Biochemical, Physiological, and Pathological Changes in Pyridoxine-Deficient Rainbow Trout (Salmo gairdneri)

1974 ◽  
Vol 31 (12) ◽  
pp. 1893-1898 ◽  
Author(s):  
Charlie E. Smith ◽  
Myron Brin ◽  
John E. Halver
Keyword(s):  
Rainbow Trout ◽  
Gastrointestinal Tract ◽  
Clinical Signs ◽  
Salmo Gairdneri ◽  
Glutamic Pyruvic Transaminase ◽  
Pathological Changes ◽  
Deficient Diet ◽  
Normochromic Anemia ◽  
Kidney Liver

Rainbow trout (Salmo gairdneri) fed a pyridoxine-deficient diet developed clinical signs of the deficiency after 8 wk of feeding. Erythrocyte and muscle glutamic pyruvic transaminase (GPT) concentrations were significantly depressed in deficient fish, while liver GPT was significantly elevated. Liver GPT was also elevated in starved trout suggesting the increase in enzyme concentrations was secondary to the deficiency. A normocyte, normochromic anemia, which responded favorably to pyridoxine, developed in pyridoxine-deficient trout. Microscopic lesions were found in gastrointestinal tract, kidney, liver, pancreas, and thymus of deficient fish.

Determination of Vitamin B6 Deficiency in Rainbow Trout (Salmo gairdneri) by Liver Enzyme Assay and HPLC Analysis

1987 ◽  
Vol 44 (1) ◽  
pp. 219-222 ◽  
Author(s):  
Ronald W. Hardy ◽  
Edmundo Casillas ◽  
Toshiro Masumoto
Keyword(s):  
Rainbow Trout ◽  
Vitamin B6 ◽  
Enzyme Assay ◽  
Clinical Signs ◽  
Salmo Gairdneri ◽  
Vitamin B ◽  
Deficient Diet ◽  
Vitamin B6 Deficiency ◽  
Stimulation Of

Rainbow trout (Salmo gairdneri), initially averaging 125 g, were fed a complete or a pyridoxine-deficient diet for 14 wk. Vitamin B6 status was evaluated biweekly by direct measurement of liver pyridoxine and pyridoxal levels by HPLC and by determining pyridoxal-5′-phosphate-enhanced liver aspartate aminotransferase (ASAT) activity. By 14 wk, mortality had severely reduced the number of fish remaining in the pyridoxine-deficient group. At 14 wk, no significant differences in liver pyridoxine and pyridoxal levels were detected between the trout fed the complete or pyridoxine-deficient diet. Significant differences between dietary groups are found in ASAT activity in liver and percent stimulation of liver ASAT by the addition of pyridoxal-5′-phosphate after 8 wk. Clinical signs of vitamin B6 deficiency including anorexia, listlessness, frantic and erratic swimming, and ataxia were observed after 11 wk of feeding a pyridoxine-deficient diet. This study shows that vitamin B6 deficiency in rainbow trout can be readily determined weeks before signs of clinical deficiency are apparent by measuring pyridoxine-enhanced liver ASAT activity. However, liver levels of pyridoxine and pyridoxal are not sensitive indicators of vitamin B6 status.

scholarly journals Some effects of vitamin E and selenium deprivation on tissue enzyme levels and indices of tissue peroxidation in rainbow trout (Salmo gairdneri)

1985 ◽  
Vol 53 (1) ◽  
pp. 149-157 ◽  
Author(s):  
J. G. Bell ◽  
C. B. Cowey ◽  
J. W. Adron ◽  
Aileen M. Shanks
Keyword(s):  
Rainbow Trout ◽  
Vitamin E ◽  
Peroxidase Activity ◽  
Cumene Hydroperoxide ◽  
Dietary Vitamin ◽  
Salmo Gairdneri ◽  
Deficient Diet ◽  
Exudative Diathesis ◽  
Malondialdehyde Formation

