ANSC 438 Home / Beginning / Milk Composition / Mammary Structure
Mammary Development / Mother & Neonate / Lactation / Mastitis

Mastitis Case Studies

Susceptibiliy to Mastitis

This resource describes the factors that affect the susceptibility to mastitis and the effects of inflammation in the gland.

Factors Affecting Susceptibility to Mastitis

This section deals with the factors that are determinants of mastitis, the timing of infection and stage of lactation, and the relationships between nutrition and mastitis.

Determinants of Mastitis

Whether or not IMI occurs depends on the interaction of host, agent, and environmental factors.

HOST FACTORS include: the presence/absence of natural resistance to mastitis, the state of defense mechanisms (are the present and are they functional), the stage of lactation, and whether there are stress factors. Jersey cow in a tie stall.
AGENT FACTORS include: the number of organisms in the gland, the pathogenicity of the organisms (they must penetrate the gland, then adhere to the tissue, and then reproduce), the presence of other virulence factors, and the state of the host defenses for resistance to infection. Bacteria (E coli).
ENVIRONMENTAL FACTORS include: the design and function of milking machine, the milking environment, the milking hygiene practices, the type of housing and bedding, and the weather. Free stalls with sawdust.

Timing of Infection and Stage of Lactation

Most environmental IMI occur during the periods of active involution and colostrogenesis in the dry cow, and during early lactation in the milking cow, however, new IMI can occur at any time.

Active involution - At the beginning of the dry period the cow is no longer milked. The mammary gland undergoes a period of active involution. Several situations which occur within the first two weeks after a cow is dried off predispose the mammary gland to mastitis:

  • The gland continues to secrete milk with maximum accumulation occurring 2 to 3 days after milk removal is stopped. Pressure in the gland can cause the streak canal to widen and the teat sphincter to dilate, allowing bacteria into the gland.
  • Bacteria are no longer removed from the gland by the milking process.
  • Teat dipping ceases.
  • Phagocytes are involved in removal of secretory cell products (fat, casein), and are not particularly efficient at removing bacteria.
  • Increasing amounts of immunoglobulins and lactoferrin (decreasing citrate : LF) in the gland improve defense, but cannot override the problems noted above.
  • Dry treatment of all quarters with antibiotics reduces streptococcal and staphylococcal (but not coliform) IMI during active involution.
  • Reducing the period of active involution by infusing colchicine (disrupts milk secretion mechanisms) decreases IMI.

Colostrogenesis - Several defense mechanisms are compromised during colostrum formation which predispose the gland to mastitis.

  • Fluid volume in the gland increases resulting in increasing pressure and dilation of the streak canal and sometimes leakage of colostrum.
  • Citrate concentration rises and lactoferrin is low (see below for antimicrobial activity of lactoferrin).
  • Phagocytic cells are not efficient at engulfing and killing bacteria in colostrum contained int eh gland at this time.
  • High immunoglobulin concentrations in the gland at this time are not effective in preventing new IMI. IgG1 is not normally an effective opsonin in the mammary gland.
  • Antibiotic concentration from dry cow therapy is too low to combat infection.
  • Teat dipping during this period is not effective in mastitis prevention.

Early lactation - Cows in early lactation are metabolically stressed. This stress can result in clinical outbreaks of subclinical infections (eg. IMI acquired during the dry period or at calving time). In addition, mastitis is sometimes associated with high concentrate feeding which accompanies early lactation.

Inflammation of the Mammary Gland

This section deals with what happens during inflammation in the mammary glandand the factors affecting the ability of the mammary gland to resist infection

What happens during inflammation in the mammary gland?

  1. Bacteria enter the gland and can multiply sufficiently to trigger the inflammatory response.
  2. Vasodilation occurs resulting in increased blood flow to the gland.
  3. There is increased vascular permeability. Inflammatory products such as prostaglandins, leukotrienes, proteases, and toxic oxygen metabolites increase capillary permeability in the gland.
  4. Swelling occurs due to filtration of fluid into the tissue.
  5. Phagocytes leave the blood vessels and enter the tissue (called diapedesis). Initially PMN (polymorphonuclear neutrophils) enter the tissue, after which macrophages predominate.
  6. Phagocytosis and destruction of the bacteria occurs.
  7. Tissue repair occurs after the bacteria have been destroyed. However, milk secreting tissue may be temporarily or permanently destroyed (resulting in scar tissue).

Factors That Affect the Ability of the Mammary Gland to Resist Infection

  1. The tissue is the terminal endpoint for the leukocytes (PMNs), and some leukocytes may be too old to be maximally effective, especially the first ones to enter during an inflammation.
  2. With a large recruitment of blood PMN into the gland, many of the PMN may be too immature (too young) to be maximally effective.
  3. Some PMN (perhaps from 1 and 2) will ingest bacteria but not kill them, thereby protecting the bacteria from further destruction and providing a source of chronic infection.
  4. Components in milk lipids and the whey fraction of milk may block immunoglobulin receptors (Fc receptors) on the leukocytes.
  5. Milk fat and casein, once ingested into the PMN, can cause the PMN to "round up," making it ineffective at ingesting bacteria.
  6. Blockage of Fc receptors may result in extra degranulation of the leukocyte's hydrolytic enzymes, increasing the severity of the inflammation in the tissue.
  7. Oxygen is needed for the oxygen-dependent microbicidal system which is part of phagocytosis, but oxygen tension in milk is low. Oxygen concentration in blood is 100 times that in milk.
  8. Phagocytes use a great deal of energy during phagocytosis and glucose is the primary source of that energy. But milk is low in glucose, the phagocytes are unable to utilize lactose, and the leukocytes found in milk contain about 38% less glycogen stores than those found in blood.
  9. Milk is relatively low in opsonins such as immunoglobulins and complement.
  10. Cow milk has essentially no lysozyme activity (lysozyme is an antimicrobial hydrolytic enzyme found in high concentrations in milk of other species).
  11. Many types of bacteria can cause mastitis and a cow may not have specific antibodies for a given strain.
  12. Some bacteria, such as S. aureus, resist intracellular killing once internalized within the leukocyte. This allows them to continue living in the gland, protected from the cow's defense mechanisms, and able to re-infect the gland.
  13. Cows in the periparturient period or cows with vitamin E or selenium deficiency have decreased ability of PMN to phagocytose or kill bacteria.

Mastitis Case Studies
Mastitis Resources