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The impact of supplemental dietary methionine sources on volatile compound concentrations in broiler excreta.

The impact of different Met sources on broiler fecal odor volatiles was determined by evaluating the types of sulfur compounds produced in broiler excreta. Two experiments were conducted using straight-run broiler chicks randomly distributed in battery cages, with 3 replicate pens of 16 birds each. The treatment groups were 1) dry Met hydroxy analogue (dry MetHA), 2) sodium methioninate aqueous solution (NaMet), 3) liquid Met hydroxy analogue (Liq MetHA), 4) D,L- Met, and 5) no supplemental Met (control group). The Met activities of each Met source were 52, 45.9, 88, and 98%, respectively. All diets were formulated to contain either 0.8% (experiment 1) total Met activity or 0.5% Met activity in the starter and 0.38% Met activity in the grower (experiment 2) (except the control group, 0.35% Met activity), but otherwise met NRC nutrient requirements (NRC, 1994). Diets were fed ad libitum from d 1 to 6 wk of age. There were no significant differences in BW among the treatments. All excreta were collected in litter pans lined with aluminum foil. In experiment 1, at wk 6, broiler excreta were collected for a 24-h period, and 4.5 g of broiler excreta from each treatment group was collected into 15-mL headspace vials. Samples were analyzed by gas chromatography/mass spectrometry (GC/MS). The volatile sulfur compounds that were identified and quantified in the broiler excreta were H2S, carbonyl sulfide (COS), methyl mercaptan (CH3SH), dimethyl disulfide (CH3SSCH3), and dimethyl trisulfide (CH3SSSCH3). The NaMet treatment group had significantly higher concentrations of H2S, COS, and CH3SSCH3 compared with all other treatment groups. The Liq MetHA group had significantly lower concentrations of H2S, COS, CH3SH, and CH3SSCH3 compared with the other treatment groups. The dry MetHA group significantly had the highest concentration of CH4SH. The D,L-Met treatment group had the significantly highest concentration of CH3SSSCH3 and the lowest concentration of H2S. The control group had the significantly lowest concentrations of CH3SH, CH3SSCH3, and CH3SSSCH3 compared with the other treatment groups. In experiment 2, at wk 6, an electronic nose was used to evaluate 15 air samples per treatment group. In addition, 15 air samples (containing 6 to 8 L of air in a Tedlar bag, 3 samples per treatment group) were collected for odor evaluation by a sensory panel. Electronic nose sensor data revealed that volatile compounds in broiler excreta from the control group were significantly different from the other 4 treatment groups. Evaluation of the air samples by a sensory panel determined that there was a statistically significant difference in odor threshold detection between the control group and the other treatment groups. The dilutions to threshold of control group, NaMet, dry MetHA, Liq MetHA, and D,L-Met were 350, 492, 568, 496, and 526 odor units, respectively. These findings demonstrate that dietary Met sources significantly influenced odorous volatile concentrations in broiler excreta.

Animals↗

Microstructure and thermal characteristics of Thai indigenous and broiler chicken muscles.

The microstructure and thermal characteristics of Thai indigenous (Gallus domesticus) and broiler chicken (commercial line CP707) biceps femoris and pectoralis muscles were determined. Perimysium thicknesses were 14.2 microm for biceps femoris muscle and 7.10 microm for pectoralis muscle of indigenous chicken muscles, thicker than those of broiler muscles, which were 9.93 microm for biceps femoris muscle and 3.87 microm for pectoralis muscle (P < 0.05). Five endothermic peaks with peak transition temperatures (Tp) of 54.9, 61.7, 65.4, 70.6, and 76.1 degrees C were obtained for broiler pectoralis muscle, whereas only 3 endothermic peaks (Tp of 56.6, 62.6, and 74.9 degrees C) were obtained for broiler biceps femoris muscle. Thai indigenous biceps femoris and pectoralis muscles had endothermic peaks with Tp ranges of 53.5 to 54.8, 60.7 to 61.9, and 75.9 to 76.9 degrees C. The fiber diameters of Thai indigenous chicken muscles were greater (P < 0.05) than those of the broiler, 31.7 vs. 20.4 microm for biceps femoris muscle and 28.9 vs. 26.6 microm for pectoralis muscle, respectively. After cooking at 80 degrees C for 10 min, the fiber diameter of indigenous chicken muscles significantly decreased while those of the broiler significantly increased. The mean of sarcomere lengths of the raw muscles ranged from 1.56 to 1.64 microm and decreased to 0.92 to 1.32 microm (P < 0.001) for broiler muscles and 1.22 to 1.35 microm (P < 0.001) for indigenous chicken muscles after cooking. The perimysium and endomysium of broiler muscles melted after cooking at 80 degrees C, however, only slight disintegration was observed in these tissues in the indigenous chicken muscles.

