Three hundred sixty, 1-d-old male broiler chicks were fed diets containing grains naturally contaminated with Fusarium mycotoxins for 56 d. The four diets included control (0.14 mg/kg deoxynivalenol, 18 mg/ kg fusaric acid, < 0.1 mg/kg zearalenone), low level of contaminated grains (4.7 mg/kg deoxynivalenol, 20.6 mg/kg fusaric acid, 0.2 mg/kg zearalenone), and high level of contaminated grains without (8.2 mg/kg deoxynivalenol, 20.3 mg/kg fusaric acid, 0.56 mg/kg zearalenone) and with (9.7 mg/kg deoxynivalenol, 21.6 mg/kg fusaric acid, 0.8 mg/kg zearalenone) 0.2% esterified-glucomannan polymer derived from Saccharomyces cerevisiae1026 (E-GM). Body weight gain and feed consumption responded in a significant quadratic fashion to the inclusion of contaminated grains during the finisher period. Efficiency of feed utilization, however, was not affected by diets. The feeding of contaminated grains in the finisher period also caused significant linear increases in blood erythrocyte count and serum uric acid concentration and a significant linear decline in the serum lipase activity. Dietary inclusion of contaminated grains resulted in a significant quadratic effect on serum albumin and y-glutamyltransferase activity. Blood hemoglobin and biliary IgA concentrations, however, responded in significant linear and quadratic fashions. Supplementation of E-GM counteracted most of the blood parameter alterations caused by the Fusarium mycotoxin-contaminated grains and reduced breast muscle redness. It was concluded that broiler chickens may be susceptible to Fusarium mycotoxicoses when naturally contaminated grains are fed containing a combination of mycotoxins.
To measure stress in caged hens, differential counts of their wing vein blood were used to determine heterophil/lymphocyte (H/L) ratios and total white blood cell counts (TWBC). The H/L values of 18-wk samples from conventionally caged hens (CC) were not statistically different from hens raised in aviaries (AV) when calculated by either of 2 methods (H/L 1 and H/L 2). However, there was a high degree of variation among samples within each cage type. The TWBC data and hematology indicated leukocytosis, leukemoid reactions, and a high frequency of atypia. Reactive lymphocytes, large plasmacytoid lymphocytes, cyanophils, coccinocytes, and atypical heterophils were common. Analysis of 77-wk data indicated significant differences among 3 cage types. The H/L 1 of enriched caged (EN) hens was twice (0.91) that of either AV (0.33) or CC (0.44) hens (P < 0.01); the H/L 2 values were also highest for EN (0.46) versus AV (0.29) and CC (0.34; P <0.01). As was the case with 18-wk samples, TWBC distributions and hematological data indicated leukocytosis, leukemoid reactions, and a high frequency of atypia. Among the likely reasons for the hematological observations was the occurrence of polymicrobial bacteremia and fungemia, both of which could account for high TWBC and atypical cells. Collectively, these observations challenge the general application of the H/L ratio method when applied alone as an indicator of stress and welfare of hens caged in modern systems.
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.
Six trials were conducted during which a total of 12 congenic lines (University of California-Davis, UCD) homozygous for various B-complex haplotypes, were challenged as neonates by intraperitoneal injection with either of two isolates of Salmonella enteritidis. Because these B haplotypes were expressed on a common genetic background (highly inbred Line UCD 003), and mortality differences among lines were statistically significant in three of the six trials, and morbidity (body weight) differences were significant in another trial; it is suggested that B-complex alleles affect the degree of immunity to these isolates. When all lines and trials were compared, line 342 (BC/BC) emerged as particularly resistant, whereas lines 253 (B18/B18) and 254 (B15/B15) were more susceptible. The remainder of the lines were of neutral (intermediate) susceptibility. Sex did not appear to influence the results of the challenge, but more resistance was observed with an increase in the age at inoculation. Although the mechanism that determined this resistance is unknown it was present as early as 3 d of age, and it is suggested that complement proteins, which have a known role in protection from bacterial infections, and are encoded by genes located within the B-complex, or acute phase proteins, may account for these observations. The results provide additional evidence for the importance of the B-complex in determining immunity to Salmonella.
A study was conducted to establish the dietary Thr requirement of Pekin ducks from 15 to 35 d of age. Experimental diets were formulated to contain 0.55, 0.60, 0.65, 0.75, and 0.85% Thr (0.57, 0.60, 0.64, 0.72, and 0.80% on an analyzed basis) and were studied in 2 experiments. In experiment 1, each diet was fed to 10 pens of 52 drakes per pen. Samples were collected at d 35 for determinations of carcass yields, serum immune parameters, and intestinal characteristics. Experiment 2 was a digestibility study, wherein 0.5% chromic oxide was mixed into the experimental diets and fed from 15 to 19 d. Ileal digesta were collected at d 19 to analyze mucin secretions and apparent ileal Thr digestibility. The results showed that feeding 0.72% versus 0.64% Thr improved 15 to 35 d BW gain by 55 g (P < 0.05), reduced feed-to-gain by 0.04 (P < 0.05), as well as increased carcass and breast meat yields by 22 and 24 g, respectively. Also, 0.72% Thr had the highest crude mucin secretion on a DM intake (DMI) basis (P < 0.05), although Thr had no effect on villus height, crypt depth, goblet cells, and MUC2 gene expression in the jejunum and ileum. In addition, serum natural IgY linearly increased (P < 0.0001) with dietary Thr increase. Using nonlinear regressions, Thr requirement was estimated to range from a low of 0.70% to maximize dry crude mucin secretion on a DMI basis to a high of 0.80% to maximize carcass weight and serum IgY production by the linear or quadratic regression. Equivalently, Thr requirement varied between a low of 0.62% to minimize mortality and a high of 0.73% to maximize dry crude mucin secretion expressed as DMI using the quadratic broken-line model. Correspondingly, the apparent ileal digestible Thr requirements were estimated to be 0.52 to 0.66% (0.70 to 0.80% dietary Thr) by quadratic and 0.47 to 0.56% (0.62 to 0.73% dietary Thr) by quadratic broken-line model.
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