Limestone particle size, calcium and phosphorus levels, and phytase effects on live performance and nutrients digestibility of broilers.

Limestone particle size (PS) affects its solubility and thus can influence broiler performance by altering the rate of calcium (Ca) release into the gastrointestinal tract. The objective of this research was to determine, using 2 × 2 × 2 factorial arrangement, the influence of PS (fine and coarse) and supplemented phytase (0 and 1,000 FYT/kg) in diets formulated with 2 Ca and Pi levels (positive control [PC]; negative control [NC]) on live performance, bone ash, and apparent ileal nutrients digestibility (AID). Starter PC: 0.9 Ca and 0.45 Pi; NC: 0.72 Ca and 0.03 Pi. Grower PC: 0.76 Ca and 0.38 Pi; NC: 0.58 Ca and 0.23 Pi. The 8 diets were assigned randomly to a total of 1,512 birds, with 21 birds per pen and 9 pens per treatment. The main effects of PS and Ca and Pi levels had no influence on feed intake (FI), body weight gain (BWG), or feed conversion ratio. Adding phytase improved BWG by 8 g and 50 g and FI by 25 g and 56 g at 0-14 D (P ≤ 0.05) and 0-35 D (P ≤ 0.05), respectively. Interaction between Ca and Pi levels and phytase improved BWG and FI for 0-14 D (P ≤ 0.05) and BWG during 15-28 D (P ≤ 0.05) for PC without phytase and for PC and NC with phytase when compared with NC without phytase. Birds fed PC without phytase, or either PC or NC with phytase were about 96 g heavier than NC without phytase. Birds fed either PC or NC diet with coarse limestone or PC with fine limestone gained approximately 14 g more (P ≤ 0.05) than birds fed NC with fine limestone for BWG at 0-14 D (P ≤ 0.05). Phytase increased tibia bone ash (14 D) by 1% (P ≤ 0.05). AID of Ca and Pi at 14 D was improved (P ≤ 0.05) by 66% when phytase was added to coarse limestone. Results indicate that phytase improved broiler performance without being affected by PS. Furthermore, phytase had greater influence on coarse limestone than on fine limestone for bone ash and AID. Ca and Pi levels were the most influential factors in determining bone ash although phytase inclusion could lead to an improvement during early days.

Improved early performance of turkey poults given an Aloe ferox leaf extract with bentonite.

AT-402 (20 g/kg), a proprietary blend of Aloe ferox leaf extract and calcium bentonite, had no adverse effect on poult body weights at 3 weeks of age. Lower body weights and lower feed consumption were observed in 4-week-old poults given 10 and 20 g/kg of AT-402 compared to poults given 0 or 5 g/kg. Floor-reared poults, given either 5 or 10 g/kg AT-402 to 4 weeks of age, were significantly heavier than controls (0 g/kg AT-402), and feed conversion ratios for AT-402 given poults were improved. Xylose uptake in 5 g/kg AT-402-fed poults was significantly greater than in poults given AT-402 at 0 and 10 g/kg, reflecting increased body weights of 5 g/kg AT-402-fed poults. Delayed access by poults to the AT-402 until 10 d of age also improved 4-week body weights, suggesting that the AT-402 might improve performance as soon as it is given. AT-402 at 5 g/kg was most efficacious as demonstrated by improved body weights and feed conversions.

Breeder age affects small intestine development of broiler chicks with immediate or delayed access to feed.

1. The relationship between breeder age and chick gastrointestinal tract development to 21 days of age, as influenced by immediate or delayed access to feed, was examined in three consecutive trials. 2. Ross 708 chicks, derived from breeder flocks at 31 (young), 40 (middle) and 63 (old) weeks of age were placed randomly into either a control group with immediate access to feed and water, or a 48 h feed delayed (FD) group with free access to water. 3. FD negatively affected body weight (BW) of chicks derived from young and old flocks through the first and second weeks of age, respectively. Chicks from the older flock absorbed more yolk in the first 48 h with no FD effect. When feed was made available, chicks from the FD group showed a large increase in small intestine weight relative to BW, surpassing (P < 0·05) the control groups across all breeder flock ages. 4. Morphological measurements in all intestinal sections had higher values in chicks derived from the middle age breeder flock. FD to newly hatched chicks from the young breeder flock shortened villi (P < 0·01), decreased crypt depth and villus surface area (P < 0·001) in the duodenum through the first week post hatch. 5. Crypt depths were maximised between 7 and 14 d post-hatch in chicks from young and old breeder flocks, but crypt depths in chicks from the middle aged flocks continued to deepen. 6. The increased crypt depth may augment the number of enterocytes available for villus growth, and facilitate longer villi and greater villus surface area, in chicks from the middle age flocks. Intestinal morphological variation was associated with breeder flock age, which accounted for differential growth in chicks derived from young, middle, and old aged breeder flocks.