Animals↗

Pulmonary and systemic hemodynamic responses to intravenous prostacyclin in broilers.

The eicosanoid vasodilator prostacyclin (PGI2) reduces resistance to pulmonary blood flow and attenuates pulmonary hypertension in mammals. However, sparse information is available regarding the responsiveness of the avian pulmonary vasculature to PGI2. Accordingly, in 3 experiments we evaluated the pulmonary vascular responses to PGI2 in male broilers. In experiment 1, infusing PGI2 (10 microg/min) into clinically healthy broilers did not reduce their pulmonary vascular resistance (PVR) but did reduce their pulmonary arterial pressure (PAP) by lowering their cardiac output. Within 4 min after stopping the PGI2 infusion, the cardiac output and PAP returned to preinfusion levels. In experiment 2, the responses to PGI2 were evaluated after arachidonic acid (AA) had been infused to preconstrict the pulmonary vasculature. The AA infusion (400 microg/min) consistently triggered dramatic, sustained pulmonary vasoconstriction (increased PVR) and pulmonary hypertension (increased PAP). Concurrent PGI2 infusions did not reduce PVR but did reduce PAP by lowering cardiac output. Within 4 min after stopping the PGI2 infusion, PAP and cardiac output returned to their previous (hypertensive) levels attributable to the ongoing AA infusion. In experiment 3, PGI2 was infused (10 microg/min) into clinically healthy (PAP < or = 24 mmHg) or subclinically hypertensive (PAP > or = 27 mmHg) broilers. Throughout this experiment broilers in the hypertensive group had higher PAP values than broilers in the healthy group. The PGI2 infusion reduced PAP in both groups but did not reduce PVR. Instead, the pulmonary hypotensive response to PGI2 infusion was associated with a reduction in cardiac output in both groups. In all 3 experiments PGI2 reduced PAP by reducing cardiac output rather than by reducing PVR. There was no evidence that PGI2 acts as an effective pulmonary vasodilator in broilers regardless of whether their pulmonary vasculature was apparently normal (clinically healthy), had been pharmacologically preconstricted (AA infusion), or initially exhibited the vasoconstriction that is typical of the pathogenesis of pulmonary hypertension syndrome in broilers (PAP > or = 27 mmHg). The consistent failure of PGI2 to elicit pulmonary vasodilation in this study suggests fundamental differences in AA metabolism or the etiology of pulmonary hypertension may exist when broilers are compared with mammals.

Adenosine Diphosphate↗

Compromised liver mitochondrial function and complex activity in low feed efficient broilers are associated with higher oxidative stress and differential protein expression.

Variations in broiler growth and efficiency have been explained in part by differences in mitochondrial function and biochemistry in broilers. To further our knowledge in this regard, 2 experiments were carried out to determine the relationships of a) mitochondrial function and activities of various electron transport chain (ETC) complexes; b) production of H2O2, a reactive oxygen species (ROS), and its association with protein oxidation; and c) mitochondrial protein expression in liver of a single line male broilers with low or high feed efficiency (FE, n = 5 to 8 per group). Mitochondrial function and complex activities were measured polarographically and spectrophotometrically, respectively. H2O2 was measured fluorimetrically, whereas oxidized protein (carbonyls) and specific mitochondrial proteins were analyzed using Western blots. Mitochondrial function (ETC coupling) and activities of ETC complexes (I, II, III, and IV) were higher in high FE compared with low FE broilers. H2O2 and protein carbonyls were higher in the livers of low FE broilers than in high FE broilers. Whereas the expression of 4 immunoreactive proteins [NAD3 (complex I), subunit VII (complex III), cytochrome c oxidase subunits (COX) II, and COX IVb (complex IV)] were higher in low FE liver mitochondria and 2 proteins [subunit 70 (complex II) and a-ATP synthase (complex V)] were higher in high FE birds, there were no differences between groups in the expression of 18 other mitochondrial proteins. In conclusion, increases in oxidative stress in low FE broilers were caused by or may contribute to differences in mitochondrial function (ETC coupling and complex activities) or the differential expression of steady-state levels of some mitochondrial proteins in the liver. Understanding the role of oxidative stress in Low FE broilers will provide clues in understanding the cellular basis of feed efficiency.

