Experimental production of gastric dilation and its association with osmoregulatory stress and biogenic amines in chinook salmon, Oncorhynchus tshawytscha (Walbaum)

Abstract

Chinook salmon smolt in fresh water fed a commercial diet known to produce minimal gastric dilation and air sacculitis (GDAS) were randomly assigned to four experimental tanks with flow-through sea water. All four groups were acclimatized to sea water for 3 weeks and fed a diet of minced fresh seafood. After 3 weeks the groups were fed either; seafood as before, a different commercial pelleted diet associated with the development of GDAS on farms, or either diet supplemented with 500 mg L(-1) putrescine, 300 mg L(-1) cadaverine and 250 mg L(-1) tyramine. Gastric dilation was produced in fish fed the commercial diet for 1 month but not by feeding a diet of minced seafood. The addition of putrescine, cadaverine and tyramine to either diet had no significant effect on the development of gastric dilation. Fish fed the commercial diet had significantly (P < 0.0001) wider weight-adjusted stomach widths, less prominent longitudinal stomach folds (P < 0.0001) and lower (P < 0.0001) stomach-width ratios than fish fed the fresh seafood diet. There was no significant difference in serum osmolality or sodium concentration between fish from groups with or without gastric dilation or fed biogenic amines.

Gastric dilation and air sacculitis in Chinook salmon,Oncorhynchus tshawytscha(Walbaum); correlation of macroscopic and microscopic lesions, and relationship of the syndrome to glomerulonephritis and serum biochemistry

“…These results again support the contention that the development of GDAS is not primarily attributable to altered osmoregulatory capability (Lumsden et al. 2002, 2003).…”

“…Gastric dilation and air sacculitis was experimentally induced in fish by feeding a diet (diet A), previously known to reproduce the syndrome (Lumsden et al. 2003), from first feeding until approximately 1 month prior to introducing the fish to salt water.…”

“…Feeding low‐cohesion diets led to a reduced rate of fluid transport from the mucosal to the serosal surface of pyloric caeca and an increase in serum osmolality, while contractility declined in cardiac stomach muscle but increased in the pyloric sphincter (Forgan & Forster 2007). Observations regarding serum osmolality are somewhat equivocal, however, other authors have noted no difference in osmolality between GDAS‐affected and non‐affected fish up to 30 days post‐transfer to salt water, despite the condition becoming grossly apparent after 10 days (Lumsden et al. 2003).…”

“…Diet has been implicated in the development of GDAS, as the syndrome can be reproduced experimentally in Chinook salmon by feeding certain types of diet. GDAS was first reproduced using a commercially produced diet, albeit with a small number of fish (Lumsden, Marshall, Gillard, Wybourne & Minamikawa 2003). Later, Forgan & Forster (2007) were also able to reproduce GDAS in a large population and show that low physical pellet cohesion was the most important dietary property responsible for inducing GDAS in saltwater‐raised Chinook salmon.…”

Development and physiology of gastric dilation air sacculitis in Chinook salmon, Oncorhynchus tshawytscha (Walbaum)

“…They refer to an earlier suggestion that biogenic amines, inadvertently included in feed pellets, may cause GDAS. However, based on their results, Lumsden et al. (2003) were able to refute this hypothesis.…”