To assume that any foreign viruses in the north pacific are product of salmon farming is here is a pretty far stretch considering what we have done previously before salmon farms were here.
EVERYBODY should not want this to be true!!! But the truth should be told.
I actually would have never made that statement. However, I will agree… I would be very surprised and not expect to find any foreign Norwegian viruses from anywhere on our Westcoast in the “North Pacific.” By definition that would be the Bering Sea and NONE of our Pacific salmon even migrate and enter the Bering Sea, unless they flat-out get lost. Therefore, you are correct it would be a “pretty (sp) far stretch” to see any “foreign viruses” by product of BC salmon lots! If they are found there, I personally would have to point my finger at Japan and/or Russia fish feed lots.
The principal arms of the Pacific Ocean are (in the north) the Bering Sea; (in the east) the Gulf of California; (in the south) Ross Sea; and (in the west) the Sea of Okhotsk, the Sea of Japan, and the Yellow, East China, South China, Philippine, Coral, and Tasman seas.
Now with that and assuming you are actually referring to Gulf of Alaska that would be a very bad and uninformed statement to make as DFO themselves have already taken samples and found ISAv in salmon in the Gulf a Alaska – see and start reading the Cohen Commission testimonies and reports! Btw…
The Gulf of Alaska, an arm of the Pacific Ocean, extends along the southeastern coastline of Alaska from the Alaska Peninsula to the Alexander Archipelago.
Then just do a search and you will find Mainstream (majority owned by the country of Norway) has already acknowledged the European strain of ISAv was transported to Chile by the Atlantic feedlot industry! It is not really hard to confirm that those feedlots transmit disease and viruses. FYI… you really believe Norway doesn’t realize they are transmitting “ALL” their viruses and diseases all over the world - That might be a little naïve.
Since this has been referring to ISA and ISAv I will gladly provide all the information your heart desires on that topic, as I have actually done quite a bit research on that myself.
I assure, and it certainly appears YOU don’t have a clue of what you are dealing with here!
SCIENTIFIC OPINION
Scientific Opinion on infectious salmon anaemia (ISA)
EFSA Panel on Animal Health and Welfare (AHAW)
European Food Safety Authority (EFSA), Parma, Italy
On request from the European Commission, Question No EFSA-Q-2012-00060, adopted on 16 November 2012.
Panel members: Edit Authie, Charlotte Berg, Anette Bøtner, Howard Browman, Ilaria Capua, Aline De Koijer, Klaus Depner, Mariano Domingo, Sandra Edwards, Christine Fourichon, Frank Koenen, Simon More, Mohan Raj, Liisa Sihvonen, Hans Spoolder, Jan Arend Stegeman, Hans-Hermann Thulke, Antonio Velarde, Ivar Vågsholm, Preben Willeberg and Stéphan Zientara. Correspondence:
AHAW@efsa.europa.eu
Acknowledgement: The Panel wishes to thank the members of the Working Group on infectious salmon anaemia: Edgar Brun, Debes Christiansen, Philippe Lemey, Niels Jørgen Olesen, Rob Raynard, Espen Rimstad, Fulvio Salati, Mike Sharp (chair until July 2012), Liisa Sihvonen and Ivar Vågsholm (chair from July 2012) for the preparatory work on this scientific opinion and EFSA staff, Per Have for the support provided to this scientific opinion.
1.4. ISAV infection
The development of more sensitive methods for virus detection by PCR during the 1990s (Mjaaland et al., 1997) enabled studies providing evidence of ISA virus infection in apparently healthy wild fish (feral Atlantic salmon, brown trout and sea trout, and escaped, farmed rainbow trout) (Raynard et al., 2001; Plarre et al., 2005).Refinements to molecular methods enabled the description of genomic sequences of ISA virus in wild salmonids which were hypothesised to show a full-length sequence of the HPR of the haemagglutinin-esterase (HE) gene (Mjaaland et al., 2002b). Thus, the hypothesis that deletions of HPR0 were required for emergence of HPR variants (HPRΔ) associated with virulent forms of ISAV was derived (Mjaaland, Hungnes, et al., 2002; Nylund et al., 2003).
ISAV can be genetically differentiated on the basis of the sequence of the HPR of genomic segment 6 which encodes the HE protein. Deletions within the HPR region (HPRΔ ISAV) have been identified in all virulent isolates causing clinical ISA disease and appear to be necessary for pathogenicity.
HPR0 ISAV appears to be widely distributed, both in areas infected with and areas free from HPRΔ ISAV and clinical disease. From a disease control point of view it is important to understand the dynamics and interrelationship between HPR0 and HPRΔ ISAV and, more particularly, the likelihood of and the reasons why HPRΔ arises from a background source of HPR0 ISAV.