Animal Feed↗

Feed withdrawal of broilers before transport changes plasma hormone and metabolite concentrations.

Two experiments were completed to observe the combined effects of feed withdrawal and the catching and transport process on stress and energy metabolism. During one experiment 192 male broilers (46 d of age) were used, and in the other we used 240 male broilers (49 d of age). The experiments consisted of 2 interventions: feed intervention and transport intervention. The feed intervention took 10 h, in which broilers had full access to feed or feed was withdrawn and, thereafter, had a transport intervention that took 3 h, in which broilers were caught, crated, loaded, transported, and then had to wait in the crates for 1 h or remained in the pens. After the transport intervention, blood samples were taken to determine plasma corticosterone, triiodothyronine, thyroxine, glucose, lactate, uric acid, nonesterified fatty acid, and triglyceride concentrations. Changes in BW were also assessed. Broilers from which feed was withdrawn before the transport intervention showed higher thyroxine concentration and lower triiodothyronine, triglyceride, glucose, and lactate concentrations compared with broilers that had access to feed before the transport intervention. These findings indicate a negative energy balance and stress. Broilers that were transported after feed withdrawal had BW losses of approximately 0.42% per hour, which is approximately 0.30% per hour more than those that had full access to feed. To continue feeding broilers until catching resulted in higher BW at the slaughterhouse and less stress, as shown by a negative energy balance and might improve meat quality.

Abattoirs↗

Effects of travel distance and the season of the year on death rates of broilers transported to poultry processing plants.

Death losses among broilers transported to processing plants are caused by poor welfare. The number of birds dying during transport and in processing plants shortly after arrival there may serve as an indicator of the quality of welfare during loading and transport. In the Czech Republic, shipments of broilers to processing plants were monitored from 1997 to 2004. It was found that the mortality of broilers during transport was 0.247%, but it varied according to the transport distance to the processing plant from 0.146% (50 km maximum) to 0.862% (>300 km). The broiler mortality in transit was also influenced by the season of the year. The highest mortality was found in summer months, especially in June, July, and August, and in winter months, especially in December, January, and February. A comparison between period 1 (1997 to 2000) and period 2 (2001 to 2004) showed a long-term adverse trend in the number of broilers dying during transport to processing plants for all of the distances monitored (except transport distances <50 km), because the overall number of dead birds on arrival to processing plants increased from 0.224 to 0.265% (index of 1.18). This difference is statistically significant (P = 0.000). The stress caused to broilers by transport to processing plants is reflected in higher transport-related mortality of the birds. Long-term trends point to an increase in death losses of broilers. Longer transport distances and transportation in summer and winter months have led to an increase in death losses among broilers transported to processing plants.

Abattoirs↗

Nitrogen emissions from broilers measured by mass balance over eighteen consecutive flocks.

Emission of nitrogen in the form of ammonia from poultry rearing facilities has been an important topic for the poultry industry because of concerns regarding the effects of ammonia on the environment. Sound scientific data is needed to accurately estimate air emissions from poultry operations. Many factors, such as season of the year, ambient temperature and humidity, bird health, and management practices can influence ammonia volatilization from broiler rearing facilities. Precise results are often difficult to attain from commercial facilities, particularly over long periods of time. Therefore, an experiment was conducted to determine nitrogen loss from broilers in a research facility under conditions simulating commercial production for 18 consecutive flocks. Broilers were reared to 40 to 42 d of age and fed diets obtained from a commercial broiler integrator. New rice hulls were used for litter for the first flock, and the same litter was recycled for all subsequent flocks with caked litter removed between flocks. All birds, feeds, and litter materials entering and leaving the facility were quantified, sampled, and analyzed for total nitrogen content. Nitrogen loss was calculated by the mass balance method in which loss was equal to the difference between the nitrogen inputs and the nitrogen outputs. Nitrogen partitioning as a percentage of inputs averaged 15.29, 6.84, 55.52, 1.27, and 21.08% for litter, caked litter, broiler carcasses, mortalities, and nitrogen loss, respectively, over all eighteen flocks. During the production of 18 flocks of broilers on the same recycled litter, the average nitrogen emission rate was calculated to range from 4.13 to 19.74 g of N/ kg of marketed broiler (grams of nitrogen per kilogram) and averaged 11.07 g of N/kg. Nitrogen loss was significantly (P < 0.05) greater for flocks reared in summer vs. winter. Results of this experiment have demonstrated that the rate of nitrogen volatilization from broiler grow-out facilities varies significantly on a flock-to-flock basis.

