Mucin dynamics may be particularly sensitive to a Thr deficiency due to the high concentration and structural importance of Thr in the mucin protein backbone. Intestinal mucin secretion, expression of mucin gene (MUC2), and histological characteristics were investigated in male broilers and White Pekin ducklings offered diets containing 3.3, 5.8, or 8.2 g of Thr/kg in 4 studies. Seventy-two birds of each species were fed a standard broiler starter diet from 1 to 14 d of age followed by assignment to 3 dietary treatments in a randomized complete block design for a 7-d feeding trial in experiment 1 (broilers) and experiment 2 (ducklings). The dietary treatments consisted of an isonitrogenous corn-soybean meal-based diet with the addition of crystalline amino acids and graded levels of Thr. Dietary treatments contained 3.3, 5.8, or 8.2 g of Thr/kg. Dietary formulation and experimental design for experiments 3 (broilers) and 4 (ducklings) were similar to experiments 1 and 2 except that birds were fed 3.3 or 8.2 g of Thr/kg for durations of 7 or 14 d. For chicks, increased dietary Thr resulted in higher levels of intestinal crude mucin excretion in experiment 1 (P=0.04) but not in experiment 3, whereas intestinal sialic acid excretion increased in experiment 3 (P=0.02) but not in experiment 1. Furthermore, there was no effect of Thr on intestinal goblet cell density or MUC2 mRNA abundance for broilers. For ducklings, there was an increase in intestinal crude mucin excretion in both experiments (P<0.05) as dietary Thr increased, although there was no effect of Thr on intestinal sialic acid excretion. There was a tendency for an increase in intestinal goblet cell density (cells/microm of villus length; P=0.09) as dietary Thr increased in experiment 2. For experiment 4, intestinal MUC2 mRNA abundance increased (P=0.03) as dietary Thr increased for the 14-d feeding trial but not for the 7-d feeding trial. The data establish a link between dietary Thr and intestinal crude mucin dynamics in chicks for experiment 1 and ducklings for both experiments.

The objective of this study was to evaluate the efficiency of a hydrated sodium calcium aluminosilicate (HSCAS) adsorbent to ameliorate the adverse effects of 0.5 to 2 mg of aflatoxin B1 (AFB1)/kg in broiler chicks. The study consisted of 8 dietary treatments, including 4 concentrations of AFB1 (0, 0.5, 1, and 2 mg/kg) with or without HSCAS (0.5%) fed to 8 replicate cages per diet (6 males chicks per cage) from 0 to 21 d of age. Cumulative feed intake, BW gain (P < 0.0001), and G:F (P = 0.004) of birds fed the 2 mg of AFB1/kg of diet were significantly lower in comparison with birds fed 0 to 1 mg of AFB1/kg. Relative liver weight was increased in the 2 mg of AFB1/kg group (P < 0.0001). Dietary HSCAS improved cumulative BW gain (main effect P = 0.06), particularly from 14 to 21 d of age (P = 0.037). Dietary HSCAS also reversed the increase in relative liver weight for birds fed AFB1 (P = 0.019). Dietary AFB1 negatively affected major serum parameters (albumin, total protein, globulin, phosphorus, glucose, alkaline phosphatase, and creatine phosphokinase), whereas supplementation with HSCAS partially alleviated the affected serum biochemistry. In addition, serum complement activity and liver gene expression were negatively affected by 2 mg of AFB1/kg. The HSCAS supplement increased the liver expression of catalase and superoxide dismutase (P < 0.05). Results from this study indicate that dietary supplementation with HSCAS can effectively improve BW gain and partially ameliorate aflatoxicosis for broiler chicks fed AFB1-contaminated feeds.

The incidence of foodborne outbreaks and product recalls is on the rise. The ability of the pathogen to adapt and survive under stressful environments of food processing and the host gastrointestinal tract may contribute to increasing foodborne illnesses. In the host, multiple factors such as bacteriolytic enzymes, acidic pH, bile, resident microflora, antimicrobial peptides, and innate and adaptive immune responses are essential in eliminating pathogens. Likewise, food processing and preservation techniques are employed to eliminate or reduce human pathogens load in food. However, sub-lethal processing or preservation treatments may evoke bacterial coping mechanisms that alter gene expression, specifically and broadly, resulting in resistance to the bactericidal insults. Furthermore, environmentally cued changes in gene expression can lead to changes in bacterial adhesion, colonization, invasion, and toxin production that contribute to pathogen virulence. The shared microenvironment between the food preservation techniques and the host gastrointestinal tract drives microbes to adapt to the stressful environment, resulting in enhanced virulence and infectivity during a foodborne illness episode.