In view of the above, the Commission is evaluating whether it is appropriate, proportionate and necessary to apply risk management measures to HPR0 ISA, in addition to those applied to HPRΔ ISAV. EFSA has been asked for a scientific opinion on the HPR0 variant of ISAV and to assess the risks posed by HPR0 ISA for the health of aquatic animals, in particular Atlantic salmon. The terms of reference (ToRs) provided by the Commission can be formulated as three questions:
1. Can HPR0 ISA cause clinical disease?
2. What is the risk of HPR-deleted ISA emerging from HPR0 ISA and, if relevant, indicating factors for such an emergence
a. What is the risk of HPR-deleted (HPRΔ) ISAV emerging from HPR0
b. What are the factors relevant for such an emergence?
2. The capability of HPR0 ISAV to cause clinical disease (ToR1)
ISA is a systemic and lethal condition and clinical signs suggest circulatory failure. So far only HPRΔ ISAV variants have been reported to cause disease in Atlantic salmon.
No experimental infection has been carried out so far with HPR0 ISAV. However, this variant has also been detected in naturally infected salmon, most often in the gills (McBeath et al., 2009; Christiansen et al., 2011). As opposed to the systemic and severe disease caused by HPRΔ ISAV, HPR0 ISAV replicates in (D.H. Christiansen, personal communication) and causes a localized infection of salmon gills with no signs of disease and only occasional spread to other organs (Christiansen et al., 2011). Parallel testing of kidney, heart and gill tissue for the presence of HPR0 ISAV by real-time RT-PCR disclosed a significantly higher overall detection in gill tissue compared with kidney and heart. Also, the load of HPR0 ISAV virus in positive gills was generally much higher than in kidneys and hearts (Christiansen et al., 2011; Lyngstad et al., 2011). Thus, HPRΔ ISAV and HPR0 ISAV show different infection patterns and tissue tropism, a pattern similar to that found in wild aquatic birds in which low-pathogenic avian influenza virus causes a subclinical, transient, mucosal infection whereas highly pathogenic influenza causes a systemic and lethal infection in poultry.
2.4. Geographical distribution of HPR0 ISAV
The first detection of HPR0 ISAV was done on gill tissue from a wild-caught Atlantic salmon in Scotland (Cunningham et al., 2002). In addition to Scotland, HPR0 ISAV has also been detected in farmed Atlantic salmon from the Faroe Islands, Norway, Canada, Chile and Denmark (N.J. Olesen, personal communication).
HPR0 has also been detected in wild Atlantic salmon in the Faroes and Norway. Three out of 88 confirmed wild Atlantic salmon caught by a Faroese research vessel at the feeding grounds in the North Atlantic were HPR0 positive (D.H. Christiansen, personal communication). Furthermore, 4 out of 305 Atlantic salmon caught in rivers in mid-Norway were found to be positive by PCR. Viral RNA from one of them was sequenced to HPR0, clustering phylogenetically with the Faroes cluster. The amount of RNA from the other three was too scarce for sequencing, but still empirically indicated the presence of HPR0. All salmon were caught in an area with on-going ISA outbreaks with virus subtypes associating with a cluster different from that identified as HPR0. The four positive ones were all from the same river and confirmed as “wild salmon” according to fish scale examination. (R. Grøntvedt and T. Lyngstad, personal communication).
The Faroe Islands documented findings of HPR0 in Atlantic salmon in their monitoring from 2005 to 2009. HPR0 was detected on gills 1–13 months post sea transfer (mean 7.7 months). The various cohorts (49) were sampled 5–12 times each year, and the presence of HPR0 on gills showed peaked transient infection profile with peak prevalence up to 100 % lasting for 4 months. Almost all of the cohorts were positive for HPR0. No clinical disease or histopathological consequences have been reported in association with this HPR0 infection in the Faroes (Christiansen et al., 2011).
In Chile, all ISAV strains detected in 2011 were identified as HPR0 (Kibenge et al., 2012). No outbreaks were observed and HPRΔ was not detected.
In a retrospective study in Norway (Lyngstad et al., 2012), ISAV was present in 23 % of 210 cohorts of marine farmed Atlantic salmon along the coast, with no suspicion of ISA. HPR0 ISAV was confirmed in 59 % of these ISAV-positive groups. The rest of the positive groups were not sequenced due to lack of RNA, but the low titres may indicate the presence of HPR0.
The groups were sampled once and at various points in time after sea transfer. In other screening studies, HPR0 has been detected in gill samples from juvenile salmon and in brood stock in the freshwater environment (M. Devold and D. H. Christiansen, personal communication). A low level of HPR0 has also been detected in ovarian fluid of farmed Atlantic salmon (D. H. Christiansen, personal communication).