Effects of sulfur amino acid supplementation on broiler chickens exposed to acute and chronic cyclic heat stress.

Chronic heat stress can result in oxidative damage from increased reactive oxygen species. One proposed method to alleviate the chronic effects of HS is the supplementation of sulfur amino acids (SAA) which can be metabolized to glutathione, an important antioxidant. Therefore, the objective of this experiment was to determine the effects of dietary SAA content on broiler chickens exposed to HS from 28 to 35 d on broiler performance, body temperature, intestinal permeability, and oxidative status. Four experimental treatments were arranged as a 2 × 2 factorial consisting of HS (6 h at 33.3°C followed by 18 h at 27.8°C from 28 to 35 d of age) and Thermoneutral (TN- 22.2°C continuously from 28 to 35 d) and 2 dietary concentrations of SAA formulated at 100% (0.95, 0.87, and 0.80% for starter, grower, and finisher diets) or 130% SAA (1.24, 1.13, and 1.04% for starter, grower, and finisher diets). A total of 648-day-old, male Ross 708 chicks were placed in 36 pens with 18 chicks/pen and 9 replicates per treatment. Data were analyzed as a 2 × 2 factorial in JMP 14 (P ≤ 0.05). No interaction effects were observed on broiler live performance (P > 0.05). As expected, HS reduced BWG by 92 g and increased FCR by 11 points from 28 to 35 d of age compared to TN, respectively (P ≤ 0.05). The supplementation of SAA had no effect on live performance (P > 0.05). Cloacal temperatures were increased by 1.7, 1.4, and 1.2°C with HS at 28, 31, and 35 d compared to TN, respectively (P ≤ 0.05) and dietary SAA did not alter cloacal temperatures. At 28 d of age, supplementation of SAA to birds exposed to HS interacted as serum FITC-dextran (an indicator of intestinal permeability) was reduced to that of the TN group (P ≤ 0.05). The interaction was lost at 31 d, but HS still increased intestinal permeability (P ≤ 0.05). By 35 d, broilers were able to adapt to the HS conditions and intestinal permeability was unaffected (P > 0.05). Potential oxidative damage was reduced by increased SAA supplementation as indicated by an improvement in the reduced glutathione to oxidized glutathione ratio of 5 and 45 % at 28 (P = 0.08) and 35 d (P ≤ 0.05). These data suggest that intestinal permeability is compromised initially and to at least three d of heat exposure before the bird can adjust. However, oxidative damage in the liver of broilers exposed to HS is more chronic, building over the entire 7 d HS period and increased dietary SAA might have some protective effects on both broiler intestinal permeability and oxidative stress responses to HS.

Effects of a direct fed microbial (DFM) on broiler chickens exposed to acute and chronic cyclic heat stress in two consecutive experiments.

Two consecutive 35 d experiments were conducted to investigate the effects of a multistrain DFM fed continuously to broiler chickens exposed to HS from 28 to 35 d on broiler performance, body composition, ileal digestibility, and intestinal permeability using serum Fluorescein Isothiocyanate Dextran (FITC-d) concentration. The treatments were arranged as a 2 × 2 factorial with temperature: Elevated (HS: 33 ± 2°C for 6 h and 27.7°C for the remaining 18 h from 28 to 35 days of age) and Thermoneutral (TN: 22 to 24°C over the entire 24-h day from 28 to 35 days of age) and diet: corn-soybean meal based with and without DFM (3-strain Bacillus; Enviva PRO) fed over the entire 35-d period as the two factors. Experimental diets were formulated to meet all nutrient recommendations based on breed standards using a starter (0-10 d), grower (10-21 d), and finisher (21-35 d) period. For each of the 2 experiments, 648 Ross 708 broiler chicks were allotted among the treatments with 9 replicate pens of 18 broilers. Data were analyzed as a 2 × 2 factorial within each experiment in JMP 14. In both experiments, cloacal temperatures were increased (P ≤ 0.05) in the broilers subjected to the HS treatment at both 28 d (acute) and 35 d (chronic). Supplementing birds with DFM reduced cloacal temperatures in the Experiment 1 at 28 d, but not at the other time periods. The HS treatment reduced body weight gain and lean tissue accretion from 0 to 35 d in both experiments (P ≤ 0.05). In Experiment 2, when the litter was reused BWG was increased by 36 g/bird with supplementation of DFM (P ≤ 0.05). Ileal digestibility at 28 d (2 h post HS) was improved with DFM supplementation in both experiments (P ≤ 0.05). Serum FITC-d increased with HS at both 28 and 35 d. Serum FITC-d was generally decreased with DFM at 28 d but the response was inconsistent at 35 d. Overall, the results suggest that HS reduced broiler performance and DFM treatment improved intestinal permeability and nutrient digestibility responses to HS in both experiments but did not improve performance until built up litter was used in Experiment 2.