Microarchitecture and spatial relationship between bacteria and ileal, cecal, and colonic epithelium in chicks fed a direct-fed microbial, PrimaLac, and salinomycin.

Direct-fed microbials (DFM) could serve as a potential alternative to the feeding of antibiotics in poultry production. In this study, the effects of providing a DFM were compared with the feeding of salinomycin on intestinal histomorphometrics, and microarchitecture was examined. Broiler chicks (n=18 per treatment; trials 1 and 2) were fed a standard starter diet (control), control+PrimaLac (DFM; 0.3% wt/wt), and control+salinomycin (SAL; 50 ppm) from hatch to 21d. The birds were euthanized on d 21, and the ileal, jejunal, cecal, and colon tissues were dissected. Samples were examined by light microscopy (jejunum and ileum; trial 1) and scanning electron microscopy (ileum, cecum, and colon; trial 2). Feeding of the DFM increased intestinal muscle thickness (P<0.05) up to 33% compared with the control treatment. The DFM group also had increased villus height and perimeter (P=0.009 and 0.003, respectively) in jejunum. Segmented filamentous-like bacteria were less numerous in DFM-treated chicks than in the control chicks. Very few segmented filamentous-like bacteria were found near other microbes in the ileum. The DFM chicks had a larger number of bacteria positioned over or near goblet cells and in intervilli spaces. Bacteria in the colon were observed to be attached primarily around and within the crypts. Mucous thickness was less, and the density of bacteria embedded in the mucous blanket appeared to be lower in DFM-treated animals than in the control in all intestinal segments. The birds fed SAL had fewer bacteria and enterocytes in the ileum than in the control-and DFM-treated birds, and they had thicker and fewer microvilli. Because gastrointestinal track colonization by the DFM organisms can prevent the attachment of pathogens to the epithelium, spatial relationships, in this study, demonstrate the functionality of DFM and probiotics in preventing disease. It also supports previous observations that the feeding of salinomycin may alter intestinal function.

Influence of selenium on heat shock protein 70 expression in heat stressed turkey embryos (Meleagris gallopavo).

Heat shock protein 70 (hsp70) family of proteins, which functions as molecular chaperones, has been associated with tolerance to stressors in avian species. Selenium (Se) is an essential trace mineral incorporated into the seleno-enzymes such as glutathione peroxidase (GSHpx). GSHpx reduces oxidized glutathione (GSSG) to reduced glutathione (GSH) in the GSH/GSSG antioxidant system and protects cells from oxidative damage. This study was conducted to examine if the relationship between dietary supplementation of selenium to turkey (Meleagris gallopavo) hens and the embryonic expression of hsp70 and GSHpx activity in heat stressed embryos. Livers of embryos developing in eggs from turkey hens fed diets with or without supplemental Se were analyzed for hsp70 concentration and GSHpx activity before and after recovery from a heating episode. Before heat stress, hsp70 concentrations were equivalent in each treatment, but GSHpx activity was maximized in the SE treatment group. After recovery from the heating episode, hsp70 concentrations were significantly higher (P<0.05) in the non-Se-supplemented groups, but in the Se-supplemented groups the hsp70 concentrations were not different from pre-stress concentrations. In the pre-stress Se-supplemented group, liver GSHpx activity was significantly higher than GSHpx activity in the non-Se-supplemented embryo livers, and in the livers from embryos recovering from heat stress, GSHpx activity in the non-Se-supplemented group was lower than the pre-stress activity and significantly lower than the GSHpx activity in liver from Se-supplemented embryos recovering from heat distress. Se supplementation to the dams resulted in a significant increase in their embryos and that condition would facilitate a decreased incidence of oxidative damage to cells. A more reduced redox status in embryos from Se-supplemented dams decreased the need for cellular protection attributed to stress induced hsp70 and presumably allows heat distressed embryos to resume normal growth and development than embryos from dams with inadequate selenium nutrition.