Air Pollutants↗

Influence of aminoguanidine, an inhibitor of inducible nitric oxide synthase, on the pulmonary hypertensive response to microparticle injections in broilers.

The pulmonary hypertensive response to pulmonary vascular obstruction caused by intravenously injected microparticles is amplified by pretreatment with N(omega)nitro-L-arginine methyl ester (L-NAME). The L-NAME prevents the synthesis of the potent vasodilator nitric oxide (NO) by inhibiting both the constitutive [endothelial NO synthase (eNOS or NOS-3)] and inducible [inducible NO synthase (iNOS or NOS-2)] forms of NO synthase. In the present study we used the selective iNOS inhibitor aminoguanidine (AG) to evaluate the role of iNOS in modulating the pulmonary hypertension (PH) triggered by microparticle injections. Experiment 1 was conducted to confirm the ability of AG to inhibit NO synthesis by iNOS in broiler peripheral blood mononuclear cells exposed to bacterial lipopolysaccharide (LPS, endotoxin). Mononuclear leukocytes treated with LPS produced 10-fold more NO than untreated (control) cells. The LPS-stimulated production of NO was partially inhibited by L-NAME and was fully inhibited by AG, thereby confirming that AG inhibits LPS-mediated iNOS activation in broilers. In Experiment 2 we evaluated the responses of male progeny from a base population (MP Base) and from a derivative line selected for one generation from the survivors of an LD50 microparticle injection (MP Select). The pulmonary arterial pressure (PAP) was lower in MP Select than in MP Base broilers. Both lines exhibited similar percentage increases in PAP after microparticles were injected, and AG modestly amplified the PH triggered by microparticles in both lines. In Experiment 3 we evaluated the responses of male progeny from a second base population (PAC Base) and from a derivative line selected for 3 generations using the unilateral pulmonary artery clamp technique (PAC Select). The PAP was lower in PAC Select than in PAC Base broilers, and both lines exhibited similar percentage increases in PAP in response to the microparticles. The PH triggered by microparticles was not amplified by AG but was doubled by L-NAME. These experiments demonstrate that during the 30 min following pulmonary vascular entrapment of microparticles, iNOS modulated the PH elicited in broilers derived from the MP pedigree line, but not in broilers from the PAC pedigree line. Different NOS-mediated responses among broiler populations may affect pulmonary hemodynamic characteristics of broiler lines selected using i.v. microparticle injections.

Animals↗

Increased calcium deposits and decreased Ca2+-ATPase in right ventricular myocardium of ascitic broiler chickens.

Right ventricular hypertrophy and failure is an important step in the development of ascites syndrome (AS) in broiler chickens. Cytoplasmic calcium concentration is a major regulator of cardiac contractile function and various physiological processes in cardiac muscle cells. The purpose of this study was to measure the right ventricular pressure and investigate the precise ultrastructural location of Ca(2+) and Ca(2+)-ATPase in the right ventricular myocardium of chickens with AS induced by low ambient temperature. The results showed that the right ventricular diastolic pressure of ascitic broilers was significantly higher than that of control broilers (P < 0.01), and the maximum change ratio of right intraventricular pressure (RV +/- dp/dt(max)) of ascitic broilers was significantly lower than that of the controls (P < 0.01). Extensively increased calcium deposits were observed in the right ventricular myocardium of ascitic broilers, whereas in the age-matched control broilers, calcium deposits were much less. The Ca(2+)-ATPase reactive products were obviously found on the sarcoplasmic reticulum and mitochondrial membrane of the control right ventricular myocardium, but rarely observed in the ascitic broilers. The data suggest that in ascitic broilers there is the right ventricular diastolic dysfunction, in which the overload of intracellular calcium and the decreased Ca(2+)-ATPase activity might be the important factors.

Animals↗

Gait analysis in laying hens and broilers with and without leg disorders.

