In the last article of this series we looked at the influence of the environment on fish health. Before we delve into the world of communicable fish diseases in forthcoming issues we will cover the heritable and nutritional aspects of fish health which in some ways can be viewed as matters concerning susceptibility and deficiency.
Disease and heritability
When we talk of disease and heritability we can break this down into two further concepts: disease conditions directly inherited from the parents, and disease which arises due to the susceptibility of the individual to that disease compared to that of other individuals – robustness. It is extremely rare to find directly inherited conditions in fish. Even conditions which have in the past been attributed to genetics such as foreshortened maxilla, siamese twins and other apparently congenital abnormalities are now understood to have their precursor in the parents diet or environment during either oogenesis or spermatogenesis.
The main role of genetics in fish disease is one of either influencing the susceptibility of the individual to disease or indeed influencing nutritional-based disorders owing to the genetic influence on growth and metabolism. This latter factor quite often represents a ‘bottle-neck’ in the expansion of farming a species.
Limits of feed
As husbandry practices are improved and the genetics modified towards increased growth then the limits of feed are often exposed. An example would be the bioavailability of phosphorous in commercial fish feed diets. This bioavailability can vary throughout the year depending on the sources used for formulating the diet. A diet which is at the limit for normal skeletal development in a fish can become an issue for a farmer who is pushing his fish as much as possible. A farmer who is growing his fish more slowly and is not overly concerned with FCR would not encounter an issue as there would be sufficient dietary phosphorous for that fishes development.
On the other hand, a farmer who has bought eggs claiming to give increased growth of 15% and who is very focused on reducing his FCR and thus reducing the availability of the mineral to the fish – will quickly expose the diets deficiency and his fish will suffer variable bone mineralization and deformity problems.
Breeding for robustness
But perhaps the most important genetic component in disease is susceptibility. In salmon, the QTL for resistance to IPN was found during 2008/2009 and for the past five years or thereabouts there has been an increase in the presence of this QTL in broodstock held by the main breeding companies. There has been a corresponding decrease in IPN outbreaks in hatcheries as a result.
However, protection against IPN does not necessarily confer protection against other diseases or parasites and the concept of robustness in breeding is one which needs to be addressed. All too often when fish are challenged under commercial conditions it is the more genetically manipulated domestic stock which is found to be more susceptible than those stocks with less breeding. This may be a direct result of breeding almost exclusively for growth and there is plenty of current work being performed in species ranging from carp and salmon through to tilapia that show there seems to be such a thing as a ‘domestic gene.’ This appears to confer protection against various pathogens in the aquatic environment and, more importantly, the fishes response to this pathogen or other stressor.
Studies in other animals have demonstrated that it is a relatively limited number of major genes including the major histocompatibility complex (MHC) which regulate the immune response. In fish there may be two areas of MHC genes which may also explain the lack of correlation between protection against viral and bacterial pathogens. This modulation of host response is important.
It has been noted, in some incidences, that the host response from a first generation wild individual to an ectoparasite such as ich or amoeba is much reduced compared to that of commercial stocks. This reduction in response actually reduces mortality as in this scenario it is the hosts ‘over-response’ in terms of cell proliferation and mucus production that actually leads to death. If fish production is to play its anticipated role in feeding the world in future generations then disease control through breeding will play an enormously important role.
Disease and nutrition
Nutrition has already been mentioned in terms of the synergetic effect between it and the genetics of an individual fish. Nutrition plays a much more direct role, however, in the fishes health from direct starvation to much more subtle health issues caused by either lack of micro-nutrients and/or anti-nutritional which may affect the digestive system.
Variation between species is large, and although species such as salmon and trout have complete available diets, the specifications of which are well understood, there are new species being grown for which the dietary requirements are little understood.
An example of this variation can be seen in the two accompanying tables from around 20 years ago which show this inter-species variation for vitamin and mineral requirements, but more importantly show the gaps in knowledge which existed in what was then a new species. Currently the dietary requirements of sea bream, for example, are much better understood, but there are new species being grown today which have very little research applied to their dietary requirements and where it is all too easy to cause or provoke disease.
Table 1. Vitamin requirements of three different cultured species.
Vitamin A (IU)
Vitamin D (IU)
Table 2. Mineral requirements of five commonly cultured species
If the reason for increased morbidity or mortality in the hatchery cannot be ascertained through diagnostic sampling by either the in-house health staff or contracted vets then the issue is normally due to husbandry, the environment or nutrition. The nutritional aspect is more often than not the most difficult to pin down. There is so much variation between species and at different stages of their life-cycles in terms of nutritional requirements that it often impossible to fully diagnose the exact cause. Some of the symptoms of mineral deficiency as an example can be seen in Table 3.
Table 3. Some mineral deficiency symptoms across fish species.
Symptom of deficiency
Reduced growth, bone demineralisation, skeletal deformity.
Reduced growth, poor FCR.
Muscular dystrophy, cataracts, anaemia, mortality.
Reduced growth, cataracts, fin erosion, depressed bone Ca & Zn content, mortality.
Reduced growth, sluggishness, convulsions, cataracts muscle and gill filament degeneration, mortality.
Reduced growth, loss of equilibrium, cataracts, mortality.
Reduced growth, cataracts.
Of course it is not just mineral deficiencies that can cause problems but their excess too. The same goes for all the dietary components from lipids to amino acids and problems can be expressed owing to both too little or too much. The increase in anti-nutritionals caused by the replacement of marine oil and protein with vegetable replacements can cause quite severe enteritis in fish such as salmon, sea bass and sea bream. As this replacement trend will only continue it is important that problems such as these are solved quickly or again this will pose a nutritional bottleneck to the industries concerned. The gut is one of the main pathogen barriers for the fish and any disruption at a cellular level can lead to increased susceptibility to viruses and bacteria.
The next installment of the fish health series will look at one of the most problematic pathogen groups for the hatchery manager – the viruses.
— Alan Dykes
Alan Dykes is Fish Health Services Manager at FishGuard Scotland.