Influence of organic selenium on hsp70 response of heat-stressed and enteropathogenic Escherichia coli-challenged broiler chickens (Gallus gallus).

The effect of dietary selenium yeast, a source of organic selenium, on heat shock protein 70 (hsp70) responses, redox status, growth and feed utilization were evaluated either in enteropathogenic Escherichia coli-challenged (EPEC) or in heat-stressed (HS) male broiler chickens grown to 42 days of age. One day-old chicks in experiment 1 were challenged orally with EPEC (10(6) cfu/chicken on day 1 and boosted by water application on days 2, 3, and 4) and fed diets with or without selenium yeast. Body weight (BW), feed conversion ratio (FCR), and total mortality were determined at 42 days of age, and this was followed by collection of ileal tissue for the quantification of total glutathione (TGSH), reduced glutathione (GSH), oxidized glutathione (GSSG), and hsp70 in randomly selected chickens from each treatment. In experiment 2, male broiler chickens were fed diets with or without selenium yeast under a thermoneutral rearing condition. At four weeks of age, blood and hepatic tissue were collected from chickens maintained in the thermoneutral environment and from chickens subjected to HS (40 degrees C for 1 h) and analyzed for TGSH, GSH, GSSG, and hsp70. Selenium yeast improved BW, FCR, and decreased mortality in both control and EPEC-challenged chicks. Selenium yeast significantly attenuated hsp70 expression in EPEC-challenged chickens and in those subjected to HS. The EPEC challenge increased TGSH and GSSG levels and decreased GSH/GSSG ratio. However, GSSG level accumulated in chickens fed diets without selenium supplementation resulting in a lower GSH/GSSG ratio in the selenium yeast-fed group. Heat stress increased GSSG level and decreased GSH/GSSG ratio. Selenium yeast-fed groups maintained higher levels of GSSG before and after HS with a resultant lower GSH/GSSG ratio. The hsp70 response was significantly less in those chickens fed selenium yeast and challenged with either EPEC or HS than in those chickens given no supplemental selenium. The results of this study suggest that selenium yeast supplementation had imparted resistance to oxidative stress associated with enteric bacteria infection and to high temperature exposure. It is believed that the resistance to the stressors was due to an improved redox status of the selenium yeast-fed chickens.

The effect of dietary phosphorus on heat shock protein mRNAs during acute heat stress in male broiler chickens (Gallus gallus).

A 2 x 2 factorially arranged completely randomized experimental design was used to study the relationship between inorganic phosphorus (Pi) and heat shock protein (HSP) mRNA expression in different organs of commercial broiler cockerels during acute heat stress (HS). Brain, heart, liver and spleen were assayed for hsp70, hsp90alpha and hsp90beta mRNA. At 1 day of age, chickens were assigned randomly to two dietary Pi treatment groups (Pi-: 0.16%; Pi+: 0.5%). At 3 weeks of age, half of the chickens in each Pi group were subjected to HS (Ta=41 degrees C, 60 min) while the other half was maintained in a thermoneutral environment (CN, Ta=25 degrees C). The results showed inter-organ variation in the expression of HSP mRNAs. Brain expressed the most HSP mRNAs while spleen expressed the least. When broilers were subjected to HS, the expression of HSP mRNAs was influenced positively by the consumption of the Pi+ diet. However, analysis of variance revealed that Ta influenced HSP transcription more than phosphorus availability. Thermal stress caused induction of hsp90alpha and hsp90beta in heart, liver and spleen, but hsp90alpha and hsp9beta mRNA levels were stable in brain. Transcription of hsp70 increased (P< or =0.05) in all organs from chickens in HS groups when compared to chickens in CN groups. Although Pi+ did not show any significant increases in the expression of hsp mRNAs, there were consistently larger HSP mRNA values in liver and spleen tissues. The high expression of hsp90alpha and hsp90beta in brain of chicks in both CN and HS conditions could be due to the involvement of hsp90 in steroid hormone receptors or the high metabolic activity of neurons in the central nervous system.

