Pathologic effects of 2,2',4,4',5,5'-and 2,3',4,4',5,5'-hexabromobiphenyl in white leghorn cockerels

Pathologic effects of 2,2',4,4',5,5'-hexabromobiphenyl (HBB), 2,3',4,4',5,5'-HBB, and a commercial mixture of polybrominated biphenyls (PBB) were compared in White leghorn cockerels. Diets containing 1, 10, or 100 ppm PBB, 4 or 10 ppm 2,3',4'4',5,5'-HBB, or 10 or 62 ppm 2,2',4,4',5,5'-HBB were fed for 28 days. Doses of 10 ppm of each chemical were used to provide a direct comparison of toxicity. Since nearly 4% of PBB consists of 2,3',4,4',5,5'-HBB and approximately 62% consists of 2,2',4,4',5,5'-HBB, effects of doses of 4 and 62 ppm, respectively, were compared with effects of 100 ppm of PBB to determine if either of the congeners were mainly responsible for the pathologic effects caused by the mixture. Liver weights were increased in cockerels fed diets containing 62 ppm of 2,2',4,4',5,5'-HBB or 10 or 100 ppm PBB. Hepatocytes were enlarged and vacuolated and lymphoid cells of the bursa of Fabricius were depleted by 10 ppm 2,3',4,4',5,5'-HBB, ppm 2,2',4,4',5,5'-HBB, and 10 or 100 ppm PBB. These dietary concentrations caused ultrastructural changes in hepatocytes consisting of vacuolation, increased smooth endoplasmic reticulum, swollen mitochondria, and disruption of mitochondrial cristae. When either of the congeners were given in concentrations relative to their concentrations in PBB, they were less toxic than the mixture. When concentrations in diets were equal, PBB caused more severe effects than 2,3',4,4',5,5'-HBB. The least effects were seen with 2,2',4,4',5,5'-HBB. Results indicate that the two congeners chosen for study are not individually as toxic as the parent mixture.     

Effect of feeding organic and inorganic sources of additional zinc on growth performance and zinc balance in nursery pigs

Three experiments were conducted to evaluate the effect of feeding pharmacological concentrations of zinc (Zn), from organic and inorganic sources, on growth performance, plasma and tissue Zn accumulation, and Zn excretion of nursery pigs. Blood from all pigs was collected for plasma Zn determination on d 14 in Exp. 1, d 7 and 28 in Exp. 2, and d 15 in Exp. 3. In Exp. 1, 2, and 3, 90, 100, and 15 crossbred (GenetiPorc USA, LLC, Morris, MN) pigs were weaned at 24+/-0.5, 18, and 17 d of age (6.45, 5.47, and 5.3 kg avg initial BW), respectively, and allotted to dietary treatment based on initial weight, sex, and litter. A Phase 1 nursery diet was fed as crumbles from d 0 to 14 in Exp. 1, 2, and 3, and a Phase 2 nursery diet was fed as pellets from d 15 to 28 in Exp. 1 and 2. The Phase 1 and Phase 2 basal diets were supplemented with 100 ppm Zn as ZnSO4. Both dietary phases contained the same five dietary treatments: 150 ppm additional Zn as zinc oxide (ZnO), 500 ppm added Zn as ZnO, 500 ppm added Zn as a Zn-amino acid complex (Availa-Zn 100), 500 ppm added Zn as a Zn-polysaccharide complex (SQM-Zn), and 3,000 ppm added Zn as ZnO. Overall in Exp. 1, pigs fed 500 ppm added Zn as SQM-Zn or 3,000 ppm added Zn as ZnO had greater ADG (P < 0.05) than pigs fed 150 ppm, 500 ppm added Zn as ZnO, or 500 ppm added Zn as Availa-Zn 100 (0.44 and 0.46 kg/d vs 0.35, 0.38, and 0.33 kg/d respectively). Overall in Exp. 2, pigs fed 3,000 ppm added Zn as ZnO had greater (P < 0.05) ADG and ADFI than pigs fed any other dietary treatment. On d 14 of Exp. 1 and d 28 of Exp. 2, pigs fed 3,000 ppm added Zn as ZnO had higher (P < 0.05) plasma Zn concentrations than pigs on any other treatment. In Exp. 3, fecal, urinary, and liver Zn concentrations were greatest (P < 0.05) in pigs fed 3,000 ppm added Zn as ZnO. On d 10 to 15 of Exp. 3, pigs fed 3,000 ppm added Zn as ZnO had the most negative Zn balance (P < 0.05) compared with pigs fed the other four dietary Zn treatments. In conclusion, feeding 3,000 ppm added Zn as ZnO improves nursery pig performance; however, under certain nursery conditions the use of 500 ppm added Zn as SQM-Zn may also enhance performance. The major factor affecting nutrient excretion appears to be dietary concentration, independent of source.     

