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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.

Poult Enteritis and Mortality Syndrome (PEMS) is a condition of yet undefined etiology. Affected flocks may exhibit 100% morbidity with mortality up to 50% or more between 2 to 4 wk of age. The current study reports the immune status of poults experimentally infected with PEMS agent(s) in various trials. When compared with the unchallenged controls, PEMS-infected poults had significant atrophy of the bursa (up to 2-fold), thymus (up to 11-fold), and spleen (up to 2-fold) (P < or = 0.05). When challenged with SRBC, PEMS-infected poults had 1 to 2 log2 lower anti-SRBC antibody titers than the controls (P < or = 0.05). Responsiveness to a mitogenic lectin, phytohemagglutinin-P, was reduced significantly in PEMS poults (P < or = 0.05). These data show that the immune system of the poults is compromised significantly during PEMS infection in terms of lymphoid organ integrity and humoral and cell-mediated immunity. These findings imply, therefore, that immune dysfunction may contribute to the mortality observed during PEMS outbreaks.

The experiment investigated the effects of limestone particle size and dietary potassium (K) on live performance, blood physiology, and muscle myopathies in broilers raised to 35 days of age. A total of 384 Ross male broilers were placed in 24 floor pens and fed four diets during the starter (0–16 days of age) and grower (17–33 days of age) periods containing two limestone particle sizes (fine: 0.2 mm and coarse: 0.9 mm), and amended with either 0% basal K (K–) or 0.2% added dietary K (K+) as potassium carbonate to complete the 2 × 2 factorial arrangement. Live performance was measured from 1–33 days of age. Blood physiology, woody breast (WB), and white striping (WS) scores were measured at 35 days of age. The K+ dietary treatment reduced (P< 0.05) feed intake and BWG when compared to K– during the starter and grower period. The K+ dietary treatment decreased blood Na (mmol/L), blood glucose (mg/dl), ionized blood Ca (mg/dl), TCO2(mmol/L), blood HCO3(mmol/L), and base excess in extracellular fluid (mmol/L) when compared to K– birds of similar body weight at 35 days of age (P≤ 0.05). Fine limestone diets tended to reduce WB scores (3.0 vs. 2.59) when compared to coarse limestone diets at 35 days of age (P= 0.08). This study demonstrated that using 0.2% of K as potassium carbonate did not negatively affect FCR even though FI and BWG were reduced. Furthermore, fine limestone has the potential to reduce WB in breast muscle tissues; however, further research is needed to confirm these outcomes.

SUMMARY Tibial dyschondroplasia (TD) is the most common skeletal anomaly associated with fast growth in broiler and turkey lines and often results in the occurrence of bone deformation and lameness. It is a fairly common cartilage defect associated with the prehypertrophic cartilage of the growth plate being retained in the metaphysis. The objective of this investigation was to determine, through the use of pathomorphological methods, the prevalence of TD lesions that lead to lameness in 3 commercial broiler lines grown in Bulgaria. The study involved 20 broiler flocks with approximately 17,000 birds per flock and included flocks of Ross 308, Cobb 500, and Pureline broiler chickens. The initial age-related occurrence of TD-associated lesions averaged 23.7 d for Ross 308 flocks from 18 to 34 d of age, 19.6 d for Cobb 500 flocks from 16 to 23 d of age, and 28.8 d for Pureline flocks from 22 to 34 d of age. The number of observed macroscopic TD lesions in the Ross 308 broilers was 355 (24.22%), of which 203 (13.74%) were found in males and 152 (10.28%) were found in females; the number of lesions for Cobb 500 broilers was 185 (24.22%), of which 73 (10.48%) were found in males and 112 (16.09%) were found in females; and the number for Pureline was 313 (27.7%), of which 187 (16.54%) were found in males and 126 (11.16%) were found in females. A comparatively high prevalence of TD lesion-associated deformities was found in the proximal tibial metaphysis. There was a relatively low prevalence of TD lesion-associated proximal tibiotarsal fractures. We suggest, based on the results of our field investigation, that macroscopic TD lesions are developing at younger ages than reported previously. In the commercial broilers involved in the study, the prevalence of TD lesion-associated proximal tibiotarsal deformities was relatively high, and this condition involving TD lesion development potentially has severe consequences leading to lameness in broiler chickens.

