An experimental means of transmitting pancreas disease in <scp>A</scp>tlantic salmon <i>Salmo salar </i><scp>L</scp>. fry in freshwater

Cano, Irene; Joiner, C.; Bayley, Amanda; Rimmer, Georgina S. E.; Bateman, Kelly S.; Feist, Stephen W.; Stone, David A.; Paley, Richard

doi:10.1111/jfd.12310

Cited by 11 publications

(10 citation statements)

References 40 publications

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“…Degenerative lesions were seen in the liver and kidney of some groups however, which are not usually observed during experimentally-induced or naturally occurring clinical SAV infections of older fish [ 12 , 15 ]. The differences of pathological presentation seen in the fry in the present study was similar to that observed by Cano and others [ 26 ] compared to previous experimental and clinical infections in adult fish [ 15 ], and may be indicative of fry being less active or having lower levels of immune competence.…”

Section: Discussionsupporting

confidence: 90%

“…This study was performed to examine the susceptibility and pattern of disease pathogenesis in diploid and triploid Atlantic salmon fry exposed to SAV1 through an IP, immersion or co-habitation route of infection. Cano and others [ 26 ] recently established an SAV1 infection in Atlantic salmon fry using an immersion route of infection. The present study is the first report of a SAV infection in both triploids and diploids using IP and co-habitation routes to infect the fish.…”

Section: Discussionmentioning

confidence: 99%

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Impact of Salmonid alphavirus infection in diploid and triploid Atlantic salmon (Salmo salar L.) fry

et al. 2017

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With increasing interest in the use of triploid salmon in commercial aquaculture, gaining an understanding of how economically important pathogens affect triploid stocks is important. To compare the susceptibility of diploid and triploid Atlantic salmon (Salmo salar L.) to viral pathogens, fry were experimentally infected with Salmonid alphavirus sub-type 1 (SAV1), the aetiological agent of pancreas disease (PD) affecting Atlantic salmon aquaculture in Europe. Three groups of fry were exposed to the virus via different routes of infection: intraperitoneal injection (IP), bath immersion, or cohabitation (co-hab) and untreated fry were used as a control group. Mortalities commenced in the co-hab challenged diploid and triploid fish from 11 days post infection (dpi), and the experiment was terminated at 17 dpi. Both diploid and triploid IP challenged groups had similar levels of cumulative mortality at the end of the experimental period (41.1% and 38.9% respectively), and these were significantly higher (p < 0.01) than for the other challenge routes. A TaqMan-based quantitative PCR was used to assess SAV load in the heart, a main target organ of the virus, and also liver, which does not normally display any pathological changes during clinical infections, but exhibited severe degenerative lesions in the present study. The median viral RNA copy number was higher in diploid fish compared to triploid fish in both the heart and the liver of all three challenged groups. However, a significant statistical difference (p < 0.05) was only apparent in the liver of the co-hab groups. Diploid fry also displayed significantly higher levels of pancreatic and myocardial degeneration than triploids. This study showed that both diploid and triploid fry are susceptible to experimental SAV1 infection. The lower virus load seen in the triploids compared to the diploids may possibly be related to differences in cell metabolism between the two groups, however, further investigation is necessary to confirm this and also to assess the outcome of PD outbreaks in other developmental stages of the fish when maintained in commercial production systems.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Impact of Salmonid alphavirus infection in diploid and triploid Atlantic salmon (Salmo salar L.) fry

et al. 2017

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“…Although viral isolates have been detected in freshwater, no outbreaks of PD in the fry stage have been recorded ( Jansen et al , 2010b ). The practicality of large-scale challenge experiments at the fry stage of the salmon lifecycle has meant that fry challenges can be used as a model for post-smolt PD outbreaks ( Cano et al , 2014 ). However, differences in behaviour, environment and physiology between the freshwater and marine stages of the salmon lifecycle mean that the genetic architecture of PD resistance could potentially differ between the two life stages.…”