Ascorbic acid decreases heat shock protein 70 and plasma corticosterone response in broilers (Gallus gallus domesticus) subjected to cyclic heat stress.

It is known that ascorbic acid (AA) supplementation can ameliorate the chicken's responses to heat stress. The influence of AA on heart heat shock protein 70 (hsp70) and plasma corticosterone (CS) was evaluated in young male broiler chickens fed either no AA (N-AA) or 500 mg AA /kg (AA) and exposed to cyclic high temperatures (21 to 30 to 21 degrees C) over a 3.5 h period on three consecutive days. Dietary AA supplementation elevated plasma AA and maintained it at high levels after heating, but in N-AA birds, only heat elevated plasma AA. In N-AA fed chickens, plasma CS was elevated and was further increased by heat stress as compared with AA-fed birds. Heart hsp70 expression was greater in N-AA-fed chickens compared to AA-fed chickens, and heat stress further elevated hsp70 in both N-AA- and AA-fed birds. The hsp70 increase after heat was two-fold greater in N-AA- vs. AA-fed birds. Plasma CS and heart hsp70 were positively correlated, plasma AA and heart hsp70 were negatively correlated, and plasma CS and AA were negatively correlated. It was concluded that chickens experience a less severe stress response after exposure to high temperatures when they are provided dietary AA.

Influence of selenium sources on age-related and mild heat stress-related changes of blood and liver glutathione redox cycle in broiler chickens (Gallus domesticus).

Selenium is an essential trace element that up-regulates a major component of the antioxidant defense mechanism by controlling the body's glutathione (GSH) pool and its major Se-containing antioxidant enzyme, glutathione peroxidase (GPX). Evidence has emerged suggesting that organic selenium, natural seleno-amino acids found in plants, grains and selenized yeast, maintains the antioxidant defense system more efficiently than inorganic selenium. Inorganic selenium is a pro-oxidant, whereas organic selenium possesses antioxidant properties itself. As a pro-oxidant, inorganic selenium is not suitable for animals or humans. Therefore, we examined the GSH-GPX system in broiler chickens and determined that organic selenium was indeed more beneficial than inorganic selenium. Chickens fed the organic selenium as Sel-Plex, a selenized yeast, had elevated GPX activity in both blood and liver in a thermoneutral environment and after heat distress. More importantly, the ability to reduce the oxidized glutathione (GSSG to 2 GSH) was enhanced and facilitated by maintenance of glutathione reductase activity. Organic selenium-fed chickens were less affected by mild heat distress than inorganic selenium-fed chickens, and this assessment was based upon less induction of heat shock protein 70 (hsp70) in organic selenium-fed chickens. Our results clearly show that heat distress, a potent inducer of oxidative stress and hsp70, can be partially ameliorated by feeding organic selenium. We attribute this observation to an enhanced GSH-GPX antioxidant system in organic selenium-fed chickens.

Effect of ascorbic acid and acute heat exposure on heat shock protein 70 expression by young white Leghorn chickens.

Dietary ascorbic acid (AA) and heat stress (HS) affect heat shock protein 70 (hsp70) and body temperature (BT) of strain cross white Leghorn chickens. At five weeks of age, chicks fed either no supplemental AA (N-AA) or 200 mg/kg AA (AA) were subjected to either HS (42 degrees C) or maintained in control (CN, 23 degrees C) ambient temperature (T(a)) for 1 h. Body temperature (BT) was recorded for each bird before collection of heart and liver for hsp70 assay. In the CN AA-fed groups, neither the lower constitutive hsc70 nor the decreased hsp70 response to HS in the heart and liver were sex-dependent. The BT was increased by HS, but neither AA nor sex of the bird affected BT response. A diet X T(a) interaction revealed that BT of CN AA-fed chickens was lower than in N-AA-fed chickens, but BT of HS AA-fed chicks was greater than BT in HS N-AA-fed chickens. The BT and hsp70 responses were positively correlated. A lower expression of hsp70 indicated less of a stress response in the AA-fed chickens.

Influence of a propionic acid feed additive on performance of turkey poults with experimentally induced poult enteritis and mortality syndrome.

