Infection with salmonid alphavirus
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Infection with salmonid alphavirus
International Common Names
- English: pancreas disease; pancreas disease of Atlantic salmon; salmon pancreas disease; salmonid alphavirus infection; sleeping disease
OverviewTop of page
Pancreas disease (PD) is a viral disease of farmed Atlantic salmon (Salmo salar L.) and rainbow trout (Oncorhynchus mykiss W.) in seawater, characterized by extensive necrosis of the exocrine pancreas (Munro et al., 1984; McVicar, 1987), and cardiac and skeletal myopathy (Ferguson et al., 1986a; Ferguson et al., 1986b; Rodger et al., 1991; McLoughlin et al., 2002). Mortality may be moderate, but this varies between farms and geographical regions. Mortality rates up to 50% have been reported (Menzies et al., 1996; Anonymous 2002). Economic losses may be high because survivors often fail to grow and may die several months after the primary outbreak (Munro et al., 1984).
A nutritional aetiology was initially considered as vitamin E and selenium deficiencies were present in diseased fish (Ferguson et al., 1986b), but the course and pattern of spread of the disease indicated an infectious aetiology (McVicar, 1987). This was later confirmed in transmission experiments using tissue homogenates from affected fish (McVicar, 1990; Raynard and Houghton, 1993). A viral aetiology was suggested as infective material was inactivated after treatment with chloroform (Murphy et al., 1995), and the spread of the infectious agent through the circulatory system was typical of a viraemia (Houghton, 1995). Although numerous attempts to propagate the causal agent in cell culture had failed, Nelson and co-workers isolated a toga-like virus from Atlantic salmon with clinical PD (Nelson et al.,1995). Re-injection of the virus into experimental fish and exposed cohabitant fish resulted in typical histological lesions of PD, and it was therefore proposed that the virus be termed salmon pancreas disease virus (SPDV). This virus has subsequently been identified as an alphavirus of the Togaviridae family (Weston et al., 1999).
Sleeping disease (SD) is a viral disease of rainbow trout Oncorhynchus mykiss (Walbaum) reared in freshwater. The disease was first observed in France (Boucher and Baudin Laurencin, 1994) and affects rainbow trout at all stages of production. SD is an emerging disease associated with increased mortality and growth retardation that has been reported as an increasing problem in Europe. It is endemic in parts of France and has been observed for many years in Italy. More recently, SD was reported in England, Scotland (Branson, 2002; Graham et al., 2003b) and Spain (Graham, Belfast UK, 2004 personal communication).
The most characteristic sign of SD is the unusual behaviour of fish which lie on their side at the bottom of the tank. The lesion responsible for this behaviour was presumed to be extensive necrosis of the skeletal red muscle. This chronic stage follows characteristic lesions of the exocrine pancreas and heart (Boucher and Laurencin, 1996). The viral aetiology of SD was suspected for some time (Boucher and Baudin Laurencin, 1994) and was recently confirmed by the isolation of the Sleeping Disease Virus (SDV) (Castric et al., 1997). SDV was subsequently characterised as an atypical alphavirus of the Togaviridae family (Villoing et al., 2000a).
SDV and SPDV are closely related isolates of the same virus species, for which the name Salmonid alphavirus is proposed (Weston et al., 2002).
[Based upon material originally published in Woo PTK, Bruno DW, eds, 1999. Fish diseases and disorders, Vol. 3 Viral, bacterial and fungal infections. Wallingford, UK: CABI Publishing.]
Hosts/Species AffectedTop of page
Pancreas Disease (PD) has typically affected farmed Atlantic salmon (Salmo salar) during their first year in seawater with the peak prevalence occurring from late July to early September (McVicar, 1987; Crockford et al., 1999). However, in recent years Atlantic salmon at all stages of the marine production cycle have been recognized as susceptible (M McLoughlin, AB Olsen personal observations). In France, PD also affects seawater-reared brown trout (Salmo trutta) (Boucher et al., 1995) and in Norway, PD severely affects seawater-reared rainbow trout (Oncorhynchus mykiss) (Olsen and Wangel 1997). Following experimental infection of seawater-reared rainbow trout, brown trout and Atlantic salmon with SPDV, rainbow trout and brown trout developed typical but less severe lesions than Atlantic salmon; brown trout was even less susceptible than rainbow trout (Boucher et al., 1995). Experimental induction of the disease in Atlantic salmon parr in freshwater and post-smolt in seawater has also been achieved (McLoughlin et al., 1995; Murphy et al., 1995; McLoughlin et al., 1996).