Section: Discussionmentioning

confidence: 99%

Mapping and validation of a major QTL affecting resistance to pancreas disease (salmonid alphavirus) in Atlantic salmon (Salmo salar)

et al. 2015

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Pancreas disease (PD), caused by a salmonid alphavirus (SAV), has a large negative economic and animal welfare impact on Atlantic salmon aquaculture. Evidence for genetic variation in host resistance to this disease has been reported, suggesting that selective breeding may potentially form an important component of disease control. The aim of this study was to explore the genetic architecture of resistance to PD, using survival data collected from two unrelated populations of Atlantic salmon; one challenged with SAV as fry in freshwater (POP 1) and one challenged with SAV as post-smolts in sea water (POP 2). Analyses of the binary survival data revealed a moderate-to-high heritability for host resistance to PD in both populations (fry POP 1 h2~0.5; post-smolt POP 2 h2~0.4). Subsets of both populations were genotyped for single nucleotide polymorphism markers, and six putative resistance quantitative trait loci (QTL) were identified. One of these QTL was mapped to the same location on chromosome 3 in both populations, reaching chromosome-wide significance in both the sire- and dam-based analyses in POP 1, and genome-wide significance in a combined analysis in POP 2. This independently verified QTL explains a significant proportion of host genetic variation in resistance to PD in both populations, suggesting a common underlying mechanism for genetic resistance across lifecycle stages. Markers associated with this QTL are being incorporated into selective breeding programs to improve PD resistance.

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“…Indeed, the loss of exocrine pancreatic tissue resulting in inappetence and defective uptake of nutrients [ 32 , 39 ] together with the loss of muscle progenitor cells slowing down the muscle regeneration might be the reason of the low growth rate observed in surviving fish. In addition, previous results mentioned that clearance of the virus did not occur in all challenged fish which might lead to persistent chronic inflammation and thus delaying even more the full recovery in surviving fish [ 30 , 31 , 40 ]. These observations are supported by the long lasting in vitro replication of SDV in trout skeletal muscle progenitors.…”

Section: Discussionmentioning

confidence: 99%

Rainbow trout (Oncorhynchus mykiss) muscle satellite cells are targets of salmonid alphavirus infection

Biacchesi

Jouvion

Mérour

et al. 2016

Vet Res

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Sleeping disease in rainbow trout is characterized by an abnormal swimming behaviour of the fish which stay on their side at the bottom of the tanks. This sign is due to extensive necrosis and atrophy of red skeletal muscle induced by the sleeping disease virus (SDV), also called salmonid alphavirus 2. Infections of humans with arthritogenic alphaviruses, such as Chikungunya virus (CHIKV), are global causes of debilitating musculoskeletal diseases. The mechanisms by which the virus causes these pathologies are poorly understood due to the restrictive availability of animal models capable of reproducing the full spectrum of the disease. Nevertheless, it has been shown that CHIKV exhibits a particular tropism for muscle stem cells also known as satellite cells. Thus, SDV and its host constitute a relevant model to study in details the virus-induced muscle atrophy, the pathophysiological consequences of the infection of a particular cell-type in the skeletal muscle, and the regeneration of the muscle tissue in survivors together with the possible virus persistence. To study a putative SDV tropism for that particular cell type, we established an in vivo and ex vivo rainbow trout model of SDV-induced atrophy of the skeletal muscle. This experimental model allows reproducing the full panel of clinical signs observed during a natural infection since the transmission of the virus is arthropod-borne independent. The virus tropism in the muscle tissue was studied by immunohistochemistry together with the kinetics of the muscle atrophy, and the muscle regeneration post-infection was observed. In parallel, an ex vivo model of SDV infection of rainbow trout satellite cells was developed and virus replication and persistence in that particular cell type was followed up to 73 days post-infection. These results constitute the first observation of a specific SDV tropism for the muscle satellite cells.

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An experimental means of transmitting pancreas disease in Atlantic salmon Salmo salar L. fry in freshwater

Cited by 11 publications

References 40 publications

Impact of Salmonid alphavirus infection in diploid and triploid Atlantic salmon (Salmo salar L.) fry

Impact of Salmonid alphavirus infection in diploid and triploid Atlantic salmon (Salmo salar L.) fry

Mapping and validation of a major QTL affecting resistance to pancreas disease (salmonid alphavirus) in Atlantic salmon (Salmo salar)

Rainbow trout (Oncorhynchus mykiss) muscle satellite cells are targets of salmonid alphavirus infection

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