8 research outputs found

    Effects of two different rearing protocols for Holstein bull calves in the first 3 weeks of life on health status, metabolism and subsequent performance

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    The aim of this study was to investigate the impact of weight gain of calves within the first 3 weeks of life on health status and subsequent performance. Holstein bull calves were reared either intensively (IR; individual hutches and ad libitum milk feeding for the first 3 weeks of life; n = 24), or according to the established protocol [ER; 4 l milk/day in hutches during week 1 and 720 g/day milk replacer (MR) from day 8 to 21 in a group pen; n = 24]. Water, hay and concentrates were freely available to all calves. From week 4, calves of both groups were housed together in a group pen and fed 720 g MR/day; step-down weaning was performed between week 5 and 10. Key metabolic blood parameters were analysed on day 2, 12, 21 and 70 of life. After weaning, all animals were fed concentrates and corn silage until slaughter at an age of 8 months. Within the first 3 weeks, average daily weight gain was threefold higher in IR calves in relation to ER calves (1.28 vs. 0.38 kg/day, p < 0.001). Neither incidence nor duration of scouring differed significantly between groups. Starter intake (week 4–10) was higher in IR calves in relation to ER calves (49.7 vs. 38.0 kg/calf, p = 0.006). Serum glucose, urea, albumin and insulin were higher at an age of 21 days in IR calves in relation to ER calves; no differences were obvious at an age of 70 days. Plasma GH and IGF-I concentrations revealed an uncoupling of the somatotropic axis in ER calves within the first 3 weeks of life. At slaughter, body weight of IR calves tended to be higher than that of the ER calves (320 vs. 309 kg, p = 0.07). In conclusion, intensive feeding and individual housing during the first 3 weeks of life had positive long-term effects on subsequent performance

    Effect of preweaned dairy calf housing system on antimicrobial resistance in commensal Escherichia coli

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    Group housing of preweaned dairy calves is a growing practice in the United States. The objective of this practice is to increase the average daily gain of calves in a healthy and humane environment while reducing labor requirements. However, feeding protocols, commingling of calves, and occurrence of disease in different calf-housing systems may affect the prevalence of antimicrobial drug-resistant bacteria. This study evaluated the effect of a group pen-housing system and individual pen-housing system on antimicrobial resistance trends in fecal Escherichia coli of preweaned dairy calves and on the prevalence of environmental Salmonella. Twelve farms from central New York participated in the study: 6 farms using an individual pen-housing system (IP), and 6 farms using a group pen-housing system (GP). A maximum of 3 fecal E. coli isolates per calf was tested for susceptibility to 12 antimicrobial drugs using a Kirby-Bauer disk diffusion assay. Calves in GP had a significantly higher proportion of E. coli resistant to ciprofloxacin and nalidixic acid, whereas calves in IP had a significantly higher proportion of E. coli resistant to ampicillin, ceftiofur, gentamycin, streptomycin, and tetracycline. Calf-housing system had an effect on resistance to individual antimicrobial drugs in E. coli, but no clear-cut advantage to either system was noted with regard to overall resistance frequency. No outstanding difference in the richness and diversity of resistant phenotypes was observed between the 2 calf-housing systems

    Hereditary Neurohypophyseal Diabetes Insipidus

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    Neurohypophyseal diabetes insipidus (DI) is most often caused by trauma, including operations, and infiltrating processes in the hypothalamic-pituitary region. Irradiation, ischemia, infections, or autoimmunity can also underlie the disease. Since the middle of the 19th century, familial forms of neurohypophyseal DI have been described. Most commonly, the disease is transmitted in an autosomal-dominant fashion; very rarely, autosomal-recessive inheritance has been observed. Hereditary neurohypophyseal DI is caused by mutations in the gene encoding the antidiuretic hormone vasopressin (AVP) and its carrier protein neurophysin II (NPII). Symptoms result from the lack of hormone, or from the inability of mutant AVP to activate its renal receptor, and respond to treatment with desmopressin (DDAVP). Dominant mutations cause retention of the hormone precursor in the endoplasmic reticulum (ER) of vasopressinergic neurons in the hypothalamus, resulting in cellular dysfunction and eventually neuronal death. This so-called "neurotoxicity hypothesis" was initially established on the basis of autopsy studies in affected humans and has been supported by heterologous cell-culture expression experiments and murine knock-in models. Current data show that retained mutants fail to be eliminated by the cell's quality control system and accumulate in fibrillar aggregations within the ER. Autosomal-dominant neurohypophyseal DI may thus be viewed as a neurodegenerative disease confined to vasopressinergic neurons

    Invited review: Influence of climatic conditions on the development, performance, and health of calves

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    Invited review: Effects of group housing of dairy calves on behavior, cognition, performance, and health

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