1. Duplicate groups of rainbow trout (Salrno gairdnert) (mean weight 11 g) were given for 40 weeks one of four partially purified diets that were either adequate or low in selenium or vitamin E or both.2. Weight gains of trout given the dually deficient diet were significantly lower than those of trout given a complete diet or a diet deficient in Se. No mortalities occurred and the only pathology seen was exudative diathesis in the dually deficient trout.3. There was significant interaction between the two nutrients both with respect to packed cell volume and to malondialdehyde formation in the in vitro NADPH-dependent microsomal lipid peroxidation system.4. Tissue levels of vitamin E and Se decreased to very low levels in trout given diets lacking these nutrients. For plasma there was a significant effect of dietary vitamin E on Se concentration.5. Glutathione (GSH) peroxidase (EC 1. 1 1. 1.9) activity in liver and plasma was significantly lower in trout receiving low dietary Se but was independent of vitamin E intake. The ratios of hepatic GSH peroxidase activity measured with cumene hydroperoxide and hydrogen peroxide were the same for all treatments. This confirms the absence of a Se-independent GSH peroxidase activity in trout liver.6. Se deficiency did not lead to any compensatory increase in hepatic GSH transferase (EC 2. 5. 1. 18) activity; values were essentially the same in all treatments.7. Plasma pyruvate kinase (EC 2. 7. 1.40) activity increased significantly in the trout deficient in both nutrients. This was thought to be due to leakage of the enzyme from the muscle and may be indicative of incipient (subclinical) muscle damage.

scholarly journals Effect of selenium deficiency on hydroperoxide-stimulated release of glutathione from isolated perfused liver of rainbow trout (Salmo gairdneri)

1986 ◽  
Vol 56 (2) ◽  
pp. 421-428 ◽  
Author(s):  
J. G. Bell ◽  
J. W. Adron ◽  
C. B. Cowey
Keyword(s):  
Hydrogen Peroxide ◽  
Rainbow Trout ◽  
Weight Gain ◽  
Peroxidase Activity ◽  
Selenium Deficiency ◽  
Salmo Gairdneri ◽  
Perfused Liver ◽  
Deficient Diet ◽  
Significant Difference ◽  
Glutathione Disulphide

1. Duplicate groups of rainbow trout (Salmo gairdneri) were each given partially purified diets which were either adequate or depleted in selenium for 40 weeks.2. Although there was no significant difference in weight gain, liver Se concentration was significantly lower in fish given the deficient diet.3. Glutathione (GSH) peroxidase (EC 1. 11. 1. 9) activity was significantly reduced in liver of Se-deficient fish but a differential assay did not indicate the presence of a non-Se-dependent GSH peroxidase activity, although liver GSH S-transferase (EC 2. 5. 1. 18) was significantly increased.4. Perfusion of livers from trout given Se-adequate diets with t-butyl hydroperoxide (BuOOH) or hydrogen peroxide caused an increase in the rate of release of glutathione disulphide (GSSG) into the perfusate.5. Perfusion of livers from Se-deficient trout with BuOOH or H2O2 did not result in any change in rate of release of GSSG into the perfusate.6. These findings confirm the absence of any compensatory non-Se-dependent peroxidase activity in Se-depleted trout.

scholarly journals Weissellosis in rainbow trout in Colombia

2020 ◽  
Vol 13 (3) ◽  
pp. 575-580
Author(s):  
Gersson Vásquez-Machado ◽  
Miguel Rubiano-Garzón ◽  
Jonny Yepes-Blandón ◽  
Daniel Gordillo-González ◽  
Jersson Avila-Coy
Keyword(s):  
Rainbow Trout ◽  
Clinical Signs ◽  
Fish Swimming ◽  
Gram Positive Bacteria ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Ocular Lesions ◽  
Intraocular Hemorrhage ◽  
Trout Farms ◽  
Kidney Liver ◽  
Corneal Rupture