Sleeping Disease (SD) has been recorded mainly in freshwater-reared rainbow trout; these can be affected at all stages of production. The disease has occasionally been recorded in Coho salmon (Boucher and Baudin Laurencin, 1994), and has been transmitted experimentally to Atlantic salmon (Boucher and Laurencin, 1996).
Present knowledge on specific risk factors for PD is limited, but general risk factors associated with other viral fish diseases are likely. In a Norwegian retrospective case-control study of PD, environmental factors such as lack of fallowing of sites and well boat traffic were associated with an increased risk for PD, whereas the season (spring or autumn) for seawater transfer of smolts did not affect prevalence nor the time from transfer to outbreak (Brun et al., 2005).
DistributionTop of page
Pancreas Disease was first recorded in 1976 in Scotland (Munro et al., 1984). Later, a similar disease was reported to affect Atlantic salmon in North America (Kent and Elston, 1987), Norway (Poppe et al., 1989), Ireland (Murphy et al., 1992), France and Spain (Raynard et al., 1992).
Sleeping Disease is endemic in parts of France (Boucher and Baudin Laurencin, 1994; Boucher and Laurencin, 1996) and has been observed for many years in Italy (G. Bovo 2003, personal communication). SD has more recently been reported in England and Scotland (Branson, 2002; Graham et al., 2003b) and in Spain (D Graham, Belfast UK, 2004 personal communication).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|France||Present||Raynard et al., 1992; Boucher and Baudin, 1994; Boucher and Laurencin, 1996|
|Ireland||Present||Murphy et al., 1992|
|Norway||Present||Poppe et al., 1989|
|Spain||Present||Raynard et al., 1992|
|UK||Present||Present based on regional distribution.|
|-England and Wales||Present||Graham et al., 2003b; Branson, 2002|
|-Scotland||Present||Munro et al., 1984|
PathologyTop of page
Pancreas Disease (PD)
The main clinical signs observed in chronological order of their appearance are sudden inappetence; lethargy; increased mortality; and ill-thrift. In the early stages of PD, the principal gross findings are no food in the stomach, yellow casts in the gut and occasional petechiae over the surface of the pyloric caeca and surrounding fat.
In the chronic stages, fish in good body condition can be seen swimming in a spiralling or circling motion, or they may appear seemingly dead at the bottom of the cage, but are still able to swim away when handled (McLoughlin et al., 2002). Examination of the latter fish show severe skeletal muscle pathology. Occasionally fish has been observed spitting out pellets of food. This was found to coincide with the appearance of degenerative lesions in the striated muscle of the oesophagus, which occasionally occurred in chronic PD outbreaks (Ferguson et al., 1986b). In chronically affected and recovering fish there is reduced caecal and body fat and long thin fish with poor body condition (runts) are more common (Fig. Normal (upper) and PD-affected (lower) Atlantic salmon of the same age).
Although a low level mortality may be recorded early in an outbreak simultaneously with inappetence and acute pancreatic necrosis, the main mortality peak is usually recorded later and is associated with the abnormal swimming behaviour and skeletal muscle lesions (McLoughlin et al., 2002). The mortalities vary significantly (see economic impact above) between sites, but usually not between years on the same site, indicating a complex multifactorial aspect to this disease. High mortalities tend to occur in high energy sites, i.e. oceanic sites or sites with strong water currents, and when the fish were returning to feed (Crockford et al., 1999).
Original histopathological descriptions of pancreas disease only recognised complete loss of exocrine pancreatic acinar tissue as the main lesion and this finding was influential in naming the disease (Munro et al., 1984; McVicar, 1987) (Fig. Pancreas from PD-affected fish showing extensive acinar necrosis to the left and less affected tissue to the right). Fibrotic tissue may replace the degenerated acinar tissue, or in recovering fish, a regeneration of exocrine tissue seems to take place (Munro et al., 1984). This may occur very rapidly with affected fish having apparently normal pancreatic architecture within 4 weeks after infection, but heart and especially skeletal muscle lesions persist for a longer period (McLoughlin et al., 2002).
