cerebralis) and furuncolosis in trout (Dobson and Foufopoulos
2001). In Norway, disease outbreaks of gyrodactyliasis (caused by
G. salaris) and furunculosis leading to severe declines in wild populations are highly correlated with the expansion of the aquaculture industry in the northwestern Atlantic and the Baltic during the first half of the 1980s (Johnsen and Jensen
1994; Heggberget et al.
1993). The scale of
G. salaris losses was so great in Norwegian salmon rivers that entire systems were treated with rotenone in an attempt to eradicate the parasite (Windsor and Hutchinson
1990).
(cont'd in next post)
