External & Internal Signs

Clinical Signs
The clinical signs of acute infection with SPDV can be difficult to detect, especially in winter conditions.

Classically there is a sudden drop in feed intake, in some cases preceded by voracious feeding.
A variable proportion of fish become lethargic and can be seen swimming around the edges and corners of the net pen.
There may be a small increase in mortalities at this viraemic stage, but the most significant mortalities usually occur 3-6 weeks after the acute phase disease at temperatures of 12-14°C.
An increase in yellow cast-like faeces is often associated with PD.
Other clinical manifestations include sudden death in large fish, fish lying motionless on the bottom of the pen, unusual swimming behaviour (including circling and spiral swimming) and spitting out feed pellets.
A variable percentage of fish become runts.

Laboratory Tests
Histopathological examination still remains the principal method for diagnosing PD.

Virus isolation remains difficult from natural outbreaks, as the wild type virus is very slow growing in cell culture and can be easily overgrown by IPNV if IPNV is not neutralised.

Serological diagnosis can be used for retrospective confirmation of a PD outbreak with SPDV-neutralising antibodies appearing from 14-21 days pi. RT-PCR analysis is available at a limited number of laboratories.

An EU research programme has just started to develop rapid diagnostic tests for this problematic disease and rapid specific immunohistochemical and serological tests will hopefully soon be available.

Post Mortal Diagnosis

Gross Pathology
In acute phase PD, which is rarely detected, there will be no food in the gut, white or yellow casts in the gut and, occasionally, petechial haemorrhages over the surface of the pyloric caecae.

In chronic phase PD, there will be a significant lack of abdominal body fat and poor condition factors in severely affected fish. Large good conditioned fish may show no gross lesions but rupture of the heart is occasionally observed.

Careful interpretation of the key histological lesions is required. At 12-14°C, acute phase PD [0-10 days post infection (pi)] will reveal:

  • Acute pancreatic acinar cell necrosis, with a rapid disappearance of the majority of pancreatic exocrine tissue.
  • A variable inflammatory reaction is observed at this stage in the peripancreatic fat.
  • Acute necrosis of heart fibres occurs concurrently with the above pancreatic lesions.
  • Cardiac muscle cells in the atrium and the compact and spongy layers of the ventricle can be affected. Affected cells become very eosinophilic and have shrunken nuclei.
  • Skeletal muscle lesions are rarely seen at this stage.

Due to the difficulty in recognising early PD, this stage is rarely presented for histological diagnosis.

In mid-stage PD, from 10-21 days pi, there will be:

  • Significant loss of exocrine pancreas in the majority of fish, with concurrent and variable cardiac myopathy.
  • Skeletal muscle lesions appear around 14 days pi and affect both red and white muscle fibres. The lesions are typical of hyaline degeneration, as described in other species, with swollen fragmented eosinophilic sarcoplasm, central migration of myocytic nuclei and subsequent invasion of the sarcoplasm by phagocytic macrophages. The distribution and severity of these muscle lesions is very variable but can be a good indicator of the prognosis for the population. If you have severe red and white muscle damage, the prognosis for survival is poor.

Differential Diagnosis
It is important to distinguish PD from IPN in marine farmed Atlantic salmon. The main differences are that:

  • IPN tends to occur within 3 months of transfer to sea.
  • Mortalities occur during the acute phase of IPN.
  • There is not the same degree of appetite loss with IPN.
  • The histological lesion profile is different in IPN, with acute pancreatic necrosis (often focal in nature) and a distinct catarrhal enteritis, which is not seen in PD.
  • No cardiac or skeletal muscle lesions are observed with IPN.
  • Confirmation by immunoperoxidase studies is possible for IPN.

It is also important to remember that concurrent infection with IPNV and SPDV can occur.

In older fish, an important differential diagnostic consideration is Cardiomyopathy Syndrome (CMS), which has been described in Scotland and Norway. No cause has yet been determined but severe PD-related cardiac lesions are very similar to those described in CMS.

In chronic phase PD, from 21-42 days pi:

  • The pancreas will be in the recovery phase. In general, if there has been a minimal inflammation or disruption of the peri-acinar tissue, the pancreas has a significant ability to regenerate. In a small percentage of fish, where severe fibrosis of the peri-acinar tissue occurs, the pancreas does not recover and these fish become runts. At this stage, pancreatic acinar tissue will appear around pancreatic ducts and in small clusters around the periphery of the periacinar supporting tissue, and this distribution will be apparent for some time after the PD outbreak.
  • The heart has a significant capacity for regeneration of damaged cardiac cells in young smolts and numerous mitotic figures may be seen, especially at the junction of the compact and spongy layers; this is less common in growers. Recovering hearts will appear very cellular with large active nuclei. There will occasionally be focal proliferation of endocardial cells and mild epicarditis. In mildly affected hearts, no obvious changes may be seen at this stage.
  • The skeletal muscle lesions will reach their peak severity at this stage and this often corresponds to peak mortality in the pen. In severely affected fish, all of the red muscle bundles are severely damaged, as are a significant proportion of the white muscle fibres. As fish must continue to swim to survive, there is no possibility of resting damaged muscle to aid recovery; therefore, severely affected fish normally die. If they are in a high energy, high current site, exhaustion will also contribute to the high mortalities usually observed on such sites.

If samples are taken after 42 days, it may be difficult to confirm a diagnosis of PD, as the most severely affected fish will have died and the remainder will be in various stages of recovery.

No consistent lesions are seen in other organs of PD-affected fish. Occasionally, single cell necrosis is seen in the liver and focal gliosis in the brain. In some fish, the striated muscle of the oesophagus is damaged, resulting in an inability to swallow; hence, the spitting behaviour.

Disease reprinted courtesy of OIE Diagnostic Manual for Aquatic Animal Diseases, OIE (World Organisation for Animal Health), Paris, France.