Mastitis, Mammary Gland Immunity, and Nutrition Daniela Resende Bruno, DVM, Phd Texas Veterinary Medical Diagnostic Laboratory - Amarillo
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The Mid-South Ruminant Nutrition Conference does not support one product over another and any mention herein is meant as an example, not an endorsement. Mastitis, Mammary Gland Immunity, and Nutrition Daniela Resende Bruno, DVM, PhD Texas Veterinary Medical Diagnostic Laboratory - Amarillo INTRODUCTION the mastitis depends on the animal response to the insult, for example the entrance and installation of the Although intensive research and prevention pathogen inside the gland, and on virulence factors measures have been carried out for decades to control present on the bacteria. bovine mastitis, it continues to cause the biggest economic impact to the dairy industry worldwide. There are various genetic, physiological, and Severe economic losses, which are estimated to be environmental factors that can compromise host approximately $200/cow/yr in the United States, are defense mechanisms during the functional transitions due to reduced milk production, discarded milk, of the mammary gland (Sordillo, 2005). Nowadays, replacement costs, extra labor, treatment, and the lactating cow has been genetically selected to veterinary service costs (Smith and Hogan, 2001). In produce more milk, which is the basis of the dairy addition, mastitis increases the risk of antibiotic industry. However this increase in milk volume residues in milk due to treatments and decreases milk metabolically stresses dairy cows and affects quality due to an increase in somatic cell count, as mammary gland immunity by impairing defense well as proteolytic and lipolytic enzymes, which mechanisms decreasing the resistance to mastitis increase the enzymatic breakdown of milk protein (Heringstad et al., 2003). In addition, the milking and fat (National Mastitis Council, 1991). procedure can cause trauma to teat and tissues, making it easier for the invasion and colonization of Intramammary infections (IMI) result in a mastitis causing pathogens in the mammary gland. typical inflammatory response characterized by an influx of somatic cells composed primarily of Housing is also a factor that aggravates the neutrophils accompanied by variable numbers of incidence of mastitis, first due to excess numbers of macrophages and lymphocytes (Rainard and Riollet, animals in a limited space; and also because of the 2003). The response is driven by the action of a use of bedding material that easily allows for variety of inflammatory mediators including bacterial survival and growth, which over exposes cytokines, chemokines, prostaglandins, and animals and challenges their immune defense leukotrienes; all of which play pivotal roles in mechanisms (Hogan and Smith, 2003). Prevention of mammary gland defenses by mediating and intramammary infections leads to better milk quality, regulating inflammation and immunity. The ensuing which in turn is beneficial for the dairy industry inflammatory response induced by entry of bacteria because high quality milk means extended shelf life, into the mammary gland is variable; the intensity increased cheese yield, and increased consumption of typically dictating an outcome ranging from dairy products. successful elimination of the pathogen to establishment of chronic infection. There are several factors both infectious and non-infectious, that can cause bovine mastitis; and There are 2 groups of bacterial pathogens that there is an increase in the evidence that nutritional can cause mastitis in dairy cows: contagious factors are associated with mastitis in cows and pathogens such as Streptococcus agalactiae, heifers (Heinrichs et al., 2009). Despite all the Mycoplasma bovis, and Staphylococcus aureus, and measures taken by dairy producers to prevent environmental pathogens such as Escherichia coli intramammary infections in their herds, it is not and Klebsiella sp. Contagious microorganisms reside always clearly understood that there is a strong on the skin of the teat and interior of the udder, and relationship between nutrition and susceptibility to are transmitted from cow-to-cow during the milking mastitis. When the consumption of minerals and procedure through milking equipment and milker’s vitamins by dairy cows is not optimal, it can have hands. Environmental pathogens are found in the negative effects on immunity. Animals become more environment, such as in the cattle shed and milking susceptible to diseases such as mastitis, because a parlor; and, in an opportunistic way, enter the teat depressed immune system is not able to fight off canal when the cow comes in contact with a bacteria that invade the udder. contaminated environment (Table 1). The severity of 2010 Mid-South Ruminant Nutrition Conference 19 Arlington, Texas