athogenesis
The organism must enter the mammary gland through the teat sphincter. (fig 102) (fig mam 004)
Coagulase-positive S. aureus can normally inhabit the skin of the teats and the population of the organism can be high if the quarter is also shedding the organism. In addition, the organism may be deposited on the teat end by contaminated wash cloths or sponges used in the normal premilking cleaning procedure. Contaminated inflations from previously milked infected quarters may easily transmit the organism. (fig mam 006)
Another factor that can potentiate the organism is damage to the epithelium of the teat end, caused by viral infection, chemical irritation from teat dips, or physical damage from excessive milking or high vacuum which will allow the organism to colonize on the teat end.
Following entry into the mammary gland of the organism, the subsequent course is determined by the ability of the neutrophils to control the growth and multiplication of the bacteria. When growth and multiplication is not prevented, the gangrenous form of staphylococcal mastitis will frequently occur. The cow can die of toxemia or the quarter may slough with this form.
If neutrophils are able to adequately control S. aureus multiplication, mild clinical signs, which are usually confined to the mammary gland, will be observed.
Repeated cycles of clinical and subclinical infection throughout the lactation period is typical of S. aureus mastitis.
The initial pathological finding is degeneration and denuding of duct epithelium with stromal swelling which decreases the size of the lumen. The alveolar secretory cells nearest the ducts decrease in numbers. Microabscesses will form in the secretory areas and the majority of viable staphylococcal organisms are found within somatic cells. These are some of the factors that make this infection difficult to treat.