Mastitis is most often associated with disease of the udder recognized as either subclinical or clinical disease resulting in reduced milk production and potentially a sick cow.
We previously defined (“Equip your toolbox for managing mastitis,” Aug. 7, 2017, issue) subclinical mastitis as an elevated somatic cell count (SCC: >200,000 cells/mL) with normal-looking milk, whereas clinical mastitis was described as the cow potentially showing clinical disease signs and with physical changes to the milk (clots, clear or reddish color) and possibly the udder (heat, swelling, redness). The impacts of mastitis extend much further than just cow disease and lost milk production.
Inflammation: Friend or foe in milk composition?
The process of mastitis is inflammatory in nature where the udder’s activated immune response induces a range of physical and biochemical changes to the collective gland secretion. We already understand that white blood cells (leukocytes) are signaled to congregate near the site of infection and migrate from blood vessels into mammary tissues and secretions, thus increasing the SCC.
These leukocytes, which are primarily neutrophils, are essentially the body’s “suicide squad” in that they attack the invading bacteria by locating, engulfing (“eating”) and destroying both the bacteria and neutrophil through release of toxic enzymes from their intracellular granules. These enzymes and other reactive substances are strong oxidizers that kill the invading bacteria and potentially the surrounding host tissue.
A balance is needed between the actions of the neutrophils and associated immune cells in activating the immune response and cellular messengers released as well as body antioxidants (vitamins A and E) to suppress the inflammatory response and subsequent tissue damage.
In addition to the inflammatory impacts on milk, mastitic milk is at risk for presence of bacteria or fungi that could impact derived milk-based products, especially products based on raw milk.
Milk from cows experiencing mastitis is also at greater risk for having antibiotic residues, which will be identified through routine comprehensive testing at the processing plant, and all this milk will be discarded from production, incurring a significant loss to the production facility and responsible producer.
Altered milk composition from mastitis
A component of this inflammatory response is also responsible for changing the permeability of the blood vessels in the surrounding affected area of the udder. Increased “leakage” of blood vessels allows for sodium, chloride, fluids and various blood proteins to enter the udder’s secretory cells, thus ending up in the harvested milk. Table 1 summarizes a number of significant compositional changes to milk when there is a high SCC.
The constituents highlighted in red are greatly increased in high-SCC milk. These increased constituents are products of the inflammatory process. The elevated sodium is why electrical conductivity can be used to detect mastitis. Increased immunoglobulins, serum albumin, lactoferrin and other whey proteins counterbalance the loss in casein content, thus typically total protein remains normal or may even increase slightly.
Lactoferrin is a specialized protein that binds iron and prevents gram-negative bacteria (coliform) growth. The immunoglobulins help fight off infection in the gland.
The milk constituents highlighted in grey typically decrease in high- SCC milk. Some of the oxidative enzymes can also remain in the milk and have adverse effects on the processing of milk products. The casein protein is the highly desirable protein in milk for making cheese, but this protein can be significantly degraded by proteolytic enzymes from inflammation, resulting in reduced cheese yield.
Other enzymes may degrade the fat in milk. Lactose may be consumed by the invading bacteria to support their growth as milk is potentially a good bacterial growth media. Although this chart suggests a dramatically decreased milk calcium content, this has not been consistent across all studies.
Implications on milk product quality
The effects of mastitis on product quality can vary according to the causative agent and the final product. The important sensory properties of milk such as the taste, smell or appearance can be affected by mastitis.
An example is a salty taste that may be observed as a result of the imbalance in the constituents of the milk, namely the increase in sodium and chloride (salt) content. Proteolytic enzymes can impart a bitter flavor to milk, whereas lipid- degrading enzymes release fatty acids that become oxidized, inducing a rancid off-flavor.
Cheese produced from high-SCC milk may have an altered texture or flavor, which poses a challenge for processors. Using higher-SCC milk in cheese production results in a 4 percent or greater loss in product yield compared with low-SCC milk, and curds have a higher moisture content.
Spore-forming bacteria potentially found in raw milk can become active during the cheese ripening process, producing gas and degrading specific products. Enzyme activity, especially plasmin that is extremely heat stable, in the finished product may continue to degrade the product, resulting in a reduced storage time or shelf life.
An increase in bulk milk SCC from 100 to 400,000 cells/mL results in more than a 3 percent reduction in revenue to the processing plants. These costs are then passed on to producers or consumers. As a consequence, many processors will pay a bonus for high-quality milk.
The goal for producers is to minimize the prevalence of subclinical and clinical mastitis in their cows in an effort to not only improve cow welfare, but provide a high-quality food product. However, producers also need to recognize that preventing mastitis is not a simple fix as many interactive management, milking, environmental and nutritional factors can contribute to mastitis.
To lower mastitis in a herd, effectively use monitoring tools to quickly and efficiently identify mastitis (see the previous article in the Aug. 7 issue); then identify underlying causes and make appropriate changes in management practices. 
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Robert Van Saun
- Professor/Extension Veterinarian
- Penn State University
- Email Robert Van Saun
