Effect of litter management systems on incidence and severity of footpad dermatitis among broilers at finisher stage.

Pododermatitis, or footpad dermatitis (FPD), is a welfare concern affecting broiler chickens globally. In the humid tropics, where high temperatures and humidity prevail, the impact of pododermatitis on broiler performance characteristics and behavior becomes even more significant hence this investigation. One hundred and eighty male broilers were used for this experiment out of 200 birds initially procured at day old. They were brooded and reared on deep litter and at 21 days of age, they were randomly allotted to the experimental unit. There were three treatments each with three replicates in a completely randomized design. The three litter management systems constituted the treatment groups. In the first treatment (t-A), litter materials were changed on a weekly basis and replaced with fresh ones while in the second treatment (t-B), the litter materials were turned or raked once a week, and in the third treatment (t-C), the litter materials were left untouched. The litter material used across all treatments was wood shavings and t-C served as control. The experimental birds were fed ad libitum during the trial. Data on daily feed intake, incidence and severity of paw lesions, and weekly body weights were taken while the experiment lasted 35 days. Test of mobility and aggression were carried out on the birds from each group on the last day of the experiment. The moisture content and pH of litter materials of each replicate were taken weekly from day 21 till the end of the experiment. Data were later subjected to analysis of variance statistically. The results revealed that broilers on t-A performed better (P < 0.05) than those on t-B and t-C for feed intake, live weight, weight gain, and feed utilization. However, FPD was pronounced among broilers on t-C and much more severe. A positive correlation was observed between the values of litter moisture content, litter pH, and incidence and severity of FPD. Birds on t-C were dull in appearance and inactive. In conclusion, FPD has a detrimental impact on the performance characteristics and behavior of broiler chickens in the humid tropics. However, the severity depends on the management system adopted. By adopting appropriate management practices such as weekly replacement of litter with fresh ones, it is possible to alleviate the negative consequences of FPD, improve broiler welfare, and enhance the sustainability of the poultry industry in these regions.

Interleukin-1alpha-induced changes in chromium-51 absorption, tissue retention, and urinary excretion in rats.

The effects of interleukin-1 alpha (IL-1alpha) on chromium-51 absorption, tissue retention, and urinary excretion were studied in adult male Sprague-Dawley rats. Ten rats were deprived of food for 12 h, injected intraperitoneally with mouse recombinant IL-1alpha (1 microg/kg of body weight in phosphate-buffered saline [PBS]) or control (0.1% bovine serum albumin [BSA] in PBS). Two hours after dosing with the IL-1alpha, rats were fed 50 microL (200 microCi, 0.36 microg Cr) of 51CrCl3 by micropipet. Blood was collected from the tail at 0.25, 0.5, 1, 2, and 4 h. Six hours after dosing with 51CrCl3, rats were exsanguinated and blood and tissues were sampled. The IL-1alpha significantly decreased chromium-51 in blood, urine, and some tissues compared to the control. The decreased absorption, retention, and urinary excretion of chromium-51 from 51CrCl3 in this study may be due to IL-1alpha-mediated increases in the production of prostaglandins and/or decreased production of gastric acid.

Absorption, retention and urinary excretion of chromium-51 in rats pretreated with indomethacin and dosed with dimethylprostaglandin E2, misoprostol or prostacyclin.

