Effects of water and diet acidification with and without antibiotics on weanling pig growth and microbial shedding

Two 5-wk experiments were conducted to determine the effects of water and diet acidification with and without antibiotics on weanling pig growth performance and microbial shedding. In Exp. 1, 204 pigs (19.2 d of age) were used in a 3 x 2 factorial, with 3 dietary treatments fed with or without water acidification (2.58 mL/L of a propionic acid blend; KEM SAN, Kemin Americas, Des Moines, IA). Dietary treatments were: 1) control, 2) control + 55 ppm of carbadox (CB), and 3) dietary acid [DA; control + 0.4% organic acid-based blend (fumaric, lactate, citric, propionic, and benzoic acids; Kemin Americas)] on d 0 to 7 followed by 0.2% inorganic acid-based blend (phosphoric, fumaric, lactic, and citric acids; Kemin Americas) on d 7 to 34. In Exp. 2, 210 pigs (average 18.3 d of age) were fed 1 of 3 dietary treatments: 1) control, 2) control + 55 ppm of CB, and 3) control + 38.6 ppm of tiamulin + 441 ppm of chlortetracycline on d 0 to 7 followed by 110 ppm of chlortetracycline on d 7 to 35 (TC) with or without dietary acidification (same as Exp. 1) in a 3 x 2 factorial arrangement of treatments. For both experiments, the pigs were allotted based on genetics, sex, and initial BW [5.5 kg (Exp. 1) or 5.6 kg (Exp. 2)]. Pigs were housed at 6 or 7 (Exp. 1) and 7 (Exp. 2) pigs/pen. Treatments were fed in 3 phases: d 0 to 7, 7 to 21, and 21 to 35 (34 d, Exp. 1). Fecal grab samples were collected from 3 pigs/pen on d 6, 20, and 33 for measurement of pH and Escherichia coli. During phase 3 and overall in Exp. 1, pigs fed CB had greater (P < 0.001) ADG (overall ADG, 389 vs. 348, and 348 g/d, respectively), ADFI (P < 0.007, 608 vs. 559, and 554 g/d, respectively), and d 34 BW (P < 0.001, 18.8 vs. 17.3, and 17.3 kg, respectively) than pigs fed NC and DA. Phase 3 ADG was improved (P < 0.01) by water acidification across all diets. In Exp. 2, pigs fed CB and TC had greater ADG (P < 0.004; 315 and 303 vs. 270 g/d, respectively), ADFI (P < 0.01), and d 35 BW (P < 0.002; 16.7 and 16.2 vs. 15.1 kg, respectively) than pigs fed NC. There was a tendency (P < 0.08) for an improvement in ADG when DA was added to the NC or TC, but decreased ADG when DA was added to CB.     

Effect of chromium picolinate and chromium propionate on glucose and insulin kinetics of growing barrows and on growth and carcass traits of growing-finishing barrows

Two experiments were conducted to determine the effects of dietary Cr tripicolinate (CrPic) or Cr propionate (CrProp) on growth, carcass traits, plasma metabolites, glucose tolerance, and insulin sensitivity in pigs. In Exp. 1, 36 barrows (12 per treatment; initial and final BW were 20 and 38 kg) were allotted to the following treatments: 1) corn-soybean meal basal diet (control), 2) as 1 + 200 ppb Cr as CrPic, or 3) as 1 + 200 ppb Cr as CrProp. Growth performance data were collected for 28 d, and then 23 pigs (seven, eight, and eight pigs for treatments 1, 2, and 3, respectively) were fitted with jugular catheters and a glucose tolerance test (500 mg glucose/kg BW) and an insulin challenge test (0.1 IU of porcine insulin/kg BW) were conducted. Both CrPic and CrProp decreased (P < 0.05) ADG and ADFI but did not affect gain:feed (P > 0.10). Fasting plasma glucose, total cholesterol, urea N, insulin, and high-density lipoprotein cholesterol:total cholesterol concentrations were not affected (P > 0.10) by either Cr source. Pigs fed CrPic had lower (P < 0.02) fasting plasma NEFA concentrations than control pigs, but plasma NEFA concentrations of pigs fed CrProp were not affected (P > 0.10). During the glucose tolerance test, glucose and insulin kinetics were not affected by treatment (P > 0.10). During the insulin challenge test, glucose clearance was increased (P < 0.01) in pigs fed CrProp but not affected (P > 0.10) in pigs fed CrPic. Glucose half-life was decreased (P < 0.03) in pigs fed CrPic or CrProp, but insulin kinetics were not affected (P > 0.10). In Exp. 2, 48 barrows (four replicates of four pigs per replicate; initial and final BW were 23 and 115 kg) were allotted to the same dietary treatments in a growing-finishing study. Average daily gain, ADFI, and gain:feed were not affected (P > 0.10) by treatments. Carcass length tended (P = 0.10) to be greater in pigs fed CrPic than in pigs fed CrProp, but other carcass measurements were not affected (P > 0.10). Glucose kinetics from the insulin challenge test indicate that both CrPic and CrProp increase insulin sensitivity and that both Cr sources are bioavailable.     