Poult enteritis and mortality syndrome (PEMS) has multiple etiological agents associated with its occurrence, including two viruses and at least three Escherichia coli isolates. Myco Curb (MC) contains organic acids and is used as a feed additive to inhibit growth of many bacteria and toxin-producing molds but not viruses. Studies evaluating the influence of MC on BW, feed conversion, and mortality indicate that turkey poults tolerate MC at 1.25% but not 2.50%, but higher MC content in feed provides greater suppression of growth of bacterial isolates commonly associated with PEMS. In two PEMS experiments, 1.25% MC was blended into poult starter feed and was maintained in the feed for the duration of the 3-wk experiments. In these experiments, 1-d-old commercial poults were placed into battery brooders and were given turkey starter feed and water ad libitum. At 6 d posthatch, PEMS-designated poults were given a 1-mL oral gavage of a 10% suspension of feces from PEMS-infected poults. BW depression due to PEMS was not alleviated by MC, although there was less variation in mean BW of the MC-fed poults, and there was a highly significant reduction in mortality (68% in PEMS-exposed with MC vs. 32.5% in PEMS-exposed without MC). The reduction in mortality in the MC-fed poults was attributed to decreased bacterial content of the gut and to maintenance of packed cell volume and hemoglobin content. It was concluded that MC might be a potential nutritional intervention during PEMS.

Isolation of a reovirus from poult enteritis and mortality syndrome and its pathogenicity in turkey poults.

Poult enteritis and mortality syndrome (PEMS) is an acute, infectious intestinal disease of turkey poults, characterized by high mortality and 100% morbidity, that decimated the turkey industry in the mid-1990s. The etiology of PEMS is not completely understood. This report describes the testing of various filtrates of fecal material from control and PEMS-affected poults by oral inoculation into poults under experimental conditions, the subsequent isolation of a reovirus, ARV-CU98, from one of the PEMS fecal filtrates, and in vivo and in vitro studies conducted to determine the pathogenicity of ARV-CU98 in turkey poults. In order to identify a filtrate fraction of fecal material containing a putative etiologic agent, poults were challenged in two independent experiments with 220- and 100-nm filtrates of fecal material from PEMS-negative and PEMS-positive poults. The 100-nm filtrate was chosen for further evaluation because poults inoculated with this filtrate exhibited mortality and significantly lower (P < or = 0.05) body weight and relative bursa weight, three clinical signs associated with PEMS. These results were confirmed in a third experiment with 100-nm fecal filtrates from a separate batch of PEMS fecal material. In Experiment 3, body weight and relative bursa and thymus weights were significantly lower (P < or = 0.05) in poults inoculated with 100-nm filtrate of PEMS fecal material as compared with poults inoculated with 100-nm filtrate of control fecal material. Subsequently, a virus was isolated from the 100-nm PEMS fecal filtrate and propagated in liver cells. This virus was identified as a reovirus on the basis of cross-reaction with antisera against avian reovirus (FDO strain) as well as by electrophoretic analysis and was designated ARV-CU98. When inoculated orally into poults reared under controlled environmental conditions in isolators, ARV-CU98 was associated with a higher incidence of thymic hemorrhaging and gaseous intestines. In addition, relative bursa and liver weights were significantly lower (P < or = 0.05) in virus-inoculated poults as compared with controls. Virus was successfully reisolated from virus-challenged poults but not from control birds. Furthermore, viral antigen was detected by immunofluorescence in liver sections from virus-challenged poults at 3 and 6 days postinfection and virus was isolated from liver at 6 days postinfection, suggesting that ARV-CU98 replicates in the liver. In addition to a decrease in liver weight, there was a functional degeneration as indicated by altered plasma alanine aminotransferase and aspartate aminotransferase activities in virus poults as compared with controls. Although this reovirus does not induce fulminating PEMS, our results demonstrated that ARV-CU98 does cause some of the clinical signs in PEMS, including intestinal alterations and significantly lower relative bursa and liver weights. ARV-CU98 may contribute directly to PEMS by affecting the intestine, bursa, and liver and may contribute indirectly by increasing susceptibility to opportunistic pathogens that facilitate development of clinical PEMS.

Effects of hen age, Bio-Mos, and Flavomycin on poult susceptibility to oral Escherichia coli challenge.

