Acute stress alters the intestinal lining of Atlantic salmon, Salmo salar L.: An electron microscopical study

Abstract

Groups of Atlantic salmon (Salmo salar L.) in feeding (guts filled with faeces) or fasted (three days of diet deprivation) states were subjected to 15 minutes of acute stress. Blood samples and intestinal tissue were collected and prepared for chemical and ultrastructural analyses at intervals post stress until 53 h of recovery. Subjecting fish to acute stress led to significant alterations of the ultrastructure of the enterocytes lining the gastrointestinal tract (GI tract). The most notable effect was substantial damage to the intercellular junctional complexes in midgut regions. These effects appeared within the first hour after stress, were maintained for at least 12 h and were more pronounced in fed than fasted fish. In contrast, hindgut was influenced less by stress and damage was rarely observed. Stress also influenced fish intestinal microbiota. Adherent bacteria decreased in both midgut and hindgut of stressed fish, and this was accompanied by a significant increase in the bacterial contents of faeces. It is suggested that this was due to the sloughing off of mucus eliminating existing microflora and allowing remaining bacteria (also pathogenic) in the gut lumen to colonize the surface of the enterocytes. Although blood haematocrit and plasma cortisol increased following stress, the response appeared to be greater in fasted fish. There were also significant differences in carbohydrate metabolism. While liver glycogen stores were depleted in fasted fish following the mobilization of glucose into plasma, liver glycogen was never depleted in fed fish. As a consequence, plasma glucose levels remained high for more than 12 h of recovery. In fed fish, plasma lactate was also higher than in fasted salmon, and the clearance rate appeared slower. Acute stress induced oxidative stress, as measured through plasma malondialdehyde, but the effect was marginal and nonsignificant.