Glycerol as a partial replacement for lactose in milk replacer for young dairy calves.

Glycerol (glycerin) is increasingly available from biodiesel manufacture and edible oil refining and it has been used successfully in diets for chickens, pigs, and adult cattle; however, less information is available on its nutritional value in young calves. Our objective was to determine the effects on calf growth and health when glycerol replaced a portion of lactose in milk replacer. Holstein calves (12 male, 12 female) born at the University of Illinois dairy unit were assigned alternately to 1 of 2 treatments (24 calves total): control milk replacer or milk replacer supplemented with 15% glycerol in replacement of lactose. The experimental base milk replacer contained greater protein, fat, minerals, and vitamins so that when glycerol was added, the composition would be the same as that of the control, except that glycerol replaced some lactose. Calves were housed in individual hutches bedded with straw, and water was freely available. Starter was offered beginning on d 36. The amount of milk replacer offered was reduced by half on d 43, and calves were weaned at d 49. Calves were fed milk replacers twice daily from d 3 of life. Milk replacers contained 28% protein (all from whey proteins), 2.6% lysine, and 15% fat. Control milk replacer contained 40% lactose, and the glycerol milk replacer contained 25% lactose. Both replacers were reconstituted to 15% solids. Glycerol (liquid) was added to reconstituted base milk replacer at each feeding. During wk 1, milk replacers were fed at a rate of 0.25 Mcal/kg of metabolic body weight (BW) (about 1.5% of BW daily as powder, or approximately 675 g/d) and from wk 2 to 6 at 0.30 Mcal/kg of metabolic BW (about 2% of BW daily, or approximately 900 to 1,200 g/d). Measurements of BW and stature were made weekly through d 56. Calf BW and average daily gain through d 35 (0.66 vs. 0.65 kg/d for controls and glycerol, respectively) did not differ significantly between treatments. Stature measurements (withers height, body length, heart girth) and measures of health (fecal scores, medical treatments) did not differ between treatments. Under the conditions of this experiment, glycerol was an acceptable replacement for at least 37.5% of the total lactose in milk replacer (15% of the formula) if economically favorable.

Rapid direct conversion of Cu(2-x)Se to CuAgSe nanoplatelets via ion exchange reactions at room temperature.

The use of template nanostructures for the creation of photovoltaic and thermoelectric semiconductors is becoming a quickly expanding synthesis strategy. In this work we report a simple two-step process enabling the formation of ternary CuAgSe nanoplatelets with a great degree of control over the composition and shape. Starting with hexagonal nanoplatelets of cubic Cu2-xSe, ternary CuAgSe nanoplatelets were generated through a rapid ion exchange reaction at 300 K using AgNO3 solution. The Cu2-xSe nanoplatelet template and the final CuAgSe nanoplatelets were analyzed by electron microscopy and X-ray diffraction (XRD). It was found that both the low temperature pseudotetragonal and the high temperature cubic forms of CuAgSe phase were created while maintaining the morphology of the Cu2-xSe nanoplatelet template. Thermal and electronic transport measurements of hot-pressed pellets of the synthesized CuAgSe nanoplatelets showed a drastic reduction in the thermal conductivity and a sharp transition from n-type (S = -45 µV K(-1)) to p-type (S = +200 µV K(-1)) semiconducting behavior upon heating above the structural transition from the low temperature orthorhombic to the high temperature super-ionic cubic phase. This simple reaction process utilizing a template nanostructure matrix represents an energy efficient, cost-efficient, and versatile strategy to create interesting materials with lower defect density and superior thermoelectric performance.

Nutritionally induced adipose hypertrophy in young pigs is transient and independent of changes in the expression of the obese and peroxisome proliferator activated receptor genes.

Previous studies have shown that piglets weaned to a liquid milk replacer (MR), rather than a typical dry diet (DD) regimen, have improved growth rates and deposit more energy as body fat. In the present study, we used this model to determine whether changes in the expression of genes linked to the regulation of adiposity were related to the accelerated fat accretion. We also determined whether the increase in body fat was sustained throughout a substantial proportion of the growth curve. At weaning (19 plus minus 2 days of age), 96 piglets were placed in 12 replicate pens per diet (4 pigs per pen, 2 barrows and 2 gilts), and fed a liquid MR or conventional DD regimen for 5 weeks. Thereafter, 6 barrows and 6 gilts pigs from each diet were killed for determination of whole body chemical composition (less gastrointestinal contents). The remaining pigs were assigned randomly to weight target groups (60, 85, and 110 kg), placed in individual pens, and fed a conventional dietary regimen until killed at their respective weight targets for tissue sampling and determination of whole body chemical composition. Over the 5-week period in which the MR was fed, the growth rate of the pigs consuming the MR exceeded that of the pigs fed the DD by 36% (P <.05). Fat gain in these pigs was increased to 1.8 times that of the pigs fed the DD, and percentage body fat was 45% greater (P <.05). Acetyl Co-A carboxylase (ACC) activity (per mg of adipose extract protein) was not different between the two diet groups at the conclusion of the 5-week period, or at 110 kg body weight. During the MR period, actual protein gain was increased (P <.05) 22% in the pigs fed the MR as well. By 110 kg of body weight, body fat was reduced (P <.05) by 7.7% (total fat mass) and 8.3% (percentage of body weight basis) in the pigs fed MR vs. the DD group. The expression of the peroxisome proliferator activated receptors (PPAR) alpha and gamma was not influenced by diet or by body weight. Expression of the obese gene was independent of diet, but was greater (P <.09) in pigs at 110 kg body weight than at 60 kg. These data provide additional evidence that piglets weaned to liquid diets have greater rates of growth and deposit more body fat, but that this difference subsides quickly when a typical dry dietary regimen is imposed. Furthermore, the biochemical changes responsible for the increased adiposity are independent of changes in the expression of the obese or PPAR genes, at least at the mRNA level.

Changes in the expression of uncoupling proteins and lipases in porcine adipose tissue and skeletal muscle during feed deprivation*(1).

The hormone-sensitive and lipoprotein lipases are critical determinants of the metabolic adaptation to starvation. Additionally, the uncoupling proteins have emerged with potential roles in the metabolic adaptations required by energy deficiency. The objective of this study was to evaluate the expression (mRNA abundance) of uncoupling proteins 2 and 3 and that of hormone-sensitive and lipoprotein lipase in the adipose tissue and skeletal muscle of the pig in relationship to feed deprivation. Thirty-two male castrates (87 kg +/- 5%) were assigned at random to fed and feed-deprived treatment groups. After 96 hr, the pigs were euthanized and adipose and skeletal muscle tissue obtained for total RNA extraction and nuclease protection assays. Feed deprivation increased uncoupling protein 3 mRNA abundance 103-237% (P < 0.01) in longissimus and red and white semitendinosus muscle. In contrast, the increase in uncoupling protein 3 mRNA in adipose tissue was only 23% (P < 0.06), and adipose uncoupling protein 2 mRNA was not influenced (P > 0.66) by feed deprivation. The increased abundance of uncoupling protein 2 mRNA in the longissimus muscle of feed-deprived pigs was small (22%), but significant (P < 0.04). The expression of hormone-sensitive lipase was increased 46% and 64% (P < 0.04) in adipose tissue and longissimus muscle, respectively, by feed deprivation, whereas adipose lipoprotein lipase expression was reduced (P < 0.01) to 20% of that of the fed group. Longissimus lipoprotein lipase expression in the feed-deprived group was 37% of that of the fed group (P < 0.01), and similar reductions were detected in red and white semitendinosus muscle. Overall, these findings indicate that uncoupling protein 3 expression in skeletal muscle is quite sensitive to starvation in the pig, whereas uncoupling protein 2 changes are minimal. Furthermore, we conclude that hormone-sensitive lipase is upregulated at the mRNA level with prolonged feed deprivation, whereas lipoprotein lipase is downregulated.

Regulation of PPARgamma but not obese gene expression by dietary fat supplementation.