Tryptophan requirement of first-cycle commercial laying hens in peak egg production.

An experiment was conducted to evaluate the digestible tryptophan (Trp) requirement of laying hens from 22 to 34 wk of age. A total of 252 Hy-line W-36 laying hens were selected at 16 wk of age and allocated by weight (P = 0.90) to 7 dietary treatments resulting in 12 replicate cages of 3 birds for each treatment. A Trp-deficient basal diet was formulated using corn, corn gluten meal, and soybean meal for each of the 3 dietary phases and supplemented with synthetic L-Trp to provide 105, 119, 133, 147, 162, 176, and 190 mg digestible Trp on a daily basis over the experimental period. To adapt the hens to experimental diets, pullets were fed complete diets that contained increasing amounts of corn gluten meal. Hens received a controlled amount of feed daily based on feed intake expected under commercial conditions. Linear and quadratic broken-line, and quadratic polynomial models were used to estimate digestible Trp requirements based on hen-housed egg production (HHEP), egg mass (EM), and feed efficiency (FE). FE was calculated using EM and feed intake. Digestible Trp requirements were estimated to be 137, 183, and 192 mg/d for HHEP; 133, 180, and 183 for EM and 133, 177, and 173 for FE using linear broken-line, quadratic broken-line, and quadratic polynomial analysis, respectively. The quadratic broken line model in this experiment resulted in the best fit (R2) for all parameters measured. Linear broken line estimates resulted in lower estimates that the other models, and HHEP resulted in higher estimated digestible Trp requirement than EM and FE.

Effect of guanidinoacetic acid supplementation on live performance, meat quality, pectoral myopathies and blood parameters of male broilers fed corn-based diets with or without poultry by-products.

Creatine is a nitrogenous compound naturally occurring in animal tissues and is obtained from dietary animal protein or de novo synthesis from guanidinoacetic acid (GAA). The dietary supply of this semi-essential nutrient could be adversely compromised when feeding purely vegetable-based diets. The objective of this experiment was to evaluate the effects of GAA supplementation in broilers fed corn-based diets with or without the inclusion of poultry by-products (PBP) on live performance, carcass and cut up yields, meat quality, pectoral muscle myopathies, differential blood count, blood clinical chemistry, serum GAA and its metabolites. The treatments consisted of PBP inclusion in the diets at 0 and 5%, with or without GAA supplementation (0 or 0.06%). A total of 1,280 one-d-old male Ross 708 broiler chicks were randomly placed in 64 floor pens with 16 replicates per treatment combination. At 0, 14, 35, 48, and 55 d, pen BW and feed intake were recorded. BW gain and FCR were calculated at the end of each phase. Individual BW was obtained at 55 d and one broiler per pen was selected for blood collection. Additionally, four broilers per pen were selected (including the chicken for blood collection) for processing. Data were analyzed as a randomized complete block design in a 2 × 2 factorial arrangement with PBP and GAA supplementation as main effects. An improvement (P < 0.05) on FCR of 0.019 (g:g) was detected at 55 d due to GAA supplementation. The probability of having breast meat with low severity of wooden breast (score 2) was increased (P < 0.05) by GAA inclusion in diets without PBP. An interaction effect (P < 0.05) was detected on GAA concentration in blood. The supplementation with GAA and PBP inclusion resulted in higher (P < 0.05) GAA serum concentration. Generally, meat quality parameters were not affected by GAA. In conclusion, GAA supplementation improved FCR regardless of dietary PBP and reduced wooden breast severity by increasing score 2 in diets without PBP.