Growth and intestinal morphology of pigs from sows fed two zinc sources during gestation and lactation

An experiment was conducted to compare the effects of organic (Zn AA complex, ZnAA) and inorganic Zn (ZnSO4) sources on sows and their progeny during gestation and lactation and on the pigs during the nursery period. The dietary treatments were 1) a corn-soybean meal diet with 100 ppm Zn from ZnSO4 (control); 2) diet 1 + 100 ppm additional Zn from ZnSO4; and 3) diet 1 + 100 ppm additional Zn from ZnAA. Dietary additions were on an as-fed basis. Thirty-one primaparous and multiparous sows were allotted to the treatment diet beginning on d 15 of gestation and continuing through lactation. At weaning (d 17 of age), 202 pigs (63, 55, and 84 pigs for treatments 1 to 3, respectively) were allotted to the same dietary treatment as their dam. The pigs were fed a 3-phase diet regimen during the nursery period: d 0 to 7 (phase I); d 7 to 21 (phase II); and d 21 to 28 (phase III). At weaning and at the end of phase III, 1 gilt per replicate was killed, and the left front foot, liver, pancreas, and entire small intestine were removed. Diet had no effect (P > 0.10) on any response during gestation. During lactation, there was an increase (P < 0.10) in litter birth weight in sows fed ZnAA compared with those fed the control or ZnSO4 diets. The sows fed ZnAA nursed more pigs (P < 0.10) than sows fed the ZnSO4 diet, and they weaned more pigs (P < 0.05) than sows fed the control diet. Jejunal villus height of the weaned pigs from sows fed ZnSO4 was increased (P < 0.05) compared with those from the sows fed the control diet. During the nursery period, growth performance was not affected (P > 0.10) by diet. Pigs fed ZnSO4 had greater duodenal villus width (P < 0.05) than those fed ZnAA, and pigs fed ZnSO4 or the control diet had greater ileal villus width (P < 0.05) than those fed ZnAA. Pigs fed ZnSO4 or ZnAA had more (P < 0.05) bone Zn than those fed the control diet. Liver Zn concentration was greatest in pigs fed ZnSO4, followed by those fed ZnAA, and then by those fed the control diet (P < 0.05). Pancreas Zn was increased (P < 0.05) in pigs fed ZnSO4 compared with those fed the control diet. These results suggest that 100 ppm Zn in trace mineral premixes provides adequate Zn for optimal growth performance of nursery pigs, but that 100 ppm additional Zn from ZnAA in sow diets may increase pigs born and weaned per litter.     

Effects of L-carnitine fed during lactation on sow and litter performance

Sows of differing parities and genetics were used at different locations to determine the effects of feeding added L-carnitine during lactation on sow and litter performance. In Exp. 1, sows (n = 50 PIC C15) were fed a lactation diet (1.0% total lysine, .9% Ca, and .8% P) with or without 50 ppm of added L-carnitine from d 108 of gestation until weaning (d 21). No differences in litter weaning weight, survivability, sow ADFI, or sow weight and last rib fat depth change were observed. Number of pigs born alive in the subsequent farrowing were not different (P>.10). In Exp. 2, parity-three and -four sows (n = 115 Large White cross) were used to determine the effect of feeding 0, 50, 100, or 200 ppm of added L-carnitine during lactation (diet containing .9% total lysine, 1.0% Ca, and .8% P) on sow and litter performance. No improvements in the number of pigs or litter weights at weaning were observed (P>.10). Sows fed added L-carnitine had increased weight loss (linear; P<.04), but no differences (P>.10) were observed in last rib fat depth change or subsequent reproductive performance. In Exp. 3, first-parity sows (n = 107 PIC C15) were fed a diet with or without 50 ppm of added L-carnitine during lactation (diet containing 1.0% total lysine). Sows fed added L-carnitine tended (P<.10) to have fewer stillborn and mummified pigs than controls (.42 vs .81 pigs). No differences were observed for litter weaning weight, survivability, or subsequent farrowing performance. Feeding 50 to 200 ppm of added L-carnitine during lactation had little effect on sow and litter performance.     