Leptin, the product of the obese gene, and peroxisome proliferator activated receptor gamma (PPARgamma) are important regulators of energy metabolism, adipogenesis, and immune function. In rodent models, both genes seem to respond at the mRNA and/or protein levels to dietary fat consumption. To determine the effect(s) of dietary saturated and polyunsaturated fatty acids on the expression (mRNA abundance) of these genes, adipose tissue was obtained from pigs fed three different dietary fat sources. Corn-soybean meal diets containing no added fat (NO, control) or 10% beef tallow (BT), safflower oil (SO), or fish oil (FO) were fed ad libitum (n = 12) for 12 weeks. The abundance of obese, PPARgamma1, and PPARgamma2 mRNA was quantified relative to 18S rRNA using ribonuclease protection assays. The gain:feed ratio was improved (P < 0.05) 21% by all fats with a corresponding reduction (P < 0.05) in feed intake. Relative to pigs fed NO, serum total cholesterol was increased (P < 0.01) in pigs fed BT and triglyceride and nonesterified fatty acid concentrations were increased (P < 0.01) by all supplemental fats. Serum insulin was increased (P < 0.10) only by SO. Neither obese nor PPARgamma1 mRNA abundance were responsive to added fat (P > 0.15). However, the abundance of PPARgamma2 mRNA was increased fourfold by SO compared with the NO diet. These data indicate that the abundance of obese mRNA is independent of dietary fat consumption per se, whether saturated or unsaturated, when feed consumption is reduced due to greater dietary caloric density. Furthermore, we provide evidence that expression of the PPARgamma2 gene in porcine adipose tissue is selectively responsive to SO (presumably linoleic acid, 18:2n-6).

Soybean isoflavones, genistein and genistin, inhibit rat myoblast proliferation, fusion and myotube protein synthesis.

The isoflavones, genistein and genistin, are cytotoxic in vitro (e.g. , inhibition of cell proliferation), due in part to inhibition of protein tyrosine kinase and DNA topoisomerase activities. Normal cell functions associated with these enzymatic activities could potentially be impaired in animals through ingestion of soybean products. In this study, cultured rat myogenic cells (L8) were used to determine whether genistein or genistin influences myoblast proliferation and fusion, and myotube protein synthesis and degradation. Genistein or genistin was dissolved in dimethylsulfoxide and included in the culture medium at 0, 1, 10 or 100 micromol/L. Myoblast proliferation was measured by methyl-3H-thymidine incorporation over 48 h. Myoblast differentiation was evaluated by the number of nuclei in multinucleated myotubes. Myotube protein synthesis was measured by 2-h 3H-amino acid incorporation into the myosin and total protein pools after acute (2 h) or chronic (24 h) exposure to similar treatments; protein degradation was measured by measuring radioactivity in protein pools following a time course of protein breakdown after myotube proteins were prelabeled with 3H-amino acids. Genistein or genistin strongly inhibited in vitro myoblast proliferation (P < 0.001) and fusion (P < 0.001) in a dose-dependent manner with effective genistein concentration as low as 1 micromol/L. Genistein or genistin inhibited protein accretion in myotubes (P < 0.001). Decreased protein accretion is largely a result of inhibition on cellular (myofibrillar) protein synthesis rate. No adverse effect on protein degradation was observed. Results suggest that if sufficient circulating concentrations are reached in tissues of animals consuming soy products, genistein/genistin can potentially affect normal muscle growth and development.

Proinflammatory cytokines regulate myogenic cell proliferation and fusion but have no impact on myotube protein metabolism or stress protein expression.

The objective of the present study was to evaluate the effect of the proinflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-alpha (IL-1a), on myoblast proliferation and fusion and on myocyte protein metabolism and stress protein expression. Proliferation was suppressed (p < 0.05) by both cytokines, alone and in combination, and at lower concentrations, the suppression was additive. Likewise, fusion was retarded (p < 0.05) by these cytokines alone and in combination. Myosin synthesis was not altered acutely or chronically by TNF-alpha alone or by the combination of this cytokine with IL-1alpha. Chronic exposure to TNF-alpha did not alter total cellular protein synthesis, but exposure to IL-1alpha and the cytokine combination resulted in an increase (14% to 19%, p < 0.05) in synthesis. Neither total cellular protein nor myosin degradation were influenced by either cytokine alone or by the combination. There was no detectable induction, acutely or chronically, of any of the stress proteins evaluated (HSC70, HSP70, or HSP60). These data suggest that cytokines may alter muscle growth and development prenatally and postnatally and that the changes in muscle protein metabolism during periods of immune challenge are not direct effects of TNF-alpha or IL-1alpha.