Drug-nutrient interactions affecting chromium were investigated in this study. Rats were injected with indomethacin to reduce endogenous prostaglandin synthesis and dosed with prostaglandin analogues or prostacyclin. Effects on absorption, tissue distribution and urinary excretion of 51Cr from 51CrCl3 were evaluated using a 2 x 4 factorial experimental design. Forty-eight adult male rats were food deprived for 12 h and then injected intraperitoneally with indomethacin (5 mg/kg body wt) or placebo. Thirty minutes later, rats were intubated and dosed with one of four treatments: a prostaglandin E1 analogue (misoprostol) at 50 microg/kg body wt; a prostaglandin E2 analogue (16,16-dimethylprostaglandin E2) at 7.5 microg/kg body wt; prostacyclin at 20 microg/kg body wt; or control (7.64 mmol/L Tween-80 suspended in 0.15 mol/L NaCl containing 0.48 mol/L ethanol). Immediately after intubation, rats were dosed with 3.7 mBq of 51CrCl3 by micropipette. Blood was collected from the tail at intervals after 51Cr dosing. Six hours after dosing, 51Cr rats were exsanguinated by cardiac puncture. Indomethacin, an inhibitor of prostaglandin synthesis, significantly increased (P < 0.05) 51Cr in blood at all time periods tested except at 15 min. In tissues, indomethacin significantly increased 51Cr retention. Urinary 51Cr excretion at 6 h was higher (P < 0.05) in indomethacin-pretreated rats than in control rats. Administration of indomethacin, which blocks prostaglandin synthesis, enhanced 51Cr absorption, whereas dosing with 16,16-dimethylprostaglandin E2 decreased 51Cr absorption.

Uptake and retention in suckling rats of 51chromium fed with human milk or infant formulas.

Optimum concentration of Cr for infant formulas has not been established. Such components as soy protein or supplemental Fe could influence absorption and retention. Suckling rat pups were used to evaluate the influence of three commercial formulas and human milk, all of which had been incubated with 51CrCl3 for 1 h, on the uptake and retention of the added 51Cr. After fasting 3 h, the pups were intubated with a single dose of 25 microCi 51CrCl3 in either a cow's milk-based formula, an Fe-supplemented cow's milk-based formula, a soy-based formula, or human milk. Six hours later, 51Cr was counted in five organs, thymus, blood, and total urine. Absorption of 51Cr was low. At 6 h, percent 51Cr in blood was < 0.2% of the dose, and total 51Cr excretion in urine was < 1.8%. The uptake and retention of 51Cr and its concentration in any of the organs, thymus, blood, and urine were not influenced by different types of formula or by human milk.

Chromium and chronic ascorbic acid depletion effects on tissue ascorbate, manganese, and 14C retention from 14C-ascorbate in guinea pigs.

Chromium (Cr) potentiates the effects of insulin and a role for insulin in ascorbic acid transport has been reported. Therefore, the effects of Cr and ascorbate depletion on tissue ascorbic acid and 14C distribution and excretion after a 14C ascorbate dose were investigated in guinea pigs. As utilization of dietary Cr is affected by interaction with other minerals, tissue manganese (Mn), zinc (Zn), copper (Cu), and iron (Fe) were examined. For 20 wk, 40 weanling animals were fed either a Cr-deficient (< 0.06 micrograms Cr/g diet, -Cr) or a Cr-adequate (2 micrograms Cr from CrCl3/g diet, +Cr) casein-based diet and were given 1 mg ascorbate/d (-C) or 10 mg ascorbate/d (+C) for 20 wk. Animals fed the Cr-depleted diet had decreased weight at 20 wk (p < 0.01). Six hours before necropsy, animals were dosed by micropipette with 1.8 microCi of L-[carboxyl-14C] ascorbic acid and placed in metabolic cages. Ascorbate supplementation increased Fe concentrations in most analyzed tissues, hepatic 14C, tissue ascorbate and Mn concentration in the adrenal and testes, but decreased the concentrations of Cu in the kidney and Mn in the spleen. Liver Mn concentration was higher and kidney Mn concentration was lower in +Cr animals. Interactions between Cr and ascorbic acid affected Mn concentrations in bone and brain. These results indicate that ascorbate and Cr may affect Mn distribution. Chromium supplementation decreased plasma cortisol, brain 14C and the amount of 14C expired as carbon dioxide. These findings suggest that dietary Cr may affect ascorbic acid metabolism and the metabolic response to stress.