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The effect of adding 0%, 1%, 2% and 5% chitin from prawn shells in the diets for Atlantic cod, Atlantic halibut and Atlantic salmon on growth was investigated. Nutrient digestibility and feed utilization was investigated in salmon and cod. Atlantic cod grew from 186 ± 29 to 383 ± 78 g ( N = 960) over 13 weeks. Dietary chitin had no effect on length, weight, condition, liver size or specific growth rate (SGR). The apparent digestibility ( ADC) for protein ranged from 84.7% to 86.5%, lipid between 88.8% and 93.1% and dry matter from 96.1% to 96.6%. Feed utilization varied between 1.08 and 1.11 and was not correlated with dietary chitin content. Atlantic salmon tripled their weight from 199 ± 9 to 615 ± 75 g ( N = 480) during the 13 weeks. High inclusions of chitin (>1%) reduced both growth rate and condition. Protein and lipid ADC was negatively correlated with dietary chitin. Feed utilization ranged between 0.86 and 0.90 and was not significantly affected by dietary chitin. Faecal protein increased significantly with increasing dietary chitin, while faecal dry matter and lipid did not. Individually tagged Atlantic halibut grew from 1300 ± 470 to 2061 ± 714 g ( N = 70) during 6 months. Individual growth rates varied within each group from being slightly negative to 0.81%·day−1. Diet had no significant effect on growth rates. Atlantic cod and Atlantic halibut seems unaffected by up to 5% chitin additions in the diet, while chitin >1% of diet negatively affects growth and nutrient utilization in Atlantic salmon. [ABSTRACT FROM AUTHOR]

This study investigated the production performance of the Atlantic salmon postsmolt ( Salmo salar L.) subjected to cyclic oxygen reductions (hypoxia) of varying severity. Triplicate groups ( N = 955) were kept at constant 80% O2 (control) or subjected to 1 h and 45 min of hypoxia (50, 60 or 70% O2, termed 80:70, 80:60 and 80:50 groups) every 6 h at 16°C for 69 days. Feed was provided in normoxia. One third of the fish were kept further for 30 days in normoxia to study possible compensatory growth. Cyclic hypoxia did not alter the oxygen uptake rates of fish, measured in night-time. Fish subjected to 50% and 60% O2 reduced feeding by 13% and 6% compared with the controls, respectively, with corresponding reductions in specific growth rates. Feed utilization was not reduced. Compensatory growth was observed in fish from the 80:50 group, but full compensation was not achieved. The main conclusions were that feeding in normoxia does not fully alleviate negative effects of cyclic hypoxia on feeding and growth, when oxygen is reduced to 60% or below in hypoxic periods, that feed utilization is maintained, and that compensatory growth may lessen negative effects. [ABSTRACT FROM AUTHOR]

In the present study the impact on autochthonous (adherent) bacteria in proximal intestine ( PI) and distal intestine ( DI) of Atlantic cod ( Gadus morhua L.) was evaluated following feeding of a control diet and a diet supplemented with 5% chitin. The autochthonous gut bacteria were investigated using denaturing gradient gel electrophoresis ( DGGE). Analysis of the microbiota associated with PI and DI of Atlantic cod indicate that dietary chitin modulate the intestinal bacterial community. For example, band 25 ( Escherichia coli-like), band 14 ( Anaerorhabdus furcosa-like) and band 29 (uncultured bacterium-like) in PI were depressed by dietary chitin ( P < 0.05). The number of bands (23.7 ± 5.4) in DI of fish fed chitin was marginally higher than the control fish (16.7 ± 2.1) ( P = 0.065), and the relative abundances of band 6 (swine faecal bacterium-like) were marginally stimulated by dietary chitin ( P = 0.095). Furthermore, the present study reports several novel sequences not previously reported in the gastrointestinal tract of Atlantic cod. Whether the dietary effect of chitin on gut bacterial community has any positive effect of fish health merits further investigations. [ABSTRACT FROM AUTHOR]

