Introduction:
Mastitis, or inflammation of the mammary gland, is the most common and the most expensive disease of dairy animals, including dairy goats and sheep, throughout most of the world. Although stress and physical injuries may cause inflammation of the gland, infection by invading bacteria or other microorganisms (fungi, yeasts and possibly viruses) is the primary cause of mastitis.The impact of mastitis goes with the milk beyond the gate of the farm. Changes in milk composition (reduction in calcium, phosphorus, protein, and fat; and increases in sodium and chlorine) reduce its quality. In addition, the antibiotics used in treating mastitis are an important industrial and public health concern. The presence of antibiotic residue in the milk interferes with the manufacturing process of many dairy products (cheese and other fermented products). Undesirable flavors reduce the value of dairy products and the presence of low levels of antibiotics may cause health problems in consumers.
Clinical and Subclinical Mastitis: In clinical mastitis, the infected udder often becomes swollen and painful to touch. The milk is visibly altered by the presence of clots, flakes, serum, and sometimes blood. In severe cases (acute mastitis), the ewe/doe has a fever, rapid pulse, loss of appetite, and a sharp decline in milk production.
In contrast, subclinical mastitis is subtle and more difficult to detect. The animal appears healthy, the udder does not show any signs of inflammation, and the milk seems normal. However, microorganisms and white blood cells (somatic cells) that fight infections are found in elevated numbers in the milk.
The loss of milk and income due to clinical mastitis are readily apparent because milk production drops sharply and milk from animals treated with antibiotics must be discarded. However, a lot more milk is lost due to subclinical mastitis:
Control of subclinical mastitis is more important than simply treating clinical cases:
Development and Transmission of the Disease: Infections begin when microorganisms penetrate the teat canal and multiply in the mammary gland. The teat itself is the first line of defense against the penetration of bacteria into the udder. Normally, the sphincter muscle closes the teat canal tightly when the ewe or doe is not being milked.
Invasion of the teat most often occurs during or right after milking. Organisms present in the milk or at the teat end are propelled into the teat canal and cistern when there is admission of undesired air in the milking unit. This happens when the milking unit slips or squawks, or when the teatcup is removed without first shutting off the vacuum. After milking, the teat canal remains dilated for 1-2 hours and the canal of a damaged teat may permanently remain partially open. Organisms from the environment (feces, bedding, etc.) or those found on injured skin at the tip of the teat may easily invade an open or partially open canal.
Bacteria first damage the tissues lining the large milk-collecting ducts. While in these ducts, the bacteria may encounter leukocytes (white blood cells) that are naturally present in small numbers in the milk. These cells are the animal’s second line of defense because they can engulf and destroy bacteria. However, during this process, the leukocytes release substances that cause the movement of additional leukocytes from the blood into the milk. This increases the somatic cell count in the milk.
If the bacteria are not entirely destroyed, they continue to multiply and begin to invade smaller ducts and alveolar (small cavity or sac) areas. Milk-secreting cells damaged by toxins and other irritants release substances that lead to increased permeability of blood vessels. Additional leukocytes move to the site of infection. They enter the alveolar tissue in great numbers by squeezing between the damaged milk secreting cells. Fluids, minerals, and clotting factors also leak into the affected area. Clotted milk may close ducts and, in effect, isolate the infected regions.
Sometimes, the microorganisms are eliminated rapidly and the infection is cleared. In these cases, the clogged ducts are opened and milk composition and production return to normal within several days. However, if the infection persists and ducts remain clogged, the entrapped milk causes the secretory cells to revert to a resting (non-producing) state and the alveoli begin to shrink. Substances released by leukocytes lead to the complete destruction of alveolar structures and replacement of the alveoli with connective and scar tissues. The destruction of milk secretory tissue could be called the animal’s third line of defense to bring the infection under control.
If the infection is not treated, the number of somatic cells in the milk becomes elevated and a reduction (potentially permanent) in milk yield can result.
Causative Agents/Treatments: Mastitis is an infection of the udder caused by two major categories of bacteria:
Diagnosis:
There are many different types of tests (C.M.T., strip test, and culture and sensitivity on the milk) that can identify mastitis in an animal. Some tests can also identify the bacterial cause of the mastitis. See Section D for additional information on the above tests.Mastitis Prevention: