Healthy cows with good immune systems will be able to fight off mastitis infections. Many mastitis pathogens are eliminated by the cow's own defense system. Assure that the diets are balanced for Vitamin E and Selenium. Immunization with J5 vaccine will not prevent infection but will decrease the severity of clinical signs.
Diets - During lactation cows should receive 400-600 IU Vit E and .3 ppm of Selenium per day. During the dry period, cows should get 1000 IU Vit E and .3 ppm Selenium per day.
J5 vaccine schedule - Immunization with E. coli mutant (J5) is reported effective. Protection extends to other coliform species. The protocol we use is 3 injections, 1st at dry off, 2nd 3 weeks later, and the 3rd injection 2-4 weeks after calving. Avoid giving immunization to cows at calving and up to two weeks after calving.
Much current research is focused on improving the cow's immune system.
Anatomy of the Mammary Gland
Cross section of the udder infused with dye. The front quarter is smaller than the rear quarters and is separated by a membrane through which bacteria and drugs do not diffuse. Each quarter is separate.
The entrance of the udder is known as the streak canal or teat canal. it is surrounded by a band of muscle tissue that keeps the canal closed. The cavity within the teat is known as the teat sinus. It is separated from the udder cistern by a ring of tissue known as the annular ring. Canals connect to the udder cistern like the branches of a tree and terminate in tiny circular areas known as alveoli which secrete milk.
A cubic inch of udder tissue contains millions of alveoli. Each alveolus is richly fed by blood vessels and surrounded by muscle fibers known as myoepithelial cells. Oxytocin acts on these cells to cause milk let down.
Bacteria overcome or penetrate the teat canal. This occurs by multiplication, propulsion during milking and perhaps other factors. These bacteria are not considered motile.
The most important factor to keep in mind to control mastitis is to keep bacteria away from the teat end.
How Does Mastitis Result?
Mastitis results when bacteria pass through the teat canal, overcome the defenses in milk and multiply. Organisms pass through the teat canal in several ways:
1. Between milkings, organisms pass through the teat canal by multiplying inside the canal.
2. During machine milking, organisms may be propelled into through the teat canal into the teat cistern and udder.
Defenses of the Cow:
1. Smooth muscle sphincter surrounding the teat canal inhibits bacterial closure. Because the teat canal lumen remains dilated for up to 2 hours after milking, feed cows after milking to keep them on their feet.
2. Keratin, a waxy substance derived from the teat canal lining partially occludes the lumen of the teat canal and inhibits bacterial penetration. Only infuse the tip of intramammary infusion cannulas into the teat canal.
3. Somatic Cells are the most important natural defense mechanism to infection. Leukocytes (mostly PMN, polymorphonuclear neutrophils) function by phagocytosing and killing bacteria. They may reach in the millions.
4. Antibodies and other soluble factors in milk. They coat bacteria and enhance PMN engulfment. They also interfere with bacterial adhesion to tissues, reducing multiplication and neutralizing toxins.
Establishment of Infection:
1. The inherent virulence of the bacterial species is often associated with is ability to adhere to mammary epithelium and remain in the gland during lactation when the udder is periodically flushed. Strep ag and Staph aureus adhere well. E. coli does not adhere well but multiplies rapidly.
2. If bacteria are eliminated by leukocytes, the infection is cleared!
3. Bacteria initially affect tissues lining the large milking collecting ducts and cisterns. They enter small ducts and alveolar areas of the gland by multiplication and via milk currents.
4. Bacteria produce toxins and irritants that cause swelling and death of alveoli. This results in the release of substances that increase blood vessel permeability and attract PMN to the affected area.
The inflammatory response is due to the influx of PMN, serum components and fluid. The first change in milk during inflammation is increase in blood proteins followed by massive movement of PMN into the gland. These changes are accompanied by edema, redness and swelling of the udder and abnormal watery secretions containing clots and red blood cells.
PMN cross blood vessels and move through tissue toward damaged tissue site. PMN accumulate around alveoli and can release enzymes that cause the destruction of the alveoli. So the presence of bacteria, toxins and PMN may cause healthy alveoli to involute. Tissue debris, bacteria and PMN clog ducts. If the bacteria are eliminated, inflammation subsides, clogged ducts are opened and milk composition returns to normal in several days. If the infection persists and ducts remain clogged, milk accumulates in alveoli exerting pressure on the alveoli. These alveoli will involute or be destroyed depending on how severe the infection. Destroyed alveoli are permanently replaced by scar tissue (fibrosis).