Selection of broiler strains for high body weight has changed the anatomical characteristics and in connection to that, the pattern of locomotion. In addition, rapid growing broilers show a high incidence of leg disorders which compromise the walking ability of the birds. Differences in the patterns of locomotion between laying hens and broilers and between broilers with and without leg disorders can be demonstrated and quantified by gait analysis. The gait pattern was recorded by videotracking. Three points of the body - the cloacal region and both feet joints - were marked by small patches of reflecting foils. The vertical and horizontal movements of the marked points were recorded by a camera in posterior position, while the bird was walking on a treadmill The camera was connected with a PC-operated videotracking system. The vertical and horizontal movements of the 3 marked points were recorded simultaneously and plotted against the time axis. Kinetograms show clearly the differences in the walking pattern between broilers and layers. Layers place the legs directly under the centre of gravity and, therefore, the body moves in a straight line. Broilers, in contrast, move the centre of gravity step by step laterally towards the position of the supporting leg. This pattern may be caused by the anatomical characteristics of broilers. Limping in broilers with leg problems can be measured by differences in the lateral and vertical movements of the right and left leg.

Animals↗

Role of volatile fatty acids in development of the cecal microflora in broiler chickens during growth.

It is known that volatile fatty acids can inhibit growth of species of the family Enterobacteriaceae in vitro. However, whether these volatile fatty acids affect bacterial populations in the ceca of chickens is unknown. Therefore, a study was conducted to investigate if changes in volatile fatty acids in ceca of broiler chickens during growth affect bacterial populations. Results showed that members of the Enterobacteriaceae and enterococci are present in large numbers in 3-day-old broilers and start to decrease when broilers grow older. Lactobacilli are present in large numbers as well in 3-day-old broilers, but they remain stable during the growth of broilers. Acetate, butyrate, and propionate increase from undetectable levels in 1-day-old broilers to high concentrations in 15-day-old broilers, after which they stabilize. Significant negative correlations could be calculated between numbers of Enterobacteriaceae and concentrations of undissociated acetate, propionate, and butyrate. Furthermore, pure cultures of Enterobacteriaceae isolated from the ceca were grown in the presence of volatile fatty acids. Growth rates and maximal optical density decreased when these strains grew in the presence of increasing volatile fatty acid concentrations. It is concluded that volatile fatty acids are responsible for the reduction in numbers of Enterobacteriaceae in the ceca of broiler chickens during growth.

Animals↗

Sources of Campylobacter spp. colonizing housed broiler flocks during rearing.

The study aimed to identify sources of campylobacter in 10 housed broiler flocks from three United Kingdom poultry companies. Samples from (i) the breeder flocks, which supplied the broilers, (ii) cleaned and disinfected houses prior to chick placement, (iii) the chickens, and (iv) the environments inside and outside the broiler houses during rearing were examined. Samples were collected at frequent intervals and examined for Campylobacter spp. Characterization of the isolates using multilocus sequence typing (MLST), serotyping, phage typing, and flaA restriction fragment length polymorphism typing was performed. Seven flocks became colonized during the growing period. Campylobacter spp. were detected in the environment surrounding the broiler house, prior to as well as during flock colonization, for six of these flocks. On two occasions, isolates detected in a puddle just prior to the birds being placed were indistinguishable from those colonizing the birds. Once flocks were colonized, indistinguishable strains of campylobacter were found in the feed and water and in the air of the broiler house. Campylobacter spp. were also detected in the air up to 30 m downstream of the broiler house, which raises the issue of the role of airborne transmission in the spread of campylobacter. At any time during rearing, broiler flocks were colonized by only one or two types determined by MLST but these changed, with some strains superseding others. In conclusion, the study provided strong evidence for the environment as a source of campylobacters colonizing housed broiler flocks. It also demonstrated colonization by successive campylobacter types determined by MLST during the life of a flock.

Animal Husbandry↗

Intake and digestion by Holstein steers consuming diets based on litter harvested after different numbers of broiler growing periods or with molasses addition before deep-stacking.