Myostatin expression in porcine tissues: tissue specificity and developmental and postnatal regulation.

The objective of this study was to establish the developmental pattern and tissue specificity of porcine myostatin expression and to evaluate expression in skeletal muscle during circumstances in which muscle growth was altered. Northern blot analysis revealed two transcripts (1.5 and 0.8 kb). Myostatin mRNA was detected in whole fetuses at 21 and 35 days and was markedly increased (P < 0.05) by 49 days. At birth, mRNA abundance in longissimus muscle had declined significantly (P < 0.05) from that at day 105 of gestation and continued to decrease (P < 0.05) to its lowest level 2 wk postnatally (4 kg body wt). Myostatin expression was higher (P < 0. 05) at 55, 107, and 162 kg body wt than at 4 kg body wt. Postnatally, myostatin mRNA was detected in skeletal muscle and mammary gland. Expression at birth was 65% higher (P < 0.04) in longissimus muscle of low-birth-weight piglets (0.57 +/- 0.052 kg body wt) vs. normal (1.37 +/- 0.077 kg body wt) littermates, irrespective of gender. However, suppression of longissimus muscle growth by food deprivation (3 days) did not alter (P > 0.15) myostatin expression in either 4- or 7-wk-old piglets. Additionally, myostatin mRNA abundance was not changed by porcine growth hormone administration in growing animals. These data indicate that myostatin expression in skeletal muscle peaks prenatally and that greater expression is associated with low birth weight. Expression in mammary gland indicates a possible role for myostatin in mammary gland development and/or lactation.

Partial cloning and expression of the bovine leptin gene.

The product of the leptin (i.e., obese) gene may be an important regulator of energy metabolism, adiposity, and reproduction, and is perhaps linked to meat quality determinants such as marbling. Molecular probes were developed using polymerase chain reaction (PCR) technology to evaluate leptin expression in adipose depots and to evaluate the tissue-dependent nature of expression reported in other species. A 438 bp fragment representing the coding region of the bovine leptin gene excluding the N-terminal secretory signal was amplified, cloned into a plasmid vector (pASK75), and expressed in E. coli. Sequence analysis of the cDNA and the corresponding polypeptide indicate that, overall, both share approximately 87% homology with the mouse and human leptin genes and polypeptides. Amino terminal sequencing (30 amino acid residues) of the recombinant bovine leptin (rBL) protein revealed 100% homology with mouse and human leptin. The bovine leptin gene is expressed as a 3,090 nt mRNA which is detected in adipose tissue, but is not found in brain (despite the appreciable fat content and lipid metabolism) or other tissues. Leptin gene expression in several adipose depots (subcutaneous, renal, and omental) was similar (P = .73) in finished cattle.

Porcine somatotropin improves growth in finishing pigs without altering calpain 3 (p94) or alpha-actin mRNA abundance and has a differential effect on calpastatin transcription products.

The objective of this study was to determine whether the improvements in growth and efficiency of gain achieved by recombinant porcine somatotropin (pST) are associated with altered expression of the p94, calpastatin, or alpha-actin genes in porcine longissimus (LD) muscle. Forty-eight barrows (initial 64.2 to 67.4 kg BW) were assigned to four treatments (n = 12) arranged as a 2 x 2 factorial in a randomized complete block design. Factors were duration of treatment (3 or 6 wk) and pST administration (0 or 3 mg x pig(-1) x d(-1)). Plasma samples were obtained 24 h after the first pST injection and at the end of the each treatment period for assays of selected variables. The LD samples were obtained at 3 and 6 wk of pST treatment. Northern blot analysis of calpastatin expression in LD muscle revealed three distinct transcription products of approximately 8.5 (CPST I), 5.5 (CPST II), and 2.5 (CPST III) kb; CPST II was reduced (P < .02) 33 and 61% by pST at 3 and 6 wk, respectively, whereas CPST I and III were not influenced (P > .12). Neither alpha-actin nor p94 was responsive to pST injection. As expected, pST resulted in higher (50%, P < .02) plasma insulin within 24 h and one- and twofold higher (P < .01) concentrations at 3 and 6 wk, respectively. Glucose was increased (P < .01) at 3 (15%) and 6 (10%) wk, whereas urea nitrogen was reduced (32 to 36%, P < .01). The efficacy of pST was evident in that ADG was improved (P < .01) 11 to 13% independent of time. Likewise, feed intake was reduced (P < .01) 10 to 11% and gain: feed improved (P < .01) approximately 26% for pigs receiving pST independent of time. These data indicate that the enhanced muscle growth achieved by pST is not associated with altered expression of p94 or alpha-actin, or an increase in the abundance of any calpastatin transcription product.

