Dissecting the Effects of Mastitis
Mastitis is a major cause of economic loss in the dairy industry with approximately 60% of this is due to decreased milk production (Akers & Nickerson, 2011). The external effects of mastitis (heat, swelling and hardness of the udder) are useful for diagnosing the disease, but it is the internal effects of mastitis on the udder that have a detrimental effect on milk quality and yield.
Normal milk production depends on both the mammary vascular and secretory systems. Milk synthesis relies on the proliferation of epithelial (udder tissue) cells and it is estimated that 400L of blood must flow through the blood vessels of the udder to produce just 1L of milk (Agricultural & Horticulture Development Board, 2016). Pathogen infection and immune response can damage these internal vascular and secretory structures, negatively impacting their function which leads to decreased milk quality and production.
Changes to Udder Structure & Function
Decreased milk production due to mastitis is the consequence of physical damage to the udder glands responsible for synthesizing milk. Some pathogens (especially Staphylococcus aureus) produce powerful toxins that damage the internal udder tissue and can make the pathogen resistant to destruction by the immune system.
Damage can also be done through the immune response when tough fibrin tissue accumulates around the ducts and glands in an effort to restrict the growth of bacteria. This can eventually form scar tissue, making the secretory cells non-functional and even forming reservoirs where pathogens can lie dormant out of the reach of immune system cells. These reservoirs are major contributors to the flare-ups of chronically infected cows.
Internal damage can also have detrimental effects on the quality of milk produced. Tissues affected by pathogenic toxins have increased vascular permeability, leading to the breakdown of the barrier between blood and milk. This results in citrate and lactose molecules diffusing into blood capillaries, lowering their concentration in milk. The decreased synthetic capacity of the mammary glands also decreases the concentrations of fat and casein in milk.
Despite continual research and improvements to mastitis control programs, the disease is still the primary cause of decreased production. Cell damage and impaired function of the udder alters the synthesis of milk and its composition. These changes do not just affect milk production during the period of infection but can persist through multiple lactations with the potential to progressively decrease a cow’s production and milk quality for the rest of her life.
Diligently monitoring your herd’s SCC can help you diagnose and treat mastitis early, enhancing your milk quality control, and giving all of your cows a better chance to contribute more to your production for a longer time.
Are you having difficulties finding a solution to reduce your milk SCC levels? We offer instant, on-farm milk testing to help you take control of your business and implement effective milk quality control. Contact us, or visit our Dairy Health Check page for more information.
About the Author
Anna is an undergraduate student at the University of Guelph, Ontario. She is responsible for researching and writing about a wide variety of topics related to dairy cow welfare and management for Dairy Quality Inc. The 10 years she spent living in Australia, as well as her love of travelling, give her a firsthand viewpoint of issues facing the international dairy community. She plans to graduate from the University’s College of Physical & Engineering Science in 2019 and pursue a career in the Life Sciences or Agriculture industry.
Agricultural & Horticulture Development Board. (2016, June 07). Udder Physiology. Retrieved from Agriculture & Horticulture Development Board: Dairy: http://dairy.ahdb.org.uk/technical-information/animal-health-welfare/mastitis/symptoms-of-mastitis/udder-physiology/#.V1b0ACnmqM8
Akers, R. M., & Nickerson, S. C. (2011). Mastitis and its Impact on Structure and Function in the Ruminant Mammary Gland. Journal of Mammary Gland Biology Neoplasia, 275-289.
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