We determined the effects on feed intake and digestibility by Holstein steers of 1) the number of broiler growing periods before litter harvest and dietary level of broiler litter and 2) level of molasses added to broiler litter before deep-stacking. In Exp. 1, eight steers (179+/-7.4 kg average BW) were used in two simultaneous 4 x 4 Latin squares (2 x 4 factorial) with 21-d periods. Broiler litter harvested after one, three, or six 6-wk growing periods (1P, 3P, and 6P, respectively) mixed with .5 or 1.5% BW of ground corn (.5C and 1.5C, respectively) was consumed ad libitum. Bermudagrass hay was fed to 1P, 3P, and 6P steers at .5% BW and was ingested ad libitum by Control steers, along with feeding of .5 or 1.5% BW of corn (DM basis). Broiler litter was 63, 43, and 35% NDF, 2.2, 3.5, and 4.1% N, and 18, 30, and 27% ash for 1P, 3P, and 6P, respectively. Total tract digestibility of NDF was 53.7, 29.4, 50.4, 58.1, 31.3, 30.8, 34.1, and 49.5% (SE 3.50), and digestible OM intake was 2.21, 1.70, 2.27, 2.39, 2.26, 3.18, 2.93, and 3.34 kg/d (SE .160) for .5C-Control, .5C-1P, .5C-3P, .5C-6P, 1.5C-Control, 1.5C-1P, 1.5C-3P, and 1.5C-6P, respectively. In Exp. 2, five steers (228+/-6.0 kg average BW) were used in a 5 x 5 Latin square with 21-d periods. Offered diets were 15% bermudagrass hay and 60% broiler litter (6P of Exp. 1; DM). Molasses was offered at 0, 3.2, or 6.7% of total DM, with the balance of the diet composed of corn. Molasses for two treatments was mixed with litter at meals, whereas for two other treatments molasses and litter were mixed before deep-stacking. Only a few minor treatment effects on intakes and digestibilities occurred. In conclusion, digestible OM intake by growing steers was less for litter harvested after one broiler growing period than after three or six when fed with only .5% BW of corn, although the effect of the number of periods was negligible with corn given at 1.5% BW. Molasses addition before deep-stacking or at meals did not enhance feeding value of litter harvested after six broiler growing periods.

Animal Feed↗

The effects of different protein and energy levels and time of change from starter to finisher ration on the performance of broiler chickens in the tropics.

Three experiments were conducted to determine the optimum protein and energy levels for starting and finishing broiler chickens and the optimum time of change from broiler starter rations to broiler chicken finisher rations. We tested four protein levels (17, 20, 23, and 26%), each fed at three energy levels (2800, 3000, and 3200 kcal/kg diet). For starting chickens, maximum weight gains, feed efficiency, and lowest feed cost per kilogram live weight gain were obtained on the rations containing 23 or 26% protein. Differences in dietary energy levels did not significantly affect weight gain and feed consumption. Feed efficiency improved with increase in dietary energy levels although the differences in feed efficiency between any two consecutive groups were not significant. Feed cost tended to increase nonsignificantly with increase in energy level. For finishing broiler chickens, dietary protein level did not have any significant effects on weight gains. The poorest weight gain, feed efficiency, and feed cost per kilogram gain were obtained on the rations containing 17% protein. The differences in feed efficiency between protein levels of 20, 23, and 26% were not significant while no two consecutive protein levels among the 20, 23, and 26% protein diets gave feed cost per kilogram gain that was significantly different from each other. Weight gain, feed consumption, and feed cost per kilogram gain were not significantly affected by dietary energy levels. Efficiency of feed conversion tended to improve with increase in dietary energy levels, although differences in feed efficiency between 3000 and 3200 kcal/kg diet were not significant. Performances of birds fed the starter ration for 0, 1, 2, 3, or 4 weeks before changing to the finisher ration were not as good as those fed the starter ration for 5 or 6 weeks before being change) to the finisher ration or those fed the starter ration for the 9 weeks experimental period. The results of the present work indicate that a protein level of 23% and energy level of 2800 to 3000 kcal/kg diet may be recommended for starting broiler chicks raised in Nigeria. For finishing broiler chickens, a protein level of 20% and energy level of 3000 kcal/kg diet may be recommended. The optimum time of change from broiler starter to broiler finisher may be recommended at 5 or 6 weeks of age.

Animal Nutritional Physiological Phenomena↗

The effect of floor type on the development of breast blisters and feather follicle infections in broilers.

The effect of floor types on the incidence of feather follicle infection and breast blisters in caged broilers was investigated in two trials. Broilers were reared on corn-soybean meal diets with warm-room brooding. Floor types included litter (control), wire, wire covered with various types of plastic mats, and wire woven with surgical tubing. In trial 1, the effect of a coccidiostat (Monensin, 120 mg/kg of feed) was investigated for broilers not on litter, and in trial 2, the effect of supplemental zinc was investigated. Broilers were processed in the laboratory processing plant when they were 51 (trial 1) and 53 days old (trial 2). Carcasses were evaluated for the occurrence of fleshing downgrades, crooked keels, feather follicle infection, and breast blisters. Incidence of feather follicle infection was low for broilers on litter or wire floor and high for broiler reared on plastic mats. Breast blisters incidence was low for broilers on litter and plastic mats and was high for broilers on the wire floor. Overall carcass quality for litter (control) was superior to any of the cage treatments. Neither the coccidiostat nor supplemental zinc affected the incidence of breast blisters or feather follicle infection.