Obese gene expression in porcine adipose tissue is reduced by food deprivation but not by maintenance or submaintenance intake.

The relationship between obese gene expression and energy intake was determined in pigs of various body weights. With ad libitum consumption, expression increased (P < 0.001) with body weight from 55 to 163 kg. Obese mRNA relative abundance was correlated with fat mass (r = 0.74, P < 0.0001) and percentage of fat (r = 0.72, P < 0. 0001). Obese expression was also evaluated at 159 kg (initial weight) and ad libitum, maintenance or 23% of maintenance intake for 28 d. Obese mRNA was independent of treatment (P > 0.78) despite considerable weight differences. Obese mRNA abundance was then compared at 136 kg (initial weight) and ad libitum or maintenance intake for 3 or 28 d. Abundance was not influenced by either duration of treatment or intake, despite a small increase (P < 0.01) in serum nonesterified fatty acids (NEFA) and a reduction (P < 0.02) in insulin attributable to maintenance intake. Finally, mRNA abundance was determined at 60 and 136 kg and conditions of food deprivation or ad libitum intake for 3 d. Food deprivation reduced (P < 0.01) serum insulin and increased (4- to 5-fold) NEFA concentrations. Obese mRNA abundance was greater (P < 0.01) in the heavier pigs and was reduced (P < 0.01) by food deprivation. We conclude that obese mRNA abundance in pigs correlates with fat mass and percentage of body fat under conditions of ad libitum intake. Furthermore, obese mRNA abundance is reduced by food deprivation, whereas lesser degrees of intake restriction do not change obese mRNA abundance, even when accompanied by appreciable weight loss.

Leptin expression in porcine adipose tissue is not increased by endotoxin but is reduced by growth hormone.

The physiologic response to infection includes reductions in tissue concentrations of anabolic growth factors as a means of reducing growth and conserving nutrients for immunologic processes. This repartitioning of nutrients is accompanied by anorexia, which has been linked to increased leptin expression. Furthermore, leptin and growth hormone (GH) concentrations are inversely related, with leptin being required for normal GH release. The objective of this study was to determine if pretreatment with GH would influence endotoxin-induced changes in leptin expression or attenuate endotoxin-induced reductions in serum insulin-like growth factor-1 (IGF-1) and IGF-1 expression in liver and longissimus muscle. In experiment 1, 40 pigs were assigned to four treatments (n = 10 per treatment) arranged as a 2x2 factorial with GH (s.c. injection, 2 mg 1 h before challenge and 2 mg 2 h after challenge) and endotoxin (single i.m. injection, 25 microg/kg body weight) as main effect variables. Pretreatment with GH resulted in a marked increase (p<0.001) in serum GH within 1 h that was sustained throughout the study. Endotoxin challenge reduced (p<0.003) serum IGF-1 independent of GH (GH x endotoxin, p>0.682), and reduced (p<0.05) IGF-1 expression in longissimus muscle but not liver. Leptin mRNA abundance was reduced 56% (p<0.005) by GH but was not affected by endotoxin (p>0.81). In experiment 2, 36 pigs (n = 12 per treatment) were either allowed ad libitum feed consumption with no injection or deprived of feed and injected twice with either saline or endotoxin 24 h apart. Feed deprivation reduced leptin expression (p<0.05). However, endotoxin did not change leptin expression but markedly increased (p<0.05) serum haptoglobin. These data indicate that changes in IGF-1 status in endotoxin-challenged pigs are independent of serum GH and that leptin expression is not increased by endotoxin challenge in the pig. These data also indicate a regulatory linkage between GH and leptin in vivo.

Effect of dietary energy source and immunological challenge on growth performance and immunological variables in growing pigs.