The effects of hen age, Escherichia coli, and dietary Bio-Mos and Flavomycin on poult performance from 1 to 21 d were studied. Day-of-hatch BUTA (BIG-6) male poults were gavaged orally (1 mL) with approximately 10(8) cfu/mL E. coli composed of four serotypes or sterile carrier broth. A mixture of the same E. coli cultures was added to the poults' water troughs to attain a concentration of approximately 10(6) cfu/mL on a weekly basis to ensure a continuous bacterial challenge. Within each E. coli split plot treatment group, poults from hens of different ages (33 and 58 wk of age) were fed diets containing Bio-Mos (1 g/kg feed), Flavomycin (2.2 mg active ingredient/kg feed), Bio-Mos plus Flavomycin, or a control diet, in a randomized complete block design. This experiment yielded eight treatments per challenge group. At Weeks 1 and 3, eight birds from each treatment from the E. coli challenged and unchallenged groups were randomly chosen for bacterial sampling of liver and intestinal tissue for coliforms, aerobic bacteria, and Lactobacillus spp. E. coli isolates from tissue samples were O serotyped. During E. coli challenge, dietary Bio-Mos and Flavomycin improved poult BW and BW gains (P < or = 0.05). When poults were not challenged with E. coli, poults from old hens had improved BW and cumulative BW gains over poults from young hens (P < or = 0.05). Cumulative 3-wk BW gains for unchallenged poults from young hens were improved by Bio-Mos and Flavomycin (P < or = 0.05) alone and in combination when compared to the control diet. Two of the four E. coli serotypes administered were recovered. Several serotypes were recovered that were not administered. It may be concluded that dietary Bio-Mos and Flavomycin can improve the overall performance of poults, especially when they are faced with an E. coli challenge.

Induction of functional defects in macrophages by a poult enteritis and mortality syndrome-associated turkey astrovirus.

The interaction of a poult enteritis and mortality syndrome (PEMS)-turkey astrovirus-Ohio State University (TAst-OSU) with the mononuclear phagocytic system cells, namely macrophages, was examined after in vitro and in vivo exposure. In vitro exposures were performed by incubating adherent turkey macrophages with various volumes of 10(6) 50% embryo infective dose (EID50)/ml TAst-OSU stock, whereas for in vivo challenge, poults were given a 200 microl inoculum of 10(6) EID50/ml TAst-OSU stock at 7 days of age. Results show that TAst-OSU in vitro exposure reduced macrophage viability relative to controls (P < 0.05) and decreased phagocytosis (P < 0.05) and intracytoplasmic killing of Escherichia coli (P < 0.05) after a 42-48-hr exposure. Poults challenged with TAst-OSU in vivo recruited almost 50% fewer Sephadex-elicited inflammatory cells in the abdominal cavity (P < 0.05) as compared with the sham controls. Similar to in vitro exposure, macrophages isolated from in vivo TAst-OSU-challenged poults exhibited reduced percentage of phagocytic macrophages (P < 0.05) as well as fewer intracytoplasmic E. coli per phagocytic macrophage (P < 0.05). TAst-OSU-challenged poults had a greater number of viable E. coli in their spleens (P < 0.05) after an intravenous E. coli challenge as compared with the non-TAst-OSU-challenged control poults. Macrophage-mediated cytokines and metabolites were also examined during this study. Both in vitro and in vivo TAst-OSU challenge resulted in reduced interleukin (IL)-1 and IL-6 activity. On the contrary, nitrite levels in macrophage culture supernatant fraction of TAst-OSU-challenged macrophages were significantly higher (P < or = 0.05). The findings of these studies indicated that TAst-OSU challenge induced defects in macrophage effector functions, implying that PEMS-turkey astrovirus can potentially impair the immune response of turkeys, thereby leading to enhanced susceptibility of turkeys to secondary, perhaps even fatal, bacterial infections.

Dietary copper effects on lipid metabolism and circulating catecholamine concentrations in finishing steers.