The effects of dietary T-2 toxin on acute herpes simplex virus type 1 infection in mice

Young male white Swiss mice were fed control diet or diet supplemented with 20 or 10 parts per million (ppm) of T-2 toxin for two or three weeks. These mice then were inoculated with herpes simplex virus type 1 (HSV-1) (9.6 x 10(6) plaque forming units) intraperitoneally. To compare the effects of T-2 toxin against a known immunosuppressive drug, cyclophosphamide was injected intraperitoneally at 150 mg/kg, 24 hours after treatment with HSV-1, into mice fed the control diet. Mice were necropsied and tissues were collected for microscopic and virologic examination. White Swiss mice which consumed a daily diet containing 20 ppm of T-2 toxin for two or three weeks were highly susceptible to HSV-1 infection and 27 of 36 (75%) died as a result of extensive hepatic and adrenal necrosis. Although HSV-1 was isolated from livers and brains of mice fed 20 ppm of T-2 toxin for two or three weeks, there was little or no inflammatory response found in the adrenals, livers, spinal cords, brains, or ganglia. The necrotizing encephalomyelitis observed in control mice was absent. High levels of dietary T-2 toxin appeared to be more immunosuppressive than cyclophosphamide because only one mouse died after treatment with HSV-1 and cyclophosphamide. Mice treated with cyclophosphamide had changes in brain, spinal cord, spleens, thymus, and bone marrow which were similar to those fed 20 ppm of T-2 toxin and infected with HSV-1, however, liver lesions were much less severe. HSV-1-infected mice on a diet with 10 ppm T-2 toxin had lesions of intermediate severity when compared with HSV-1-infected mice fed a diet with 20 ppm T-2 toxin and HSV-1-infected mice on control diets. Necrosis was less extensive in the livers and adrenals. The infrequent isolation of virus from liver and brain was consistent with the lack of intranuclear inclusion bodies and a more marked inflammatory response. Ten ppm of dietary T-2 toxin only depressed bone marrow and splenic red pulp to a mild or moderate degree. This may have enhanced the necrotizing encephalomyelitis observed in mice killed on days 6 and 8 after HSV-1 infection. Liver lesions were mild and those of the adrenals were moderate in mice fed control diet. The rare isolation of HSV-1 from the liver and brain and the findings of a moderate to severe necrotizing encephalomyelitis in these mice was consistent with an essentially functional immune system.     

Selenium elimination in pigs after an outbreak of selenium toxicosis.

In May 1996, 150 grower pigs in 5 California counties were exposed to selenium-contaminated feed distributed by a single feed company. Feed samples from 20 herds had a mean selenium concentration of 121.7 ppm dry weight (range, 22.1-531 ppm). In San Luis Obispo County, 52 pigs in 24 herds were exposed to the feed, and 8 pigs died with signs of paralysis. Bilateral symmetrical poliomyelomalacia involving the ventral horns of the cervical and lumbar intumescence was evident on histologic examination of spinal cord from affected pigs. Of 44 surviving exposed pigs, 33 (75%) exhibited signs of selenosis, including anorexia, alopecia, and hoof lesions. Thirty-nine of 44 pigs (88.6%) had elevated (>1 ppm) blood selenium concentrations. Surviving exposed pigs were changed to a standard commercial ration containing approximately 0.5 ppm (dry weight) selenium. Blood selenium concentrations were determined weekly for 46 days following removal of the contaminated feed and were compared with values of 20 control pigs fed a standard commercial ration. Mean (+/-SD) blood selenium concentrations of exposed pigs were 3.2 +/- 2.6 ppm at the initial sampling and 0.4 +/- 0.1 ppm after 46 days. Mean blood selenium concentrations of < or = 0.3 ppm for control pigs at all samplings were significantly lower (P < 0.001) than concentrations for exposed pigs. Muscle and liver samples of 22 of the 44 exposed pigs were collected at slaughter approximately 72 days after withdrawal of the selenium-contaminated feed. Muscle samples had a mean selenium concentration of 0.36 ppm (wet weight). Liver samples had a mean selenium concentration of 1.26 ppm (wet weight). One liver sample had a selenium value in the toxic range for pigs (3.3 ppm wet weight; reference range, 0.4-1.2 ppm). A 1-compartment pharmacokinetic model of selenium elimination in exposed pigs was generated, and the geometric mean blood selenium elimination half-life was estimated to be 12 days. The 60-day withdrawal time recommended by the Food Animal Residue Avoidance Database was considered sufficient to allow safe human consumption of tissues from exposed pigs.     