Forty-eight growing pigs (23 kg BW) were assigned to four treatments (n = 12) arranged as a 2 x 2 factorial. Dietary energy source (conventional [CON] vs high-oil corn [HOC]), with or without an immunological challenge (IC) regimen constituted main effects. The IC regimen consisted of injection of endotoxin (E. coli lipopolysaccharide [LPS]) and vaccination for porcine respiratory and reproductive syndrome (PRRS). Growth performance data were collected over a 5-wk period and are presented as prechallenge (d 1 to 14; d 1 was the 1st d of the study), challenge (d 15 to 21), and postchallenge (d 22 to 36) periods, and overall. Overall, the pigs fed HOC consumed less feed (P < .11) and gained more efficiently (P < .03). During the immunological challenge period, ADG was depressed 21% and feed intake 15% (P < .01). The IC resulted in lower (P < .01) serum alpha-1-acid glycoprotein (AGP) concentrations on d 22, and the magnitude of the reduction was greater in the pigs fed the CON diet (energy source x immune challenge, P < .10). Serum AGP concentrations remained lower (P < .08) in challenged pigs on d 36. Immunoreactive prostaglandin concentrations were higher (55%, P < .08) in the pigs fed HOC immediately following the IC period (d 22). The data reported herein indicate that the performance of pigs fed HOC is satisfactory, and that feeding HOC does not compromise growth performance during or after an immunological challenge.

Influence of protein intake, energy intake and stage of gestation on growth, reproductive performance, nitrogen balance and carcass composition in gestating gilts.

Thirty-six crossbred gilts were fed three levels of protein (146, 255 and 364 g/d) and two levels of energy (6,200 and 7,440 kcal of digestible energy/d) throughout gestation in a 3 x 2 factorial arrangement of treatments. Five-day N balance studies were conducted in early (0 to 30 d), mid- (30 to 60 d) and late (60 to 90 d) gestation. At slaughter (90 d of gestation), reproductive tracts were weighed and evaluated for reproductive performance and samples of the reproductive tract, liver and semimembranosus muscle (SM) were analyzed for crude protein. The right half of the carcass was subjected to a physical separation of fat, lean and bone. Neither dietary protein nor energy level significantly affected weight gain or reproductive performance. Nitrogen retention increased as dietary protein level increased and stage of gestation progressed (linear effect, P less than .01), but efficiency of N utilization and dry matter digestibility decreased with increasing protein intakes (quadratic effect, P less than .05 and linear effect, P less than .01, respectively). Nitrogen retention (P less than .01), efficiency of N retention (P less than .05) and dry matter digestibility (P less than .01) were higher in gilts fed high (H) energy compared with gilts receiving moderate (M) energy diets. Increasing dietary protein increased total carcass separable lean tissue (quadratic effect, P less than .01), liver weight (linear effect P less than .01) SM weight (quadratic effect, P less than .05) and SM percentage M (linear effect P less than .10). Similarly, total carcass N and carcass lean N increased as protein level increased (quadratic effect, P less than .10, P less than .05, respectively). In contrast to the increase in muscle N, N in uterine tissue and fluids was not affected by dietary protein level. The results of this experiment suggest that 146 g of crude protein/d during gestation is just as effective as higher levels of crude protein for litter size or storage of N in reproductive tissue, but 255 to 364 g of protein/d are required to maximize muscle N.

Amino acid utilization as influenced by antibacterial and anticoccidial drugs.

Utilization of amino acids, sulfur-containing amino acid (SAA) in particular, is little affected by antibiotic and anticoccidial compounds. Coccidiosis (i.e., Eimeria acervulina infection) likewise seems to have little effect on SAA utilization. Copper sulfate, a commonly used antibacterial-antifungal compound (used at levels of 100-250 mg/kg diet), interacts with SAA. Hence, at upper levels of copper ingestion (i.e., 250 mg/kg and higher), copper binds SH compounds such as cysteine and reduced glutathione. Dietary SAA requirements are increased in both chicks and rats by dietary copper levels of 250 or 500 mg/kg. Hepatic copper deposition is enhanced by copper feeding and also by E. acervulina infection. These two effects, moreover, appear to be additive. The organic arsenic compound, roxarsone, interacts with SAA also, but in a different way. Thus, whereas added dietary cysteine partially ameliorates copper toxicity due to the binding of copper by cysteine-SH with subsequent excretion, roxarsone toxicity (i.e., 500 mg/kg diet) is exacerbated by supplemental cysteine.