The lesion profile of PD was extended by the description of severe cardiac as well as skeletal myopathy which was often associated with high PD-mortality (Ferguson et al.,1986a,b; McVicar, 1987; McCoy et al., 1994; Rodger et al., 1994; McLoughlin et al., 2002). The major cardiac lesions are characterized by necrosis of the ventricular myocardium that affects both the spongy and compact layers. The striation of the muscle may disappear with an increased eosinophilia and degeneration of myocardial fibres. The atrial myocardium seems to be less affected (Ferguson et al., 1986a). Similar lesions are found in the skeletal muscle, which usually affects all red fibres, especially along the lateral line, and white muscle to a more variable degree (Rodger et al., 1991). The muscle lesions are prevalent in fish in the chronic and recovery stages of the disease. In the recovery stage red muscle may show significant inflammation and fibrosis, with a significant number of regenerating muscle fibres also present. Table 1 summarise the location of tissue lesions at different stages of PD.
Table 1. The location of tissue lesions at different stages of PD
Stage of PD
- / +
Sleeping Disease (SD)
The most characteristic sign of the disease is the unusual behaviour of fish which lie on their side at the bottom of the tank. If they are disturbed, they swim for some time and then return down to the bottom. Extensive necrosis of the skeletal red muscle is probably responsible for this behaviour. There are usually no macroscopic lesions, but occasionally petechiae on the pyloic caeca are found (Boucher and Baudin Laurencin 1994). The sequential development of lesions in pancreas, heart and muscle as well as the quality of those lesions are similar to PD (Boucher and Laurencin 1996).
DiagnosisTop of page
Pancreas Disease (PD)
Early clinical signs are increased appetite prior to a sudden drop in appetite which is indicative of acute PD. However, these signs are not always present or observed. Some weeks later, abnormal swimming behaviour and increased mortality are usually observed, indicating a chronic phase of the disease. PD tends to recur in affected sites and regions.
Careful observation and selection of clinically diseased fish for diagnostic examinations will enhance the probability of the detection of PD, as compared to random sampling in cages with diseased fish.
At autopsy, yellow mucus in the gut is a common finding, but this may also be seen in fish that have not eaten for a variety of reasons. In some fish, fine petechiae in the pyloric fat tissue can be observed, resembling acute infectious pancreatic necrosis (IPN). Patchy pale discolouration of muscle may indicate PD related pathology. Thin, slender fish (runts) are often found one to several months after the onset of mortality, when the majority of the surviving fish usually appear clinically healthy.
For several years, the diagnosis of PD was based on clinical signs, autopsy and the detection of characteristic lesions in pancreas, heart and muscle as seen by histopathology (McLoughlin et al., 2002). Recently, several additional diagnostic tools have been established. Some methods are currently used for research and some are being validated for diagnostic use. The choice of methods will depend on the purpose of the examinations, and it is important to take into account that the suitability of different methods may depend upon the stage of the disease development. In general, the use of several methods based upon biologically different principles will give the most reliable diagnoses.
Histopathology is still the basic method used to identify PD (McLoughlin et al., 2002) and to differentiate PD from similar diseases (Table "Location of tissue lesions in salmonid fish diseases with similar pathologies"). PD is a slowly developing disease, and the characteristic lesions in the different tissues in a single fish do not develop simultaneously. Therefore, different patterns of lesions characterise the different stages of PD (Table "Location of tissue lesions at different stages of PD" in the Pathology section). To detect SPDV in tissue sections, an immunohistochemical procedure has been established, using a monoclonal antibody against E1 glycoprotein as a primary antibody. It detects SPDV in acute pancreatic necrosis and can thus be used to differentiate PD from acute IPN. However, this method does not identify SPDV in PD-related lesions in sub-acute and late stage PD and is therefore of limited use (Taksdal et al., 2003).
Recently, a rapid virus neutralization test for the detection of specific antibodies against SPDV in blood samples has been developed (Graham et al., 2003a). The test has been used for examination of a large number of farmed as well as wild salmonids and is a reliable method for confirming that fish have been exposed to SPDV and SDV. Neutralizing antibodies are usually first detected approximately 3 weeks after first detection of SPDV in a fish farm or in experimental infection (McLoughlin et al., 1996). Examination of serum samples collected 2-4 weeks apart will add valuable information about the time scale of the outbreak, as rising antibody titres could indicate a recent infection. After the first detection of antibodies during an outbreak, a high prevalence of antibody-positive fish has been detected throughout the following production cycle (Graham et al. 2005).