Weissellosis is an emergent disease caused by Weissella, a Gram-positive bacteria correlated with hemorrhagic illness and mortality in farm-raised trout in several countries. The current study reports the first outbreaks of weissellosis by Weissella ceti in rainbow trout (Oncorhynchus mykiss), which caused severe mortalities in trout farms in Colombia between May 2016 to June 2019. The disease occurred in several farms irrigated by the same river where temperatures were above 17 °C. Symptoms of the disease were limited almost exclusively to trout above 250 g. The clinical signs consisted of lethargic and anorexic fish, swimming in circles at the surface or against the walls. Pathological findings were mainly ocular lesions like bilateral exophthalmia, periocular and intraocular hemorrhage, lenticular opacity and corneal rupture usually leading to blindness, muscular hemorrhages and necrosis. Microbial isolating from eye, brain, kidney, liver and muscle was performed and W. ceti was confirmed by amplification and sequencing of the 16S rRNA. The aim of this work was to characterize the Weisellosis by Weissella ceti in trouts in Colombia, including microbiological isolating, molecular analysis, gross and microscopic characterization.

Spontaneous Nephroblastoma in a Rainbow Trout (Salmo gairdneri)

1973 ◽  
Vol 30 (4) ◽  
pp. 549-551 ◽  
Author(s):  
P. H. Odense ◽  
V. H. Logan ◽  
S. R. Baker
Keyword(s):  
Rainbow Trout ◽  
Kidney Disease ◽  
Clinical Signs ◽  
Salmo Gairdneri ◽  
Renal Tubules ◽  
Simultaneous Presence ◽  
Etiological Factors ◽  
Fibrous Stroma ◽  
First Case ◽  
Hatchery Stock

A neoplasm in a rainbow trout (Salmo gairdneri) identified as a nephroblastoma is described and its possible pathological implications discussed. The characteristic conditions of abortive renal tubules and glomeruli in a fibrous stroma were observed; however, metastases were absent. The simultaneous presence of inflammatory kidney disease made association of clinical signs with the neoplasm impossible. This is the first case of nephroblastoma in Canadian hatchery stock. The etiological factors are unknown.

scholarly journals Toxicity Effects of Microplastics Individually and in Combination the Fish Pathogen Yersinia Ruckeri on the Rainbow Trout (Oncorhynchus Mykiss)

2021 ◽  
Author(s):  
Elham Alsadat Banihashemi ◽  
Siyavash Soltanian ◽  
Amin Gholamhosseini ◽  
Mahdi Banaee
Keyword(s):  
Rainbow Trout ◽  
Bacterial Infections ◽  
Low Density Lipoprotein ◽  
Clinical Signs ◽  
Density Lipoprotein ◽  
Pathogen Transmission ◽  
Clinical Parameters ◽  
Glutamic Pyruvic Transaminase ◽  
Yersinia Ruckeri ◽  
Cholesterol Levels

Abstract Exposure to xenobiotics such as Yersinia ruckeri can significantly affect bacterial infections in fish. Microplastics (MPs) may predispose fish to infection and act as carriers in pathogen transmission. Therefore, this study is designed to evaluate MPs' effect on damage caused by exposure to Y. ruckeri in rainbow trout. In this study, blood biochemical parameters and hepatic oxidative biomarkers as clinical signs were measured in the fish co-exposed to Y. ruckeri (5 and 10% LD50) and MPs (500 and 1000 mg Kg-1) for 30 days. There were no significant changes in the creatinine, triglyceride, cholesterol levels, and glutamic-pyruvic transaminase activity in the blood of fish infected with Y. ruckeri. In contrast, exposure to MPs had a significant effect on most clinical parameters. The total protein, albumin, globulin, total immunoglobulins, High-density lipoprotein, low-density lipoprotein, cholesterol levels, and γ-glutamyltransferase activity decreased, whereas glucose, triglyceride, and creatinine levels, and glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased in the plasma of fish after co-exposure to MPs and Y. ruckeri. Dietary MPs combined with a bacterial challenge decreased catalase activities, glutathione peroxidase, and total antioxidant levels. However, the superoxide dismutase activity and malondialdehyde contents in the hepatocytes increased in the hepatocyte of fish co-exposed to MPs and Y. ruckeri. In conclusion, this study showed that fish exposure to MPs and simultaneous challenge with Y. ruckeri could have a synergistic effect on clinical parameters.

