Abstract

Production of juvenile Atlantic cod ( Gadus morhua) in Norway has made progress during the past few years; however, high mortality in the larval stage is still one of the bottlenecks in commercial mass production. “Distended gut syndrome (DGS)” is often seen before and during phases of high mortality in the larval stage. The syndrome, which may affect various larval stages, is characterized by low activity and reduced appetite. The gut lumen becomes opaque, distended and filled with fluid. This study reports an outbreak of DGS in a commercial cod hatchery and employed histology and transcriptomics to characterize differences between DGS-affected larvae and well-performing larvae. During commercial larval production in autumn 2008, samples were collected regularly from two of the rearing tanks, enabling us to follow a typical outbreak of DGS. During the outbreak of DGS, larvae were sampled from the water surface (floating larvae, with typical DGS symptoms) and from the water column (swimming larvae, apparently unaffected, as an internal control), and they were compared with well-performing larvae from spring 2008 (as an external control). Histological sections showed extraordinarily many exfoliated epithelial cells in the gut of DGS larvae. There was also hydropic degeneration of hepatocytes in the liver of most of the larvae (from both DGS and internal control). Microarray analysis revealed several genes which were differentially regulated in DGS larvae. A literature search for genes with large differences in expression revealed that the genes which are related to redox balance and inflammation response were affected. The data indicate that oxidative stress is one of the underlying mechanisms of DGS and that the primary problems occur in the liver while secondary effects develop in the gut.

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