A 14-d study was conducted to evaluate the effects of cultured aflatoxin B1 (AFB1) on performance, serum biochemistry, serum natural antibody and complement activity, and hepatic gene expression parameters in Pekin ducklings. A total of 144 male Pekin ducklings were weighed, tagged, and randomly allotted to 4 dietary treatments containing 4 concentrations of AFB1 (0, 0.11, 0.14, and 0.21 mg/kg) from 0 to 14 d of age (6 cages per diet; 6 ducklings per cage). Compared with the control group, there was a 10.9, 31.7, and 47.4% (P < 0.05) decrease in cumulative BW gain with 0.11, 0.14, and 0.21 mg of AFB1/kg of diet, respectively, but feed efficiency was not affected. Increasing concentrations of AFB1 reduced cumulative BW gain and feed intake both linearly and quadratically, and regression equations were developed with r(2) ≥0.73. Feeding 0.11 to 0.21 mg of AFB1/kg reduced serum glucose, creatinine, albumin, total protein, globulin, Ca, P, and creatine phosphokinase linearly, whereas serum urea N, Cl, alkaline phosphatase, and aspartate amino transferase concentrations increased linearly with increasing AFB1 (P < 0.05). Additionally, 0.11 to 0.21 mg of AFB1/kg diets impaired classical and alternative complement pathways in the duckling serum when tested by lysis of rabbit, human type O, and horse erythrocytes, and decreased rabbit and horse agglutinins (P < 0.05). Liver peroxisome proliferator activated receptor α (PPARα) expression was linearly downregulated by AFB1 (P < 0.01). Results from this study indicate that for every 0.10 mg/kg increase in dietary AFB1, cumulative feed intake and BW gain decrease approximately 230 and 169 g per duckling from hatch to 14 d; and that AFB1 at very low concentrations can significantly impair liver function and gene expression, and innate immune dynamics in Pekin ducklings.

In 2 experiments, a total of 184 pigs (PIC, initial BW of 10.3 and 9.7 kg for Exp. 1 and 2, respectively) were used to develop an available P (aP) release curve for commercially available Escherichia coli-derived phytases. In both experiments, pigs were fed a corn-soybean meal basal diet (0.06% aP) and 2 diets with added inorganic P (iP) from monocalcium phosphate (Exp. 1: 0.075 and 0.15% aP; Exp. 2: 0.07 and 0.14% aP) to develop a standard curve. In Exp. 1, 100, 175, 250, or 500 phytase units (FTU)/kg of OptiPhos 2000 or 200, 350, 500, or 1,000 FTU/kg of Phyzyme XP were added to the basal diet. In Exp. 2, 250, 500, 750, or 1,000 FTU/kg of OptiPhos 2000; 500, 1,000, or 1,500 FTU/kg of Phyzyme XP; or 1,850 or 3,700 FTU/kg of Ronozyme P were added to the basal diet. One FTU was defined as the amount of enzyme required to release 1 µmol of iP per minute from sodium phytate at 37°C. For all phytase products, the manufacturer-guaranteed phytase activities were used in diet formulation. All diets were analyzed for phytase activity using both the Phytex and AOAC methods. Pigs were blocked by sex and BW and allotted to individual pens with 8 pens per treatment. Pigs were killed on d 21, and fibulas were collected and analyzed for bone ash. In both experiments, increasing iP improved (linear, P < 0.01) G:F and percentage bone ash. Pigs fed increasing OptiPhos had improved (Exp. 1: linear, P < 0.001; Exp. 2: quadratic, P < 0.001) percentage bone ash, as did pigs fed increasing Phyzyme XP (linear, P < 0.001). In Exp. 2, increasing Ronozyme P improved (quadratic, P < 0.01) percentage bone ash. Using analyzed values from the AOAC method and percentage bone ash as the response variable, an aP release curve was developed for up to 1,000 FTU/kg of E. coli-derived phytases (OptiPhos 2000 and Phyzyme XP) in P-deficient diets. The prediction equation was Y = -0.000000125X(2) + 0.000236X + 0.016, where Y = aP release (%) and X = analyzed phytase (FTU/kg) in the diet.