Involvement of ATP‐sensitive K+ channels in the peripheral antinociceptive effect induced by ketamine

ObjectiveTo investigate the contribution of K⁺ channels on peripheral antinociception induced by ketamine.Study designProspective experimental study.Animals110 male Wistar rats weighing 160–200 g.MethodsThe paw pressure required to elicit limb flexion was designated as the nociceptive threshold. Hyperalgesia was induced by intraplantar injection of prostaglandin E₂. All drugs were administered locally into the right hind paw of rats. Ketamine was administered into the right hind paw 2 hours and 55 minutes after local injection of PGE₂. Tetraethylammonium was administered 30 minutes prior to ketamine and the other K⁺ channel blockers, glibenclamide, dequalinium and paxilline, were administered 5 minutes prior to ketamine.ResultsProstaglandin E₂ (2 μg per paw) induced hyperalgesia. Ketamine (10, 20, 40 and 80 μg per paw) elicited a local peripheral antinociceptive effect that was antagonized by a specific blocker of ATP‐sensitive K⁺ channels, glibenclamide (20, 40 and 80 μg per paw). In another experiment, the non‐selective voltage‐dependent K⁺ channel blocker tetraethylammonium (30 μg per paw) and small and large conductance blockers of Ca²⁺‐activated K⁺ channels, dequalinium (50 μg per paw) and paxilline (20 μg per paw), were ineffective at blocking the effect of a local ketamine injection.Conclusions and clinical relevanceAnalysis of these results provides evidence that ketamine, may in part, induce peripheral antinociceptive effects by ATP‐sensitive K⁺ channel pathway activation.     

Skeletal deformities associated with nutritional congenital rickets in newborn lambs

Abstract

CASE HISTORY: A group of 545 pregnant rising 2-year-old Coopdale ewes on a Southland sheep farm were grazed over winter on a fodder beet (Beta vulgaris) crop. Subsequently, 45 out of approximately 750 lambs were born with a variety of skeletal deformities, including shortened limbs, varus and valgus angular limb deformities, palmar grade stance and cranial bowing of the carpus. Analysis of the crop showed the fodder beet contained a low percentage of phosphorus. In addition, 60 out of 460 rising 2-year-old ewes that had been grazed on the fodder beet crop as 1-year-olds had incisor abnormalities and malocclusion.

PATHOLOGICAL FINDINGS: Two affected lambs (1-day-old and 3-days-old) with representative clinical signs examined postmortem were found to have markedly enlarged costochondral junctions, and noticeably enlarged long bone metaphyses. In addition, one lamb had a dense band of metaphyseal sclerosis beneath the physes of all long bones examined. Histopathological findings included small islands and columns of chondrocytes and eosinophilic cartilage matrix present in the metaphysis. Metaphyseal trabeculae were disorganised and often lined by accumulations of pale pink osteoid; similar pale pink osteoid was also present in the cortices. Unerupted molar teeth in the affected lambs lacked a layer of enamel, and the dentine was irregular with globular basophilia.

DIAGNOSIS: The gross and histopathological lesions were consistent with a diagnosis of rickets.

CLINICAL RELEVANCE: Nutritional congenital rickets has not been previously diagnosed in sheep, but is a recognised disease of human infants with vitamin D deficient mothers. The rickets in affected lambs was most likely associated with phosphorus deficiency as a result of the pregnant ewes grazing fodder beet during gestation. While vitamin D deficiency was not definitively ruled out in these cases, practitioners are alerted to the possible effects of feeding phosphorus-deficient fodder beet to ewes for long periods during gestation and to 1-year-old sheep during important growth periods.     

Detection of Aphanomyces invadans and epizootic ulcerative syndrome in the Murray‐Darling drainage

Epizootic ulcerative syndrome was diagnosed, and the presence of Aphanomyces invadans confirmed, from an outbreak of clinical disease in wild‐caught bony bream (Nematalosa erebi) from the Darling River near Bourke, in New South Wales, Australia, during 2008. This confirms a significant extension of the agent beyond its historical range.     

Femtosecond dynamics of electron localization at interfaces

The dynamics of two-dimensional small-polaron formation at ultrathin alkane layers on a silver(111) surface have been studied with femtosecond time- and angle-resolved two-photon photoemission spectroscopy. Optical excitation creates interfacial electrons in quasi-free states for motion parallel to the interface. These initially delocalized electrons self-trap as small polarons in a localized state within a few hundred femtoseconds. The localized electrons then decay back to the metal within picoseconds by tunneling through the adlayer potential barrier. The energy dependence of the self-trapping rate has been measured and modeled with a theory analogous to electron transfer theory. This analysis determines the inter- and intramolecular vibrational modes of the overlayer responsible for self-trapping as well as the relaxation energy of the overlayer molecular lattice. These results for a model interface contribute to the fundamental picture of electron behavior in weakly bonded solids and can lead to better understanding of carrier dynamics in many different systems, including organic light-emitting diodes.