Carry-over of sulphadimidine in the faeces and urine of pigs fed medicated feed

In two experiments sulphadimidine-free pigs were placed in pens previously occupied by pigs fed a diet containing 100 ppm sulphadimidine. Faeces, urine and spilled feed had been removed by scraping the surface of the pens before the new pigs were introduced. The concentration of sulphadimidine in the tissues of the medicated pigs fell below 100 ng/g within 72 hours of withdrawal of the medicated diet and in the fluids the concentration fell below 500 ng/ml within 96 hours. The concentrations in the tissues of the pigs housed in the contaminated pens exceeded 100 ng/g for up to 24 hours but then fell to acceptable concentrations; the concentration of sulphadimidine in body fluids occasionally exceeded 500 ng/ml.     

Effect of dietary nutrients on osteochondrosis lesions and cartilage properties in pigs

OBJECTIVE: To evaluate dietary ingredients involved in cartilage and bone metabolism and their influence on osteochondrosis lesions in swine. ANIMALS: 80 crossbred gilts (mean initial weight, 39 kg). PROCEDURES: Pigs (10 pigs/treatment) were fed a corn-soybean meal basal (control) diet or the basal diet supplemented with additional minerals (copper and manganese or silicon), amino acids (proline and glycine; a combination of leucine, isoleucine, and valine; or methionine and threonine), or fatty acids (provided by fish oil) for 84 days. Pigs were then slaughtered and the distal portion of the left femur was collected for determination of osteochondrosis lesions at the femoral condyle. After evaluation of external joint surfaces, the distal portion of the femur was sectioned to evaluate lesions in the growth plate and articular cartilage. Additionally, a cartilage specimen was obtained from the patella for analysis. RESULTS: Pigs fed diets containing high amounts of methionine and threonine or the diet containing all additional ingredients had significantly lower total severity scores, compared with scores for pigs fed the control diet or a diet supplemented with fish oil. Pigs fed diets containing additional proline and glycine, copper and manganese, methionine and threonine, or all additional ingredients had significantly lower overall scores, compared with scores for pigs fed the control diet or a diet supplemented with fish oil. CONCLUSIONS AND CLINICAL RELEVANCE: Dietary manipulation decreased the severity of osteochondrosis lesions, compared with results for pigs fed a control diet. However, additional research on optimal concentrations and combinations of dietary components is needed.     

Comparison of growth performance and zinc absorption, retention, and excretion in weanling pigs fed diets supplemented with zinc-polysaccharide or zinc oxide

Fifty weanling crossbred pigs averaging 6.2 kg of initial BW and 21 d of age were used in a 5-wk experiment to evaluate lower dietary concentrations of an organic source of Zn as a Zn-polysaccharide (Zn-PS) compared with 2,000 ppm of inorganic Zn as ZnO, with growth performance, plasma concentrations of Zn and Cu, and Zn and Cu balance as the criteria. The pigs were fed individually in metabolism crates, and Zn and Cu balance were measured on individual pigs (10 replications per treatment) from d 22 to 26. The basal Phase 1 (d 0 to 14) and Phase 2 (d 14 to 35) diets contained 125 or 100 ppm added Zn as Zn sulfate, respectively, and met all nutrient requirements. Treatments were the basal Phase 1 and 2 diets supplemented with 0, 150, 300, or 450 ppm of Zn as Zn-PS or 2,000 ppm Zn as ZnO. Blood samples were collected from all pigs on d 7, 14, and 28. For pigs fed increasing Zn as Zn-PS, there were no linear or quadratic responses (P > or = 0.16) in ADG, ADFI, or G:F for Phases 1 or 2 or overall. For single degree of freedom treatment comparisons, Phase 1 ADG and G:F were greater (P < or = 0.05) for pigs fed 2,000 ppm Zn as ZnO than for pigs fed the control diet or the diet containing 150 ppm Zn as Zn-PS. For Phase 2 and overall, ADG and G:F for pigs fed the diets containing 300 or 450 ppm of Zn as Zn-PS did not differ (P > or = 0.29) from pigs fed the diet containing ZnO. Pigs fed the diet containing ZnO also had a greater Phase 2 (P < or = 0.10) and overall (P < or = 0.05) ADG and G:F than pigs fed the control diet. There were no differences (P > or = 0.46) in ADFI for any planned comparison. There were linear increases (P < 0.001) in the Zn excreted (mg/d) with increasing dietary Zn-PS. Pigs fed the diet containing ZnO absorbed, retained, and excreted more Zn (P < 0.001) than pigs fed the control diet or any of the diets containing Zn-PS. In conclusion, Phase 2 and overall growth performance by pigs fed diets containing 300 or 450 ppm Zn as Zn-PS did not differ from that of pigs fed 2,000 ppm Zn as ZnO; however, feeding 300 ppm Zn as Zn-PS decreased Zn excretion by 76% compared with feeding 2,000 ppm Zn as ZnO.     