Performance of healthy and Eimeria acervulina-infected chicks as influenced by anticoccidial drugs and source of dietary protein.

Four experiments were conducted to evaluate an alleged interaction between the anticoccidial drugs, monensin and lasalocid, and dietary protein source. Chicks were fed practical diets (approximately 24% crude protein) containing from 0 to 13% animal-source protein supplied by either a fish meal-meat and bone meal combination or by feather meal. Monensin (121 mg/kg) and lasalocid (125 mg/kg) were evaluated for anorexigenic activity in health birds and for growth-enhancement activity in E. acervulina-infected birds. Diet-by-coccidiostat interactions were not detected in any of these experiments. The addition of monensin or lasalocid depressed performance significantly in only one of the experiments, but the magnitude of depression was similar regardless of level of animal-source protein. Efficacy of the coccidiostats, as judged by performance of chicks infected with E. acervulina, was not altered by diet type.

Eimeria acervulina infection in the chicken: a model system for estimating nutrient requirements during coccidiosis.

Eimeria maxima inoculations of 5 X 10(4) oocysts and E. acervulina inoculations of 2 X 10(5) to 4 X 10(5) oocysts were shown to depress growth by 15 to 20% in young chicks fed crystalline amino acid (CAA) diets. The intestinal lesions produced were typical of light to moderate coccidiosis. In one experiment, the performance of chicks fed monensin was increased in the presence, but not in the absence, of E. acervulina. Thus, monensin prevented the negative effects of E. acervulina on chick performance. This coccidiosis X monensin interaction was also indicative of an active coccidiosis infection. Severe E. acervulina infections were produced by inoculations of 1 X 10(6) or 2 X 10(6) oocysts. Under these conditions, gain was depressed by 30 to 40% and the intestinal lesions produced were indicative of severe coccidiosis. Also, E. acervulina infections were more severe in birds fed CAA diets than in birds fed corn-soybean meal diets. Trypsin incubation of the oocysts prior to inoculation had no significant effect on performance regardless of diet type. Based upon growth rate, intestinal lesions, and responses to anticoccidial drugs, it was clearly demonstrated that coccidiosis of varying severity cn be produced in birds fed CAA diets. In addition, it was observed that the CAA diet, with 24.58% amino acids, contained adequate levels of all indispensable nutrients, even during coccidiosis. This assures that the diet can be used effectively for nutrient requirement studies during coccidiosis.

Eimeria acervulina infection in the chicken: sulfur amino acid requirement of the chick during acute coccidiosis.

Five assays were conducted to determine whether Eimeria acervulina infection would alter the chick's sulfur amino acid (SAA) requirement. Chicks were housed in heated starter batteries with raised wire floors and fed completely purified crystalline amino acid diets. With light to moderate E. acervulina infection, data were somewhat inconclusive. In Assay 1, infected birds responded to levels of SAA above those required by healthy birds; but in two subsequent assays no difference in SAA requirements due to infection could be detected. Therefore, two additional assays were conducted in birds inoculated with a heavy dose of E. acervulina oocysts. In neither of these assays did E. acervulina infection show any indication of altering SAA utilization. When data from the five studies are viewed together, it is clear that E. acervulina infection did not increase the chick's SAA requirement.

Interaction between dietary protein/amino acid level and parasitic infection: morbidity in amino acid deficient or adequate chicks inoculated with Eimeria acervulina.

In a series of experiments designed to assess the chick's sulfur amino acid (SAA) requirement during acute coccidiosis, a striking and unexpected infection X SAA interaction was discovered. When chicks were fed diets severely deficient in SAA, Eimeria acervulina infection produced a marked growth response, while birds consuming SAA-adequate diets exhibited the expected severe growth depression when given the same dose of E. acervulina oocysts. Although the interaction was originally demonstrated in birds fed crystalline amino acid diets, it was subsequently demonstrated with intact protein diets as well. The interaction was also shown not to be unique to the SAA. Thus, lysine and E. acervulina interacted in the same manner. In fact, when birds were fed diets severely deficient in lysine, E. acervulina infection brought about a doubling of both rate and efficiency of weight gain. It was also established that the growth response to infection resulted from E. acervulina per se and not from any other component of the infective inoculum.