What this "new" disease dilemma does is to highlight the relative lack of investigative tools when it comes to attempting to answer such questions and a lack of consensus amongst those making the diagnoses.
By comparison the array of methods available to human and mammalian diagnosticians is overwhelming.
Clearly fish reside near the bottom of the evolutionary ladder, literally and in terms of applied diagnostic research; although there are good economic reasons for this lack of research relative to human and veterinary medicine.
For example, in order to decide on whether an infection is recent and active or old and convalescent, in human and veterinary medicine one can look for different types of specific indicators called antibodies (immunoglobulins referred to as Ig's). These are produced by an animal in response to an infectious agent as part of what is termed the specific immune response.
If one detects a type of antibody called IgM then this indicates a recent infection. As an infection proceeds through to the convalescent phase then another class of antibody called IgG is produced. Unless an active disease process continues the IgM will slowly disappear thereby allowing an attempt at deciding how long an infection may have been present.
Unfortunately and to the best of my knowledge the ability to discriminate between these 2 different types of antibodies is not possible (as yet) in salmonids; only an IgM type is detectable.
In fish farming we tend to deal with populations rather than individuals and another accepted method employed in human or veterinary medicine to help decide generally whether an infection is new ie developing or old ie reducing is to sample an individual on a couple of occasions over an interval of a few weeks and test for evidence of a significant increase in levels of antibodies.
In the Aquaculture environment this approach is less practical in situations where there may be 20,000 plus fish per cage and there is no easy way to isolate an individual fish for repeat sampling. Although it may be possible to isolate fish within a cage using a smaller box net arrangement there are a number of very good reasons why one might not want to do this eg increased risk of fish spreading any infectious disease by not removing sick fish, restricted space for fish may lead to lesion development and further disease, welfare implications ie stress on fish and the possibility that fish become a focus for sea lice recruitment.
In the case of HSMI or SPDV infections, the ability to discriminate between acute and chronic disease states would lend more confidence to any diagnosis made and exclude the possibility of another concurrent disease being present.
Recently published reports by Norwegian scientists working on HSMI suggest that it is indeed a new infectious disease and that the differential diagnosis of HSMI and SPDV infections will depend on the absence of pancreatic pathology and the presence of heart, skeletal muscle and liver damage in HSMI. They also include Cardiomyopathy Syndrome (CMS) in their differential diagnosis stating that CMS causes heart and variable liver necrosis and again no pancreatic damage.
In defence of their assertion that HSMI is caused by a different virus, they have looked directly for SPDV using sophisticated genetic techniques but possibly missed the boat as they tested experimentally infected fish 4 and 8 weeks into the infection and the SPD virus is only around for 2 - 3 weeks in the initial stages of the infection. They have not yet managed to isolate any virus by cell culture to date.
They have yet to look for specific SPDV antibodies or attempt to neutralise HSMI infectivity using SPDV antibodies both of which would support their case that HSMI is indeed a new disease and quite separate from SPDV. Further no-one to my knowledge has yet looked to see whether an SPDV vaccine can protect against HSMI.
For a number of years in Scotland we have seen fish suffering what we believe to be SPDV infections but showing variable pathology including heart and/or skeletal muscle changes, and sometimes liver necrosis, but no obvious pancreas pathology. These fish regularly show detectable levels of SPDV antibodies so by our diagnostic criteria we would deduce that fish were suffering or had suffered SPDV infection -but are they?
Marian McLoughlin, a highly respected Veterinary Pathologist maintains, and I agree, that the variable pathology seen in fish with SPDV infections is most probably down to a combination of factors including age and strain of fish, environmental conditions, stressors etc. The other major factor affecting the extent and degree of the pathology seen is the stage of disease present in fish at the time of sampling eg pancreas damage may only last for 3-4 weeks before resolving.
In conclusion, debilitating SPDV infections in salmon in seawater and presenting as Sleeping Disease in rainbow trout in freshwater appear to be on the increase and will only rise over time. Future work is urgently required:
In the short term, assessment of effective mitigating strategies eg best feeding practices, identification of useful feed additives and the feasibility of pre-digested feed should be explored.
In the longer term, it must answer the question of whether HSMI is indeed a new disease and if this is indeed the case then isolation of the infectious agent and assessment of vaccination feasibility must be investigated as a matter of priority.