Animals↗

The individual and combined effects of aflatoxin and ochratoxin A on various processing parameters of broiler chickens.

Male broilers (Hubbard X Hubbard) were placed at hatching into a completely randomized 2 X 2 X 2 factorial experimental design with the treatments consisting of 0 and 2.5 micrograms aflatoxin/g of feed (ppm) and 0 and 2.0 ppm ochratoxin A. In Trial 1, there were four replicate pens of 10 broilers per replicate at each treatment level. At 3 weeks of age two replicate pens were randomly selected and placed on control feed (0 to 3 weeks), the remaining two replicate pens were maintained on treatment (full-term). In Trial 2, there were three replicates of 38 broilers per replicate at each treatment level. At 3 weeks of age 13 broilers from each replicate pen were randomly selected and placed in separate housing and fed control diets (0 to 3 weeks). The remaining 25 broilers were kept on mycytoxin treatments until the conclusion of this trial (full-term). Data collected in these trials indicate that body weights of broilers were significantly (P less than .05) decreased by aflatoxin, ochratoxin A, and the combination treatments of the full term feeding regimen. Broilers partially recovered body weight in the 0 to 3-week feeding regimen; however, recovery was less rapid during ochratoxicosis compared to aflatoxicosis. Body weights of broilers in the combination treatment remained significantly (P less than .05) depressed throughout the trials. As body weight decreased, parts weights decreased accordingly. Carcass yield was significantly (P less than .05) decreased by all treatments, primarily by a decrease in breast yield.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

Body temperature of acclimated broilers during exposure to high temperature.

Short-term acclimation to high temperatures increased resistance of broilers to heat exposure. Two trials were conducted to determined the effect of acclimation on body temperature (Tb) during heat exposure. Broilers, 46-days old, were maintained at control or acclimating temperatures for 4 days. The control temperature was a constant 21 C with a 10 C dewpoint, and the acclimating temperature was a diurnal cycle of 24-35-24 C with a constant 21 C dewpoint. During the 4th day, broilers of both groups were exposed to temperatures of 41 C and 23 C dewpoint for 210 min. Body temperature was determined at the beginning of the heat exposure and at 30-min intervals until the end of the exposure. The Tb of both groups increased throughout heat exposure, but acclimated broilers had significantly lower Tb than control broilers from 90 through 210 min. Acclimated broilers had significantly lower heat stress mortality. The data show that acclimated broiler's Tb rises upon exposure to heat but that acclimation gives the capacity to stabilize Tb above normal Tb. The data also suggest Tb is preferable to mortality as a measure of acclimation in broilers.

Acclimatization↗

Effects of monensin feeding and withdrawal time on growth and carcass composition in broiler chickens.

Four experiments were conducted to evaluate the effect of monensin feeding and withdrawal on broiler performance and carcass characteristics. It was shown that monensin (100 ppm) feeding depressed growth. Withdrawal of monensin from the feed for 5 or 7 days produced higher feed consumption and weight gain values compared with those of unmedicated broilers. Increasing the withdrawal period to 10 days did not produce greater growth improvement. Whole body composition of protein, water, lipid, and ash were not significantly affected by monensin feeding or withdrawal. Abdominal fat pads of unmedicated female broilers were significantly larger than those of broilers medicated with monensin even when expressed as a percentage of body weight (3.53 vs. 2.99%). Amount of lipid per fat pad was also higher in unmedicated broilers than in medicated broilers (43.5 vs. 30.6 g). Values for fat pad weight (as a percentage of body weight) and grams of lipid per fat pad of unmedicated birds were not different from those measures in medicated birds after 5 or 7 days of withdrawal. Fat pad weights and lipids per fat pad of birds after 10 days of monensin withdrawal were intermediate between those of unmedicated and monensin-medicated broilers. Monensin feeding or its withdrawal for 5 or 10 days did not influence the female broiler abdominal fat pad lipid fatty acid composition when compared with that of unmedicated fat pad lipid.

Animal Nutritional Physiological Phenomena↗