Forty-eight Angus and Hereford x Angus steers were used to determine the effects of copper (Cu) on lipid and catecholamine metabolism. Steers were stratified by weight within breed and randomly assigned to treatments. Treatments consisted of 0 (control, no supplemental Cu), 10, or 40 mg of supplemental Cu (from Cu2(OH)3Cl)/kg DM. Steers were fed a corn silage-soybean meal-based growing diet for 42 d. Animals were then switched to a high-concentrate finishing diet and remained on the same dietary treatments. On d 70, indwelling jugular catheters were nonsurgically inserted into five steers per treatment. Blood samples were obtained from steers after a 24-h period of feed withdrawal, 1 h after feeding, and after i.v. administration of norepinephrine and were subsequently analyzed for nonesterified fatty acid (NEFA) and catecholamine concentrations. Average daily gain over the finishing period was higher (P < 0.06) in steers receiving supplemental Cu. Serum total cholesterol concentrations were reduced (P < 0.05) on d 84 and 112 in steers supplemented with Cu. Serum norepinephrine (P < 0.14) and NEFA concentrations following feed withdrawal tended (P < 0.12) to be higher in Cu-supplemented steers. Postfeeding norepinephrine concentrations tended to be higher (P < 0.14) in Cu-supplemented steers. Nonesterifled fatty acid concentrations were lower (P < 0.10) in Cu-supplemented steers after norepinephrine administration. Backfat depth was decreased (P < 0.10) and longissimus muscle polyunsaturated fatty acid percentages were increased (P < 0.10) in steers receiving supplemental Cu. These results indicate that Cu addition to a finishing diet containing 5 mg Cu/kg DM alters lipid metabolism. The reduction in backfat depth may be due to copper altering catecholamine metabolism in steers.

D-xylose absorption as a measurement of malabsorption in poult enteritis and mortality syndrome.

Severe wasting of body tissues, diarrhea, high morbidity and mortality, and stunting are all characteristics of poult enteritis and mortality syndrome (PEMS). The wasting of musculature and loss of nearly all adipose tissue suggested that even though the PEMS-infected poults were eating some feed, nutrient intake was not sufficient to meet body requirements for maintenance and growth. Because epithelial cells in the gastrointestinal tract appeared to be a target of the undefined etiological agent (or agents) that causes PEMS, a study was conducted in which PEMS-infected poults were evaluated for malabsorption through 3 wk of age. D-Xylose, a poorly metabolized pentose, was given per os as a bolus, and blood samples were obtained from the ulnar vein in the wing of control and PEMS-infected poults over a 3-h period to estimate intestinal absorption. D-Xylose absorption in control poults peaked 30 to 60 min after the oral treatment, similar to results reported earlier. The PEMS-infected poults did not show a peak in absorption. The PEMS-infected poults showed significant delays in D-xylose absorption at 4, 7, and 11 d after PEMS challenge. The severe malabsorption and metabolic deficiency problem associated with PEMS was postulated to be a direct effect of the undefined infectious agent or agents that cause the disease.

Influence of BioChrome on the response of metabolic hormones in PEMS-infected poults.

Poult enteritis and mortality syndrome (PEMS), a disease that affects turkeys between 7 and 28 d of age, causes a severe inflammation of the intestinal tract and is characterized in poults by severe diarrhea, high morbidity, mortality, and stunting. The PEMS-associated mortality and growth depression is related to malabsorption and decreased metabolic activity caused, in part, by a possible insulin deficiency or insensitivity. Insulin receptors are stimulated by the glucose tolerance factor (GTF) that incorporates Cr. Body Cr deficiency can be exacerbated by dietary deficiency and by increased excretion due to stress associated with a diarrheal disease such as PEMS. BioChrome (BC) contains natural, preformed GTF, the bioactive form of Cr. Experiments were conducted in which BC was blended into poult starter feed at 400 ppb during the first 21 d posthatch. Body weights were determined at 1, 7, 14, and 21 d of age, and weekly feed conversions were calculated for each treatment group (control, BC, PEMS, and BC+PEMS). At 6 d post-hatch, each PEMS-designated poult was given a 0.1-mL oral gavage of a 10% suspension of feces from PEMS-infected poults. Blood samples were taken via cardiac puncture from four birds per treatment group at 7, 10, 14, 17, and 21 d of age. Radioimmunoassays were conducted for plasma insulin, glucagon, thyroxine (T4), and triiodothyronine (T3). Plasma insulin levels were depressed in PEMS-infected poults from Days 10 through 17, but plasma glucagon levels in the PEMS-infected poults were significantly elevated at 14 and 17 d, after which they returned to control levels in both of the PEMS-infected groups. The T3 and T4 levels were depressed through Day 21 in PEMS-infected poults, but with BC treatment these blood hormone levels rebounded by Day 21. Body weights of PEMS-infected poults were increased significantly by the BC treatment but not to the level of noninfected controls.

