Salmon pancreas disease virus, originally described as “Togavirus-like” in 1995, was the first alphavirus to be recorded in fish (in 1999) and recent studies have indicated that it is very similar to ‘Sleeping disease virus’ of rainbow trout.
While the first isolate was made in Ireland, it has also been isolated in Scotland and Norway. Preliminary studies would indicate that these isolates are closely related.

Various groups have shown that PD can be reproduced experimentally via intraperitoneal and oral routes and, while mortality is not a huge feature of the experimental model, all the key histological lesions are reproduced.


Host range, geographic distribution:
Atlantic salmon (Salmo salar L) is considered to be the most susceptible host but published experimental challenges have shown that brown trout (Salmo trutta) and rainbow trout (Oncorhynchus mykiss) are also susceptible; however, the lesion profile is considerably less severe in these latter species. However, in in-house experimental challenge studies, we found that rainbow trout and Atlantic salmon had equally severe lesions.

Pancreas Disease has been described in Scotland, Norway, Ireland, France and the west coast of the USA in farmed Atlantic salmon. Due to the difficulty of isolating SPDV from natural outbreaks of PD and the widespread distribution of Infectious Pancreatic Necrosis virus (IPNV), which can mask the SPDV and the disease in farmed salmon, PD is significantly under diagnosed in the field.

All stages of marine-reared Atlantic salmon are susceptible, including S0, S½ and S1 smolts. There is strong evidence of a high level of acquired life-long immunity to PD as recurrent outbreaks have not been recorded. While experimental PD can be reproduced in fresh water salmon parr, no natural outbreaks of PD have been recorded in freshwater.

The epidemiology of PD was intensively studied in Ireland from 1989-1994 and PD was revealed to be the most serious cause of mortalities and production losses during that period. The study showed that the majority of cases occurred during the period of August to October following transfer of smolts in the spring. Mortality ranged from 0.1% to 63% and it was significantly higher if the PD outbreak occurred early in the production cycle. Higher losses tended to occur in high energy off shore or tidal sites. The mean duration of a PD outbreak was 112 days. Since that study, the pattern and outcome of PD outbreaks has become less predictable with disease occurring during all months of the year and in all sizes of fish in Ireland, Scotland and Norway.

There could be a number of explanations for this observation. Since the mid 90's site management practices such as fallowing, single generation rearing, all in-all out stocking policies, slaughtering fish away from the growing site, vaccination and better sea lice control, have improved disease control generally. This may have contributed to the perceived reduced occurrence and losses from PD.

In general, the sea temperatures during recent summers in Ireland, Scotland and some parts of Norway have been higher than previously recorded, remaining above 15°C over the summer period. SPDV is similar to other fish viruses in that it does not multiply rapidly at temperatures over 15°C. It's preferred temperature range is 9-12°C. When PD occurs at winter temperatures, it is very insidious in nature, takes a long time to spread throughout a cage and site, and there is a prolonged recovery phase. From a production point of view, winter PD is potentially much more damaging than a PD outbreak shortly after transfer, as, while mortalities may be less, there is a significant loss of growth over a prolonged period.

Transmission is primarily due to direct fish to fish contact, but the involvement of other marine reservoirs such as molluscs, crustaceans and wild fish, or vectors such as sea lice, cannot be ruled out.

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