| 1. |
|
|
| 2. |
- Jutfelt, Fredrik, 1975, et al.
(författare)
-
Translocation of viable Aeromonas salmonicida across the intestine of rainbow trout, Oncorhynchus mykiss (Walbaum)
- 2006
-
Ingår i: Journal of Fish Diseases. - : Wiley. - 0140-7775 .- 1365-2761. ; 29:5, s. 255-262
-
Tidskriftsartikel (refereegranskat)abstract
- The pathogenic bacterium Aeromonas salmonicida is the causative agent of the destructive disease furunculosis in salmonids. Horizontal transmission in salmonids has been suggested to occur via the skin, gills and/or intestine. Previous reports are contradictory regarding the role of the intestine as a route of infection. The present study therefore investigates the possibility of bacterial translocation across intestinal epithelia using Ussing chamber technology, in vitro. Intestinal segments were exposed for 90 min to fluorescein isothiocyanate-labelled pathogenic A. salmonicida. Sampling from the serosal side of the Ussing chambers showed that bacteria were able to translocate across the intestinal epithelium in both the proximal and distal regions. Plating and subsequent colony counting showed that the bacteria were viable after translocation. During the 90 min exposure to A. salmonicida, the intestinal segments maintained high viability as measured by electrical parameters. The distal region responded to bacterial exposure by increasing the electrical resistance, indicating an increased mucus secretion. This study thus demonstrates translocation of live A. salmonicida through the intestinal epithelium of rainbow trout, suggesting that the intestine is a possible route of infection in salmonids.
|
|
| 3. |
- Olsen, R. E., et al.
(författare)
-
Acute stress alters intestinal function of rainbow trout, Oncorhynchus mykiss (Walbaum)
- 2005
-
Ingår i: Aquaculture. - : Elsevier BV. - 0044-8486. ; 250:1-2, s. 480-495
-
Tidskriftsartikel (refereegranskat)abstract
- Groups of rainbow trout (Oncorhynchus mykiss Walbaum) in feeding (guts filled with digesta) or food-deprived (3 days of diet deprivation) states were subjected to 15 min of acute stress. Blood samples and intestinal tissue were collected and prepared for physiological, chemical and ultrastructural analysis immediately before stress, and at 4 and 48 h post-stress. Haematocrit, plasma cortisol and lactate levels increased following stress, and the response appeared to be more pronounced in food-deprived than in fed fish. Plasma glucose appeared to increase more in fed fish. Stress did not seem to cause massive tissue damage as measured by cellular leakage of transaminase enzymes into the blood. Furthermore, the plasma oxidative stress marker malondialdehyde did not increase markedly following stress. The content of malondialdehyde did not change following stress neither in midgut nor hindgut sections, and nor did membrane lipid class and fatty acid compositions. Ultrastructural studies showed that stress caused significant widening of the tight junctions between enterocytes in the midgut, with little effect seen in the hindgut. Fed fish appeared to experience more damage than food-deprived fish as judged by the ultrastructural analysis. But these changes were to a large extent transient and cellular organization in the midgut had returned to normal values within 2 days. Intestinal paracellular permeability of the midgut increased 4 h post-stress and was further increased 48 h post-stress of food-deprived fish, whereas no effect was seen in fed trout. In hindgut of food-deprived fish, the permeability appeared to increase sometime after 4 h and was still elevated 48 h after stress. No change in permeability occurred in fed fish. The adherent microbial population level and composition in hindgut was significantly reduced following stress, while the level increased in faeces. This suggests that substantial amounts of mucus are peeled off following stress. It is concluded that, under the present experimental conditions, acute stress causes cellular alteration in rainbow trout gastrointestinal tract. Ultrastructural damages are mainly observed in midgut, but most changes appear to be transient returning to normal levels within 48 h. Changes in adherent intestine microbial population level and compositions together with increased intestinal paracellular permeability following acute stress suggest a possible increased susceptibility to bacterial infections after stress and that active feeding may have a protective role. (C) 2005 Elsevier B.V. All rights reserved.
|
|
| 4. |
- Olsen, R.E., et al.
(författare)
-
The acute stress response in fed and food deprived Atlantic cod, Gadus morhua L.
- 2008
-
Ingår i: Aquaculture. - : Elsevier BV. - 0044-8486. ; 280:1-4, s. 232-241
-
Tidskriftsartikel (refereegranskat)abstract
- The aim of the present study was to evaluate the effect of stress and nutritional state (fed vs food deprived) on the generalized stress response and intestinal integrity in Atlantic cod (Gadus morhua L.). Cod in feeding or food deprived states were subjected to 15 min of acute stress (exhaustive exercise). Blood was collected at 9 intervals from before stress (t = 0), to t = 48 h post stress and analysed for blood haematocrit and haemoglobin, and plasma cortisol, lactate, glucose, osmolality, chloride, as well as the tissue damage indicators glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and thiobarbituric acid reactive substances. Intestinal segments were prepared for histology with the same intervals, while assessment of intestinal integrity and microbiology was performed at t = 0, 4 and 48 h post stress. Subjecting cod to exhaustive stress initiated a standard stress response including increased blood Hct and plasma cortisol, glucose, chloride, osmolality and lactate. Food deprived fish did in general have reduced stress resistance compared to fed fish. For many parameters, cod returned slowly to basal levels. Cellular indicators of tissue damage and oxidative stress increased in a biphasic manner following stress. Stress did not affect gut histology but did transiently increase gut permeability. Furthermore, stress had no effect on the adherent bacterial population level in midgut, but did cause a small decrease in hindgut (non-significant) and hindgut chamber (p < 0.05). Isolates belonging to Carnobacterium were predominant but not affected by stress. In conclusion, food deprived cod are less resistant to stress than fed cod. The magnitude of the response is less than in salmonids, but the effects are persistent (including tissue damage indicators and oxidative stress) and may have negative long term consequences. The gut is relatively resistant to stress, there is however a transient increase in the intestinal permeability and alterations in microbiota that may indicate lower protection against invading pathogens.
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
- Ringø, Einar, et al.
(författare)
-
Damaging effect of the fish pathogen Aeromonas salmonicida ssp salmonicida on intestinal enterocytes of Atlantic salmon (Salmo salar L.)
- 2004
-
Ingår i: Cell and Tissue Research. - : Springer Science and Business Media LLC. - 0302-766X .- 1432-0878. ; 318:2, s. 305-312
-
Tidskriftsartikel (refereegranskat)abstract
- In fish, bacterial pathogens can enter the host by one or more of three different routes: (a) skin, (b) gills and (c) gastrointestinal tract. Bacteria can cross the gastrointestinal lining in three different ways. In undamaged tissue, bacteria can translocate by transcellular or paracellular routes. Alternatively, bacteria can damage the intestinal lining with extracellular enzymes or toxins before entering. Using an in vitro (Ussing chamber) model, this paper describes intestinal cell damage in Atlantic salmon (Salmo salar L.) caused by the fish pathogen Aeromonas salmonicida ssp. salmonicida, the causative agent of furunculosis. The in vitro method clearly demonstrated substantial detachment of enterocytes from anterior region of the intestine (foregut) upon exposure to the pathogen. In the hindgut (posterior part of the intestine), little detachment was observed but cellular damage involved microvilli, desmosomes and tight junctions. Based on these findings, we suggest that A. salmonicida may obtain entry to the fish by seriously damaging the intestinal lining. Translocation of bacteria through the foregut (rather than the hindgut) is a more likely infection route for A. salmonicida infections in Atlantic salmon.
|
|