Viral detection in cell culture by inoculation of tissue homogenates from diseased fish has been difficult (Christie et al., 1998) and requires considerable experience in detecting SAV cytopathic effects (CPE) in cell culture. However, during work with the neutralization test (Graham et al., 2003a) it was revealed that viraemic fish could be detected using serum from diseased fish in CHSE-214 cell cultures in combination with immunperoxidase staining. In this case, virus could be detected in advance of any development of CPE in the cell cultures. This method has been much more efficient in isolating new SPDV and SD isolates from serum samples than from other tissues. Several new field isolates of SPDV and SDV have been obtained by this method (Jewhurst et al., 2004). Moreover, recent experience from Norway is that cell culture SPDV isolation from kidney of PD-diseased fish is quite easily obtained if isolation is done ahead of the increase in antibody response (Dannevig, personal communication). SPDV has now been isolated from several Norwegian outbreaks, and both CHSE-214 and BF-2 cell cultures are useful for primary isolation of SPDV.
Different protocols for reverse transcription-polymerase chain reaction (RT-PCR) detection of SPDV have been established at several laboratories. Primer selection will depend on whether identification of all or single genotypes of the virus is required (Hodneland et al., 2005). RT-PCR with primers adjusted to Norwegian isolates of SPDV has efficiently detected SPDV in kidney or pooled heart and kidney from fish diagnosed with acute, sub-acute and chronic PD in Norway (Taksdal et al., 2005).
A summary of the available diagnostic panel for PD is presented in table 2
Sleeping Disease (SD) diagnostic tests are in principle similar to those for PD, with minor modifications. The main clinical sign is the detection of fish "sleeping" at the bottom of the tank. Histopathological lesions are similar to those of PD. By immunohistochemistry, SDV can be detected in acute pancreatic lesions and in muscle lesions in chronically diseased fish, which indicates that immunohistochemical methods may be worth further investigation (Kerbart Boscher 2004 personal observation). Methods for detection of antibodies to SDV and for the detection of SDV by RT-PCR and by cell culture have also been established (Villoing et al. 2000b; Kerbart Boscher et al., in press)
Table 2: Diagnostic Panel for PD & SD
Days post Infection*
* Days are dependent on several biological factors and may vary. It must also be noticed that not all fish in a cage will be infected simultaneously. The information in this table is based upon published and unpublished experiments and field observations.
There are a number of economically important conditions in Atlantic salmon which share similar pathological lesions with PD (Table 3 below). Infectious pancreatic necrosis (IPN) (see appropriate Datasheet) caused by a birnavirus can cause significant pancreatic lesions similar to PD, but can readily be distinguished from PD by the absence of heart and muscle lesions and the presence of catarrhal enteritis and liver lesions in freshwater and marine salmonids (Roberts and Pearson, 2005).
Cardiomyopathy syndrome (CMS) (see appropriate Datasheet) a condition of unknown aetiology of seawater-reared Atlantic salmon, has been recorded in both Norway and Scotland (Ferguson et al.1990, Rodger and Turnbull, 2000). It is a chronic progressive heart disease associated with sudden heart failure. Severe myocardial degeneration of the atrium and spongy ventricular muscle is characteristic of this condition and similar lesions have been seen in severe cases of PD (McLoughlin and Olsen, 2005 Personal communication).
More recently a condition known as heart and skeletal muscle inflammation (HSMI) has been described in Norway and Scotland (Kongtorp et al., 2004a, b; Ferguson et al., 2005). In this condition heart and skeletal muscle lesions which are histologically very similar to PD have been described in field and experimental studies. Pancreas lesions have not been associated with either CMS or HSMI. The aetiologies of CMS and HSMI are not known at present.
Table 3. Location of tissue lesions in salmonid fish diseases with similar pathologies.
PD & SD
PD = Pancreas disease, SD = Sleeping disease, IPN = Infectious pancreatic necrosis, CMS = Cardiomyopathy syndrome, HSMI = Heart and skeletal muscle inflammation
List of Symptoms/SignsTop of page
|Finfish / Cessation of feeding - Behavioural Signs||Aquatic:All Stages||Sign|
|Finfish / Darkened coloration - Skin and Fins||Aquatic:All Stages||Sign|
|Finfish / Emaciation - Body||Aquatic:All Stages||Sign|
|Finfish / Generalised lethargy - Behavioural Signs||Aquatic:All Stages||Sign|
|Finfish / Haemorrhaging - Body Cavity and Muscle||Aquatic:All Stages||Sign|
|Finfish / Mortalities -Miscellaneous||Aquatic:All Stages||Sign|
|Finfish / Pancreas - white-grey patches (haemorrhage / necrosis / tissue damage) - Organs||Aquatic:All Stages||Sign|
Disease CourseTop of page
Pathogenesis and immunity
Pancreas Disease (PD) and Sleeping Disease (SD) affect many organs and the interpretation of the histological changes can often be complicated. Studies of pathogenesis have, until recently, been difficult since no specific methods for the detection of the viral agent were available. The studies have therefore been mainly based on histological examination of samples collected from natural outbreaks and from transmission experiments.