Normal or elevated selenium status of broilers, which is influenced by dietary selenium sources, improves the bird’s ability to overcome the adverse effects of reactive oxygen metabolites. The objective of this study was to evaluate the effects of feeding graded levels of peroxidized poultry fat on blood and hepatic glutathione peroxidase (GSH-Px), and hepatic glutathione reductase activity in broiler chickens fed either inorganic sodium selenite (SEL) or organic selenium enriched in the organic selenium yeast product Sel-Plex (SP). Nine starter diets, varying in levels of oxidized fat (0, 3, and 6 mEq/kg) and dietary selenium sources, were fed to 360 male chicks from hatch to 21 d of age. Sel-Plex or SEL was added to the basal diet to provide either 0 or 0.2 ppm of supplemental selenium in the diets. Blood and hepatic samples were obtained for each treatment group at 21 d of age. Neither peroxidized fat nor selenium source significantly altered the activity of hepatic glutathione reductase (P ≤ 0.05). Blood GSH-Px was influenced significantly by both fat and selenium source (P ≤ 0.05), but the fat × selenium source interaction was not significant (P ≥ 0.3). A selenium source effect on the hepatic GSH-Px activity (P ≤ 0.05) was evidenced by higher GSH-Px activity, even in the basal diet with no added peroxidized fat. An increase in GSH-Px activity was seen in the erythrocyte and hepatic samples in both the SEL and SP treatments when peroxidized fat was given at 3 mEq/kg, but in the erythrocytes and in the hepatic tissues from SEL-supplemented birds, there was an apparent inhibition of GSH-Px activity. This inhibition was not seen in the hepatic tissue samples from SP-fed birds. Because elevated GSH-Px activity is indicative of oxidative stress, it was concluded that dietary SP supplementation resulted in better selenium and redox status in broilers than did SEL. These results indicate that the dietary selenium supplied in an organic form (selenium yeast as SP) improved the selenium and redox status in broilers, leading to greater resistance to oxidative stress than when the inorganic form of selenium (SEL) was fed.

Positive responses attributed to selenomethionine in Se-yeast (Sel-Plex [SP], Alltech, Inc., TM Nicholasville, KY 40356)-supplemented feed have increased the interest in use of SP in all phases of poultry production. Experiments to test the influence of SP on performance parameters in broiler males (Arbor Acres X Arbor Acres) in floor pens were conducted. A completely randomized experimental design incorporated four Se-supplementation treatment groups [(1) No Se, (2) sodium selenite (NaSe; 0.2 ppm), (3) SP (0.2 ppm), and (4) NaSe (0.1 ppm)+SP (0.1 ppm)]. Body weights (BW), feed conversions (FCR), cut-up carcass yield, breast meat drip loss and serum thyroid hormones were measured through 6 wk of age. BW of SP-fed broilers were increased compared to No Se or NaSe treatment groups and the combination of NaSe and SP was no more effective than SP alone. FCR improved with Se supplementation with the SP and SP+NaSe being superior to NaSe only treatment. Feather yield was increased by SP treatment compared to all other treatments. Carcass weight, yields of viscera, feet, leg and thigh and neck were higher in SP-treated birds Increased breast meat drip loss was induced by NaSe. The serum thyroxin (T ) levels were higher in birds 4 within No Se treatment as compared to NaSe or SP. The ratios between serum T and tri-iodothyronine (T ) 4 3 indicate that SP treatment facilitated the conversion of T to T . The results suggest that Se from SP was used 4 3 more efficiently for performance in fast growing, high yielding broiler chickens.

SummaryThe storage and cooking quality of meat is dictated by the ability of muscle cells to effectively hold water. If this ability is diminished, then presentation at time of purchase is poorer, as the packaging fills with watery exudates (termed ‘drip loss’), which is detrimental to sales. In addition, these losses affect cooking and eating sensory qualities. It is known that antioxidants play a major role in ensuring robustness of the cell membrane in muscle, and within this, selenium (Se) plays a major part, being an essential component within an antioxidant enzyme system and its interaction with vitamin E within membranes. The following review examines the body of evidence for Se as an antioxidant to preserve water holding capacity, especially with reference to using a chemically organic form of the mineral which is akin to those forms found in natural feed materials.