The role of sulphide and sulphide oxidation in the copper molybdenum antagonism in rats and guinea pigs

The sulphide metabolism of rats fed molybdate up to levels of 1000 ppm molybdenum was examined and large decreases in hepatic sulphite oxidase activity observed; overall sulphide oxidation capacity was also reduced. Molybdate but not tungstate caused increases in the total plasma copper of guinea pigs but in particular the appearance of a new TCA-insoluble fraction. The effect was increased by the addition of 500 ppm sulphur as sulphide, to the molybdate diet whereas the addition of 500 ppm S as sulphate was ineffective. 100 ppm Mo was less effective as thiomolybdate (MoS4=) than as molybdate. The significance of these results in relation to the role of sulphide in the Cu-Mo-S interaction is discussed.     

Effects of source and level of copper on performance and liver copper stores in weanling pigs

Five 28- to 33-d experiments involving 460 crossbred pigs weaned at 28 +/- 2 d of age (initial weight, 6.7 to 8.1 kg) were conducted to determine the effects of feeding high dietary levels of Cu sulfate (CuSO4) or Cu oxide (CuO) on rate and efficiency of gain and liver Cu stores of weanling pigs. The pigs were housed in groups of five to six/pen and fed a fortified, unmedicated, corn-soybean meal-dried whey basal diet (1.1% lysine, 30 ppm Cu). In Exp. 1 and 2, pigs (eight replicates) were fed the basal or the basal plus 125 or 250 ppm Cu from CuSO4 or CuO for 28 d. In Exp. 3 and 4, four replications were fed the same diets as in Exp. 1 and 2 plus two additional diets (500 ppm Cu from CuSO4 or CuO). In Exp. 5, dietary levels of 0, 125, 250, 375 or 500 ppm Cu from CuSO4 were evaluated using four replications. At the end of each experiment, the liver from one pig in each pen was collected for Cu analysis. Overall, rate and efficiency of gain were improved (P less than .01) by feeding 125 or 250 ppm Cu as CuSO4, with the 125 ppm dietary level being about 75% as effective in stimulating growth as 250 ppm. Performance of pigs was not different from controls when the highest (500 ppm) level of Cu (from CuSO4) was fed. Liver Cu increased 10- to 70-fold when 250 to 550 ppm Cu from CuSO4 was included in the feed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of giving enrofloxacin in the diet to pigs experimentally infected with Actinobacillus pleuropneumoniae

Three groups of 16 pigs were exposed individually when four weeks old to intranasal infection with 10(8.9) viable Actinobacillus pleuropneumoniae (serovar 3, strain 2/(10P2); a fourth group was kept in isolation from the others as uninfected controls. Seven days later the 62 surviving animals were killed and necropsied. The organism had caused typical, mainly subacute disease in 12 of the 16 unmedicated animals but in only two of the 16 which had had continuous access to a diet containing 150ppm of enrofloxacin from four hours before exposure to infection, and in six of the 16 given 32 ppm enrofloxacin. However, only 150 ppm enrofloxacin produced marked control of the infection in terms of reduced average severity of thoracic lesions and much reduced prevalence of the organism in the lung at necropsy, and the mean weight gain (1.55 kg) and feed conversion efficiency (2.08) of this infected group over seven days were similar to those of the unmedicated, uninfected controls (1.67 kg and 2.25). The infected but untreated group on average produced detectable antibody seven days after infection whereas in the infected and medicated groups a specific response against serovar 3 was absent.     

