Pathogenesis: A Microscopic Look at Mastitis
The external progression of mastitis is well known by farmers, veterinarians and researchers alike.
A cow picks up a pathogen, somatic cell count increases, the udder becomes inflamed and milk quality and production decreases. Less widely known however is what is actually occurring at a cellular level inside the udder in response to the infection.
A cow’s main external defense mechanism is the keratin plug in the teat that provides a physical barrier to prevent bacteria migrating into the teat. Due to the time taken for the plug to reform after milking (30 mins to 2 hours), as well as any chemical, physical, or thermal injury to the teat, there are still opportunities for pathogens to invade. Once the bacteria penetrate the teat and migrate into the udder glands and cisterns, the immune system is responsible for identifying and fighting the infection.
Somatic cells are a mixture of epithelial cells (naturally shed from the udder lining) and leukocytes (immune cells). Some leukocytes are always present in the udder and can be further subdivided 3 types of cells- lymphocytes, macrophages and neutrophils. Macrophages are responsible for circulating throughout the udder and recognizing any foreign cells such as pathogens. They then release chemical signals which trigger the movement of neutrophils from blood vessels into the udder to destroy the pathogens.
This increase in the number of immune cells manifests externally as elevated SCC in cows with mastitis as well as the appearance of flakes and clots in the milk seen in clinical cases. However, both the actual infection by the pathogens and the associated immune response have the potential to cause extensive tissue damage and have a detrimental effect on the secretory ability of the udder glands to synthesize milk.
When the initial immune response is ineffective, a prolonged response is initiated which includes the release of cytokines. Cytokines are components that promote cellular inflammation, manifesting as the telltale external sign of clinical mastitis—a hot, inflamed udder. The cellular inflammation is induced to make the udder environment hostile to the invading bacteria, which are unable to exist at high temperatures (usually around 40⁰C - 45⁰C).
The high temperature causes structural proteins of the bacteria to break down. However, this inflammation also denatures the milk proteins, leading to decreased manufacturing properties and lower quality products.
Understanding mastitis at a cellular level helps make sense of the external physical changes seen as clinical mastitis. Having the whole picture gives a greater understanding of the risk factors, disease progression and long-term effects of the disease, so you can implement an effective milk quality control program.
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.
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About the Author
Anna Schwanke 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.
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