Exploration of the hypothalamic–pituitary–adrenal function as a tool to evaluate animal welfare

Intramammary infections of dairy cows with Gram-positive bacteria such as Staphylococcus aureus (major cause of mastitis) have received a lot of attention because of their major economic impact on the dairy farm through production losses induced by an increase in somatic cell count. Management strategies, including greater awareness for efficient milking and hygienic measures, have limited the spread of Gram-positive bacteria and resulted in a significant decrease of proportion of S. aureus isolates and subclinical mastitis worldwide. Other organisms such as coliform subspecies and Streptococcus uberis, both environmental bacteria that cause clinical mastitis, have received less attention. Escherichia coli causes inflammation of the mammary gland in dairy cows around parturition and during early lactation with striking local and sometimes severe systemic clinical symptoms. This disease affects many high producing cows in dairy herds and may cause several cases of death per year in the most severe cases. It is well known that bacterial, cow and environmental factors are interdependent and influence mastitis susceptibility. Many studies, executed during the last decade, indicate that the severity of E. coli mastitis is mainly determined by cow factors rather than by E. coli pathogenicity. During E. coli mastitis, the host defense status is a cardinal factor determining the outcome of the disease. Today, we know that the neutrophil is a key factor in the cows' defense against intramammary infection with E. coli. Effective elimination of the pathogen by neutrophils is important for the resolution of infection and the outcome of E. coli mastitis. This review is a compilation of some major findings over the last 15 years concerning mainly host factors that modulate and influence neutrophil function and the mammary inflammatory reaction. The individual chapters address: virulence factors of E. coli strains, how neutrophils kill E. coli, connection between endotoxins, tumor necrosis factor-alpha and nitric oxide, severity classification of E. coli mastitis, lifespan of neutrophils, host factors that influence severity, tissue damage and production loss.

https://hal.archives-ouvertes.fr/hal-00902764/document

Severity of E. coli mastitis is mainly determined by cow factors

Migration of polymorphonuclear neutrophil leukocytes (PMN) into the mammary gland provide the first line of defense against invading mastitis pathogens. Bacteria release potent toxins that activate white blood cells and epithelial cells in the mammary gland to secrete cytokines that recruit PMN that function as phagocytes at the site of infection. While freshly migrated PMN are active phagocytes, continued exposure of PMN to inhibitory factors in milk such as fat globules and casein, leads to altered PMN morphology and reduced phagocytosis. In the course of phagocytosing and destroying invading pathogens, PMN release chemicals that not only kill the pathogens but that also cause injury to the delicate lining of the mammary gland. This will result in permanent scarring and reduced numbers of milk secretory cells. The life span of PMN is limited by the onset of apoptosis. To minimize damage to mammary tissue, PMN undergo a specialized process of programmed cell death known as apoptosis. Macrophages quickly engulf and phagocytose apoptotic PMN, thereby minimizing the release of PMN granular contents that are damaging to tissue. The PMN possess an array of cell surface receptors that allow them to adhere and migrate through endothelium and to recognize and phagocytose bacteria. One receptor found on phagocytes that is receiving considerable attention in the control of infections by Gram-negative bacteria is CD14. Binding of lipopolysaccharide (LPS) to membrane bound CD14 causes release of tumor necrosis factor-alpha and sepsis. Binding of LPS to soluble CD14 shed from CD14-bearing cells results in neutralization of LPS and rapid recruitment of PMN to the site of infection. Recent advances in the fields of genomics and proteomics should greatly enhance our understanding of the PMN role in controlling intramammary infections in ruminants. Further, manipulation of PMN, through either recombinant proteins such as soluble CD14 that enhance PMN response or agents that mediate PMN apoptosis, may serve as novel therapeutics for the treatment of mastitis.

/pdf/the-bovine-neutrophil-structure-and-function-in-blood-and-dmtklxina0.pdf

The bovine neutrophil: Structure and function in blood and milk.

I. Introduction MILK and colostrum contain a variety of proteins, peptides, and steroids that possess biological activity. In studies in which the concentration of hormone/growth factor has been measured in both colostrum and milk, the highest concentrations occur in colostrum (1). This review will discuss pituitary, hypothalamic, pancreatic, thyroid, parathyroid, adrenal, gonadal, and gut hormones as well as growth factors, prostaglandins, and neuropeptides found in milk (see Table 1). Other biologically important proteins and peptides in milk such as the immunoglobulins, allergins, opiates, enzymes, casomorphins, and cyclic nucleotides will not be addressed. The reader is referred to excellent recently published reviews regarding hormones and other bioactive substances present in milk (2–4). Of the hormones and growth factors present in milk many exist in concentrations that exceed those found in maternal plasma (see Table 2). Some are rapidly transported into milk from the maternal circulation unchange...

Hormones and Growth Factors in Milk

Somatic cells of goat and sheep milk: Analytical, sanitary, productive and technological aspects ☆

Effect of Parity, Stage of Lactation, and Intramammary Infection on Concentration of Somatic Cells and Cytoplasmic Particles in Goat Milk

SummaryA mammary quarter in each of 4 cows was infused with 0.5 mg E. coli endotoxin to determine its effect on plasma corticosteroids, circulating leukocytes and milk somatic cells. At 1.5 hr following endotoxin infusion, segmented neutrophils decreased 23%, and by 5 hr dropped 93%. A shift left in the differential circulating leukocyte count began at 2.5 hr and reached maximum proportions between 18-24 hr postendotoxin infusion. Circulating lymphocytes, monocytes and eosinophils were all depressed in response to endotoxin. Plasma corticosteroid concentrations increased (P < 0.01) 2 hr following endotoxin infusion, reached maximum concentrations at 4 hr, then returned to prein-fusion concentrations by 12 hr. The initial decrease in circulating lymphocytes at 2.5 hr was not attributed to the lytic effect of the plasma corticosteroids, since depressions in circulating lymphocytes occurred too soon (0.5 hr) after the increase in plasma corticosteroids. The high plasma corticosteroid concentration appeared t...

WD Schultze

Papers

Effect of Parity, Stage of Lactation, and Intramammary Infection on Concentration of Somatic Cells and Cytoplasmic Particles in Goat Milk

Plasma corticosteroid, circulating leukocyte and milk somatic cell responses to Escherichia coli endotoxin induced mastitis

Mastitis infection from abrupt loss of milking vacuum.

Development of natural defense mechanisms

Effect of intramammary device on new infection rate milk yield, and milk somatic cell counts in Maryland dairy herds