微粒蒙脱石对猪组织铅水平、红细胞生成和肝脏ALA-D酶活性及铅诱导的脂质过氧化的影响

选60头体质量约33kg的“杜长大”杂交猪，随机分成2组，每组3个重复，一组饲以基础日粮＋10mg/kg铅＋0.5％微粒蒙脱石，另一组饲以基础日粮＋10mg／kg铅作为对照。研究结果表明：添加微粒蒙脱石组与对照组相比，明显降低了猪全血、脑、肝、肾、骨和毛等组织中铅含量：通过血细胞计数、血红素和血球容积测定表明，添加微粒蒙脱石组的红细胞生成显著增高，且肝脏中ALA—D酶活性显著提高。铅对肝脏的损伤作用明显。表现为丙二醛（MDA）含量显著升高（17．08％），过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）含量分别降低85．73％、52．17％、47．56％，而在日粮中添加微粒蒙脱石可以显著改善铅诱导的上述损伤。结果提示，微粒蒙脱石对铅中毒有潜在的治疗作用。     

Effect of inorganic selenium supplementation on selenosis in postweaning swine

A total of 72 pigs weaned at 4 wk of age were allotted by litter and weight to nine treatment groups and fed 20% protein cornsoybean meal diets supplemented with various levels of inorganic Se during a 37-d postweaning period. Eight groups were fed diets with 0, 2.5, 5.0, 7.5, 10, 15, 20 or 40 ppm Se provided as sodium selenite, while a ninth was offered the 0- and 40-ppm Se diets in separate feeders. Gains and feed intakes were similar during the trial for the 0- and 2.5-ppm Se diets. Both gain and feed intake declined as dietary Se levels above 5.0 ppm increased. At a dietary Se concentration of 40 ppm, feed consumption ceased within a few days of feeding and subsequent gains were negative. Pigs offered both the 0- and 40-ppm Se diets preferentially selected the basal as compared with the 40-ppm Se diet. When the feeders were switched at 28 d they refused the 40-ppm Se diet within a few hours. After a 17-d period, pigs fed the 20- or 40-ppm Se diet were not able to coordinate their walk, with many exhibiting an inability to stand. Alopecia was demonstrated in pigs fed 15 ppm Se or higher at 17 d, but was evident in the 5.0-ppm group at 37 d. At the termination of the trial, abnormal hoof formation at the coronary band was evident in pigs fed diets containing Se greater than or equal to 5 ppm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of various inclusion rates of organic zinc either as polysaccharide or proteinate complex on the growth performance, plasma, and excretion of nursery pigs

Three experiments were conducted to evaluate the effects of feeding dietary concentrations of organic Zn as a Zn-polysaccharide (Quali Tech Inc., Chaska, MN) or as a Zn-proteinate (Alltech Inc., Nicholasville, KY) on growth performance, plasma concentrations, and excretion in nursery pigs compared with pigs fed 2,000 ppm inorganic Zn as ZnO. Experiments 1 and 2 were growth experiments, and Exp. 3 was a balance experiment, and they used 306, 98, and 20 crossbred pigs, respectively. Initially, pigs averaged 17 d of age and 5.2 kg BW in Exp. 1 and 2, and 31 d of age and 11.2 kg BW in Exp. 3. The basal diets for Exp. 1, 2, and 3 contained 165 ppm supplemental Zn as ZnSO4 (as-fed basis), which was supplied from the premix. In Exp. 1, the Phase 1 (d 1 to 14) basal diet was supplemented with 0, 125, 250, 375, or 500 ppm Zn as Zn-polysaccharide (as-fed basis) or 2,000 ppm Zn as ZnO (as-fed basis). All pigs were then fed the same Phase 2 (d 15 to 28) and Phase 3 (d 29 to 42) diets. In Exp. 2, both the Phase 1 and 2 basal diets were supplemented with 0, 50, 100, 200, 400, or 800 ppm Zn as Zn-proteinate (as-fed basis) or 2,000 ppm Zn as ZnO (as-fed basis). For the 28-d Exp. 3, the Phase 2 basal diet was supplemented with 0, 200, or 400 ppm Zn as Zn-proteinate, or 2,000 ppm Zn as ZnO (as-fed basis). All diets were fed in meal form. In Exp. 1, 2, and 3, pigs were bled on d 14, 28, or 27, respectively, to determine plasma Zn and Cu concentrations. For all three experiments, there were no overall treatment differences in ADG, ADFI, or G:F (P = 0.15, 0.22, and 0.45, respectively). However, during wk 1 of Exp. 1, pigs fed 2,000 ppm Zn as ZnO had greater (P < or = 0.05) ADG and G:F than pigs fed the basal diet. In all experiments, pigs fed a diet containing 2,000 ppm Zn as ZnO had higher plasma Zn concentrations (P < 0.10) than pigs fed the basal diet. In Exp. 1 and 3, pigs fed 2,000 ppm Zn as ZnO had higher fecal Zn concentrations (P < 0.01) than pigs fed the other dietary Zn treatments. In conclusion, organic Zn either as a polysaccharide or a proteinate had no effect on growth performance at lower inclusion rates; however, feeding lower concentrations of organic Zn greatly decreased the amount of Zn excreted.     