Munro et al. (1984) described the pathogenesis of the pancreatic lesions of PD in Atlantic salmon and divided the development into three phases with respect to histological changes in the pancreas: pre-acute, acute and post-acute phase. The pre-acute phase is characterized by a predominance of pancreatic acinar type B cells which have a densely basophilic cytoplasm and contain few zymogen granules. Vacuolation of the acinar cells can also be observed. There are no changes in haematocrit values, erythrocyte morphology and serum proteins in the pre-acute phase.
The acute phase is characterized by massive loss of pancreatic acinar cells. Erythrocyte morphology and haematocrit values are normal, but leucocyte hyperplasia in the head kidney and a drop in serum protein concentration can be observed. Pancreatic lesions seem to affect nearly all fish in a population over a five week period after the initial infection.
In the post-acute phase, a large proportion of fish from affected populations show normal or recovering pancreas, while in a small proportion of the fish, fibrotic tissue has replaced the exocrine pancreatic tissue. Fish that show no recovery of pancreatic tissue are unlikely to recover, they develop into runts and are usually culled.
The development of cardiac and skeletal myopathy has been studied in Atlantic salmon by monitoring pathological changes for six to nine months following seawater transfer (Murphy et al., 1992; McLoughlin et al., 2002). The prevalence of heart lesions is highest among fish with pancreatic lesions, but cardiomyopathy has been observed in fish with both normal and affected pancreas before the appearance of lethargy and increased mortality. Skeletal myopathy is most prominent in the red (aerobic) muscle beneath the skin and appears only in fish in the chronic stage or in the recovery stage of the disease (Rodger et al., 1991; Murphy et al., 1992; McLoughlin et al., 2002). However, these muscle lesions were not found in all cases (McVicar, 1987; Rodger et al.,1994) and it was suggested that they may represent secondary effects, for example such as induced vitamin E deficiency as a response to changes in the nutritional status of the fish due to pancreatic damage and reduced feeding. Furthermore, vitamin E deficiency has been observed in PD-diseased fish (Ferguson et al., 1986b; Raynard et al., 1991) and it was suggested that this deficiency could induce myopathy. However, other reports do not support this hypothesis as pancreatic lesions and myopathy occur simultaneously even with high tissue vitamin E concentrations (McCoy et al., 1994). Low plasma levels of vitamin E also occur in Atlantic salmon suffering from infectious pancreatic necrosis (IPN) (Taksdal et al., 1995), a disease that has not been connected to any muscle lesions.
An increased concentration of lipase in plasma occurs in early PD-affected fish (Grant et al., 1994), while the levels of the digestive enzymes trypsin and chymotrypsin in pyloric caeca tissue decline significantly during the development of the disease, both in experimentally and naturally infected Atlantic salmon (Pringle et al., 1992). The presence of digestive enzymes in the plasma can be explained by leakage of enzymes from acinar cells due to the pathological changes in the tissue. The decrease in enzyme levels in digestive tissues correlates well with the histological changes and may be used as an early indicator of reduced feeding and exocrine pancreatic dysfunction.
The progression of lesions in experimentally infected freshwater Atlantic salmon parr is similar to that in naturally infected seawater post smolts (McLoughlin et al.,1995; 1996). Loss of appetite occurs simultaneously with the acute pancreatic lesions (Taksdal, unpublished). Blood plasma of Atlantic salmon was infectious from day 1 after intraperitoneal injection of PD-infective kidney homogenate (Houghton, 1995). Leucocytes from blood, spleen and kidney became infective from approximately day 3 post infection. The appearance of infectivity in cells and organs was temperature dependent. The infectivity remained high until pancreatic lesions were observed. Thereafter the plasma, leucocytes or kidney were not infective, indicating an early and short lived viraemia.
Evidence for a protective immune response against SPDV has been reported, both in naturally (Murphy et al., 1995; Graham et al., 2003a; Graham et al., 2005) and experimentally (Houghton, 1994) infected farmed Atlantic salmon.
