4C - Mastitis

Question 1

general understanding

Answer 1

Inflammation of the mammary gland
30% of cultured cases have no growth
yeast and protozoa can also infect the udder
costliest disease of the US Dairy Industry
#1 cause for use of antimicrobials on dairies
has direct impact on the quality of milk sold off the farm
causes increased culling

Question 2

udder anatomy (importance to disease)

Answer 2

low oxygen present
large amount of carbohydrates in fluid (lactose)
different tyoes of tissue present, creating varied environments for bacterial growth and colonization (canal, ducts, aveolus)

Question 3

defenses of the udder

Answer 3

Physical - Derma, keratin sphincter (traps bacteria, antibacterial)
Cellular - Macrophage, Lymphocytes, Neutrophils
Humoral - IgM, IgG (1 &2), IgA
Non-Specific - Lactoferrin, Complement, Lysozyme, Defensins

Question 4

Cellular udder defenses

Answer 4

Macrophage - phagocytic antigen-presenting cell, initiates the host response, attracts other immune cells
Lymphocytes - T-cells (TH and T-suppressors), B-cells (antibody production)
Neutrophils - phagocytosis and microbicidal action, undergo margination and migration into the secretory tissues via chemokines released by other immune cells, or the presence of LPS released by G (-) bacteria, release oxidizing microbicidal agents, critical

Question 5

Humoral udder defenses

Answer 5

IgM - predominant opsonin
IgG1 - neutralizes toxins, not an opsonizer, highest % Ab in healthy udders
IgG2 - majority of opsonizing Ig in an infected udder, leaks into udder from systemic response to mastitis
IgA - produced locally in SIgA form, blocks pathogen adherence to udder tissues

Question 6

Non-Specific udder defenses

Answer 6

Lactoferrin - bacteriostatic via iron chelation
Complement - assistance with phagocytosis
Lysozyme - cell wall cleavage of G(+) and outer wall cleavage G(-) bacteria
Defensins - aggregation of pathogens, pore formation, and interference with cell wall synthesis

Question 7

types of mastitis

Answer 7

clinical and subclinical

Question 8

Major differences betwen clinical and subclinical mastitis

Answer 8

C - can be diagnosed by stripping the teat, possible systemic illness
SC - milk appears normal, must perform diagnotics to ID infected quarters (SCC)

Question 9

SCC

Answer 9

Somatic Cell Count Testing
count of the cells (WBCs, epithelial cells) per ml of milk, an indicator of infection when increased
generally performed in milk quality labs, although technology may allow this on farm soon
gives us an accurate cells/ml count, either from bulk tank sample, or from individual cows

Question 10

SCC averages/levels

Answer 10

non-infected cows = 100,000/ml
infected = 200,000/ml
US legal limit = 750,000/ml
European, Australian, Canadian = 400,000/ml

Question 11

contagious mastitis

Answer 11

spreads through milking equipment

Question 12

Enviornmental mastitis

Answer 12

from the environment, between milkings

Question 13

mastitis management and prevention

Answer 13

• must manage risk
• Interventions in human behavior in the parlor, environmental management, and the use of pharmaceuticals and biologics are important in managing mammary infections

Question 14

teat health/milking procedures

Answer 14

• milking machinery must be properly maintained
• minimize injection of anything into the teat (only use FDA approved treatments)
• culturing of high SCC cows is critical

Question 15

milking routine

Answer 15

1 - fore-strip teat, pre-dip, wipe off dip, attach machine

2 - automatic take off, post-dip, exit parlor

Question 16

how steps of the milking routine prevents mastitis

Answer 16

Pre-dip should be applied on entry to the parlor (this helps control environmental pathogens like Streptococcus species and E. coli)
Fore-stripping of the teats helps with milk let-down (oxytocin release) and is critical for identification of clinical mastitis
Post-dipping of teats helps prevent contagious pathogens, in addition to environmental bugs.

Question 17

Vaccinations for mastitis

Answer 17

Vaccines for prevention of disease in E. Coli cases have been very successful. Several products exist on the market.
E. coli vaccines for mastitis are rough-mutant bacterins –
Vaccination exists for S. aureus mastitis, however it is not efficacious in preventing infections OR disease

Question 18

toxic environmental mastitis

Answer 18

E. coli infections are typically waning or gone by the time the infection is noticed
Klebsiella infections are typically resistant to approved intramammary medications
Fluid therapy and anti-inflammatories are the most important treatments.
For cases of septicemia, antibiotics are warranted

Question 19

contagious mastitis

Answer 19

For pathogens like S. aureus and Mycoplasma bovis, treatment is usually futile
Segregation and eventual culling is the end result for these infections
For Streptococcus agalactiae, mass treatment with antibiotics can help eliminate outbreaks.

Question 20

dry cow therapy

Answer 20

Placement of antibiotics into the udder at the time of dry-off (cessation of milking prior to next calving)
Dry cow therapy has led to progress in reducing SCC over several decades
A great tool for reducing environmental mastitis picked up during the dry period
Blanket dry cow therapy is under increasing scrutiny
Use of non-antibiotic barriers is very beneficial!