SummaryThe importance of selenium as a key component of antioxidant systems in animals is well recognised due to much research about this mineral in many species. Selenium is required as part of the antioxidant enzyme structure and plays a major role in various protective systems in animal physiology, including immunity, cellular stability and DNA protection. The following review is the first in a series of three which details the importance of selenium in animal nutrition, and how the chemically organic form, which is akin to the form of the mineral in natural feed materials, can provide increased benefits in utilisation, storage and metabolism compared to inorganic sources.

SummarySelenium is an important mineral required in the antioxidant system in animals, which is involved with oxidative stability in tissues, particularly membranes, and is involved in various aspects of meat quality and stability on the shelf, due to its protective properties on lipids, preventing rancidity. Se can be supplied in an inorganic or chemically organic form, and it is well known that the latter has beneficial properties and improved functionality in physiological systems compared to the former. Research has shown that organic Se is associated with increased tenderness and the prevention of certain problems in pale exudative meat, discolouration and off-flavours and odours in meat, although this depends on other components of the antioxidant system, such as vitamin E, being present as well. The change in prominence of glutathione peroxidase forms in their interaction with vitamin E in cell membranes is also noted. The following review (the third in a series) details the research that has been conducted into the role of Se in meat stability and related factors, with specific focus on organic forms of Se, namely the commercial product Sel-Plex™(Alltech Inc, Nicholasville, KY, USA), which is derived from yeast and in which selenium replaces sulphur in methionine forming selenomethionine in yeast protein.

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.

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.

Trypsin modulating oostatic factor (TMOF), a peptide hormone originally isolated from the ovaries of adult Aedes aegypti , is currently under commercial development as a new pesticide chemistry with a novel mode of action for the control of larval mosquitoes. The objective of the current research is to evaluate potential risks of the use of TMOF as an insecticide on non-target organisms. TMOF (YDPAP 6 ) was degraded in vitro (as determined by HPLC and LC/MS) to DPAP 6 , PAP 6 , and then AP 6 by leucine aminopeptidase, a pancreatic enzyme found in the digestive system of vertebrates. The rate of degradation of TMOF and PAP 6 was significantly greater than that of DPAP 6 , while no metabolism of AP 6 was found. TMOF technical insecticide was produced on a commercial scale by recombinant yeast (heat-killed before application). The technical TMOF when administered in a single dose by gavage to male and female mice at 2000 mg dry weight/kg body weight produced no negative effects as compared to controls up to 12 days after treatment. When male and female mallard ducks were treated by gavage with 1250 mg dry weight of technical TMOF/kg body weight each day for 5 days, again no toxic effects were noted through 35 days after the last treatment. TMOF technical insecticide was also applied to the shaved skin of male and female rabbits at the rate of 2000 mg/kg for 1–2 days, with no effect. The end point observations in these in vivo experiments were mortality; changes in growth rate, behavior, body structure, and color; and possible lesions observed during necropsy. Finally, Daphnia incubated with technical TMOF in rearing water at the level of 1.0 × 10 6 yeast cells/ml (10 mg/ml) also demonstrated no negative effects on mortality, growth, molting, time to first brood, and production of viable neonates. It appears from these studies that TMOF can be degraded by vertebrate digestive proteases and technical TMOF is not toxic to the non-target organisms examined.

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.

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 °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.

Wheat varies in apparent metabolizable energy N-corrected (AMEn) due to the presence of non- starch polysaccharides (NSP), which can be improved by dietary enzyme supplementation. Poults from 0-17 d-age were fed diets containing various wheat sources (WS) with or without Natugrain Blend® (NB) (BASF, Germany). Five replicate cages of 10 poults were assigned to each eight-soybean-meal/wheat treatment diets and a control soybean-meal/corn diet. The treatments were a factorial arrangement of 4 WS (A, B, C, D) and 2 enzyme levels (0 and 200 mg NB/kg). The WS differed by the degree of frost damage during seed development. Regardless of the source of wheat, NB increased 17 d BW (351 vs 381 g, P < 0.001) , decreased 1-17 d FCR (1.55 vs 1.49, P < 0.05), increased AMEn (2,204 vs 2,455 kcal/kg, P < 0.001), and increased apparent nitrogen retention (ANR) (35.0 vs 41.4 %, P < 0.05). No effects of WS were seen on growth performance, but WS A and B had higher (P < 0.05) AMEn than sources C and D (2,396 and 2,460 vs 2,246 and 2,216 kcal/kg, respectively). Gut viscosity was higher (P < 0.05) in poults fed wheat-based diets than the control diet. Enzyme supplementation to the wheat-based diets decreased viscosity (5.57 vs 3.98 cP, P < 0.05) to a level similar to the corn-based control diet, and it resulted in equivalent growth performance. Viscosities were negatively correlated with AMEn. The results demonstrated a positive effect of enzyme supplementation on nutrient utilization and performance of turkeys.