Early- and traditionally weaned nursery pigs benefit from phase-feeding pharmacological concentrations of zinc oxide: effect on metallothionein and mineral concentrations.

Benefits of feeding pharmacological concentrations of zinc (Zn) provided by Zn oxide (ZnO) to 21-d conventionally weaned pigs in the nursery have been documented; however, several management questions remain. We conducted two experiments to evaluate the effect on growth from feeding 3,000 ppm Zn as ZnO during different weeks of the nursery period. In Exp. 1 (n = 138, 11.5 d of age, 3.8 kg BW) and Exp. 2 (n = 246, 24.5 d of age, 7.2 kg BW), pigs were fed either basal diets containing 100 ppm supplemental Zn (adequate) or the same diet with an additional 3,000 ppm Zn (high) supplied as ZnO. Pigs were fed four or two dietary phases in Exp. 1 and 2, respectively, that changed in dietary ingredients and nutrient content (lysine and crude protein) to meet the changing physiological needs of the pigs for the 28-d nursery period. Dietary Zn treatments were 1) adequate Zn fed wk 1 to 4, 2) high Zn fed wk 1, 3) high Zn fed wk 2, 4) high Zn fed wk 1 and 2, 5) high Zn fed wk 2 and 3, and 6) high Zn fed wk 1 to 4. In Exp. 1 and 2, pigs fed high Zn for wk 1 and 2 or the entire 28-d nursery period had the greatest (P < .05) ADG. During any week, pigs fed high Zn had greater concentrations of hepatic metallothionein and Zn in plasma, liver, and kidney than those pigs fed adequate Zn (P < .05). In summary, both early- and traditionally weaned pigs need to be fed pharmacological concentrations of Zn provided as ZnO for a minimum of 2 wk immediately after weaning to enhance growth.     

The effect of dietary ractopamine concentration and duration of feeding on growth performance, carcass characteristics, and meat quality of finishing pigs

A total of 400 barrows from Dekalb EB and 83 terminal sires mated to 43 and 45 maternal lines were used to evaluate the effects of dietary ractopamine (RAC; Paylean, Elanco Animal Health, Greenfield, IN) concentrations (0, 5, 10, or 20 ppm; as-fed basis) and feeding durations (6 to 34 d) on growth, efficiency, carcass, and meat quality characteristics of finishing pigs. Barrows were weighed and sorted into five weight blocks, each block consisting of 16 pens (five pigs per pen). Weight blocks were allocated to feeding duration treatments and assigned consecutively by weight from lightest to heaviest to represent 34, 27, 20, 13, and 6 d on test, respectively. The lightest and heaviest blocks averaged 79.8 and 103.8 kg, respectively, at the start of the test. Within a weight block, pens (four per treatment) were randomly assigned to one of four dietary concentrations of RAC in a basal diet containing 18.5% CP and 1.13% lysine. The experiment-wide target slaughter weight was 109 kg, and pigs and feeders were weighed weekly. Weight blocks (80 barrows per block) were slaughtered at a commercial packing plant after 6, 13, 20, 27, or 34 d on test. Overall, RAC supplementation improved (P < 0.05) ADG; however, ADG was not different (P > 0.08) from controls for pigs fed 5, 10, and 20 ppm RAC for 27, 34, and 6 d, respectively. During each feeding period, RAC-fed pigs had improved (P < 0.05) G:F, and, after 20, 27, and 34 d on test, pigs fed 20 ppm RAC had greater (P < 0.05) G:F compared with those fed 0 or 5 ppm RAC. Hot carcass weight was increased (P < 0.05) by RAC feeding after 13 and 27 d of feeding, and by feeding 10 and 20 ppm RAC after 20 d of feeding. After 34 d, pigs fed 20 ppm RAC had heavier (P < 0.05) hot carcass weight than pigs fed 10 ppm RAC. Fat-free lean estimates and the 10th-rib LM area were increased (P < 0.05) by feeding 10 and 20 ppm RAC after 27 d, and by feeding 20 ppm RAC after 34 d compared with controls. Japanese and American color scores, as well as L*, a*, and b* values of the LM, were not affected (P > 0.11) by 5 and 10 ppm RAC compared with controls during each feeding period. Visual marbling score for the LM was decreased (P < 0.05) when RAC was fed at 10 and 20 ppm compared with 0 ppm RAC when fed for 34 d. Dietary RAC improved growth performance at all feeding durations, whereas carcass composition was improved at longer feeding durations. In addition, 5 and 10 ppm RAC did not affect objective and subjective measures of pork quality.     