In the latter case, PD-challenged fish acquired a resistance to PD that lasted at least nine months after the primary infection. Humoral factors seemed to be involved in the immune response as passive immunization with serum from recovered fish protected parr against PD when challenged with PD-infective material (Murphy et al., 1995). Antisera collected from experimentally infected Atlantic salmon up to 15 weeks post infection neutralized PD-infective material when tested in transmission experiments (Houghton and Ellis, 1996). Neutralizing activity was found in sera from fish infected both by injection and cohabitation (Houghton and Ellis, 1996).
After natural infection, seroconversion has been identified, and the prevalence of fish with antibodies against SPDV remained high (66-90%) until slaughter, 7-9 months after the PD outbreaks (Graham et al., 2005).
After experimental infection of rainbow trout with kidney homogenates from either SD- or PD-affected fish, the fish successively developed similar pancreatic, heart and muscle lesions in both populations, although the SD-injected population was the most severely affected (Boucher and Laurencin 1996). An acquired cross protection was observed against PD and SD after initial injection with PD- and SD-infective material, a result that supported the idea that the two diseases are closely related (Boucher and Baudin Laurencin 1996).
EpidemiologyTop of page
The natural reservoir(s) of the viruses is unknown. However, the fact that Pancreas Disease (PD) outbreaks have only been recorded in seawater-reared salmonids suggests a marine reservoir of salmon pancreas disease virus (SPDV), as opposed to Sleeping Disease (SD) that has only been recorded in freshwater.
Field data provide evidence for horizontal waterborne transmission of PD (McVicar, 1987), and this has been demonstrated experimentally both for PD (Raynard and Houghton, 1993; McLoughlin et al., 1995; Murphy et al., 1995) and for SD (Boucher and Baudin Laurencin, 1994 ; Boucher et al., 1995 ; Castric et al., 1997). In farms or fjord systems where PD has been introduced, the disease frequently persists (McVicar, 1987; Crockford et al., 1999; Anonymous 2002) indicating that farmed or wild fish, technical equipment etc. may harbour the virus after introduction.
There is no clinical evidence for vertical transmission of SPDV from brood fish to offspring. However, a recent experiment suggests that such transmission may be possible for sleeping disease virus (SDV) in rainbow trout (Castric, 2005, personal communication).
Outbreaks are recorded all year round, but most frequently between March and October (McLoughlin et al., 2003; Brun et al., 2005). Experimentally, the incubation period has been 6 days at water temperatures of 11-14°C (McVicar, 1990; McLoughlin et al., 1995). The dynamics of transmission between cages in an affected fish farm are less well known, but a single outbreak in a population of farmed Atlantic salmon may last for up to 3-6 months (Crockford et al., 1999; McLoughlin et al., 2003; Anonymous 2002). After fish have been transferred to seawater, PD is diagnosed on average 24 weeks later in Ireland and 35 weeks later in Norway (McLoughlin et al., 2003; Brun et al., 2005).
Impact SummaryTop of page
|Fisheries / aquaculture||Negative|
Impact: EconomicTop of page
The economic impact varies and is associated with mortality during the outbreak, poor post infection growth, occasionally downgrading at slaughter and general disturbances of normal farming practice. In Ireland, mortality rates from 10 to 50 % have been reported (Menzies et al., 1996). The average Pancreas Disease (PD)- related mortality in Ireland during the years 2002-2003 was 12 % with a range of 1 to 42 % (McLoughlin et al., 2003). In these years, it was estimated that PD cost the Irish industry €12 million loss of profit. In Norway, mortalities may vary from negligible to more than 50 %. At cage level, mortalities of 80 % have been recorded and a PD outbreak in Norway may cost the farmer between €0.3 and 1.7 million (Anonymous 2002).
Impact: EnvironmentalTop of page
No environmental impact has been detected. In a survey of returning wild salmonids to the majority of river systems in Northern Ireland between 2000 and 2002, neutralizing antibodies against salmon pancreas disease virus (SPDV) were never detected (Graham et al., 2003a), suggesting that SPDV has been absent from wild salmonids returning to fresh water to spawn in this area.
Impact: SocialTop of page
The economic impact of Pancreas Disease has resulted in closure of single fish farms in Ireland (McLoughlin, 2005 personal communication) and may thus indirectly contribute to unemployment in some rural areas.
ReferencesTop of page
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McVicar AH, 1987. Pancreas disease of farmed Atlantic salmon, Salmo salar, in Scotland: epidemiology and early pathology. Aquaculture, 67(1/2):71-78
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