Performance, meat quality, and pectoral myopathies of broilers fed either corn or sorghum based diets supplemented with guanidinoacetic acid.

One experiment was conducted to evaluate the effects of guanidinoacetic acid (GAA) supplementation in broilers fed corn or sorghum-based diets on live performance, carcass and cut up yields, meat quality, and pectoral myopathies. The treatments consisted of corn or sorghum-based diets with or without the addition of GAA (600 g/ton). A total of 800 one-d-old male Ross 708 broiler chicks were randomly placed in 40 floor pens with 10 replicates (20 birds per pen) per each of the four treatments. At hatch, 14, 35, and 50 d, BW and feed intake were recorded. BW gain and FCR were calculated at the end of each phase. Four broilers per pen were selected and slaughtered at 51d and 55d of age to determine carcass and cut up yields, meat quality and myopathies (spaghetti muscle, white striping, and wooden breast) severity in the Pectoralis major. Data were analyzed as a randomized complete block design in a 2 × 2 factorial arrangement with grain type and GAA supplementation as main effects. At 50 d, diets containing GAA improved (P < 0.01) FCR (1.682 vs. 1.724 g: g) independently of grain type. At 55 d, broilers fed corn diets with GAA had higher breast meat yield (P < 0.05) compared to corn without GAA. Drip and cook loss, and shear force (Warner-Bratzler) were not affected (P > 0.05) by GAA supplementation at any slaughter ages. However, GAA decreased (P < 0.05) the ultimate pH at 51 and 55 d in breast meat samples compared to unsupplemented diets. At 51 d, broilers supplemented with GAA had double (P < 0.05) breast meat fillets without wooden breast (score 1) compared with broilers fed non-supplemented diets, therefore reducing the severity of this myopathy. In conclusion, GAA supplementation improved broiler live performance in broilers raised up to 50 d independently of grain source, increased breast meat yield in corn-based diets and reduced the severity of wooden breast myopathy.

Pathogenesis of Enterococcal Spondylitis Caused by Enterococcus cecorum in Broiler Chickens.

Enterococcal spondylitis (ES) is a disease of commercial broiler chickens, with a worldwide distribution. Symmetrical hind limb paralysis typical of ES results from infection of the free thoracic vertebra (FTV) by pathogenic strains of Enterococcus cecorum . To determine the pathogenesis of ES, birds with natural and experimental ES were studied over time. In natural disease, case birds (n = 150) from an affected farm and control birds (n = 100) from an unaffected farm were evaluated at weeks 1-6. In control birds, intestinal colonization by E. cecorum began at week 3. In case birds, E. cecorum was detected in intestine and spleen at week 1, followed by infection of the FTV beginning at week 3. E. cecorum isolates recovered from intestine, spleen, and FTV of case birds had matching genotypes, confirming that intestinal colonization with pathogenic strains precedes bacteremia and infection of the FTV. Clinical intestinal disease was not required for E. cecorum bacteremia. In 1- to 3-week-old case birds, pathogenic E. cecorum was observed within osteochondrosis dissecans (OCD) lesions in the FTV. To determine whether OCD of the FTV was a risk factor for ES, 214 birds were orally infected with E. cecorum, and the FTV was evaluated histologically at weeks 1-7. Birds without cartilage clefts of OCD in the FTV did not develop ES; while birds with OCD scores ≥3 were susceptible to lesion development. These findings suggest that intestinal colonization, bacteremia, and OCD of the FTV in early life are crucial to the pathogenesis of ES.