The adverse effects of non-starch polysaccharides (NSP) on turkeys fed wheat-based diets may be alleviated by dietary supplementation of endoxylanase (to reduce the adverse effects of digesta viscosity) or phospholipase (to improve the digestibility of fat). BUTA toms were fed wheat-based diets containing one of 5 enzyme treatments: unsupplemented control, Natugrain Blend® (> 5,500 EXU/kg diet; NB), Lyxasan®-50 (> 2,250 EXU/kg diet; LX50), Lyxasan®-100 (> 5,500 EXU/kg diet; LX100), and Phospholipase (> 500 PLU/kg diet; PL) (BASF, Germany). Each treatment group was assigned to 8 pens containing 12 birds to evaluate growth performance (1-128 d), and 2 pens of 12 birds (excluding LX50) for the apparent metabolizable energy N-corrected (AMEn) and ileum viscosity determination (56-128 d). All enzyme treatments improved growth performance. In comparison to the control, dietary enzyme increased (P < 0.05) BW and decreased 1-128 d feed/gain (2.45 vs 2.37, P < 0.005). PL was most effective in reducing feed/gain during the starting phase and LX100 during the finishing phase, while NB had intermediate benefits throughout the experiment. PL increased AMEn from 9 to 12 wk, while NB and LX-100 resulted in the highest AMEn during the later finishing period. Viscosity was significantly higher for PL than the other treatments (13.5 vs 7.07 cP, P < 0.001). Growth performance and energy utilization of turkeys fed wheat-based diets can be significantl y enhanced by phospholipase supplementation of starter feeds and endoxylanase supplementation of growing and finishing feeds. However, enzyme blends may provide a positive response regardless of turkey age.

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.

SUMMARY A comparison of performance and P reduction in litter and manure from broilers fed rations with and without phytase enzyme was made with chickens reared on litter or in cages. Low-activity phytase supplemented as a dry powder to mash diets did not affect performance, but litter P accumulation was decreased 14 to 21% in the finisher phase. Manure P content of broilers in cages was reduced 14 to 19% during the starter and grower phases. Liquid phytase applied postpelleting to diets with 0.5% total P (0.3% available P) reduced litter P accumulation (14 to 19%) and reduced manure P content in starter, grower, and finisher phases of the study. Phosphorus content in raw manure was decreased by 55% during the finisher phase. Feed conversions of broilers in cages and on conventional litter-covered floors were improved significantly with postpellet application of liquid phytase. Feed conversion improvement was greater in birds in cages. Postpellet application of dry phytase was shown to be feasible based upon performance and reduction in litter P accumulation. Feed conversions were improved by 7 to 8 points (P < 0.05) when compared to those of birds given a normal P level (0.72% total P) diet without phytase. Litter P accumulation was reduced between 20.5 and 28.5% with dry phytase applied postpelleting. With liquid phytase applied postpelleting, litter P accumulation was reduced 26.6%. These reductions in litter P content represent about 4 lb of P per ton of litter.

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 (Por = 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 (Por = 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 (Por = 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.

1. 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.2. 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.3. 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.4. 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.5. 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.6. AT-402 at 5 g/kg was most efficacious as demonstrated by improved body weights and feed conversions.