Alterations in macrophage-produced cytokines and nitrite associated with poult enteritis and mortality syndrome.

Poult enteritis and mortality syndrome (PEMS) is an acute, transmissible, infectious intestinal disease associated with high mortality and morbidity in turkey poults. Earlier studies demonstrated immune dysfunction, involving both humoral and cell-mediated immunity, associated with PEMS. The current study examined cytokines and metabolites produced by macrophages from poults exposed to PEMS agent(s). Six trials were conducted with six separate hatches of poults. Poults in the PEMS group were exposed to PEMS agent(s) via contact exposure at 7 days of age whereas uninfected poults served as control poults. Abdominal macrophages were harvested from control (uninfected) and PEMS poults at various times postexposure and cultured for 18-24 hr in the presence of Escherichia coli lipopolysaccharide. Interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) bioactivities and nitrite levels in macrophage culture supernatants were quantified. Macrophage supernatants from PEMS poults had greater IL-1-mediated stimulation index compared with the macrophage supernatants from uninfected control poults in both trials. However, this increase was significant only in trial 1. IL-6 activity tested in three separate trials was significantly higher in PEMS macrophage supernatants over the controls. On the contrary, TNF-alpha production by macrophages was decreased in PEMS macrophage culture supernatants. Nitrite levels in PEMS macrophage culture supernatants were significantly higher in two out of three trials. These findings suggest that the enhanced production of proinflammatory cytokine/metabolites by activated macrophages in PEMS poults may be responsible, at least in part, for the physiological intestinal inflammation, gut motility, and anorexia that characterize this disease.

Tryptophan methylester modulation of poult responses to Bordetella avium.

On the day of hatching, four groups of poults [Control, L-tryptophan methylester (LTME), Bordetella avium-infected, and B. avium-infected plus LTME] were established and placed into heated metal brooding batteries. Bordetella avium infection caused a significant depression in body temperature within 24 h after intranasal challenge with the W strain, and the hypothermia persisted through 21 d of age. L-Tryptophan methylester, a water-soluble form of tryptophan, was given by oral gavage daily in saline at a concentration of 50 mg per poult beginning 4 d after hatch. Within 2 d after initiation of LTME treatments, colonic temperature of B. avium-infected poults was elevated to the level of Controls and remained at that level throughout the experimental period. The BW of B. avium-infected poults were reduced significantly. The LTME treatment caused a significant BW increase in the B. avium-infected poults, but the increase was not to the level of Controls. The anti-sheep red blood cell antibody titers in B. avium-infected poults were not affected significantly. However, LTME treatment induced a significant increase in anti-sheep red blood cell antibody titers in both the infected and Control poults. Based upon data reported herein, it was concluded that feed intake depression associated with development of bordetellosis caused the poults to react more specifically to a mild tryptophan deficiency than to other nutrient deficiencies. The tryptophan deficiency caused a growth depression that was only partially alleviated by daily supplementation of LTME. The physiological responses to daily supplementation of LTME to B. avium-infected poults suggested that growth depression and poor performance was not limited to dietary deficiency of tryptophan.

Heat conditioning induces heat shock proteins in broiler chickens and turkey poults.

Peripheral leukocyte heat shock proteins (HSP: HSP90, HSP70, and HSP23) from broiler chickens and turkey poults were induced by in vitro and in vivo high temperature exposure. Heat conditioning, via a daily 1 h exposure to 41 C, enhanced in vitro HSP expression in leukocytes from chickens heat-conditioned for 1 to 2 wk, and a similar response was found in turkey poults with 3 wk of heat conditioning causing the greatest HSP expression. In vivo heat exposure trials caused maximization of HSP expression after 1 wk of daily heat conditioning exposures in broilers, but no additional enhancement was seen in chickens heat conditioned for 2 wk. Enhancement in HSP expression was evident for periods up to 4 wk after termination of the daily heat conditioning episodes.