Stephen J. LeBlanc

Bio: Stephen J. LeBlanc is an academic researcher from University of Guelph. The author has contributed to research in topics: Dairy cattle & Ice calving. The author has an hindex of 47, co-authored 197 publications receiving 11123 citations. Previous affiliations of Stephen J. LeBlanc include Ontario Veterinary College & Wellington Management Company.

Monitoring Metabolic Health of Dairy Cattle in the Transition Period

Abstract: This paper reviews the importance of energy metabolism in transition dairy cows, its associations with disease and reproduction, and strategies for monitoring cows under field conditions during this critical time. Essentially all dairy cattle experience a period of insulin resistance, reduced feed intake, negative energy balance, hypocalcemia, reduced immune function, and bacterial contamination of the uterus soon before, or in the weeks after calving. One-third of dairy cows may be affected by some form of metabolic or infectious disease in early lactation. Routine, proactive actions, observations, or analysis are intended to accurately and efficiently provide early detection of problems, to provide an opportunity for investigation and intervention in order to limit the consequences and costs of health problems and reduced animal performance or welfare. Methods of early detection include monitoring of disease and culling records, feed intake, milk production, body condition, and simple metabolic tests. Methods, strategies, and interpretation of measurement of peripartum concentrations of non-esterified fatty acids (NEFA) and beta-hydroxybutyrate (BHB) as indicators of aspects of energy status and disease risk are reviewed. High NEFA (> 0.4 mmol/l) in the last 7 to 10 days before expected calving is associated with increased risk of displaced abomasum (DA), retained placenta, culling before 60 days in milk, and less milk production in the first 4 months of lactation. Subclinical ketosis (serum BHB >1200 to 1400 micromol/l) in the first or second week after calving is associated with increased risk of DA, metritis, clinical ketosis, endometritis, prolonged postpartum anovulation, increased severity of mastitis, and lower milk production in early lactation. There are several validated and practical tools for cow-side measurement of ketosis.

Nutrient requirements of dairy cattle

Abstract: Nutrient requirements of dairy cattle , Nutrient requirements of dairy cattle , مرکز فناوری اطلاعات و اطلاع رسانی کشاورزی

Defining Postpartum Uterine Disease and the Mechanisms of Infection and Immunity in the Female Reproductive Tract in Cattle

Abstract: Uterine microbial disease affects half of all dairy cattle after parturition, causing infertility by disrupting uterine and ovarian function. Infection with Escherichia coli, Arcanobacterium pyogenes, and bovine herpesvirus 4 causes endometrial tissue damage. Toll-like receptors on endometrial cells detect pathogen-associated molecules such as bacterial DNA, lipids, and lipopolysaccharide (LPS), leading to secretion of cytokines, chemokines, and antimicrobial peptides. Chemokines attract neutrophils and macrophages to eliminate the bacteria, although persistence of neutrophils is associated with subclinical endometritis and infertility. Cows with uterine infections are less likely to ovulate because they have slower growth of the postpartum dominant follicle in the ovary, lower peripheral plasma estradiol concentrations, and perturbation of hypothalamic and pituitary function. The follicular fluid of animals with endometritis contains LPS, which is detected by the TLR4/CD14/LY96 (MD2) receptor complex on granulosa cells, leading to lower aromatase expression and reduced estradiol secretion. If cows with uterine disease ovulate, the peripheral plasma concentrations of progesterone are lower than those in normal animals. However, luteal phases are often extended in animals with uterine disease, probably because infection switches the endometrial epithelial secretion of prostaglandins from the F series to the E series by a phospholipase A2-mediated mechanism, which would disrupt luteolysis. The regulation of endometrial immunity depends on steroid hormones, somatotrophins, and local regulatory proteins. Advances in knowledge about infection and immunity in the female genital tract should be exploited to develop new therapeutics for uterine disease.