SUMMARY A majority of the broilers produced around the world are sexed on the basis of rapid-feathering females or slow-feathering males, which is facilitated by the presence of the sex-linked, auto-sexing, slow-feathering K gene in males. Recent advances in materials have allowed development of a caging system that is a viable alternative to the traditional floor-rearing regimen. In this study, a comparison was made between the traditional floor- and cage-rearing environments and their influence on feathering of auto-sexing, sex-linked male and female broilers fed at 0.2 mg/kg of feed either NaSe or an organic selenium yeast (OR). Feed conversion ratios, BW, and mortality were not affected by Se source. Feather tracts on the back, breast, thigh, wing, neck, and wing were scored subjectively based on feather size and skin surface covered. Feather scores ranged from 0 (no feathering) to 5 (best feathering) for each tract. The OR induced more rapid whole body feathering in the slow-feathering males as well as in the normal-feathering females. The influence of OR was evident from 21 through 42 d of age. Females had a faster feathering rate than did males. Females approached full feathering at 35 d of age, but males lagged behind females even at 42 d. Feathering of broilers in the conventional house was slightly faster than the feathering of broilers in the cage house. The mechanism for improved feathering rate in normal-feathering females and slow-feathering males given OR has not been determined.

Inorganic sodium selenite (NaSe; 0.1 and 0.3 ppm) and organic selenium yeast (Sel Plex 50: OR; 0.1 and 0.3 ppm) were provided in the diets of broilers placed on four different litter types: 1) ACR paper (diced recycled low-density fiber paper treated with boric acid, 4.5%), 2) shavings (pine wood shavings), 3) diced/cross-cut news print, or 4) 50% mixture of ACR and shavings, in a 32-pen broiler house with curtain side walls. Subjective body feathering scores ranging from 0 (no feathers) to 5 (best) were determined at 3, 5, and 6 wk of age. In experiment 1, feather scores at 6 wk of age were improved significantly with OR supplementation at 0.3 ppm compare to all other selenium treatments, and in Experiment 2 both levels of OR supplementation were associated with improved feathering compared to NaSe supplementation. ACR paper caused reduced feathering in both experiments, and neither NaSe nor OR were sufficient to overcome the problem. In both experiments, OR was associated with better feathering for broilers on all litters at all ages. Performance parameters such as feed conversion ratios were not affected by selenium source even though feathering, an energetically expensive function, was improved in the OR-fed birds.

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.

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.

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.

A metabolic dysfunction contributes to the poor performance and mortality associated with Poult Enteritis and Mortality Syndrome (PEMS). Within 2 d after contact-exposed poults were removed from the presence of PEMS-infected poults and returned to their respective treatment rooms to infect experimental poults, the experimental poults began to huddle together and show signs of the disease. When separated from the huddle, body temperatures of exposure poults were depressed significantly. Body temperatures decreased progressively through 8 d after exposure with a maximum depression of 2 C and returned to a normal level at 18 d after PEMS exposure. Similar decreasing patterns in serum glucose, inorganic phosphorus, triiodothyronine, and thyroxine were observed, with maximum decreases in these serum constituents being found between 8 and 13 d after PEMS exposure. There were significant correlations among decreasing body temperatures, decreasing serum constituents, and mortality in the PEMS-exposed poults. Daily mortality rates associated with PEMS began at 6 d and peaked at 9 d after PEMS exposure. Mortality rates decreased from 9 to 15 d after experimental PEMS exposure. Depressions in serum constituents, body temperature, and increased mortality rates did not coincide with decreased feed intake associated with PEMS. Therefore, it was concluded that the agent(s) causing PEMS may have a direct effect on energy metabolism in afflicted poults.

Studies were conducted to determine the influence of the interactions among litter moisture (high [HiM]> or =40% vs low [LoM]< or =20%), brooding temperature (high [HiB] = 38 C vs normal [NrB] = 34 C), and development of poult enteritis and mortality syndrome (PEMS) as indicated by body weights, relative weights of lymphoid organs, and mortality in Control [C] vs Infected [I] groups. There was a significant interaction between litter moisture and brooding temperature that had a significant influence on BW. The brooding temperature main effect was not significant, but there was a significant litter moisture effect on BW. Body weights were suppressed by PEMS infection, but infected poults brooded at HiB on LoM had significantly greater BW than those brooded at NrB and HiB on HiM. Main effects showed that there were significant litter moisture- and brooding temperature-mediated responses for BW. Relative weights of lymphoid organs revealed significant disease main effects but no effect due to brooding temperature and litter moisture. There was a significant effect of disease and brooding temperature with regard to mortality. The results from this study suggest that litter moisture influences productivity and mortality associated with PEMS, but brooding temperature has the greatest influence on PEMS-associated mortality. Therefore, higher brooding temperature for turkey poults being placed into a facility where they may be at risk for PEMS exposure is recommended.

