of inflammation and fibrosis of endomysium can be
observed with recovering basophilic red muscle fibres
(Fig. 5.36). Creatine phosphokinase (CPK) levels are
initially low but increase during the chronic stages.
In surviving fish the pancreas can recover, with regeneration of the exocrine tissues occurring as early as 4 weeks
after infection. However, some fish can develop chronic
pancreatic lesions with significant loss of acinar cells with
or without fibroplasia of the surrounding tissue; a situation
more usually found associated with fish that become runts.
PD in salmon primarily occurs during the first year at sea,
but other year classes are also susceptible. Outbreaks are
common between late June and November, although the
disease can recur at any time in sea water. In SD all ages
are susceptible to infection but natural outbreaks appear
almost exclusively when water temperatures are around
10
C. The disease is serious in fingerlings (10–15 g) with
mortality reaching up to 50 %. As with PD, older fish can be
infected without showing any clinical signs and may become
long term carriers of the virus.
Sub-clinical SAV infection with negligible clinical signs,
no significant mortalities and relatively mild histopathological
lesions have been described, suggesting a complex situation
where several aspects influence the severity of the outbreaks in
a given population, including environmental, host and/or pathogen. Furthermore, disease outbreaks tend to reappear in consecutive fish groups introduced onto historically infected sites,
irrespective of the length of the fallowing period implying
there is a marine SAV reservoir or a freshwater carrier state.
Common dab have tested positive for SAV by PCR and
phylogenetic analysis of an E2 dataset has confirmed a subtype
V-like sequence.
Fig. 5.33 Increased cellularity at the junction of the ventricle compactspongy layer in Atlantic salmon with pancreas disease. Medium power
Fig. 5.34 Focal necrosis and inflammation of cardiomyocytes in
spongy myocardium in farmed Atlantic salmon with pancreas disease.
Medium power
Fig. 5.35 Myofibre degeneration with swollen and fragmented sarcoplasm in Atlantic salmon with pancreas disease. Medium power
Fig. 5.36 Inflammation and fibrosis of endomysium with recovering
red muscle fibres in Atlantic salmon with pancreas disease. Medium
power
66
5 Viral Diseases
observed with recovering basophilic red muscle fibres
(Fig. 5.36). Creatine phosphokinase (CPK) levels are
initially low but increase during the chronic stages.
In surviving fish the pancreas can recover, with regeneration of the exocrine tissues occurring as early as 4 weeks
after infection. However, some fish can develop chronic
pancreatic lesions with significant loss of acinar cells with
or without fibroplasia of the surrounding tissue; a situation
more usually found associated with fish that become runts.
PD in salmon primarily occurs during the first year at sea,
but other year classes are also susceptible. Outbreaks are
common between late June and November, although the
disease can recur at any time in sea water. In SD all ages
are susceptible to infection but natural outbreaks appear
almost exclusively when water temperatures are around
10
C. The disease is serious in fingerlings (10–15 g) with
mortality reaching up to 50 %. As with PD, older fish can be
infected without showing any clinical signs and may become
long term carriers of the virus.
Sub-clinical SAV infection with negligible clinical signs,
no significant mortalities and relatively mild histopathological
lesions have been described, suggesting a complex situation
where several aspects influence the severity of the outbreaks in
a given population, including environmental, host and/or pathogen. Furthermore, disease outbreaks tend to reappear in consecutive fish groups introduced onto historically infected sites,
irrespective of the length of the fallowing period implying
there is a marine SAV reservoir or a freshwater carrier state.
Common dab have tested positive for SAV by PCR and
phylogenetic analysis of an E2 dataset has confirmed a subtype
V-like sequence.
Fig. 5.33 Increased cellularity at the junction of the ventricle compactspongy layer in Atlantic salmon with pancreas disease. Medium power
Fig. 5.34 Focal necrosis and inflammation of cardiomyocytes in
spongy myocardium in farmed Atlantic salmon with pancreas disease.
Medium power
Fig. 5.35 Myofibre degeneration with swollen and fragmented sarcoplasm in Atlantic salmon with pancreas disease. Medium power
Fig. 5.36 Inflammation and fibrosis of endomysium with recovering
red muscle fibres in Atlantic salmon with pancreas disease. Medium
power
66
5 Viral Diseases