Intensive fish production worldwide has increased the risk of infectious diseases. However, before any infection can be established, pathogens must penetrate the primary barrier. In fish, the three major routes of infection are the skin, gills and gastrointestinal (GI) tract. The GI tract is essentially a muscular tube lined by a mucous membrane of columnar epithelial cells that exhibit a regional variation in structure and function. In the last two decades, our understanding of the endocytosis and translocation of bacteria across this mucosa, and the sorts of cell damage caused by pathogenic bacteria, has increased. Electron microscopy has made a valuable contribution to this knowledge. In the fish-farming industry, severe economic losses are caused by furunculosis (agent, Aeromonas salmonicida spp. salmonicida) and vibriosis [agent, Vibrio ( Listonella) anguillarum]. This article provides an overview of the GI tract of fish from an electron microscopical perspective focusing on cellular damage (specific attack on tight junctions and desmosomes) caused by pathogenic bacteria, and interactions between the ‘good’ intestinal bacteria [e.g. lactic acid bacteria (LAB)] and pathogens. Using different in vitro methods, several studies have demonstrated that co-incubation of Atlantic salmon ( Salmo salar L.) foregut (proximal intestine) with LAB and pathogens can have beneficial effects, the cell damage caused by the pathogens being prevented, to some extent, by the LAB. However, there is uncertainty over whether or not similar effects are observed in other species such as Atlantic cod ( Gadus morhua L.). When discussing cellular damage in the GI tract of fish caused by pathogenic bacteria, several important questions arise including: (1) Do different pathogenic bacteria use different mechanisms to infect the gut? (2) Does the gradual development of the GI tract from larva to adult affect infection? (3) Are there different infection patterns between different fish species? The present article addresses these and other questions. [ABSTRACT FROM AUTHOR]

Fish farms may attract wild fish that feed on waste feed from the cages. Saithe, Pollachius virens L., are particularly numerous around salmon cages in northern Europe and may obtain a significant proportion of their diet from waste feed. It has been claimed that these fish are of inferior quality to saithe that feed on natural diets; differences are said to include soft muscle tissue and a different taste. In order to document such changes in quality we performed a feeding experiment. Young wild saithe were collected and fed either a lipid-rich salmon diet or a lean cod diet for 8 months. All fish were individually tagged and growth was monitored throughout the experiment. Parameters related to flesh quality were measured. Diet clearly influenced the growth rate of the fish, and many fish reached a very high hepatosomatic index when fed on a salmon diet. However, many fish had a low feed intake and thus a low rate of growth. There were some differences in skin and muscle colour, pH and in sensory parameters between wild-caught and artificially fed saithe at the end of the experiment. Those fed the cod diet were more similar to wild saithe than those fed the salmon diet. [ABSTRACT FROM AUTHOR]

Atlantic salmon ( Salmo salar L.) were fed fishmeal protein for 46 days, and 500 g kg−1 of fishmeal protein substituted with meal from Northern krill ( Meganyctiphanes norvegica). No differences were observed in weight gain, length gain, feed conversion or specific growth rate between the groups that could be attributed to dietary manipulation. The adherent microbiota in the hindgut of the two rearing groups were further investigated. By substituting fishmeal with krillmeal, the total viable counts of aerobic and facultative aerobic bacteria colonizing the hindgut of Atlantic salmon increased from 8.5 × 104 to 2.2 × 106. Furthermore, dietary krillmeal affected the adherent hindgut microbiota. The Gram-positive bacteria Carnobacteria piscicola, Microbacterium oxydans, Microbacterium luteolum and Staphylococcus equorum spp. linens and the Gram-negatives Psychrobacter spp. and Psychrobacter glacincola were not isolated from hindgut of fish fed the krill diet. On the other hand, Pseudomonas fulgida, Pseudomonas reactans and Stenotrophomonas maltophila were not isolated from the control group fed fishmeal. Acinetobacter lwoffi, which is not normally found in the fish gut, was isolated from both feeding groups. Transmission electron microscopy showed bacteria-like profiles between the hindgut microvilli in both feeding groups indicating autochthonous microbiota. When fish were fed the krill diet, hindgut enterocytes were replete with numerous irregular vacuoles. These vacuoles were not observed in fish fed the fishmeal protein. [ABSTRACT FROM AUTHOR]