Atlantic salmon reared in sea-cages in Atlantic Canada and Iceland experience temperatures as low as 1oC during the winter months, and such conditions have been associated with large-scale mortalities in both countries in recent years. However, most of our knowledge of this species’ biology/physiology is from fish reared at warmer temperatures (10-25°C), and there is very limited data and information on the cause of these winter mortalities.
Commercially reared Atlantic salmon (~300 g) of St. John River (New Brunswick, Canada) origin were exposed to a gradual decrease in temperature from 8 to 3oC, and held at the latter temperature for 6 weeks. By the end of this period, mortalities had reached 25%, with moribund animals all displaying the same symptoms. These fish were lethargic and swimming vertically near the water’s surface. They suffered from significant damage to/erosion of their snout and jaws, and there was often damage to the fins (caudal, pectoral, and anal) and body wall (mostly under the pectoral fins). Finally, these fish had a hepatosomatic index much greater (by ~ 2-fold), and pale livers, as compared to asymptomatic individuals.
To better understand the physiological changes associated with the development of this condition, blood (plasma) samples from symptomatic and asymptomatic fish were analyzed (n=9) for enzymes associated with tissue damage, as well as ion, metabolite and cortisol levels. The symptomatic fish exhibited increased plasma ion levels (Na+, Cl-) and osmolality that was likely due to the skin and fin erosion, and they possessed high circulating cortisol (~100 ng mL-1) levels indicative of severe stress. Further, indices of tissue damage (plasma creatine kinase, aspartate aminotransferase and lactate dehydrogenase) were all elevated for the individuals in the later stages of the condition.
The enlarged pale liver, erratic swimming/lethargy, and changes in enzymatic biomarkers of tissue damage are very typical of what is observed in sea bream and yellow drum experiencing ‘Winter Syndrome’, which is associated with ‘fatty liver disease’. Further, the dermal erosion and sores observed in our symptomatic fish were similar to that recently reported for salmon experiencing low temperatures (4-6oC) at cage-sites in Norway, and possibly related to Tenacibaculum sp. infection. Better understanding of the etiology of both of these pathologies associated with cold temperatures, and how to prevent them, should be a priority for the Atlantic salmon industry. This would allow for better health management and fish welfare in regions that experience prolonged low water temperatures.