Two colonial types (1 and 2) of Escherichia coli are represented predominantly in cultures isolated from turkey poults with poult enteritis and mortality syndrome (PEMS). Biotype codes determined using two systems (BBL: 36570 and 34560 for colony types 1 and 2, respectively; API-20E: 5144572 and 5144512 for colony types 1 and 2, respectively) clearly establish these organisms as E. coli. These isolates were not clearly divergent from the general profile for E. coli, but colony type 2 differs from colony type 1 with regard to its negative reactions for ornithine decarboxylase and the fermentation of dulcitol, rhamnose, sucrose, and melibiose, suggesting that it is atypical. Colony type 1 is nonserotypable and nonmotile, whereas colony type 2 is serotyped as O136: motile because it has H antigens associated with flagella. Capsular antigens were not found, but thin capsules were seen on cells from both colony types in stained preparations. Cultural morphology was different with colony type 1 having a circular, mucoid, raised morphology and colony type 2 having an irregular, flat, rough morphology. Colony type 1 has a doubling time at 37 C of about 20 min, whereas colony type 2 doubles in 30 min. Furthermore, colony type 1 is a potent colicin producer, but colony type 2 is not a colicin producer. Both E. coli isolates have resistance profiles for multiple antibiotics. Each strain responds to third generation fluoroquinolone antibiotics by changing their biotypes and become resistant after culturing once in their presence. These E. coli are proposed as possible etiological links in the complex series of events that take place in poults susceptible to PEMS.

Cytosolic glutathione S-transferase (GST) activities toward 1-chloro-2,4-dinitro-benzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), ethacrynic acid (EA), 1,2-epoxy-3-(p-nitrophenoxyl)propane (EPNP), trans-4-phenyl-3-buten-2-one(t-PBO), delta 5-androstene-3,17-dione (ASD) and trans-stilbene oxide (t-SO); cytosolic glutathione peroxidase activity toward cumene hydroperoxide (CuOOH); and microsomal GST activity toward CDNB were examined in liver, kidney, brain, and lung of adult male and female Japanese quail. In all cases, the renal specific activity per milligram protein was higher than the hepatic activity and was the highest among the four tissues examined. No consistent sex differences in GST activity were observed. The GSTs were purified from quail liver cytosol by S-hexylglutathione and glutathione affinity chromatography. Total GSTs eluted from the S-hexylglutathione affinity column were further separated by chromatofocusing, and the microheterogeneity of the GST isozymes was shown by high-resolution native isoelectrofocusing (IEF) in polyacrylamide slab gels and by SDS-PAGE. Five subunits were identified: QL1 (30.5 kDa), QL2 (27.2 kDa), QL3a (26.8 kDa), QL3b (26.5 kDa), and QL4 (25.5 kDa). Western blot analysis revealed that QL1 and QL2 reacted with antibodies raised against the rat Mu class GSTs (Yb1 and Yb2), and QL3a and QL3b reacted with those raised against the Alpha class (rat Ya and mouse a). Substrate specific activity of each isoform was determined with CDNB, DCNB, CuOOH, EA, t-PBO, ASD, and t-SO. QL3a and QL3b have high reactivity toward CuOOH, while QL1 and QL2 showed high activity toward t-SO. The N-terminal amino acid sequence of QL2 was identical to that of the chicken Mu class GST subunit CL2. However, no sequence was obtained with QL1 due to possible N-terminal blockage.

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.

Broiler chicken exposed to 41°C and 50% relative humidity for 60 min induced hsp70 mRNA in blood leukocytes, testes, and bursa of Fabricius. Daily heat conditioning for 3 weeks maximized expressed of testicular hsp70 mRNA. Greater amounts of hsp70 mRNA transcripts were observed in testes and bursa of Fabricius of large-comb cockerels than in small-comb cockerels. Expression of hsp70 mRNA appeared to be associated with acquired thermoresistance in chickens.

