Table 1.
Ingredients and chemical composition of experimental diets.
Table 2.
Profile of amino acids (% of complete diet) in experimental diets.
Table 3.
Summary of growth parameters in eight treatments at the end of the growth experiment.
Different superscripts across the rows represent the variance between treatments were calculated by Duncan multirange test of one-way ANOVA at P < 0.05.
Table 4.
Chemical composition of muscles in eight treatments at the end of the growth experiment.
Different superscripts across the rows represent the variance between treatments were calculated by Duncan multirange test of one-way ANOVA at P < 0.05.
Table 5.
Essential amino acids (EAA) and non-essential amino acids (NEAA) contents from fish muscles from eight treatments at the end of the growth experiment; expressed as %.
Different superscripts across the rows represent the variance between treatments were calculated by Duncan multirange test of one-way ANOVA at P < 0.05.
Table 6.
Determination of digestive enzymes in fish intestine samples from all eight treatments at the end of the growth experiment.
Different superscripts across the rows represent the variance between treatments were calculated by Duncan multirange test of one-way ANOVA at P < 0.05.
Fig 1.
Analysis of hematological parameters in eight treatments at the end of the growth experiment and after bacterial challenge.
Different superscripts represent the variance between treatments were calculated by Duncan multirange test of one-way ANOVA at P < 0.05. different treatments are as follows: T0; control, T1; Tryptophan, T2; Lysine; T3; Methionine: T4; Tryptophan + Methionine, T5; Lysine +Tryptophan, T6; Methionine +Lysine, T7; Lysine + Tryptophan +Methionine. Hemoglobin (Hb), white blood cells (WBC), red blood cells (RBC), mean corpuscle volume (MCV), haematocrit (HCT), mean corpuscular hemoglobin (MCH), μL–microliter, fL- femtoliter.
Table 7.
Analysis of biochemical parameters of blood in eight treatments eight treatments at the end of the growth experiment and after the bacterial challenge.
Different superscripts across the rows represent the variance between treatments were calculated by Duncan multirange test of one-way ANOVA at P < 0.05.
Table 8.
Analysis of catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA) from fish blood serum of eight treatments at the end of the growth experiment and after bacterial challenge.
Different superscripts across the rows represent the variance between treatments were applied as a result of one way (Duncan multirange test) at P < 0.05.
Fig 2.
Kaplan-Meier survival curves of striped catfish following infection by immersion challenge with S.
aureus. The results correspond to the survival percentage during 15 days post-infection of three replicates (n = 15/treatment). Kaplan-Meier survival data was analyzed by OriginPro software.
Fig 3.
Histological changes in gills.
Light micrographs of a paraffin section stained with eosin (40x). a; gills in -ve T0, b; gills t in +ve T0, c; gills T1, d; gills in T2, e; gills in T3, f; gills in T4, g; gills in T5, h; gills in T6, I; gills in T7. Primary lamellae, SL; Secondary lamellae, FSL; Fusion of secondary lamellae, DSL; Degeneration of secondary lamellae, HT; Hypertrophy, DPL; Degeneration of primary lamellae, TD; Tissue debris, A; Aneurism, BC; Blood congestion, V; vacuolation.
Fig 4.
Light micrographs of a paraffin section stained with eosin (40x). a; gut in -ve T0, b; gut in +ve T0, c; gut in T1, d; gut in T2, e; gut in T3, f; gut in T4, g; gut in T5, h; gut in T6, I; gut in T7. GC; Goblet cells, LP; Laminar propria, N; Nucleus, L; Lumen, CE; Columnar epithelium, FV; Fusion of villi, LL; Large lumen, FLV; Flattened villi, DCML; Damaged circular muscle layer, DL; Distended lumen, DLML; Damaged longitudinal muscle layer, VF; Vacuole formation, SLP; Swelling of lamina propria, CCA; Cracked clay appearance of the tissues, SLML; Swelling of longitudinal muscle layer, DGC; Damaged goblet cells, DMM; Disarrangement of muscularis mucosa.
Fig 5.
Fig 6.
Histological changes in liver.
Light micrographs of a paraffin section stained with eosin (40x). a; liver in -ve T0, b; liver in +ve T0, c; liver in T1, d; liver in T2, e; liver in T3, f; liver in T4, g; liver in T5, h; liver in T6, I; liver in T7. NH; Normal hepatocytes, GC; Granular cytoplasm, BC; Blood congestion HD; Hepatocyte generation, CSN; Central spheroidal hepatocyte nucleus, N; Cell necrosis, PN; Pyknotic nuclei, CD; Cytoplasmic degeneration, IEF; Infiltration of oedematous fluid, rCV; Rupturing of the central vein, V; Vacuolization of hepatocytes. DHC; degeneration of hepatocytes.
Fig 7.
Histological changes in kidney.
Light micrographs of a paraffin section stained with eosin (40x). a; kidney in -ve T0, b; kidney in +ve T0, c; kidney in T1, d; kidney in T2, e; kidney in T3, f; kidney in T4, g; kidney in T5, h; kidney in T6, I; kidney in T7. G; Glomerulus, CD; Collecting duct, DG; Degenerative glomerulus, IBS; Increased bowman space, FRT; Fusion of renal tubule, DRT; Degenerative renal tubule, CG; Congestion of glomerulus, N; Necrosis, H; Hemorrhage, A; Atrophy.