The effect of oxytetracycline on the severity of airsacculitis in chickens infected with Mycoplasma gallisepticum

Four groups of mycoplasma-free commercial broilers were challenged with the R strain of Mycoplasma gallisepticum (MG) at 14 days of age. Groups received feed containing either no medication, or 500 ppm or 1000 ppm oxytetracycline (OTC) beginning at age 13 days, or 1000 ppm OTC beginning at age 15 days. All broilers were vaccinated with a live mild Massachusetts infectious bronchitis vaccine at 17 days of age. Air sac lesions were scored at age 24 days. In two almost identical experiments, all OTC treatment groups had significantly lower mean air sac lesion scores than the unmedicated challenged controls. Groups that were fed 1000 ppm OTC in feed had significantly lower mean air sac lesion scores than groups that were fed 500 ppm OTC in feed. There was no significant difference in mean air sac lesion scores between the groups fed 1000 ppm OTC in feed beginning at 13 days of age and those fed 1000 ppm OTC in feed beginning at 15 days of age.     

Survival and postweaning performance of pigs from sows fed fat during late gestation and lactation

Sows were fed a control corn-soybean meal gestation diet to d 80 of gestation. One group of sows (n = 25) continued receiving the control diet until the end of lactation, whereas two groups were placed on other treatments. One group (n = 27) was fed a diet containing 5% added solid fat pellets from gestation d 80 through lactation, whereas another group (n = 25) was fed a diet with 10% added solid fat pellet from gestation d 100 through d 14 of lactation. Feed supply was 2.27 kg/d during gestation and to appetite during lactation. Pigs from sows fed the control diet or 5% solid fat pellet diet were weaned with an age range of 22 to 28 d and immediately allotted in a 2 x 3 factorially designed 4-wk feeding trial. Pigs from these two sow groups were fed diets 1) without fat, 2) with 4.5% choice white grease or 3) with 5% solid fat pellet. Sow weight loss, backfat change and pig weights were not different at weaning among treatments. Survival rates of all pigs to 21 d averaged 90% with no significant differences between treatments. Pigs from fat-fed sows had more (P less than .05) glycogen per gram of liver, 41% more total liver glycogen and 16% more serum glucose at birth. Weanling pigs from fat-fed sows grew slower (P less than .05) than pigs from control sows. Supplemental fat during gestation increased liver glycogen of pigs, which should help survival, but the feeding of fat throughout lactation had a negative effect on ADG during a 4-wk postweaning period.     

Experimental polychlorinated biphenyl toxicosis in germfree pigs.

The effects of polychlorinated biphenyls were studied in eight germfree pigs. Beginning at fourteen days of age, two pigs each were fed daily 12.5, 25, 50 and 100 mg/kg body weight of polychlorinated biphenyls as Aroclor 1254. Three germfree pigs were negative controls. Clinically the treated pigs had inappetance, a hemorrhagic diarrhea, erythema of the nose and the anus, retarded growth, distended abdomen and at the higher dose levels, incoordination and coma followed by death. Deaths occurred in 11 to 35 days after exposure. At necropsy, the piglets exhibited grossly enlarged mottled liver, erosions of the gastric mucosa, hemorrhages through the mesentery and the intestinal wall, a fibrinous pericarditis, a hypoplastic thymus and congested swollen thyroid glands. The histopathological lesions included hepatic centrolobular necrosis, interstitial myocarditis, endocarditis, myopathy of the muscles, gastric erosions and colitis. All of the organs examined for polychlorinated biphenyls had elevated residue levels which were particularly high in the fat, liver, psoas muscle, brain and kidney and were higher than has been reported in conventional pigs fed approximately equal concentrations of polychlorinated biphenyls. The severity of clinical signs, pathological changes and tissue concentrations were directly related to the dose administered and were more pronounced in the germfree pigs than has been described in conventional pigs.