Relative Contributions of Dietary and Waterborne Zinc in the Rainbow Trout, Salmo gairdneri

1988 ◽  
Vol 45 (1) ◽  
pp. 32-41 ◽  
Author(s):  
D. J. Spry ◽  
P. V. Hodson ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Plasma Protein ◽  
Body Burden ◽  
Normal Growth ◽  
Toxic Effects ◽  
Whole Body ◽  
Salmo Gairdneri ◽  
Deficient Diet ◽  
Zinc Concentrations ◽  
Waterborne Zinc

Rainbow trout, Salmo gairdneri, were fed purified diets with zinc concentrations ranging from deficient to excessive (1, 90, 590 μg Zn∙g−1) and simultaneously exposed to a range of waterborne [Zn] (7, 39, 148, 529 μg Zn∙L−1). After 1 wk, fish fed the deficient diet, at ambient waterborne [Zn], had low plasma [Zn] which decreased further during the 16-wk experiment. Growth ceased after 12 wk; hematocrit and plasma protein were depressed. Both whole body [Zn] and body burden decreased by 16 wk, but most other elements were elevated. Increasing waterborne [Zn] alone increased plasma [Zn], whole body [Zn], and growth in a graded manner and normalized hematocrit, plasma protein, and other whole body elements. Increasing dietary [Zn] to 90 μg Zn∙g−1 at ambient waterborne [Zn] prevented depression of plasma [Zn] and permitted normal growth and whole body [Zn]. Zinc uptake from water, probably across the gills, was independent of uptake from the diet since at any dietary [Zn], increasing the waterborne [Zn] resulted in increased whole body [Zn]. Even when dietary [Zn] was adequate, the waterborne contribution was as high as 57%, and 100% when the dietary [Zn] was deficient. There were no toxic effects on any of the variables measured.

scholarly journals Studies on the nutrition of rainbow trout (Salmo gairdneri) Magnesium deficiency: the effect of feeding with a Mg-supplemented diet

1983 ◽  
Vol 50 (1) ◽  
pp. 121-127 ◽  
Author(s):  
D. Knox ◽  
C. B. Cowey ◽  
J. W. Adron
Keyword(s):  
Rainbow Trout ◽  
Magnesium Deficiency ◽  
Control Diet ◽  
Plasma Concentrations ◽  
Complete Recovery ◽  
Salmo Gairdneri ◽  
Control Group ◽  
Deficient Diet ◽  
Bone Ash ◽  
And Control

1. For a period of 8 weeks, rainbow trout (Salmo gairdneri), mean initial weight 21 g, were given either a low-magnesium or control diet containing 0·03 and 0·58 g Mg/kg diet respectively. Both groups of trout were then given the control diet for a further 11 weeks.2. Weight gains over the initial 8-week period were lowest in the Mg-deficient trout. Feeding the deficient fish the control diet rapidly improved growth rate until it was the same as that of the control trout.3. Plasma Mg was significantly lower in the Mg-deficient trout at week 8. Feeding with the control diet for 11 weeks did not increase plasma Mg. Few changes were observed in the plasma concentrations of the other electrolytes.4. Renal calcium concentrations were unaffected by dietary Mg levels. Similarly, the renal levels of phosphorus, sodium and potassium all fell within the range found in normal rainbow trout.5. Muscle Mg concentrations were reduced in those trout given the Mg-deficient diet. Feeding with the control diet for a further 11 weeks increased muscle Mg but the level was still significantly lower than that found in trout given the control diet for 19 weeks.6. The bone ash Mg concentration was significantly lower, and the Ca higher, in the deficient fish at week 8, when compared with the control group.7. When compared with the value at the start of the experiment, total bone Mg fell slightly in the deficient trout over the initial 8-week period, but increased in the control group of fish. Feeding with the control diet for a further 11 weeks increased total bone Mg in both Mg-deficient trout and control trout.8. The results show that the Mg deficiency imposed on the rainbow trout was of limited severity and almost complete recovery was obtained when the control diet was fed.

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