The Mid-South Ruminant Nutrition Conference does not support one product over another and any mention herein is meant as an example, not an endorsement. Table 1: Differences between contagious and environmental mastitis Contagious Environmental Microorganisms Staphylococcus aureus Escherichia coli Streptococcus agalactiae Klebsiella pneumoniae Mycoplasma bovis Klebsiella oxytoca Streptococcus uberis Streptococcus disgalactiae Enterococcus faecalis Enterococcus faecium Candida, yeast Corynebacterium pyogenes Primary source Udders of infected cows The environment of the cow Indicators of problem Bulk tank SCC > 300,000 cells/ml; High rate of clinical mastitis, usually in early Frequent cases of clinical mastitis, often in lactation or during hot weather; the same cows; and Large numbers of dry cows that have mastitis Bacterial culturing results shows S. during the early dry period; and agalactiae and/or S. aureus infections. Increase in the herd's somatic cell. Control Develop program to prevent the spread of Reduce the number of bacteria to which the bacteria at milking time. teat end is exposed. Eliminate existing infections by treating all Improve cleanliness of cow surroundings, cows at dry-off and culling chronic cows. especially in late dry period and at calving. Improve pre-milking procedures to ensure clean, dry teats are being milked. Researchers have studied the relationship On the other hand, the acquired immunity also known between the supplementation of trace minerals and as specific immunity, is the basis of vaccination. It vitamins and immune system function and mammary recognizes specific determinants of a pathogen that gland health. Several studies have shown that activate a selective response leading to its susceptibility to intramammary infections can be elimination. Antibodies, macrophages, and influenced by the levels of vitamins A and E and lymphocytes recognize pathogenic factors and incite minerals such as Se, Cu, and Zn in the diet. The a response. This type of immunity has memory, and results obtained from those experiments were used to is increased by repeated exposure to the same establish the daily intake requirements of minerals pathogen. and vitamins for dairy cows, and are published in the most recent dairy cattle version of the National As part of the innate immune system, physical Research Council (NRC, 2001). barriers of the udder, including teat skin, teat sphincter muscle, and keratin plug, work together to IMMUNITY OF THE MAMMARY GLAND prevent bacterial entrance (Figure 1). However, failure in their normal function results in Defense mechanisms can be divided into innate intramammary infection. Abrasion and cracks on teat immunity and acquired immunity. The innate skin favor bacterial colonization, increasing the risk immunity, also known as non-specific immunity, is of bacterial entrance, mainly between milking the predominant defense during early stages of procedures when the duct is dilated. Another infection. This first defense is activated quickly at the protective factor on the teat is the keratin plug, which site of infection by numerous stimuli; however, it is secreted by cells that line the teat. This substance does not have memory and is not increased by has bactericidal properties, and also entraps and repeated exposure to the same insult. This non- prevents the upward movement of bacteria into the specific defense is initiated at the teat end, which is a mammary gland decreasing the chance of physical barrier, and continues with immune cells intramammary infections, consequently decreasing such as macrophages, neutrophils, natural killer (NK) somatic cell count (SCC) (Kellogg et al., 2004). cells, and by other soluble factors, such as cytokines. 2010 Mid-South Ruminant Nutrition Conference 20 Arlington, Texas The Mid-South Ruminant Nutrition Conference does not support one product over another and any mention herein is meant as an example, not an endorsement. the teat breaks down and the teat canal is open for the entrance of mastitis pathogens (Figure 2). In addition to impaired neutrophil function, decreased lymphocyte responsiveness to mitogen stimulation contributes to this increased susceptibility to new intramammary infections (Mallard et al., 1998). Increased production of reactive oxygen species (ROS), the so called free radicals, is expected in late pregnancy, parturition, and initiation of lactation due to metabolic demands on these stages of lactation Figure 1: Physical barriers of the mammary gland (Sordillo and Aitken, 2009). New intramammary infections during the periparturient period have a For the best protection of the mammary gland significant impact on milk production efficiency due against intramammary infections, innate and acquired to the damage on milk producing cells (Oliver and immune systems must interact in a synchronized Sordillo,