In the present paper, we report the unexpected discovery of a new virus in samples from chicken and turkey flocks with clinical disorders such as tenosynovitis, enteric problems, or runting and/or stunting-like conditions. Since 1987, several virus isolation attempts on samples from these flocks resulted in the same macroscopic characteristic lesions in embryonated specific pathogen free eggs, being mortality with bright-red discolouration of legs and wing-tips, a swollen dark-red liver and oedema. Initial work suggested the presence of an agent with characteristics of a non-enveloped RNA virus. Further work, which is described in this paper, showed that the isolated strains formed a new group of avian nephritis viruses, which is genetically and antigenically distinct from known avian astroviruses. Inoculation of a representative strain (isolate 19) of this new group of avian nephritis viruses, provisionally named avian nephritis virus-3, in specific pathogen free layer chicks resulted in diarrhoea, runting and stunting, and even mortality.

The tolerance of chickens to acute heat stress may be modified by diet. Broiler chickens fed calcium-adequate (0.90% Ca) or -deficient (0.45% or 0.15% Ca) diets were either fed or not fed for 24 h and exposed to increasing temperatures (from 24 to 41 degrees C). Diets were fed for 7 d before heat stress in Experiment 1 and for 14 d before heat stress in Experiment 2. Body temperature, blood ionized Ca, pH, pCO2, plasma inorganic phosphate and total Ca were determined. During heat stress, Ca+2 and inorganic phosphate were depressed in all treatments. Feeding the 0.45% Ca diet for 7 d reduced hyperthermic body temperature of fed chickens but had no effect on body temperature of unfed chickens relative to the groups fed 0.90% Ca. No further improvement in body temperature response to heat stress was obtained by lowering the dietary Ca level to 0.15% or extending the feeding period to 14 d. Food deprivation was more effective in counteracting the heat-induced rise in body temperature than a dietary Ca deficiency. Heat-induced changes in body temperature, Ca+2, inorganic phosphate and blood pH were highly correlated (P < 0.001). The change in Ca+2 followed a pattern similar to that of changes in body temperature, but changes in inorganic phosphate seemed to be more indicative of changes in pH. Control birds fed 0.90% Ca exhibited the highest changes in Ca+2 and body temperature values. Feeding Ca-deficient diets reduced changes in both Ca+2 and body temperature. Unfed birds, regardless of dietary Ca level, showed the lowest changes in Ca+2 and body temperature.(ABSTRACT TRUNCATED AT 250 WORDS)

1. 1. During acute in vivo heat stress, a normal heat shock protein (HSP) response was not inducible in chickens deficient in inorganic phosphorus (P I -deficient). 2. 2. Small quantities of HSP 70 and HSP 90 were induced, but little or no HSP 23 was induced in P i -deficient chickens compared to P i -adequate chickens. 3. 3. Increased susceptibility of P i -deficient chickens to acute heat stress was attributed to their inability to produce an adequate HSP response.

The solubilized parasporal crystalline proteins (SPCP) of Bacillus thuringiensis subsp. israelensis when administered to Japanese quail by intraabdominal (IA) injection were toxic with an LD 50 at 24 hr of 22.8 mg/kg. No deaths were noted by intranasal, subcutaneous, and intravenous administration. SPCP were highly hemolytic against quail red blood cells but this SPCP-induced hemolysis was inhibited by preincubation of SPCP with quail serum. Electrocardiographic analyses of IA-injected quail demonstrated cardiac dysfunction consistent with bradycardia. Hypothermia was also positively correlated with heart rate reduction. SPCP IA injection reduced serum lipid levels and alkaline phosphatase, and increased serum glucose, creatine phosphokinase, and lactate dehydrogenase. Induction of a septic shock-like condition may be the toxic mode of action of IA-injected SPCP in Japanese quail.

1. Catecholamines suppress cutaneous basophil hypersensitivity (CBH) to intradermal phytohemagglutinin (PHA-P) challenge in chickens. 2. E. coli 0127: B8 endotoxin, reserpine, and propranolol prevented a norepinephrine-induced suppress of CBH. 3. PHA-P induced CBH appeared to be mediated through a β-adrenergic receptor mechanism associated with plasma corticosterone in chickens.

1. 1. Liver tryptohan 2,3-dioxygenase (TPO) activity was depressed significantly by the Bordetella avium infection localized in the trachea of the turkey poult. 2. 2. Tryptophan, given orally, induced a significant increase in TPO activity in both control and infected poults. 3. 3. Hydrocortisone induced TPO activity in the turkey in a dose dependent manner.

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

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.

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.